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Trippy depression treatment? Hopes and hype for ketamine
703-844-0184 | Ketamine Treatment Center | Fairfax , VA 22306 | Loudon, Va
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Lauren Pestikas sits as she receives an infusion of the drug ketamine during a 45-minute session at an outpatient clinic in Chicago on July 25, 2018. Pestikas struggled with depression and anxiety and made several suicide attempts before starting ketamine treatments earlier in the year. (AP Photo/Teresa Crawford)

CHICAGO (AP) — It was launched decades ago as an anesthetic for animals and people, became a potent battlefield pain reliever in Vietnam and morphed into the trippy club drug Special K.

Now the chameleon drug ketamine is finding new life as an unapproved treatment for depression and suicidal behavior. Clinics have opened around the United States promising instant relief with their “unique” doses of ketamine in IVs, sprays or pills. And desperate patients are shelling out thousands of dollars for treatment often not covered by health insurance, with scant evidence on long-term benefits and risks.

Chicago preschool teacher Lauren Pestikas long struggled with depression and anxiety and made several suicide attempts before trying ketamine earlier this year.

The price tag so far is about $3,000, but “it’s worth every dime and penny,” said the 36-year-old.

Pestikas said she feels much better for a few weeks after each treatment, but the effects wear off and she scrambles to find a way to pay for another one.

For now, ketamine has not received approval from the U.S. Food and Drug Administration for treating depression, though doctors can use it for that purpose.

Some studies show ketamine can provide relief within hours for tough-to-treat depression and suicidal behavior and clinics promising unproven benefits have popped up nationwide. But more research is needed to know long-term benefits and risks. (Oct. 31)

Ketamine has been around since the 1960s and is widely used as an anesthesia drug during surgery because it doesn’t suppress breathing. Compared to opioids such as morphine, ketamine isn’t as addictive and doesn’t cause breathing problems. And some studies have shown that ketamine can ease symptoms within hours for the toughest cases.

Its potential effects on depression were discovered in animal experiments in the late 1980s and early 1990s showing that glutamate, a brain chemical messenger, might play a role in depression, and that drugs including ketamine that target the glutamate pathway might work as antidepressants.

Conventional antidepressants like Prozac target serotonin, a different chemical messenger, and typically take weeks to months to kick in — a lag that can cause severely depressed patients to sink deeper into despair.

703-844-0184 | Ketamine Treatment Center | Fairfax , VA 22306 | Loudon, Va
A vial of ketamine, which is normally stored in a locked cabinet, on display in Chicago on July 25, 2018. AP Photo/Teresa Crawford)

Ketamine’s potential for almost immediate if temporary relief is what makes it so exciting, said Dr. Jennifer Vande Voort, a Mayo Clinic psychiatrist who has used ketamine to treat depression patients since February.

“We don’t have a lot of things that provide that kind of effect. What I worry about is that it gets so hyped up,” she said.

The strongest studies suggest it’s most useful and generally safe in providing short-term help for patients who have not benefited from antidepressants. That amounts to about one-third of the roughly 300 million people with depression worldwide.

“It truly has revolutionized the field,” changing scientists’ views on how depression affects the brain and showing that rapid relief is possible, said Yale University psychiatrist Dr. Gerard Sanacora, who has done research for or consulted with companies seeking to develop ketamine-based drugs.

But to become standard depression treatment, he said, much more needs to be known.

Last year, Sanacora co-authored an American Psychiatric Association task force review of ketamine treatment for mood disorders that noted the benefits but said “major gaps” remain in knowledge about long-term effectiveness and safety. Most studies have been small, done in research settings and not in the real world.

When delivered through an IV, ketamine can cause a rapid increase in heart rate and blood pressure that could be dangerous for some patients. Ketamine also can cause hallucinations that some patients find scary.

“There are some very real concerns,” Sanacora said. “We do know this drug can be abused, so we have to be very careful about how this is developed.”

Dr. Rahul Khare, an emergency medicine specialist in Chicago, first learned about ketamine’s other potential benefits a decade ago from a depressed and anxious patient he was preparing to sedate to fix a repeat dislocated shoulder.

“He said, ‘Doc, give me what I got last time. For about three weeks after I got it I felt so much better,’” Khare recalled.

Khare became intrigued and earlier this year began offering ketamine for severe depression at an outpatient clinic he opened a few years ago. He also joined the American Society for Ketamine Physicians, formed a year ago representing about 140 U.S. doctors, nurses, psychologists and others using ketamine for depression or other nonapproved uses.

703-844-0184 | Ketamine Treatment Center | Fairfax , VA 22306 | Loudon, Va
Dr. Rahul Khare poses for a portrait at his outpatient Chicago clinic on July 25, 2018. (AP Photo/Teresa Crawford)

There are about 150 U.S. ketamine clinics, compared with about 20 three years ago, said society co-founder Dr. Megan Oxley.

Khare said the burgeoning field “is like a new frontier” where doctors gather at meetings and compare notes. He has treated about 50 patients with depression including Pestikas. They’re typically desperate for relief after failing to respond to other antidepressants. Some have lost jobs and relationships because of severe depression, and most find that ketamine allows them to function, Khare said.

Typical treatment at his clinic involves six 45-minute sessions over about two weeks, costing $550 each. Some insurers will pay about half of that, covering Khare’s office visit cost. Patients can receive “booster” treatments. They must sign a four-page consent form that says benefits may not be long-lasting, lists potential side effects, and in bold letters states that the treatment is not government-approved.

At a recent session, Pestikas’s seventh, she leaned back on a reclining white examining-room chair as a nurse hooked her up to a heart and blood pressure monitor. She grimaced as a needle was slipped into the top of her left palm. Khare reached up with a syringe to inject a small dose of ketamine into an IV bag hanging above the chair, then dimmed the lights, pulled the window curtains and asked if she had questions and was feeling OK.

“No questions, just grateful,” Pestikas replied, smiling.

Pestikas listened to music on her iPhone and watched psychedelic videos. She said it was like “a controlled acid trip” with pleasant hallucinations. The trip ends soon after the IV is removed, but Pestikas said she feels calm and relaxed the rest of the day, and that the mood boost can last weeks.

Studies suggest that a single IV dose of ketamine far smaller than used for sedation or partying can help many patients gain relief within about four hours and lasting nearly a week or so.

Exactly how ketamine works is unclear, but one idea is that by elevating glutamate levels, ketamine helps nerve cells re-establish connections that were disabled by depression, said ketamine expert Dr. Carlos Zarate, chief of experimental therapies at the National Institute of Mental Health.

A small Stanford University study published in August suggested that ketamine may help relieve depression by activating the brain’s opioid receptors.

Janssen Pharmaceuticals and Allergan are among drug companies developing ketamine-like drugs for depression. Janssen leads the effort with its nasal spray esketamine. The company filed a new drug application in September.

Meanwhile, dozens of studies are underway seeking to answer some of the unknowns about ketamine including whether repeat IV treatments work better for depression and if there’s a way to zero in on which patients are most likely to benefit.

Until there are answers, Zarate of the mental health institute said ketamine should be a last-resort treatment for depression after other methods have failed.

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Introduction

What comes to mind when you think of Ketamine? A drug of abuse? A horse tranquiliser? An anaesthetic agent? In reality it is all three. It usually has short-term hallucinogenic effects or causes a dissociative feeling (e.g. detachment from reality, sedation, or  inability to move). However, with frequent use over time it can cause permanent problems such as ‘ketamine bladder’, resulting in pain and difficulty passing urine.

What we already know

 

Ketamine’s effects are mainly mediated via NMDA (N-methyl-D-aspartate) receptor antagonism, although it is also an agonist at some opioid receptors and interacts with various other receptors, including noradrenaline, serotonin and muscarinic cholinergic receptors.

It is a class B illicit substance and was, in fact, upgraded from class C in June 2014 following a review of its harmful effects. Ketamine (either intramuscularly or intravenously) is licensed for use as an anaesthetic agent in children, young people and adults, but over the last few years interest has been growing in the role of Ketamine as an antidepressant agent. It is not currently licensed for this purpose.

side effects of accutane 40 mg Areas of uncertainty

A study published in 2013 suggested that a single injected dose of Ketamine was associated with a rapid-onset antidepressant effect in patients with treatment-resistant depression (Murrough et al). The biggest challenge in terms of research with ketamine is that it remains tricky to compare against a placebo, given the fairly obvious side effects of taking a hallucinogenic drug, but this study compared Ketamine with Midazolam and this is probably the best comparator so far.

The following year, an open label study was published, which found similar antidepressant effects but a whole host of adverse effects were identified (Diamond et al), including anxiety and panic symptoms, increased suicidal ideation, vomiting, headaches and the anticipated feelings of detachment, confusion and dissociative symptoms.

There was a paucity of good quality information until, in 2015, a systematic review and meta-analysis of 21 studies  showed that single ketamine infusions produced a significant anti-depressant effect for up to seven days. Beyond this time, there was no evidence to suggest a prolonged effect.

What’s in the pipeline

There is some evidence to suggest that Ketamine may also work for Post-Traumatic Stress Disorder and Obsessive Compulsive Disorder. Another proposed use for Ketamine (currently being researched at the University of Manchester) is as an adjunct for Electroconvulsive Therapy (ECT), potentially minimizing the cognitive impairments experienced post-ECT.

Ketamine remains one of the most promising new treatments for depression, both unipolar and bipolar, but it is not without its problems. Requiring specialist referral and a stay in hospital overnight for a single dose clearly has financial and logistical implications far beyond those of antidepressant tablets with a stronger evidence base behind them. We also need more information about safety and adverse effects, before it can be introduced to a wider market.

References

Coyle, C. M. and Laws, K. R. (2015), The use of ketamine as an antidepressant: a systematic review and meta-analysis. Hum. Psychopharmacol Clin Exp. [Abstract]

Diamond PR, Farmery AD, Atkinson S, Haldar J, Williams N, Cowen PJ, Geddes JR and McShane R. Ketamine infusions for treatment resistant depression: a series of 28 patients treated weekly or twice weekly in an ECT clinic (PDF). J Psychopharmacol, 0269881114527361, first published on April 3, 2014. [PDF]

Murrough, J.W.; Iosifescu, D.V.; Chang, L.C.; Al Jurdi, R.K.; Green, C.E.; Perez, A.M. et al. (2013). Antidepressant efficacy of ketamine in treatment-resistant major depression; a two-site randomized controlled trial. Am J Psychiatry, 170, 1134-1142. [Abstract]

The antidepressant effects of ketamine are confirmed by a new systematic review and meta-analysis

shutterstock_18453376In recent times, few drugs have caused more excitement among clinical researchers than ketamine. It’s well known for its role in anaesthesia and veterinary surgery (“horse tranquilizer”), as well as its illicit use, but progress has been ongoing for about 15 years to repurpose it as an antidepressant.

As a consequence, many new studies are published every month that evaluate to what extent ketamine lives up to its promise as a new antidepressant drug (Aan Het Rot, Zarate, Charney, & Mathew, 2012). To make sense of the flood of new information, naturally intrigued mental elves clearly need researchers to provide timely updates of the current state of knowledge. To this end, Coyle and Laws (2015) have recently published an extensive systematic review and the first meta-analysis that summarises the latest, methodologically sound research.

The key questions of interest to these researchers were:

  • Does ketamine have an immediate effect in reducing depressive symptoms?
  • Are the antidepressant effects of ketamine sustained over time?
  • Are repeat infusions more effective in reducing depressive symptoms?
  • Do primary diagnosis and experimental design moderate the impact of ketamine on depressive symptoms?
  • Do men and women experience differences in the antidepressant effect of ketamine?

This review looked at how well the effects of ketamine are maintained over

This review looked at how well the effects of ketamine are maintained over 4 hours, 24 hours, 7 days and 12-14 days.

Methods

The authors followed PRISMA guidelines and scanned all relevant medical databases for studies assessing the antidepressant potential of ketamine in patients with major depressive disorder (MDD) and bipolar disorder (BD). To evaluate possible methodological factors and design variables, the authors also specifically assessed whether studies were: repeat/single infusion, diagnosis, open-label/participant-blind infusion, pre-post/placebo-controlled design and patients’ sex.

Effect sizes were calculated either relative to placebo or relative to baseline, in case no control group was provided. To correct for bias in small studies, a Hedge’s g procedure with random effects was used. Statistical heterogeneity, publication bias and moderator variables were assessed to have an idea of other variables that might influence the reported antidepressant potential of ketamine. Statistical heterogeneity among studies was assessed using I² values, with values above 50% generally representing substantial heterogeneity.

Results

In total, 21 studies enrolling 437 patients receiving ketamine were identified that satisfied inclusion criteria:

  • 17 were single infusion studies and the majority reported data collected at 4h (11) and 24h (13) after ketamine treatment
  • 6 studies had follow-up for 7 days
  • 4 studies had follow-up for 12-14 days

In general, there are grounds to assume publication bias for single infusion studies at 4h and 24h.

Of the 21 included studies, 2 were judged to be at a high risk of bias, 13 medium risk and 6 low risk of bias.

  • In general, ketamine had a large statistical effect on depressive symptoms that was comparable across all time points
  • Effect sizes were significantly larger for repeat than single infusion at 4 h, 24 h and 7 days
  • For single infusion studies, effect sizes were large and significant at 4 h, 24 h and 7 days
  • The overall pooled effect sizes for single and repeated ketamine infusions found no difference at any time point, suggesting that the antidepressant effects of ketamine are maintained for at least 12-14 days

table3

Moderator analyses suggest that responsiveness to ketamine may vary according to diagnosis. Specifically, while ketamine produced moderate to large effects in both MDD and BD patients, the effect of a single infusion was significantly larger in MDD than BD after 24h. On the other hand, after 7 days, this pattern reversed and ketamine showed higher efficacy in BD patients. However, the small number of studies makes it tricky to draw any conclusions.

In addition, single-infusion pre-post comparisons did not differ in effect size estimation from placebo-controlled designs except for at 12-14 days, where only one study was available. In a similar vein, there were no effect size differences between single infusion studies with open-label and blinded infusions.

Of note, the meta-analysis found the percentage of males in the group was positively associated with ketamine’s antidepressant effects after 7 days, although this finding warrants replication with more data points.

There's huge room for improvement in the primary research, but this analysis shows ketamine in a promising light as an antidepressant.

There’s plenty of room for improvement in the primary research, but this meta-analysis shows ketamine in a promising light as an antidepressant.

Conclusions

The authors conclude:

Single ketamine infusions elicit a significant anti-depressant effect from 4h to 7days; the small number of studies at 12-14 days post infusion failed to reach significance. Results suggest a discrepancy in peak response time depending upon primary diagnosis – 24 h for MDD and 7 days for BD. The majority of published studies have used pre-post comparison; further placebo-controlled studies would help to clarify the effect of ketamine over time.

Limitations

This meta-analysis suffers from several limitations that are inherent in the available studies:

  • For one, there were only four studies that assessed the effect of repeated ketamine infusions, which is a shame given that maintenance of antidepressant effects is one of the key drawbacks of rapidly acting interventions
  • In addition, the authors note that their results suggest publication bias, which may be taken to indicate that several negative findings have not been published and thus could not be included in this meta-analysis
  • Also, more information about adverse effects would have been useful, especially to evaluate whether ketamine can be safely applied in a broader clinical context

Summary

This is the first meta-analysis to evaluate ketamine’s antidepressant effects. For single infusion specifically, ketamine exerts large antidepressant effects in MDD as well as BD patients that seem to last at least 7 days, while too few studies are available beyond this time point.

It’s noteworthy that the effect sizes did not differ between time points, which indicates that the effect of a single infusion remains relatively stable in the short-term. While repeated infusions were shown to provide higher effects than single infusions at least for the first week, more studies are needed to corroborate the supremacy of repeated treatment.

Before ketamine can become a clinically viable treatment option, however, this review makes it clear that more methodologically refined studies (especially RCTs with adequate placebo controls) need to be conducted. With this in mind, researchers should take these findings as an incitement to action!

High quality

High quality placebo controlled trials are needed to drive forward progress in this field.

Links

Primary paper

Coyle, C. M. and Laws, K. R. (2015), The use of ketamine as an antidepressant: a systematic review and meta-analysisHum. Psychopharmacol Clin Exp, doi: 10.1002/hup.2475. [PubMed abstract]

Other references

Aan Het Rot, M., Zarate, C. a, Charney, D. S., & Mathew, S. J. (2012). Ketamine for depression: where do we go from here? Biological Psychiatry72(7), 537–47. doi:10.1016/j.biopsych.2012.05.003

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CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

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The VA Recognizes Ketamine As An Emergency Treatment For PTSD And Depression Patients At High Suicide Risk

CLEARWATER, Fla., Sept. 27, 2018 /PRNewswire/ — Long used as an safe and effective sedative for surgery, Ketamine has found new life as a treatment for severe depression, PTSD and suicidal ideation. Praised by some mental health experts, the drug so far has achieved very good results in clinical trials. The military now recognizes its’ potential, and last fall Brooke Army Medical Center in San Antonio became part of study on its effects. BAMC will treat active-duty troops with Ketamine, while a VA hospital near Yale will treat veterans. Another study is currently underway at a Veterans Affairs medical center in Cleveland, Ohio. The VA is trying to stem the tide of rising suicide rates among veterans, which average 22 per day – that’s one suicide every 65 minutes.

A staff psychiatrist at the Louis Stokes Cleveland VA Medical Center in Ohio, Dr. Punit Vaidya stated “30% of individuals with major depression don’t respond to traditional medications, so people can become desperate for things that work, because they can have a huge impact on their quality of life, and their overall functioning. The effects of the ketamine infusion can often be seen within a day, if not hours,” Vaidya explained. “If you look at their depression ratings and suicidal ratings given right before treatment and even four hours later you can see a significant reduction and I think that’s really quite remarkable,” Vaidya said.

Dr. Ashraf Hanna, a board certified physician and director of pain management at the Florida Spine Institute in Clearwater, Florida discusses PTSD and Treatment-Resistant Depression: “There are many forms of depression that can be treated by a psychiatrist with various modalities, anti-depressants and psychotherapy. IV Ketamine therapy is only reserved for those patients that have Treatment-Resistant Depression that have failed conventional therapy. IV Ketamine infusion therapyhas offered a new hope to patients that had no hope.”

When asked what prompted his use of IV Ketamine for PTSD and Depression and if any universities were involved in its development, Dr. Hanna went on to say: “There have been multiple universities involved in the research such as Harvard, Yale and Stanford that have proven the success rate of IV Ketamine for treatment-resistant depression. Since I was already successfully using IV Ketamine for CRPS/RSD,FibromyalgiaNeuropathy, and Post-Treatment Lyme Disease Syndrome, with over 10,000 infusions to date, I wanted to expand the treatment for PTSD, Depression, bipolar and Obsessive Compulsive Disorders. Since I am not a psychiatrist, I do not treat depression, but I work with qualified psychiatrists, and if he or she feels the patient has failed other treatment modalities, I then administer IV Ketamine for treatment-resistant depression.”

Dr. Bal Nandra and Ketamine patient Jason LaHood on how Ketamine is redefining the way patients are treated for depression

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Links for Ketamine Articles

  1. NYMag.com – What It’s Like to Have Your Severe Depression Treated With a Hallucinogenic Drug
    http://nymag.com/scienceofus/2016/03/what-its-like-to-treat-severe-depression-with-a-hallucinogenic-drug.html
  2. Huffington Post – How Ketamine May Help Treat Severe Depression
    http://www.huffingtonpost.com.au/2017/04/05/how-ketamine-may-help-treat-severe-depression_a_22027886/
  3. Murrough, Iosifescu, Chang et al. Antidepressant Efficacy in Treatment-Resistant Major Depression: A Two-Site Randomized Controlled Trial  Am J Psychiatry. 2013 Oct 1, 170(10): 1134-1142
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3992936/
  4. Murrough, Perez, Pillemer, et al.. Rapid and Longer0Term Antidepressant Effects of Repeated Ketamine Infusions in Treatment-Resistant Major Depression Biol Psychiatry 2013 Aug 15; 74(4): 250-256
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725185/
  5. Murrough, Burdick, Levitch et al. Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial Neuropsychopharmacology 2015 Apr; 40(5): 1084-1090
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367458/
  6. Feder, Parides, et al. Efficacy of Intravenous Ketamine for Treatment of Chronic Posttraumatic Stress Disorder A Randomized Clinical Trial Jama Psychiatry 2014 June;71(6): 681-8
    http://jamanetwork.com/journals/jamapsychiatry/fullarticle/1860851
  7. Schwartz, Murrough, Iosifescu Ketamine for treatment-resistant depression: recent developments and clinical applications Evid Based Ment Health 2016 May; 19(2):35-8
    http://ebmh.bmj.com/content/ebmental/19/2/35.full.pdf
  8. Rodriguez, Kegeles, et al Randomized Controlled Crossover Trial of Ketamine in Obsessive-Compulsive Disorder: Proof-of-Concept Neuropsychopharmacology 2013 Nov; 38(12): 2475-2483
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799067/pdf/npp2013150a.pdf
  9. Singh, Fedgchin, Daly et al. A Double-Blind, Randomized, Pacebo-Controlled, Dose-Frequency Study of Intravenous Ketamine in Patients With Treatment-Resistant Depression American Journal of Psychiatry 2016 August; 173(8): 816-826
    http://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.2016.16010037
  10. Taylor,  Landeros-Weisenberger, Coughlin et al. Ketamine for Social Anxiety Disorder: A Randomized, Placebo-Controlled Crossover Trial  Neuropsychopharmacology 2017 August;
    https://www.ncbi.nlm.nih.gov/pubmed/28849779

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WHAT CAN I EXPECT AT AN INFUSION VISIT?

We will ask you to fast for 8 hours before your infusion. Once you have checked in, you will complete a questionnaire to assess your current status. The IV will be started in your hand or your arm using a small catheter. This may feel like a sting from a small bug bite. The Ketamine will be administered through your IV over a period of 40 minutes. We will take your vital signs before, during, and after the infusion. After resting for an additional 15-20 minutes after the infusion, you will be discharged home with your driver.

  1. What is Ketamine? 
    Ketamine is an anesthetic drug that has been available since the 1960’s. In high doses, it can cause a ‘dissociative anesthesia” which induces hypnosis like states as well as unconsciousness. Around 2000, scientists started looking at Ketamine IV infusions carefully when its clinical usefulness was expanded to include a role in the management of mood disorders as well as chronic pain.
  2. Why can I not drive the day of the infusion?
    Ketamine is a potent anesthetic. As with any anesthetic, we advise our patients to NOT operate any heavy machinery for the remainder of the day due to potential residual effects.
  3. What are the side effects?
    Less than 2% of people will experience side effects. Some of the common side effects are: drowsiness, nausea, dizziness, poor coordination, blurred vision, and feeling strange or unreal. Most of these symptoms dissipate after the first hour of receiving the infusion.
  4. Are there certain conditions that are contra-indications for Ketamine treatment?
    Yes. If you have a history of cardiovascular disease, uncontrolled hypertension, history of psychosis, history of failed Ketamine infusion treatment, history of substance abuse or dependence within the year (patients will undergo a screening process) you will not qualify for Ketamine infusion treatments.
  5. How will I know if I need a booster infusion and how frequently will I require them?
    The duration of antidepressant efficacy after the initial treatment is different for everyone. The studies show that the variance can be 15 days to indefinitely. This is quite a range and unfortunately, there are no predictors for the duration.
  6. Is there a guarantee that this will work for me?
    Unfortunately, we cannot give guarantees.  Studies have shown that 70% of people will obtain efficacy.  After the first 2 infusions, we will be able to ascertain whether the infusions will work for you. We will not advise you to continue your treatment after the first 2 infusions if we do not see a certain amount of improvement.
  7. Isn’t Ketamine addictive? 
    Ketamine has the potential to be addictive. Studies have shown that at these doses and frequency, Ketamine is not addictive.
  8. Do I have to continue my current treatments for depression? 
    Yes. We advise that you alert your current health care provider that you are undergoing these treatments and that you maintain your current regimen.  It can be dangerous to stop taking your medications without the care of a physician. Our patients have a brighter outlook and a positive drive after their treatment that has allowed them to have higher success rates with psychotherapy. We will be happy to work with your current health care provider to provide the optimal outcome.

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CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

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The IV Medical Center - IV Vitamin Drips for wellness and recovery


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Magnesium is essential for our health. It is a key cofactor for our energy regulation, and in plants it is the center of the chlorphyll molecule. Low magnesium in people is associated with depression. Among the treatments we provide at the IV Medical Center is Ketamine infusions. In the process of our treatments, we assess patients for toher medical conditions that may lead to refractory depression and low magnesium is one of them.

 

 

Ketamine, an anesthetic and street drug known as “Special K” has garnered a lot of attention for it’s ability, in some, to relieve the symptoms of very severe depression in a matter of minutes. A recent study has demonstrated how it might work, but before you go signing up for a clinical trial (and there are currently many going on in the US), it’s important to understand the downsides to the drug. One major problem is that the effects wear off, usually within 10 days, leaving you just as depressed as before. It can cause urinary incontinence, bladder problems, addiction, and, with chronic use, it can worsen mental health problems, causing more depression, anxiety, and panic attacks.

Ketamine seems to have a remarkable, short term ability to heal the synapses injured by chronic stress. However, anything that acts that quickly and successfully usually has a long-term cost. All powerfully addictive drugs work on our own natural receptors and neurons. Cocaine, for example, causes immediate racing euphoria by inhibiting the natural neurotransmitter dopamine from being recycled, leaving bunches of dopamine in the synaptic cleft. In the very short term, you feel great. In the long term, you tax the system by driving the neurotransmitter system far out of balance in an aggressive way.

Nicotine has a similar effect on the alpha-7 nicotinic receptor. It activates it in a pleasing way, but unfortunately desensitizes the receptor so much that only nicotine will keep it firing. A nutrient found in foods such as egg yolks called choline activates the same receptor, but without desensitizing it.  Long term, regular ingestion of choline keeps the receptor functional and happy, helping with certain brain tasks. Long term, regular use of nicotine activates the receptor but forces you to take more nicotine to keep the receptor working, leaving you foggy-headed and less sharp if you go without cigarettes.

So is there a less dramatic, “natural” version of ketamine, something we can safely ingest every day, but might be a little depleted in our modern diets? Nothing taken in physiologic amounts would reverse a depression in half an hour like ketamine, but could another chemical we find in food and mineral water help with resilience to stress, synaptic repair, and make us more resistant to depression and anxiety symptoms? Sure—that chemical is the mineral magnesium. Magnesium, like ketamine, acts as an antagonist to the NMDA receptor, which means it is a counter to glutamate, the major excitatory neurotransmitter in the brain. The exact mechanisms are complex, but both ketamine and magnesium seem to help glutamate do its job, activating the receptor, without damaging the receptor with too much activation, which, chronically, leads to excitotoxicity, synaptic degradation, inflammation, and even cell death.

One of the exciting things about ketamine is that it works in some people with severe treatment resistant depression who have failed the traditional therapies. Treatment-resistant individuals tend to have lower intracellular magnesium levels than normal (1). Ketamine and magnesium may also work synergistically, complementing each other. Ketamine leads to an increase of intracellular magnesium, and ketamine will reverse the normally seen magnesium decreases after brain trauma (2). There is some evidence also that more standard antidepressant medications, such as imipramine, work in part by reversing the magnesium-depleting effects of chronic stress, suggesting that adding magnesium supplementation to standard antidepressant regimens might help the medications work better (at least in rodents) (3).

It’s great to see an interesting compound like ketamine be taken seriously and thoroughly studied for its action in serious, resistant depression. Ultimately its usefulness may be limited to hospitalized patients who can be closely monitored for the side effects, and who also may benefit the most from the quick mechanism of action, while the longer term risks may be outweighed by the short term benefit in such a critical, serious situation. I would love to see a much safer compound, the mineral magnesium, be studied as an adjunct treatment.

In the mean time, magnesium supplementation is generally safe for most folks with normal kidney function. Many folks eating a normal Western Diethave a low intake of the mineral (4). Those with bowel obstructions, very slow heart rate, or dangerously low blood pressure should not take it. Magnesium can interfere with the absorption of certain medicines (digoxin, nitrofurantoin, bisphosphanates, and some anti malaria drugs). Here are some excellent food sources of magnesium (though remember that both nuts and grains have phytates, which bind minerals, so the magnesium you absorb may not be quite as much as the magnesium you ingest.) Magnesium is also available in many mineral waters.

 

Lets digress over Choline. Choline has impact on decreasing schizophrenia in the children of mother’s who supplement the right amount during pregnancy:

Recently in the American Journal of Psychiatrya new paper was published tying nutrient supplementation in pregnant women to positive changes in the brains of their offspring. One of the nutrients that may be less predominant in our modern diets than in traditional diets is the phospholipid known as choline. Phospholipids are exceedingly important for brain development and neuron signaling.

In the current study, 100 pregnant women were randomized to receiving a daily choline supplement (equivalent to the amount of choline found in 3 large eggs) or placebo. After the babies were born, the choline babies continued to get a supplement equal to 100mg of choline daily (the institutes of medicine recommend total daily choline in infants to be 125mg daily), and at measurements of “cerebral inhibition” were taken at about one month and three months of age. Cerebral inhibition is a term used to describe the ability of the brain to tune out a stimulus that happens over and over. For example, if you are trying to work, and someone is running a jackhammer on the street outside, if you have intact cerebral inhibition, your brain will respond less and less to the sound of the jackhammer as it continues. Presumably this change would allow you to focus on more important things, such as the work at hand.

Source: http://www.flickr.com/photos/anniemole/5268772776/sizes/m/

In some brain disorders, such as schizophrenia, cerebral inhibition is impaired. For someone with schizophrenia, the signal from the jackhammer would be just as strong the second and the third and the seventh and the eighth times. You can imagine how you might be affected if you couldn’t tune anything out, if your brain was constantly taking in more stimulation and unable to sort through what was necessarily important or not. It could be this lack of cerebral inhibition (which begins with brain development in utero and early infancy) is one of the central causes of developing schizophrenia later on. The brain, so overwhelmed with stimuli, stops making sense of it, leading to psychosis and eventually the degeneration of neurons.

Cerebral inhibition is typically measured by a test called the p50 evoked potential. Electrodes are placed on the scalp, and then the subject is exposed to a sensory stimulus, in this case, paired sounds. With intact cerebral inhibition, the second time the brain processes the sound, the wave amplitude of the auditory evoked potential 50 milliseconds after the sound will be much less than the first time. (Go to this image from the American Journal of Psychiatry to see what the waveforms look like in healthy controls and subjects with schizophrenia.

P50 evoked potential abnormalities can be seen in infants, and genes that are associated with a higher risk of schizophrenia are also associated with these abnormal evoked potential tests. Choline is known to cross the placenta and help with the brain development of certain receptors that normalize cerebral inhibition. In the study of pregnant women receiving choline supplements, 76% of the infants whose mothers got choline had normal p50 evoked potential tests at age one month. Only 43% of the infants of the mothers who received placebo had tests consistent with intact cerebral inhibition. In addition, a gene known as CHRNA7 correlated with diminished cerebral inhibition in the placebo group of infants, but not in the choline group. That means that it is possible (though there is way too little data to know) the choline supplementation could reduce the risk of schizophrenia in these infants. The ScienceDaily write up of the study can be found here.

Schizophrenia risk is higher in the offspring of malnourished mothers. There is also a known gene that reduces choline levels that is associated with a higher risk of schizophrenia. Choline is also sequestered in the mother’s liver during trauma, anxiety, or depression, depriving the fetus. Measures of developmental delay and other developmental problems are also associated with later risk of schizophrenia.

Nicotine activates but also profoundly desensitizes the same receptor that choline seems to protect and activate (the alpha-7 nicotinic receptor). 90% of people with schizophrenia smoke, and smoking normalizes p50 evoked potential tests is schizophrenia. Smoking in mothers has been associated with poorer infant cerebral inhibition and later childhood behavioral problems, whereas choline has only been shown to be beneficial for brain development. One difference between the two compounds (among many!) is that choline does not desensitize the alpha-7 nicotinic receptor at all, leaving it active so it can play its presumed role in helping with intact cerebral inhibition.

While choline supplementation is the interest of researchers, I’m more interested in having pregnant women eat their meat and egg yolks, the best sources of choline in the diet. Egg yolks are jam packed with great nutrients for the brain, not only choline, but also B vitamins and other fatty acids important for nerve growth. Bananas also have more choline than you would expect for a fruit. Choline levels in the diet have fallen recently with folks restricting their egg and organ meat consumption. These traditional foods have some important nutrients that we don’t want to skimp on in our diets.

 

Choline supplementation during pregnancy presents a new approach to schizophrenia prevention

Choline, an essential nutrient similar to the B vitamin and found in foods such as liver, muscle meats, fish, nuts and eggs, when given as a dietary supplement in the last two trimesters of pregnancy and in early infancy, is showing a lower rate of physiological schizophrenic risk factors in infants 33 days old. The study breaks new ground both in its potentially therapeutic findings and in its strategy to target markers of schizophrenia long before the illness itself actually appears. Choline is also being studied for potential benefits in liver disease, including chronic hepatitis and cirrhosis, depression, memory loss, Alzheimer’s disease and dementia, and certain types of seizures.

Robert Freedman, MD, professor and chairman of the Department of Psychiatry, University of Colorado School of Medicine and one of the study’s authors and Editor of The American Journal of Psychiatry, points out, “Genes associated with schizophrenia are common, so prevention has to be applied to the entire population, and it has to be safe. Basic research indicates that choline supplementation during pregnancy facilitates cognitive functioning in offspring. Our finding that it ameliorates some of the pathophysiology associated with risk for schizophrenia now requires longer-term follow-up to assess whether it decreases risk for the later development of illness as well.”

Normally, the brain responds fully to an initial clicking sound but inhibits its response to a second click that follows immediately. In schizophrenia patients, deficient inhibition is common and is related to poor sensory filtering and familial transmission of schizophrenia risk. Since schizophrenia does not usually appear until adolescence, this trait — measurable in infancy — was chosen to represent the illness.

Half the healthy pregnant women in this study took 3,600 milligrams of phosphatidylcholine each morning and 2,700 milligrams each evening; the other half took placebo. After delivery, their infants received 100 milligrams of phosphatidylcholine per day or placebo. Eighty-six percent of infants exposed to pre- and postnatal choline supplementation, compared to 43% of unexposed infants, inhibited the response to repeated sounds, as measured with EEG sensors placed on the baby’s head during sleep.

 


Journal Reference:

  1. Randal G. Ross et al. Perinatal Choline Effects on Neonatal Pathophysiology Related to Later Schizophrenia RiskAmerican Journal of Psychiatry, 2013; DOI: 10.1176/appi.ajp.2012.12070940
  2. Perinatal Choline Effects on Neonatal Pathophysiology Related to Later Schizophrenia Risk

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Ketamine, magnesium and major depression–from pharmacology to pathophysiology and back.

Ketamine, magnesium and major depression e From pharmacology to pathophysiology and back

Abstract

The glutamatergic mechanism of antidepressant treatments is now in the center of research to overcome the limitations of monoamine-based approaches. There are several unresolved issues. For the action of the model compound, ketamine, NMDA-receptor block, AMPA-receptor activation and BDNF release appear to be involved in a mechanism, which leads to synaptic sprouting and strengthened synaptic connections. The link to the pathophysiology of depression is not clear. An overlooked connection is the role of magnesium, which acts as physiological NMDA-receptor antagonist: 1. There is overlap between the actions of ketamine with that of high doses of magnesium in animal models, finally leading to synaptic sprouting. 2. Magnesium and ketamine lead to synaptic strengthening, as measured by an increase in slow wave sleep in humans. 3. Pathophysiological mechanisms, which have been identified as risk factors for depression, lead to a reduction of (intracellular) magnesium. These are neuroendocrine changes (increased cortisol and aldosterone) and diabetes mellitus as well as Mg(2+) deficiency. 4. Patients with therapy refractory depression appear to have lower CNS Mg(2+) levels in comparison to health controls. 5. Experimental Mg(2+) depletion leads to depression- and anxiety like behavior in animal models. 6. Ketamine, directly or indirectly via non-NMDA glutamate receptor activation, acts to increase brain Mg(2+) levels. Similar effects have been observed with other classes of antidepressants. 7. Depressed patients with low Mg(2+) levels tend to be therapy refractory. Accordingly, administration of Mg(2+) either alone or in combination with standard antidepressants acts synergistically on depression like behavior in animal models.

CONCLUSION:

On the basis of the potential pathophysiological role of Mg(2+)-regulation, it may be possible to predict the action of ketamine and of related compounds based on Mg(2+) levels. Furthermore, screening for compounds to increase neuronal Mg(2+) concentration could be a promising instrument to identify new classes of antidepressants. Overall, any discussion of the glutamatergic system in affective disorders should consider the role of Mg(2+)

 

So back to the magnesium and Ketamine issue: As above, Low magnesium seems to be present in individuals who are depressed and have sleeping disorders. The magnesium is not the type measured by standard blood tests as most magnesium is intracellular. Magnesium may play an important role by antagomizing the NMDA receptors as does Ketamine. Our deficient diets in Magnesium may be increasing our rates of depression!

Magnesium as the original Chill Pill

Source: http://www.flickr.com/photos/derekskey/3219004793/

Magnesium is a vital nutrient that is often deficient in modern diets. Our ancient ancestors would have had a ready supply from organ meats, seafood, mineral water, and even swimming in the ocean, but modern soils can be depleted of minerals and magnesium is removed from water during routine municipal treatment. The current RDA for adults is between 320 and 420mg daily, and the average US intake is around 250mg daily.

Does it matter if we are a little bit deficient? Well, magnesium plays an important role in biochemical reactions all over your body.  It is involved in a lot of cell transport activities, in addition to helping cells make energy aerobically or anaerobically. Your bones are a major reservoir for magnesium, and magnesium is the counter-ion for calcium and potassium in muscle cells, including the heart. If your magnesium is too low, you can experience muscle cramps, arrythmias, and even sudden death. Ion regulation is everything with respect to how muscles contract and nerves send signals. In the brain, potassium and sodium balance each other. In the heart and other muscles, magnesium pulls some of the load.

That doesn’t mean that magnesium is unimportant in the brain. Au contraire!In fact, there is an intriguing article entitled Rapid recovery from major depression using magnesium treatment, published in Medical Hypothesis in 2006. Medical Hypothesis seems like a great way to get rampant (but referenced) speculation into the PubMed database. Fortunately, I don’t need to publish in Medical Hypothesis, as I can engage in such speculation in my blog, readily accessible to Google. Anyway, this article was written by George and Karen Eby, who seem to run a nutrition research facility out of an office warehouse in Austin, Texas – and it has a lot of interesting information about our essential mineral magnesium.

Magnesium is an old home remedy for all that ails you, including “anxiety, apathy, depression, headaches, insecurity, irritability, restlessness, talkativeness, and sulkiness.” In 1968, Wacker and Parisi reported that magnesium deficiency could cause depression, behavioral disturbances, headaches, muscle cramps, seizures, ataxia, psychosis, and irritability – all reversible with magnesium repletion.

Stress is the bad guy here, in addition to our woeful magnesium deficient diets. As is the case with other minerals such as zinc, stress causes us to waste our magnesium like crazy – I’ll explain a bit more about why we do that in a minute.

Let’s look at Eby’s case studies from his paper:

A 59 y/o “hypomanic-depressive male”, with a long history of treatable mild depression, developed anxiety, suicidal thoughts, and insomnia after a year of extreme personal stress and bad diet (“fast food”). Lithium and a number of antidepressants did nothing for him. 300mg magnesium glycinate (and later taurinate) was given with every meal. His sleep was immediately restored, and his anxiety and depression were greatly reduced, though he sometimes needed to wake up in the middle of the night to take a magnesium pill to keep his “feeling of wellness.” A 500mg calcium pill would cause depression within one hour, extinguished by the ingestion of 400mg magnesium.

A 23 year-old woman with a previous traumatic brain injury became depressed after extreme stress with work, a diet of fast food, “constant noise,” and poor academic performance. After one week of magnesium treatment, she became free of depression, and her short term memory and IQ returned.

A 35 year-old woman with a history of post-partum depression was pregnant with her fourth child. She took 200mg magnesium glycinate with each meal. She did not develop any complications of pregnancy and did not have depression with her fourth child, who was “healthy, full weight, and quiet.”

A 40 year-old “irritable, anxious, extremely talkative, moderately depressed” smoking, alchohol-drinkingcocaine using male took 125mg magnesium taurinate at each meal and bedtime, and found his symptoms were gone within a week, and his cravings for tobacco, cocaine, and alcoholdisappeared. His “ravenous appetite was supressed, and … beneficial weight loss ensued.”

Eby has the same question about the history of depression that I do – why is depression increasing? His answer is magnesium deficiency. Prior to the development of widespread grain refining capability, whole grains were a decent source of magnesium (though phytic acid in grains will bind minerals such as magnesium, so the amount you eat in whole grains will generally be more than the amount you absorb). Average American intake in 1905 was 400mg daily, and only 1% of Americans had depression prior to the age of 75. In 1955, white bread (nearly devoid of magnesium) was the norm, and 6% of Americans had depression before the age of 24. In addition, eating too much calcium interferes with the absorption of magnesium, setting the stage for magnesium deficiency.

Beyond Eby’s interesting set of case studies are a number of other studies linking the effects of this mineral to mental health and the stress response system. When you start to untangle the effects of magnesium in the nervous system, you touch upon nearly every single biological mechanism for depression. The epidemiological studies (1) and some controlled trials (2)(3) seem to confirm that most of us are at least moderately deficient in magnesium. The animal models are promising (4). If you have healthy kidneys, magnesium supplementation is safe and generally well-tolerated (up to a point)(5), and many of the formulations are quite inexpensive. Yet there is a woeful lack of well-designed, decent-sized randomized controlled trials for using magnesium supplementation as a treatment or even adjunctive treatment for various psychiatric disorders.

Let’s look at the mechanisms first. Magnesium hangs out in the synapse between two neurons along with calcium and glutamate. If you recall, calcium and glutamate are excitatory, and in excess, toxic. They activate the NMDA receptor. Magnesium can sit on the NMDA receptor without activating it, like a guard at the gate. Therefore, if we are deficient in magnesium, there’s no guard. Calcium and glutamate can activate the receptor like there is no tomorrow. In the long term, this damages the neurons, eventually leading to cell death. In the brain, that is not an easy situation to reverse or remedy.

And then there is the stress-diathesis model of depression, which is the generally accepted theory that chronic stress leads to excess cortisol, which eventually damages the hippocampus of the brain, leading to impaired negative feedback and thus ongoing stress and depression and neurotoxicity badness. Murck tells us that magnesium seems to act on many levels in the hormonal axis and regulation of the stress response. Magnesium can suppress the ability of the hippocampus to stimulate the ultimate release of stress hormone, it can reduce the release of ACTH (the hormone that tells your adrenal glands to get in gear and pump out that cortisol and adrenaline), and it can reduce the responsiveness of the adrenal glands to ACTH. In addition, magnesium can act at the blood brain barrier to prevent the entrance of stress hormones into the brain. All these reasons are why I call magnesium “the original chill pill.”

If the above links aren’t enough to pique your interest, depression is associated with systemic inflammation and a cell-mediated immune response. Turns out, so is magnesium deficiency. In addition, animal models show that sufficient magnesium seems to protect the brain from depression and anxiety after traumatic brain injury (6), and that the antidepressants desipramine and St. John’s Wort (hypericum perforatum) seem to protect the mice from the toxic effects of magnesium deficiency and its relationship to anxious and depressed behaviors (4).

The overall levels of magnesium in the body are hard to measure. Most of our body’s magnesium is stored in the bones, the rest in the cells, and a very small amount is roaming free in the blood. One would speculate that various mechanisms would allow us to recover some needed magnesium from the intracellular space or the bones if we had plenty on hand, which most of us probably don’t. Serum levels may be nearly useless in telling us about our full-body magnesium availability, and studies of levels and depression, schizophrenia, PMS, and anxiety have been all over the place (7). There is some observational evidence that the Mg to Ca ratio may be a better clue. Secondly, the best sources of magnesium in the normal Western diet are whole grains (though again, phytates in grains will interfere with absorption), beans, leafy green veggies, and nuts. These happen to be some of the same sources as folate, and folate depletion is linked with depression, so it may be a confounding factor in the epidemiological studies.

Finally, magnesium is sequestered and wasted via the urine in times of stress. I’m speculating here, but in a hunter-gatherer immediate stress sort of situation, maybe we needed our neurons to fire on all cylinders and our stress hormones to rock and roll through the body in order for us to survive. Presumably we survived or didn’t, and then the stressor was removed, and our paleolithic diets had plenty of magnesium to replace that which went missing. However, it may not be overall magnesium deficiency causing depression and exaggerated stress response – it may just be all that chronic stress, and magnesium deficiency is a biomarker for chronic stress. But it doesn’t hurt to replete one’s magnesium to face the modern world, and at least the relationships should be studied thoroughly. Depression is hugely expensive and debilitating. If we could alleviate some of that burden with enough mineral water… we should know whether that is a reasonable proposition.

As I mentioned before, there are only a few controlled trials of magnesium supplementation and psychiatric disorders. A couple covered premenstrual dysphoria, cravings, and other symptoms (8)(9). Another small study showed some improvement with magnesium supplementation in chronic fatigue syndrome (10). Two open-label studies showed some benefit in mania (11)(12). There is another paper that postulates that magnesium deficiency could exacerbate the symptoms of schizophrenia. However, there is nothing definitive. Which is, of course, quite troubling. How many billions of dollars have we spent on drug research for depression, bipolar disorder, and schizophrenia, when here is a cheap and plausibly helpful natural remedy that hasn’t been properly studied?

So everyone get out there and take some magnesium already!  Whew.  Well, just a few more things to keep in mind before you jump in.

There are some safety considerations with respect to magnesium supplementation. If you have normal kidney function, you do not have myasthenia gravis, bowel obstruction, or bradycardia, you should be able to supplement without too many worries. In addition, magnesium interferes with the absorption of certain pharmaceuticals, including dixogin, nitrofurantoin, bisphosphanates, and some antimalaria drugs. Magnesium can reduce the efficacy of chloropromazine, oral anticoagnulants, and the quinolone and tetracycline classes of antibiotics.

Magnesium oxide is the cheapest readily available formulation, as well as magnesium citrate, which is more likely to cause diarrhea in excess. (In fact, magnesium is a great remedy for constipation). The oxide is not particularly bioavailable, but the studies I’ve referenced above suggest that you can top yourself off after about a month of daily supplementation. Those with short bowels (typically due to surgery that removes a large section of bowel) may want to supplement instead with magnesium oil. You can also put some Epsom salts in your bath. In addition to diarrhea, magnesium can cause sedation, and symptoms of magnesium toxicity (again, quite unlikely if your kidneys are in good shape) are low blood pressure, confusion, arrythmia, muscle weakness, and fatigue. Magnesium is taken up by the same transporter as calcium and zinc, so they can fight with each other for absorption. Jaminet and Jaminet recommend total daily levels (between food and supplements) of 400-800mg. Most people can safely supplement with 200-350mg daily without any problems (again, don’t proceed without a doctor’s supervision if you have known kidney disease or if you are elderly).

People looking for good (but not all paleo) food sources can go here (also a good link for more information on the other formulations of magnesium – there are many!), here, and here.

 

Following are some foods and the amount of magnesium in them:[23]

 

MAGNESIUM  

Magnesium Webpage as below

 

Summary

Magnesium plays important roles in the structure and the function of the human body. The adult human body contains about 25 grams of magnesium. Over 60% of all the magnesium in the body is found in the skeleton, about 27% is found in muscle, 6% to 7% is found in other cells, and less than 1% is found outside of cells (1).

Function

Magnesium is involved in more than 300 essential metabolic reactions, some of which are discussed below (2).

Energy production

The metabolism of carbohydrates and fats to produce energy requires numerous magnesium-dependent chemical reactions. Magnesium is required by the adenosine triphosphate (ATP)-synthesizing protein in mitochondria. ATP, the molecule that provides energy for almost all metabolic processes, exists primarily as a complex with magnesium (MgATP)(3).

Synthesis of essential molecules

Magnesium is required for a number of steps during synthesis of deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and proteins. Several enzymes participating in the synthesis of carbohydrates and lipids require magnesium for their activity. Glutathione, an important antioxidant, requires magnesium for its synthesis (3).

Structural roles

Magnesium plays a structural role in bone, cell membranes, and chromosomes (3).

Ion transport across cell membranes

Magnesium is required for the active transport of ions like potassium and calcium across cell membranes. Through its role in ion transport systems, magnesium affects the conduction of nerve impulses, muscle contraction, and normal heart rhythm (3).

Cell signaling

Cell signaling requires MgATP for the phosphorylation of proteins and the formation of the cell-signaling molecule, cyclic adenosine monophosphate (cAMP). cAMP is involved in many processes, including the secretion of parathyroid hormone (PTH) from the parathyroid glands (see the articles on Vitamin D and Calcium for additional discussions regarding the role of PTH) (3).

Cell migration

Calcium and magnesium levels in the fluid surrounding cells affect the migration of a number of different cell types. Such effects on cell migration may be important in wound healing (3).

Nutrient interactions

Zinc

High doses of zinc in supplemental form apparently interfere with the absorption of magnesium. One study reported that zinc supplements of 142 mg/day in healthy adult males significantly decreased magnesium absorption and disrupted magnesium balance (the difference between magnesium intake and magnesium loss) (4).

Fiber

Large increases in the intake of dietary fiber have been found to decrease magnesium utilization in experimental studies. However, the extent to which dietary fiber affects magnesium nutritional status in individuals with a varied diet outside the laboratory is not clear (2, 3).

Protein

Dietary protein may affect magnesium absorption. One study in adolescent boys found that magnesium absorption was lower when protein intake was less than 30 grams/day, and higher protein intakes (93 grams/day vs. 43 grams/day) were associated with improved magnesium absorption in adolescents (5).

Vitamin D and calcium

The active form of vitamin D (calcitriol) may slightly increase intestinal absorption of magnesium (6). However, it is not clear whether magnesium absorption is calcitriol-dependent as is the absorption of calcium and phosphate. High calcium intake has not been found to affect magnesium balance in most studies. Inadequate blood magnesium levels are known to result in low blood calcium levels, resistance to parathyroid hormone (PTH) action, and resistance to some of the effects of vitamin D (2, 3).

Deficiency

Magnesium deficiency in healthy individuals who are consuming a balanced diet is quite rare because magnesium is abundant in both plant and animal foods and because the kidneys are able to limit urinary excretion of magnesium when intake is low. The following conditions increase the risk of magnesium deficiency (1):

  • Gastrointestinal disorders: Prolonged diarrhea, Crohn’s diseasemalabsorption syndromesceliac disease, surgical removal of a portion of the intestine, and intestinal inflammation due to radiation may all lead to magnesium depletion.
  • Renal disorders (magnesium wasting): Diabetes mellitus and long-term use of certain diuretics (see Drug interactions) may result in increased urinary loss of magnesium. Multiple other medications can also result in renal magnesium wasting (3).
  • Chronic alcoholism: Poor dietary intake, gastrointestinal problems, and increased urinary loss of magnesium may all contribute to magnesium depletion, which is frequently encountered in alcoholics.
  • Age: Several studies have found that elderly people have relatively low dietary intakes of magnesium (7, 8). Intestinal magnesium absorption tends to decrease with age and urinary magnesium excretion tends to increase with age; thus, suboptimal dietary magnesium intake may increase the risk of magnesium depletion in the elderly (2).

Although severe magnesium deficiency is uncommon, it has been induced experimentally. When magnesium deficiency was induced in humans, the earliest sign was decreased serum magnesium levels (hypomagnesemia). Over time, serum calcium levels also began to decrease (hypocalcemia) despite adequate dietary calcium. Hypocalcemia persisted despite increased secretion of parathyroid hormone (PTH), which regulates calcium homeostasis. Usually, increased PTH secretion quickly results in the mobilization of calcium from bone and normalization of blood calcium levels. As the magnesium depletion progressed, PTH secretion diminished to low levels. Along with hypomagnesemia, signs of severe magnesium deficiency included hypocalcemia, low serum potassium levels (hypokalemia), retention of sodium, low circulating levels of PTH, neurological and muscular symptoms (tremor, muscle spasms, tetany), loss of appetite, nausea, vomiting, and personality changes (3).

The Recommended Dietary Allowance (RDA)

In 1997, the Food and Nutrition Board of the Institute of Medicine increased the recommended dietary allowance (RDA) for magnesium, based on the results of recent, tightly controlled balance studies that utilized more accurate methods of measuring magnesium (2Table 1). Balance studies are useful for determining the amount of a nutrient that will prevent deficiency; however, such studies provide little information regarding the amount of a nutrient required for chronic disease prevention or optimum health.

Table 1. Recommended Dietary Allowance (RDA) for Magnesium
Life Stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months 30 (AI) 30 (AI)
Infants 7-12 months 75 (AI) 75 (AI)
Children 1-3 years 80 80
Children 4-8 years 130 130
Children 9-13 years 240 240
Adolescents 14-18 years 410 360
Adults 19-30 years 400 310
Adults 31 years and older 420 320
Pregnancy 18 years and younger 400
Pregnancy 19-30 years 350
Pregnancy 31 years and older 360
Breast-feeding 18 years and younger 360
Breast-feeding 19-30 years 310
Breast-feeding 31 years and older 320

Disease Prevention

Metabolic syndrome

Low magnesium intakes have been associated with the diagnosis of metabolic syndrome. The concomitant presentation of several metabolic disorders in an individual, including dyslipidemia, hypertensioninsulin resistance, and obesity, increases the risk for type 2 diabetes mellitus and cardiovascular disease. Systemic inflammation, which contributes to the development of metabolic disorders, has been inversely correlated with magnesium intakes in a cross-sectional study of 11,686 middle-aged women; the lowest prevalence of metabolic syndrome was found in the group of women with the highest quintile of magnesium intakes (median intake, 422 mg/day) (9).

Hypertension (high blood pressure)

Large epidemiological study studies suggest a relationship between magnesium and blood pressure. However, the fact that foods high in magnesium (fruit, vegetables, whole grains) are frequently high in potassium and dietary fiber has made it difficult to evaluate the independent effects of magnesium on blood pressure. A prospective cohort study of more than 30,000 male health professionals found an inverse association between dietary fiber, potassium, and magnesium and the development of hypertension over a four-year period (10). In a similar study of more than 40,000 female registered nurses, dietary fiber and dietary magnesium were each inversely associated with systolic and diastolic blood pressures in those who did not develop hypertension over the four-year study period, but neither dietary fiber nor magnesium was related to the risk of developing hypertension (11). The Atherosclerosis Risk in Communities (ARIC) study examined dietary magnesium intake, magnesium blood levels, and risk of developing hypertension in 7,731 men and women over a six-year period (12). The risk of developing hypertension in both men and women decreased as serummagnesium levels increased, but the trend was statistically significant only in women.

However, circulating magnesium represents only 1% of total body stores and is tightly regulated; thus, serum magnesium levels might not best reflect magnesium status. A recent prospective study that followed 5,511 men and women for a median period of 7.6 years found that the highest levels of urinary magnesium excretion corresponded to a 25% reduction in risk of hypertension, but plasma magnesium levels were not correlated with risk of hypertension (13). In cohort of 28,349 women followed for 9.3 years, the risk of hypertension was 7% lower for those with the highest magnesium intakes (434 mg/day vs. 256 mg/day) (14). The relationship between magnesium intake and risk of hypertension suggests that magnesium supplementation might play a role in preventing hypertension; however, randomized controlled trials are needed to assess whether supplemental magnesium might help prevent hypertension in high-risk individuals.

Diabetes mellitus

Public health concerns regarding the epidemics of obesity and type 2 diabetes mellitus and the prominent role of magnesium in glucose metabolism have led scientists to investigate the relationship between magnesium intake and type 2 diabetes mellitus. A prospective study that followed more than 25,000 individuals, 35 to 65 years of age, for seven years found no difference in incidence of diabetes mellitus when comparing the highest (377 mg/day) quintile of magnesium intake to the lowest (268 mg/day) (15). However, inclusion of this study in a meta-analysis of eight cohort studies showed that risk of type 2 diabetes was inversely correlated with magnesium intake (15). A second meta-analysis found that an increase of 100 mg/day in magnesium intake was associated with a 15% decrease in the risk of developing type 2 diabetes (16). The most recent meta-analysis of 13 observational studies, published in the last 15 years and including almost 540,000 individuals and 24,500 new cases of diabetes, found higher magnesium intakes were associated with a lower risk of diabetes (17).

Insulin resistance, which is characterized by alterations in both insulin secretion by the pancreas and insulin action on target tissues, has been linked to magnesium deficiency. An inverse association between magnesium intakes and fasting insulin levels was evidenced in a meta-analysis of 11 cohort studies that followed more than 36,000 participants without diabetes (18). It is thought that pancreatic β-cells, which regulate insulin secretion and glucose tolerance, could become less responsive to changes in insulin sensitivity in magnesium-deficient subjects (19). A randomizeddouble-blindplacebo-controlled trial, which enrolled 97 individuals (without diabetes and with normal blood pressure) with significant hypomagnesemia (serum magnesium level ≤0.70 mmoles/L), showed that daily consumption of 638 mg of magnesium (from a solution of magnesium chloride) for three months improved the function of pancreatic β-cells, resulting in lower fasting glucose and insulin levels (20). Increased insulin sensitivity also accompanied the correction of magnesium deficiency in patients diagnosed with insulin resistance but not diabetes (21). Another study found that supplementation with 365 mg/day of magnesium (from magnesium aspartate hydrochloride) for six months reduced insulin resistance in 47 overweight individuals even though they displayed normal values of serum and intracellular magnesium (22). This suggests that magnesium might have additive effects on glucose tolerance and insulin sensitivity that go beyond the normalization of physiologic serum concentrations in deficient individuals.

Cardiovascular disease

A number of studies have found decreased mortality from cardiovascular disease in populations who routinely consume “hard” water. Hard (alkaline) water is generally high in magnesium but may also contain more calcium and fluoride than “soft” water, making the cardioprotective effects of hard water difficult to attribute to magnesium alone (23). One large prospective study (almost 14,000 men and women) found a significant trend for increasing serum magnesium levels to be associated with decreased risk of coronary heart disease (CHD) in women but not in men (24). However, the risk of CHD in the lowest quartile of dietary magnesium intake was not significantly higher than the risk in the highest quartile in men or women. This prospective study was included in a meta-analysis of 14 studies that found a 22% lower risk of CHD (but not fatal CHD) per 200 mg/day incremental intake in dietary magnesium (25). In another prospective study, which followed nearly 90,000 female nurses for 28 years, women in the highest quintile of magnesium intake had a 39% lower risk of fatal myocardial infarction (but not nonfatal myocardial infarction) compared to those in the lowest quintile (>342 mg/day versus <246 mg/day) (26). Higher magnesium intakes were associated with an 8%-11% reduction in stroke risk in two meta-analyses of prospective studies, each including over 240,000 participants (27, 28). Additionally, a meta-analysis of 13 prospective studies in over 475,000 participants reported that the risk of total cardiovascular events, including stroke, nonfatal myocardial infarction, and CHD, was 15% lower in individuals with higher intakes of magnesium (29). Finally, a meta-analysis of six prospective studies found no association between magnesium intake and cardiovascular mortality risk (30). However, a recent prospective study that followed 3,910 subjects for 10 years found significant correlations between hypomagnesemia and all-cause mortality, including cardiovascular-related mortality (31). Presently, well-controlled intervention trials are required to assess the benefit of magnesium supplementation in the prevention of cardiovascular disease.

Stroke

Occurrence of hypomagnesemia has been reported in patients who suffered from a subarachnoid hemorrhage caused by the rupture of a cerebral aneurysm (32). Poor neurologic outcomes following an aneurysmal subarachnoid hemorrhage (aSAH) have been linked to inappropriate calcium-dependent contraction of arteries (known as cerebral arterial vasospasm), leading to delayed cerebral ischemia (33). Magnesium sulfate is a calcium antagonist and potent vasodilator that has been considered in the prevention of vasospasm after aSAH. Several randomized controlled trials have assessed the effect of intravenous (IV) magnesium sulfate infusions. A meta-analysis of nine randomized controlled trials found that magnesium therapy after aSAH significantly reduced vasospasm but failed to prevent neurologic deterioration or decrease the risk of death (34). The most recent meta-analysis of 13 trials in 2,413 aSAH patients concluded that the infusion of magnesium sulfate had no benefits in terms of neurologic outcome and mortality, despite a reduction in the incidence of delayed cerebral ischemia (35). At present, the data advise against the use of intravenous magnesium in clinical practice for aSAH patients after normalization of their magnesium status.

Complications of heart surgery

Atrial arrhythmia is a condition defined as the occurrence of persistent heart rate abnormalities that often complicate the recovery of patients after cardiac surgery. The use of magnesium in the prophylaxis of postoperative atrial arrhythmia after coronary artery bypass grafting has been evaluated as a sole or adjunctive agent to classical antiarrhythmic molecules (namely, β-blockers and amiodarone) in several prospective, randomized controlled trials. A meta-analysis of 21 intervention studies showed that intravenous magnesium infusions could significantly reduce postoperative atrial arrhythmia in treated compared to untreated patients (36). However, a meta-analysis of five randomized controlled trials concerned with rhythm-control prophylaxis showed that intravenous magnesium added to β-blocker treatment did not decrease the risk of atrial arrhythmia compared to β-blocker alone and was associated with more adverse effects (bradycardia and hypotension) (37). Presently, the findings support the use of β-blockers and amiodarone, but not magnesium, in patients with contraindications to first-line antiarrhythmics.

Osteoporosis

Although decreased bone mineral density (BMD) is the primary feature of osteoporosis, other osteoporotic changes in the collagenous matrix and mineral components of bone may result in bones that are brittle and more susceptible to fracture. Magnesium comprises about 1% of bone mineral and is known to influence both bone matrix and bone mineral metabolism. As the magnesium content of bone mineral decreases, apatite crystals of bone become larger and more brittle. Some studies have found lower magnesium content and larger apatite crystals in bones of women with osteoporosis compared to women without the disease (38). Inadequate serum magnesium levels are known to result in low serum calcium levels, resistance to parathyroid hormone (PTH) action, and resistance to some of the effects of vitamin D (calcitriol), all of which can lead to increased bone loss (see the articles on Vitamin D and Calcium). A study of over 900 elderly men and women found that higher dietary magnesium intakes were associated with increased BMD at the hip in both men and women. However, because magnesium and potassium are present in many of the same foods, the effect of dietary magnesium could not be isolated (39). A cross-sectional study in over 2,000 elderly individuals reported that magnesium intake was positively associated with total-body BMD in white men and women but not in black men and women (40). More recently, a large cohort study conducted in almost two-thirds of the Norwegian population found the level of magnesium in drinking water was inversely correlated with risk of hip fracture (41).

Few studies have addressed the effect of magnesium supplementation on BMD or osteoporosis in humans. In a small group of postmenopausal women with osteoporosis, magnesium supplementation of 750 mg/day for the first six months followed by 250 mg/day for 18 more months resulted in increased BMD at the wrist after one year, with no further increase after two years of supplementation (42). A study in postmenopausal women who were taking estrogen replacement therapy and also a multivitamin found that supplementation with an additional 500 mg/day of magnesium and 600 mg/day of calcium resulted in increased BMD at the heel compared to postmenopausal women receiving only estrogen replacement therapy (43). Evidence is not yet sufficient to suggest that supplemental magnesium could be recommended in the prevention of osteoporosis unless normalization of serum magnesium levels is required. Moreover, it appears that high magnesium levels could be harmful to skeletal health by interfering with the action of the calciotropic hormones, PTH and calcitriol (44). Presently, the potential for increased magnesium intake to influence calcium and bone metabolism warrants more research with particular attention to its role in the prevention and treatment of osteoporosis.

Disease Treatment

The use of pharmacologic doses of magnesium to treat specific diseases is discussed below. Although many of the cited studies utilized supplemental magnesium at doses considerably higher than the tolerable upper intake level (UL), which is 350 mg/day set by the Food and Nutrition Board (see Safety), it is important to note that these studies were all conducted under medical supervision. Because of the potential risks of high doses of supplemental magnesium, especially in the presence of impaired kidney function, any disease treatment trial using magnesium doses higher than the UL should be conducted under medical supervision.

Pregnancy complications

Preeclampsia and eclampsia

Preeclampsia and eclampsia are pregnancy-specific conditions that may occur anytime after 20 weeks of pregnancy through six weeks following birth. Approximately 7% of pregnant women in the US develop preeclampsia-eclampsia. Preeclampsia (sometimes called toxemia of pregnancy) is defined as the presence of elevated blood pressure (hypertension), protein in the urine, and severe swelling (edema) during pregnancy. Eclampsia occurs with the addition of seizures to the triad of symptoms and is a significant cause of perinatal and maternal death (45). Although cases of preeclampsia are at high risk of developing eclampsia, one-quarter of eclamptic women do not initially exhibit preeclamptic symptoms (46). For many years, high-dose intravenous magnesium sulfate has been the treatment of choice for preventing eclamptic seizures that may occur in association with preeclampsia-eclampsia late in pregnancy or during labor (47, 48). A systematic review of seven randomized trials compared the administration of magnesium sulfate with diazepam (a known anticonvulsant) treatment on perinatal outcomes in 1,396 women with eclampsia. Risks of recurrent seizures and maternal death were significantly reduced by the magnesium regimen compared to diazepam. Moreover, the use of magnesium for the care of eclamptic women resulted in newborns with higher Apgar scores; there was no significant difference in the risk of preterm birth and perinatal mortality (46). Additional research has confirmed that infusion of magnesium sulfate should always be considered in the management of preeclampsia and eclampsia to prevent initial and recurrent seizures (49).

Perinatal neuroprotection

While intravenous magnesium sulfate is included in the medical care of preeclampsia and eclampsia, the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine support its use in two additional situations: specific conditions of short-term prolongation of pregnancy and neuroprotection of the fetus in anticipated premature delivery (50). The relationship between magnesium sulfate and risk of cerebral damage in premature infants has been assessed in observational studies. A meta-analysis of six case-control and five prospective cohort studies showed that the use of magnesium significantly reduced the risk of cerebral palsy, as well as mortality (51). However, the high degree of heterogeneity among the cohort studies and the fact that corticosteroid exposure (which is known to decrease antenatal mortality) was higher in the cases of children exposed to magnesium compared to controls imply a cautious interpretation of the results. However, a meta-analysis of five randomized controlled trials, which included a total of 6,145 babies, found that magnesium therapy given to mothers delivering before term decreased the risk of cerebral palsy and gross motor dysfunction, without modifying the risk of other neurologic impairments or mortality in early childhood (52). Another meta-analysis conducted on five randomized controlled trials found that intravenous magnesium administration to newborns who suffered from perinatal asphyxia could be beneficial in terms of short-term neurologic outcomes, although there was no effect on mortality (53). Nevertheless, additional trials are needed to evaluate the long-term benefits of magnesium in pediatric care.

Cardiovascular disease

Hypertension (high blood pressure)

While results from intervention studies have not been entirely consistent (2), the latest review of the data highlighted a therapeutic benefit of magnesium supplements in treating hypertension. A recent meta-analysis examined 22 randomizedplacebo-controlled trials of magnesium supplementation conducted in 1,173 individuals with either a normal blood pressure (normotensive) or hypertension, both treated or untreated with medications. Oral supplementation with magnesium (mean dose of 410 mg/day; range of 120 to 973 mg/day) for a median period of 11.3 months significantly reduced systolic blood pressure by 2-3 mm Hg and diastolic blood pressure by 3-4 mm Hg (54); a greater effect was seen at higher doses (≥370 mg/day). The results of 19 of the 22 trials included in the meta-analysis were previously reviewed together with another 25 intervention studies (55). The systematic examination of these 44 trials suggested a blood pressure-lowering effect associated with supplemental magnesium in hypertensive but not in normotensive individuals. Magnesium doses required to achieve a decrease in blood pressure appeared to depend on whether subjects with high blood pressure were treated with antihypertensive medications, including diuretics. Intervention trials on treated subjects showed a reduction in hypertension with magnesium doses from 243 mg/day to 486 mg/day, whereas untreated patients required doses above 486 mg/day to achieve a significant decrease in blood pressure. While oral magnesium supplementation may be helpful in hypertensive individuals who are depleted of magnesium due to chronic diuretic use and/or inadequate dietary intake (56), several dietary factors play a role in hypertension. For example, adherence to the DASH diet — a diet rich in fruit, vegetables, and low-fat dairy and low in saturated and total fats — has been linked to significant reductions in systolic and diastolic blood pressures (57). See the article in the Spring/Summer 2009 Research Newsletter, Dietary and Lifestyle Strategies to Control Blood Pressure.

Myocardial infarction (heart attack)

Results of a meta-analysis of randomizedplacebo-controlled trials indicated that an intravenous (IV) magnesium infusion given early after suspected myocardial infarction(MI) could decrease the risk of death. The most influential study included in the meta-analysis was a randomized, placebo-controlled trial in 2,316 patients that found a significant reduction in mortality (7.8% all-cause mortality in the experimental group vs. 10.3% all-cause mortality in the placebo group) in the group of patients given intravenous magnesium sulfate within 24 hours of suspected myocardial infarction (58). Follow-up from one to five years after treatment revealed that the mortality from cardiovascular disease was 21% lower in the magnesium treated group (59). However, a larger placebo-controlled trial that included more than 58,000 patients found no significant reduction in five-week mortality in patients treated with intravenous magnesium sulfate within 24 hours of suspected myocardial infarction, resulting in controversy regarding the efficacy of the treatment (60). A US survey of the treatment of more than 173,000 patients with acute MI found that only 5% were given IV magnesium in the first 24 hours after MI, and that mortality was higher in patients treated with IV magnesium compared to those not treated with magnesium (61). The most recent systematic review of 26 clinical trials, including 73,363 patients, concluded that IV magnesium likely does not reduce mortality following MI and thus should not be utilized as a treatment (62). Thus, the use of IV magnesium sulfate in the therapy of acute MI remains controversial.

Endothelial dysfunction

Vascular endothelial cells line arterial walls where they are in contact with the blood that flows through the circulatory system. Normally functioning vascular endothelium promotes vasodilation when needed, for example, during exercise, and inhibits the formation of blood clots. Conversely, endothelial dysfunction results in widespread vasoconstriction and coagulation abnormalities. In cardiovascular disease, chronic inflammation is associated with the formation of atherosclerotic plaques in arteries. Atherosclerosis impairs normal endothelial function, increasing the risk of vasoconstriction and clot formation, which may lead to heart attack or stroke (reviewed in 63). Research studies have indicated that pharmacologic doses of oral magnesium may improve endothelial function in individuals with cardiovascular disease. A randomizeddouble-blindplacebo-controlled trial in 50 men and women with stable coronary artery disease found that six months of oral magnesium supplementation (730 mg/day) resulted in a 12% improvement in flow-mediated vasodilation compared to placebo (64). In other words, the normal dilation response of the brachial (arm) artery to increased blood flow was improved. Magnesium supplementation also resulted in increased exercise tolerance during an exercise stress test compared to placebo. In another study of 42 patients with coronary artery disease who were already taking low-dose aspirin (an inhibitor of platelet aggregation), three months of oral magnesium supplementation (800 to 1,200 mg/day) resulted in an average 35% reduction in platelet-dependent thrombosis, a measure of the propensity of blood to clot (65). Additionally, a study in 657 women participating in the Nurses’ Health Study reported that dietary magnesium intake was inversely associated with E-selectin, a marker of endothelial dysfunction (66)In vitro studies using human endothelial cells have provided mechanistic insights into the association of low magnesium concentrations, chronic inflammation, and endothelial dysfunction (67). Finally, since magnesium can function as a calcium antagonist, it has been suggested that it could be utilized to slow down or reverse the calcification of vessels observed in patients with chronic kidney disease. The atherosclerotic process is often accelerated in these subjects, and patients with chronic kidney disease have higher rates of cardiovascular-related mortality compared to the general population (68). Additional studies are needed to assess whether magnesium may be of benefit in improving endothelial function in individuals at high risk for cardiovascular disease.

Diabetes mellitus

Magnesium depletion is commonly associated with both insulin-dependent (type 1) and non-insulin dependent (type 2) diabetes mellitus. Reduced serum levels of magnesium (hypomagnesemia) have been reported in 13.5% to 47.7% of individuals with type 2 diabetes (69). One cause of the depletion may be increased urinary loss of magnesium, which results from increased urinary excretion of glucose that accompanies poorly controlled diabetes. Magnesium depletion has been shown to increase insulin resistance in a few studies and may adversely affect blood glucose control in diabetes (70). One study reported that dietary magnesium supplements (390 mg/day of elemental magnesium for four weeks) improved glucose tolerance in elderly individuals (71). Another small study in nine patients with type 2 diabetes reported that supplemental magnesium (300 mg/day for 30 days), in the form of a liquid, magnesium-containing salt solution, improved fasting insulin levels but did not affect fasting glucose levels (72). Yet, the most recent meta-analysis of nine randomizeddouble-blind, controlled trials concluded that oral supplemental magnesium may lower fasting plasma glucose levels in individuals with diabetes (73). One randomized, double-blind, placebo-controlled study in 63 individuals with type 2 diabetes and hypomagnesemia found that those taking an oral magnesium chloride solution (638 mg/day of elemental magnesium) for 16 weeks had improved measures of insulin sensitivity and glycemic control compared to those taking a placebo (74). Large-scale, well-controlled studies are needed to determine whether magnesium supplementation has any long-term therapeutic benefit in patients with type 2 diabetes. However, correcting existing magnesium deficiencies may improve glucose metabolism and insulin sensitivity in those with diabetes.

Migraine headaches

Individuals who suffer from recurrent migraine headaches have lower intracellular magnesium levels (demonstrated in both red blood cells and white blood cells) than individuals who do not experience migraines (75). Additionally, the incidence of ionized magnesium deficiency has been found to be higher in women with menstrualmigraine compared to women who don’t experience migraines with menstruation (76). Oral magnesium supplementation has been shown to increase intracellular magnesium levels in individuals with migraines, leading to the hypothesis that magnesium supplementation might be helpful in decreasing the frequency and severity of migraine headaches. Two early placebo-controlled trials demonstrated modest decreases in the frequency of migraine headaches after supplementation with 600 mg/day of magnesium (75, 77). Another placebo-controlled trial in 86 children with frequent migraine headaches found that oral magnesium oxide (9 mg/kg body weight/day) reduced headache frequency over the 16-week intervention (78). However, there was no reduction in the frequency of migraine headaches with 485 mg/day of magnesium in another placebo-controlled study conducted in 69 adults suffering migraine attacks (79). The efficiency of magnesium absorption varies with the type of oral magnesium complex, and this might explain the conflicting results. Although no serious adverse effects were noted during these migraine headache trials, 19% to 40% of individuals taking the magnesium supplements have reported diarrhea and gastric (stomach) irritation.

The efficacy of magnesium infusions was also investigated in a randomized, single-blind, placebo-controlled, cross-over trial of 30 patients with migraine headaches (80). The administration of 1 gram of intravenous (IV) magnesium sulfate ended the attacks, abolished associated symptoms, and prevented recurrence within 24 hours in nearly 90% of the subjects. While this promising result was confirmed in another trial (81), two additional randomized, placebo-controlled studies found that magnesium sulfate was less effective than other molecules (e.g., metoclopramide) in treating migraines (82, 83). The most recent meta-analysis of five randomized, double-blind, controlled trials reported no beneficial effect of IV magnesium for migraine in adults (84). However, the effect of magnesium should be examined in larger studies targeting primarily migraine sufferers with hypomagnesemia (85).

Asthma

The occurrence of hypomagnesemia may be greater in patients with asthma than in individuals without asthma (86). Several clinical trials have examined the effect of intravenous (IV) magnesium infusions on acute asthmatic attacks. One double-blindplacebo-controlled trial in 38 adults with acute asthma, who did not respond to initial treatment in the emergency room, found improved lung function and decreased likelihood of hospitalization when IV magnesium sulfate was infused compared to a placebo (87). However, another placebo-controlled, double-blind study in 48 adults reported that IV infusion of magnesium sulfate did not improve lung function in patients experiencing an acute asthma attack (88). A systematic review of seven randomized controlled trials (five adult and two pediatric) concluded that IV magnesium sulfate is beneficial in patients with severe, acute asthma (89). In addition, a meta-analysis of five randomized placebo-controlled trials, involving 182 children with severe asthma, found that IV infusion of magnesium sulfate was associated with a 71% reduction in the need for hospitalization (90). In the most recent meta-analysis of 16 randomized controlled trials (11 adult and 5 pediatric), IV magnesium sulfate treatment was associated with a significant improvement of respiratory function in both adults and children with acute asthma treated with β2-agonists and systemic steroids (91). At present, available evidence indicates that IV magnesium infusion is an efficacious treatment for severe, acute asthma; however, oral magnesium supplementation is of no known value in the management of chronic asthma (92-94). Nebulized, inhaled magnesium for treating asthma requires further investigation. A meta-analysis of eight randomized controlled trials in asthmatic adults showed that nebulized, inhaled magnesium sulfate had benefits with respect to improved lung function and decreased hospital admissions (91). However, a recent systematic review of 16 randomized controlled trials, including adults, children, or both, found little evidence that inhaled magnesium sulfate, along with a β2-agonist, improved pulmonary function in patients with acute asthma (95).

Sources

Food sources

A large US national survey indicated that average magnesium intake is about 350 mg/day for men and about 260 mg/day for women — significantly below the current recommended dietary allowance (RDA). Magnesium intakes were even lower in men and women over 50 years of age (8). Such findings suggest that marginal magnesium deficiency may be relatively common in the US.

Since magnesium is part of chlorophyll, the green pigment in plants, green leafy vegetables are rich in magnesium. Unrefined grains (whole grains) and nuts also have high magnesium content. Meats and milk have an intermediate content of magnesium, while refined foods generally have the lowest. Water is a variable source of intake; harder water usually has a higher concentration of magnesium salts (2). Some foods that are relatively rich in magnesium are listed in Table 2, along with their magnesium content in milligrams (mg). For more information on the nutrient content of foods, search the USDA food composition database.

Table 2. Some Food Sources of Magnesium
Food Serving Magnesium (mg)
Cereal, all bran ½ cup 112
Cereal, oat bran ½ cup dry 96
Brown rice, medium-grain, cooked 1 cup 86
Fish, mackerel, cooked 3 ounces 82
Spinach, frozen, chopped, cooked ½ cup 78
Almonds 1 ounce (23 almonds) 77
Swiss chard, chopped, cooked ½ cup 75
Lima beans, large, immature seeds, cooked ½ cup 63
Cereal, shredded wheat 2 biscuits 61
Peanuts 1 ounce 48
Molasses, blackstrap 1 tablespoon 48
Hazelnuts 1 ounce (21 hazelnuts) 46
Okra, frozen, cooked ½ cup 37
Milk, 1% fat 8 fluid ounces 34
Banana 1 medium 32

Supplements

Magnesium supplements are available as magnesium oxide, magnesium gluconate, magnesium chloride, and magnesium citrate salts, as well as a number of amino acidchelates, including magnesium aspartate. Magnesium hydroxide is used as an ingredient in several antacids (96).

Safety

Toxicity

Adverse effects have not been identified from magnesium occurring naturally in food. However, adverse effects from excess magnesium have been observed with intakes of various magnesium salts (i.e., supplemental magnesium) (6). The initial symptom of excess magnesium supplementation is diarrhea — a well-known side effect of magnesium that is used therapeutically as a laxative. Individuals with impaired kidney function are at higher risk for adverse effects of magnesium supplementation, and symptoms of magnesium toxicity have occurred in people with impaired kidney function taking moderate doses of magnesium-containing laxatives or antacids. Elevated serum levels of magnesium (hypermagnesemia) may result in a fall in blood pressure (hypotension). Some of the later effects of magnesium toxicity, such as lethargy, confusion, disturbances in normal cardiac rhythm, and deterioration of kidney function, are related to severe hypotension. As hypermagnesemia progresses, muscle weakness and difficulty breathing may occur. Severe hypermagnesemia may result in cardiac arrest (2, 3). The Food and Nutrition Board (FNB) of the Institute of Medicine set the tolerable upper intake level (UL) for magnesium at 350 mg/day (Table 3); this UL represents the highest level of daily supplemental magnesium intake likely to pose no risk of diarrhea or gastrointestinal disturbance in almost all individuals. The FNB cautions that individuals with renal impairment are at higher risk for adverse effects from excess supplemental magnesium intake. However, the FNB also notes that there are some conditions that may warrant higher doses of magnesium under medical supervision (2).

Table 3. Tolerable Upper Intake Level (UL) for Supplemental Magnesium
Age Group UL (mg/day)
Infants 0-12 months Not possible to establish*
Children 1-3 years 65
Children 4-8 years 110
Children 9-13 years 350
Adolescents 14-18 years 350
Adults 19 years and older 350
*Source of intake should be from food and formula only.

Drug interactions

Magnesium interferes with the absorption of digoxin (a heart medication), nitrofurantoin (an antibiotic), and certain anti-malarial drugs, which could potentially reduce drug efficacy. Bisphosphonates (e.g., alendronate and etidronate), which are drugs used to treat osteoporosis, and magnesium should be taken two hours apart so that the absorption of the bisphosphonate is not inhibited. Magnesium has also been found to reduce the efficacy of chlorpromazine (a tranquilizer), penicillamine, oral anticoagulants, and the quinolone and tetracycline classes of antibiotics. Because intravenous magnesium has increased the effects of certain muscle-relaxing medications used during anesthesia, it is advisable to let medical staff know if you are taking oral magnesium supplements, laxatives, or antacids prior to surgical procedures. High doses of furosemide (Lasix) and some thiazide diuretics (e.g., hydrochlorothiazide), if taken for extended periods, may result in magnesium depletion (96, 97). Moreover, long-term use (three months or longer) of proton-pump inhibitors (drugs used to reduce the amount of stomach acid) may increase the risk of hypomagnesemia (98, 99). Many other medications may also result in renal magnesium loss (3).

Linus Pauling Institute Recommendation

The Linus Pauling Institute supports the latest RDA for magnesium intake (400-420 mg/day for men and 310-320 mg/day for women). Following the Linus Pauling Institute recommendation to take a daily multivitamin/mineral supplement may ensure an intake of at least 100 mg of magnesium/day. Few multivitamin/mineral supplements contain more than 100 mg of magnesium due to its bulk. Because magnesium is plentiful in foods, eating a varied diet that provides green vegetables, whole grains, and nuts daily should provide the rest of an individual’s magnesium requirement.

Older adults (>50 years)

Older adults are less likely than younger adults to consume enough magnesium to meet their needs and should therefore take care to eat magnesium-rich foods in addition to taking a multivitamin/mineral supplement daily. Since older adults are more likely to have impaired kidney function, they should avoid taking more than 350 mg/day of supplemental magnesium without medical consultation (see Safety).

magnesium-flashcard

 

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“I definitely was feeling what I would consider suicidal, not really wanting to live, not really wanting to die, just numb. That’s not a healthy place for me,” McCombie said.

She said she has lived with depression and Bipolar disorder for 30 years, has tried dozens of medications and supplements to combat it, but nothing, she said, has worked as well as the Ketamine infusions she gets at Rise Wellness Center.

She’s had six of them in ten months.”I had the right attitude and wanted to be healed and believing that it was going to happen for me and my brain. It happened. It cut down the mood stabilizers and antidepressants I had been on for years. I don’t take them at all,” she said.

More studies,like this one, are finding that Ketamine may be more effective and work faster than traditional antidepressants.

A local team of anesthesiologists had used the drug before, as an anaesthetic inside the operating room, but after seeing its potential to treat depression, they opened Rise Wellness Center, which specializes in Ketamine infusions.

“We get people that are so far down and so dark that we need this to get them out, to get them up, to get them moving. No drug does that like Ketamine,” said Dr.  Renaud Rodrigue, a pain management physician at Rise Wellness Center.

Experts say Ketamine can be dangerous, even deadly, if abused or taken in large doses.

Even though it’s not FDA-approved to treat depression, Dr. Rodrigue said, when given in small doses and in a clinical setting, 90 percent of his patients with severe depression reported long-term benefits.

Researchers at the University of Illinois published this study about how Ketamine may trigger a depression-fighting protein in the brain.

“This protein changed the game for us. We know now there’s something that is created just by the drug itself, which is staying in the central nervous system and is exerting this affect way beyond the duration of the drug,” said Dr. Rodrigue.

McCombie said Ketamine saved her life.

Could Ketamine conquer Treatment resistant depression?

A notorious drug that can cause dangerous hallucinations and even death when abused may be the key to treating severely depressed patients when used under proper physician care. UT Southwestern’s Dr. Lisa Monteggia has uncovered how the drug Ketamine works so rapidly and why patients are seeing success when other treatments have failed.

Transcript

{Video opens with music and pictures of UTSW patient Megan Joyce along with her mother and with her husband.}

Megan Joyce: Everything in my life seems great.

Narrator: Megan Joyce’s life may look picture perfect.

Megan: I graduated college. I got married. He’s an amazing person. He is incredibly supportive.

Narrator: But what these happy photos hide is a relentless inner struggle.

Megan: This is not something that I love to admit, but I fight for my life every single day.

Narrator: The 27-year-old has spent more than a decade battling severe depression. It triggers for no obvious reason.

Megan: They have defined my bipolar illness as treatment resistant.

Narrator: She says she tried every medication in the books … as well as checking into inpatient and outpatient treatment centers. Nothing worked. Until doctors at UT Southwestern Medical Center tried something bold. Ketamine infusion therapy.

Megan: I don’t know if I would be here without the Ketamine treatment. I drive from Austin every 10 days, and I come for treatment, and I’m in the hospital for about 5 hours, and then I go home the same day.

Narrator: Several studies show ketamine can quickly stabilize severely depressed patients. But it does come with risks.

Dr. Madhukar Trivedi: There is a risk for addiction so that if people start taking Ketamine on their own on the black market, then that can be very dangerous. There are toxic effects in the brain if you overdose. On the other hand, for patients who do well on this and are getting the right dose under the guidance of a physician, it can be life saving.

Megan: When I have the IV in, it’s for 40 minutes, and then I stay for 2 hours after because it is an anesthetic so they want to make sure you don’t have adverse side effects.

Narrator: Dr. Madukhar Trivedi is closely monitoring Joyce … as well as the work his colleagues are doing at the bench.

Dr. Trivedi: At UT Southwestern, we have the whole breadth of work being done. There are people working like Dr. Monteggia in basic research. Understanding the exact mechanism of how Ketamine changes molecularly and changes the mechanism of action.

Dr. Lisa Monteggia: We got involved with how Ketamine triggers an anti-depressant effect because of the real need. Some of the recent clinical data has really shown that about a third of all patients don’t respond to anti-depressants. So, what do you do for treatment for those individuals?

Narrator: UT Southwestern’s Dr. Lisa Monteggia is a neuroscientist whose lab pinpointed a key protein that helps tigger Ketamine’s rapid antidepressent effects in the brain. Whereas traditional antidepressents can take up to 8 weeks to work, the effects of ketamine are seen within 60 to 90 minutes.

Dr. Monteggia: The idea of trying to understand how you generate a rapid anti-depressant response in patients … it’s really the first time we’ve been able to study it.

Narrator: Her study, published in the prestigious journal Nature, shows that ketamine blocks a protein responsible for a range of normal brain functions.

Dr. Monteggia: How we think Ketamine triggers an anti-depressant effect, this blocking the NMDA receptor, we think may also be causing the side effects associated with Ketamine. One of the things we’re working on is to try and see if we can identify compounds, slight derivatives perhaps, that may have the beneficial effects of Ketamine, in terms of triggering anti-depressant effects, without the side effects.

Narrator: In the meantime, Joyce remains optimistic for her future and the millions of others trying to defeat depression.

Megan: That’s why I really sought out Ketamine is I really wanted to give back and just have a chance at a semi-normal life.

Depression Patients Turning to Local Doctor’s Ketamine Therapy

The deaths of designer Kate Spade on Tuesday and TV Chef Anthony Bourdain Friday morning are bringing new attention to depression and suicide.

A new Center for Disease Control and Prevention report reveals suicide rates have risen 30 percent across much of the country since 1999.

But right here in San Diego, there is hope for a category of patients some doctors call “the untreatable.”

This patient, we’ll call Lisa, is composing a letter to the editor about her 20-year fight to stay alive.

“I know how tall the bridge is. I know how many seconds it takes to land,” Lisa said.

Lisa is an attorney with severe depression. Conventional medicines could not suppress her suicidal thoughts.

“It’s awful,” she said. “The day starts with waking up thinking ‘Can I even get out of bed?’ You just fight it to exhaustion every single day.”

She was referred to Dr. David Feifel who NBC 7 first also spoke to three years ago. Patients travel from as far away as Canada to undergo his Ketamine therapy.

“Sort of a psychedelic experience. It’s also been termed dissociative experience because it is sort of an out-of-body feeling,” Dr. Feifel said of his therapy.

Dr. Feifel says low doses of Ketamine have an almost immediate effect on his patients, unlike conventional anti-depressants that can take weeks to build up a therapeutic level.

While Ketamine doesn’t stay in the body more than a day, its effects can last for months.

“It seems to be able to vaporize people’s sense of wanting to take their life.” Dr. Feifel said.

Lisa has received some 35 treatments over the last four months.

“I walk in here crappy, I’ll leave happy. It is a remarkable, remarkable experience that in 20 years nothing has ever come close” Lisa said.

Her goal is to need fewer treatments and experience longer-lasting effects.

Lisa’s hope for the so-called “untreatable community” of depressed people is they find help.

Ketamine-Associated Brain Changes – A Review of the Neuroimaging Literature

KEY POINTS:

                  Ketamine-Associated Brain Changes: A Review of the Neuroimaging Literature

Subanesthetic doses of ketamine have rapid (within hours), robust (across a variety of symptoms), and relatively sustained (typically up to one week) antidepressant effects—even in patients with TRD (treatment resistant depression). Clinical studies show that about 50% of patients with TRD have a significant decrease in symptoms within 24 hours of a single intravenous subanesthetic ketamine dose.

Animal models show that ketamine’s antidepressant effects are likely mediated by its antagonism of N-methyl-D-aspartate (NMDA) receptors through increased α-amino-3-hydroxy-5- methyl-4-isoxazolepropionic acid (AMPA)–mediated glutamatergic signaling. This triggers activation of intracellular synaptogenic pathways, most notably in the mechanistic target of rapamycin (mTOR)–signaling pathway, which also has implications in many other psychiatric disorders.

With regard to MDD patients, decreased glutamate has been noted in various prefrontal regions, including the dorsolateral prefrontal cortex (dlPFC), dorsomedial PFC (dmPFC), and anterior cingulate cortex (ACC), when compared to controls.8–10 This shortage of glutamate makes ketamine an ideal treatment for MDD; by creating a surge in glutamate levels in regions of the brain that suffer from a glutamate deficit, ketamine may provide some normalization of glutamate levels in patients with MDD. This “glutamate surge” hypothesis has dominated as the primary theory of ketamine’s antidepressant mechanism.

Ketamine may work through additional receptors, as it is known to have effects on several opioid receptors, adrenergic receptors, and several serotonin and norepinephrine transporters.17–19 It is also possible that acute dissociative side effects of ketamine may be mediating antidepressant response.

One salient biological metric that may provide insight into ketamine’s mechanism of action is related to dissociation. Dissociative side effects begin from infusion, reach a peak typically within an hour of infusion, and are completely diminished 230 minutes after infusion.20 The same study has shown that increased dissociation and psychotomimetic symptoms immediately following infusion may predict antidepressant response. (Luckenbaugh DA, Niciu MJ, Ionescu DF, et al. Do the dissociative side effects of ketamine mediate its antidepressant effects? J Affect Disord 2014;159:56–61Do the dissociative side effects of ketamine mediate its antidepressant effects.)

Certain themes have emerged with Ketamine. First are our findings of convergent brain regions implicated in MDD and how ketamine modulates those areas. Specifically, the subgenual ACC has been a region of interest in many previous studies. In relation to emotion and cognition, ketamine appears to reduce brain activation in regions associated with self-monitoring, to increase neural regions associated with emotional blunting, and to increase neural activity in reward processing.

Overall, ketamine’s effects were most notably found in the subgenual ACC, PCC, PFC, and hippocampus. Abnormalities in overlapping regions (specifically, the dorsal and subgenual ACC, amygdala, hippocampus, and ventral striatum) have been implicated, via a growing body of neuroimaging literature, in the pathophysiology of depression.  The subgenual ACC, in particular, has been a frequently studied area of interest concerning ketamine and MDD.

FMRI found significant reductions in subgenual ACC coupling with hippocampus, retrosplenial cortex, and thalamus. Immediate reductions in subgenual ACC blood flow and focal reductions in OFC blood flow strongly predicted dissociation.

NIMH studies using PET 120 minutes postinfusion found that increased metabolism in the subgenual ACC was positively correlated with improvements in depression scores post-ketamine. (Neural correlates of rapid antidepressant response to ketamine in bipolar disorder..)

Analysis of resting-state scans in healthy volunteers further suggests that dissociation may be responsible for ketamine’s antidepressant effects because it may disconnect the “excessive effects of an aversive visceromotor state on cognition and the self”—a hallmark of depression.40(p 163) Related, one study found that ketamine may dampen brain regions involved in rumination (the repetitive focusing of attention on negative feelings and thoughts in response to negative mood) by reducing the functional connectivity between the pregenual ACC and the dorsal PCC, and decreasing connectivity between the left and right executive-control networks.  (. Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35 .Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network.)

Taken together, these studies suggest that ketamine may cause a “disconnect” in several circuits related to affective processing, perhaps by shifting focus of attention away from the internal states of anxiety, depression, and somatization, and more toward the perceptual changes (e.g., hallucinations, visual distortions, derealization) induced by ketamine. Similarly, during an emotion task, ketamine attenuated responses to negative pictures, suggesting that the processing of negative information is specifically altered in response to ketamine. (Scheidegger M, Henning A, Walter M, et al. Ketamine administration reduces amygdalo-hippocampal reactivity to emotional stimulation. Hum Brain Mapp 2016;37:1941–52.Ketamine administration reduces amygdalo‐hippocampal reactivity to emotional stimulation)

By taking the focus off “oneself” and placing it on other stimuli, it is possible that ketamine decreases awareness of negative experiences and consequently improves mood.

Perhaps most interesting are ketamine’s effects on brain connectivity as it relates to self-monitoring behaviors. Reduced connectivity between the pregenual ACC and dorsal PCC was associated with increased dissociation during infusion, and reduced activation in the left superior temporalcortex was associated with impaired self-monitoring56,65—which is disruptive to patients with psychotic illness—especially those with chronic symptoms of psychosis. By contrast, the transient dissociation experienced by depressed patients during a ketamine infusion may have the effect of dampening what the hyperactive self-monitoring associated with depressive illness (Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. b)

During ketamine administration, subjects experience emotional blunting, which may be associated with reduced limbic responses to emotional stimuli.54,55 It is possible that by decreasing the activity of deep limbic structures (thought to be involved in the pathophysiology of depression, such as the amygdala), ketamine acutely disables the emotional resources required to perpetuate the symptoms of depression. (Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine and fMRI BOLD signal: distinguishing between effects mediated by change in blood flow versus change in cognitive state. Hum Brain Mapp 2003;18:135–45. Ketamine and fMRI BOLD signal Distinguishing between effects mediated by change in blood flow versus change in cognitive state|||| Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine alters neural processing of facial emotion recognition in healthy men: an fMRI study. Neuroreport 2003;14:387–91 Ketamine alters neural processing of facial emotion recognition in healthy men an fMRI study.)

Ketamine may play a role in reactivating reward areas of the brain in patients with MDD. This reactivation may be especially important, as reward areas in MDD have been characterized by decreased subcortical and limbic activity and by an increased cortical response to reward paradigms. (Zhang WN, Chang SH, Guo LY, Zhang KL, Wang J. The neural correlates of reward-related processing in major depressive disorder: a meta-analysis of functional magnetic resonance imaging studies. J Affect Disord 2013;151:531–9.)

In resting-state scans, BOLD activation in the cingulate gyrus, hippocampus, insula, thalamus, and midbrain increased after ketamine.( Stone J, Kotoula V, Dietrich C, De Simoni S, Krystal JH, Mehta MA. Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe. J Psychopharmacol 2015;29:1025–8.Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe)

In addition, ketamine increases neural activation in the bilateral MCC, ACC, and insula, as well as the right thalamus.  Activation of these areas is consistent with activation of reward-processing areas, suggesting that ketamine may play a role in activating reward neurocircuitry. (Hoflich A, Hahn A, Kublbock M, et al. Ketamine-dependent neuronal activation in healthy volunteers. Brain Struct Funct 2017;222:1533–42.)

Though no single brain area has been singled out as the locus of depression, ketamine affects different areas of the brain in various ways, which may contribute to overall mood improvements. For example, at baseline, patients with MDD, compared to healthy volunteers, had reduced global connectivity in the PFC and increased connectivity in the posterior cingulate, precuneus, lingual gyrus, and cerebellum; postketamine, responders had increased connectivity in the lateral PFC, caudate, and insula. (Abdallah CG, Averill LA, Collins KA, et al. Ketamine treatment and global brain connectivity in major depression. Neuropsychopharmacology 2017;42:1210–9.Ketamine Treatment and Global Brain Connectivity in Major Depression.)

These findings may reflect ketamine’s ability to reclaim frontal control over deeper limbic structures, thus strengthening the cognitive control of emotions and decreasing depressive symptoms. Similarly, TRD patients, compared to healthy volunteers, had reduced insula and caudate responses to positive emotions at baseline, which normalized in the caudate post-ketamine. (Murrough JW, Collins KA, Fields J, et al. Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder. Transl Psychiatry 2015;5:e509 Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder.)

Improvements are correlated with increased metabolism in the hippocampus, dorsal ACC, and decreased metabolism in the OFC. (Lally N, Nugent AC, Luckenbaugh DA, Niciu MJ, Roiser JP, Zarate CA Jr. Neural correlates of change in major depressive disorder anhedonia following open-label ketamine. J Psychopharmacol 2015;29:596–607 Neural correlates of change in major depressive disorder anhedonia following open-label ketamine.)

Specifically, based on this review, future studies should likely focus on ketamine’s action in the subgenual ACC, PCC, PFC, and hippocampus. Another promising direction for research builds on the view that depression is the product of underactive prefrontal and limbic mood-regulation networks and overreactive subcortical limbic networks, which are involved in emotional and visceral responses. (Drevets WC, Price JL, Furey ML. Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression. Brain Struct Funct 2008; 213:93–118 Brain structural and functional abnormalities in mood disorders.)

Ketamine’s potential use in both research and treatment is promising indeed.

 

Neural correlates of exercise training in individuals with schizophrenia and in healthy individuals A systematic review.

Mechanisms of Ketamine Action as an Antidepressant

Ketamine and Ketamine Metabolite Pharmacology Insights into Therapeutic Mechanisms.

Ketamine and other N-methyl-D-aspartate receptor antagonists in the treatment of depression a perspective review

THE NEUROBIOLOGY OF ketamine and addiction

Psychedelic-Assisted Psychotherapy – A Paradigm Shift in Psychiatric Research and Development

KETAMINE FOR TREATMENT-RESISTANT UNIPOLAR AND BIPOLAR MAJOR DEPRESSION – CRITICAL REVIEW AND IMPLICATIONS FOR CLINICAL PRACTICE.

Ketamine for the treatment of addiction Evidence and potential mechanisms  <<<<<<<<<<<<<<<<<<<<<<<<<<<

REVIEW OF KETAMINE ABUSE AND DIVERSION

Cognitive behavior therapy may sustain antidepressant effects of intravenous ketamine in treatment-resistant depression

The Effect of a Single Dose of Intravenous Ketamine on suicidal ideation – systemic review and meta-analysis

Rapid-Acting Antidepressants Mechanistic Insights and Future Directions.

Ketamine and rapid-acting antidepressants a new era in the battle against depression and suicide.

Molecular and Cellular Mechanisms of Rapid-Acting Antidepressants Ketamine and Scopolamine

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

New Targets for Rapid Antidepressant Action

Role of copper in depression. Relationship with ketamine treatment

Ketamine normalizes brain activity during emotionally valenced attentional processing in depression.

Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine.

Recognizing Depression from the Microbiota⁻Gut⁻Brain Axis. b

Psychobiotics and the gut–brain axis in the pursuit of happines

Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion

Default Mode Connectivity in Major Depressive diosrder measured up to 10 days after Ketamine administration

S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life

S-Adenosyl Methionine in the Therapy of Depression and Other Psychiatric Disorders.

Ketamine for Depression, 2 Diagnostic and Contextual Indications.

Ketamine’s antidepressant efficacy is extended for at least four weeks in subjects with a family history of an alcohol use disorder

Predictors of Response to Ketamine in Treatment Resistant Major Depressive Disorder and Bipolar Disorder

The role of adipokines in the rapid antidepressant effects of ketamine.

response to ketamine and prediction of treatment outcome

What is the mechanism of Ketamine’s rapid‐onset antidepressant effect A concise overview of the surprisingly large number of possibilities

Medical comorbidity in bipolar disorder The link with metabolic-inflammatory systems.

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Role of neuro-immunological factors in the pathophysiology of mood disorders.

Anti-inflammatory agents in the treatment of bipolar depression a systematic review and meta-analysis

The role of tryptophan metabolism and food craving in the relation between obesity and bipolar disorder

Immune-based strategies for mood disorders facts and challenges

Metabolic syndrome in psychiatric patients implications

Genetic Studies on the Tripartite Glutamate Synapse in the Pathophysiology and Therapeutics of Mood Disorders

The Impact of a Single Nucleotide Polymorphism in SIGMAR1 on Depressive Symptoms in Major Depressive Disorder and Bipolar Disorder.

Case–control association study of 14 variants of CREB1, CREBBP and CREM on MDD and bipolar

Metabolic syndrome in psychiatric patients overview, mechanisms, and implications.

Peripheral inflammation, Physical Activity and Cognition in Bipolar Disorder

The putative role of oxidative stress and inflammation in the pathophysiology of sleep dysfunction across neuropsychiatruc disorders – chronic fatigue bipolar MS

Bipolar Disorder and Inflammation.

Pharmacologic implications of inflammatory comorbidity in bipolar disorder.

Minding the brain- the role of pharmacotherapy in substance-use disorder treatment

Molecular and Cellular Effects of Traumatic Stress Implications for PTSD

Synaptic Loss and the Pathophysiology of PTSD Implications for Ketamine as a Prototype Novel Therapeutic

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Ketamine Consultants Blog

Ketamine has much support in the use of hard-to-treat depression and suicidal behaviors. Below are studies and their links, including a meta-analysis, which demonstrate the effect of Ketamine. Also a recent trial by Carlos Zarate shows the heterogenous nature of response to Ketamine . It is difficult to say who is going to be lifted from their depression completely or partially respond, but in the study, Dr. Zarate showed that patients with a long history of suicidal thinking and self-harm will have less of a response in some cases.

NOVA Health Recovery | 703-844-0184 | Fairfax, Virginia 22304
NOVA Health Recovery | 703-844-0184 | Fairfax, Virginia 22304

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients << Article link 

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients

Repeat intravenous treatment with low doses of the anesthetic drug ketamine quickly reduced suicidal thoughts in a small group of patients with treatment-resistant depression. In their report receiving Online First publication in the Journal of Clinical Psychiatry, a team of Massachusetts General Hospital (MGH) investigators report the results of their study in depressed outpatients who had been experiencing suicidal thought for three months or longer.

“Our finding that low doses of ketamine, when added on to current antidepressant medications, quickly decreased suicidal thinking in depressed patients is critically important because we don’t have many safe, effective, and easily available treatments for these patients,” says Dawn Ionescu, MD, of the Depression Clinical and Research Program in the MGH Department of Psychiatry, lead and corresponding author of the paper. “While several previous studies have shown that ketamine quickly decreases symptoms of depression in patients with treatment-resistant depression, many of them excluded patients with current suicidal thinking.”

It is well known that having suicidal thoughts increases the risk that patients will attempt suicide, and the risk for suicide attempts is 20 times higher in patients with depression than the general population. The medications currently used to treat patients with suicidal thinking — including lithium and clozapine — can have serious side effects, requiring careful monitoring of blood levels; and while electroconvulsive therapy also can reduce suicidal thinking, its availability is limited and it can have significant side effects, including memory loss.

Primarily used as a general anesthetic, ketamine has been shown in several studies to provide rapid relief of symptoms of depression. In addition to excluding patients who reported current suicidal thinking, many of those studies involved only a single ketamine dose. The current study was designed not only to examine the antidepressant and antisuicidal effects of repeat, low-dose ketamine infusions in depressed outpatients with suicidal thinking that persisted in spite of antidepressant treatment, but also to examine the safety of increased ketamine dosage.

The study enrolled 14 patients with moderate to severe treatment-resistant depression who had suicidal thoughts for three months or longer. After meeting with the research team three times to insure that they met study criteria and were receiving stable antidepressant treatment, participants received two weekly ketamine infusions over a three-week period. The initial dosage administered was 0.5 mg/kg over a 45 minute period — about five times less than a typical anesthetic dose — and after the first three doses, it was increased to 0.75 mg/kg. During the three-month follow-up phase after the ketamine infusions, participants were assessed every other week.

The same assessment tools were used at each visit before, during and after the active treatment phase. At the treatment visits they were administered about 4 hours after the infusions were completed. The assessments included validated measures of suicidal thinking, in which patients were directly asked to rank whether they had specific suicide-related thoughts, their frequency and intensity.

While only 12 of the 14 enrolled participants completed all treatment visits — one dropped out because of ketamine side effects and one had a scheduling conflict — most of them experienced a decrease in suicidal thinking, and seven achieved complete remission of suicidal thoughts at the end of the treatment period. Of those seven participants, two maintained remission from both suicidal thinking and depression symptoms throughout the follow-up period. While there were no serious adverse events at either dose and no major differences in side effects between the two dosage levels, additional studies in larger groups of patients are required before any conclusions can be drawn.

“In order to qualify for this study, patients had to have suicidal thinking for at least three months, along with persistent depression, so the fact that they experienced any reduction in suicidal thinking, let alone remission, is very exciting,” says Ionescu, who is an instructor in Psychiatry at Harvard Medical School. “We only studied intravenous ketamine, but this result opens the possibility for studying oral and intranasal doses, which may ease administration for patients in suicidal crises.”

She adds, “One main limitation of our study was that all participants knew they were receiving ketamine. We are now finishing up a placebo-controlled study that we hope to have results for soon. Looking towards the future, studies that aim to understand the mechanism by which ketamine and its metabolites work for people with suicidal thinking and depression may help us discover areas of the brain to target with new, even better therapeutic drugs.”

 

Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine: Secondary Analysis of an Open-Label Study  << Article in Clinical Psychiatry

Ketamine for Rapid Reduction of Suicidal Thoughts in Major Depression: A Midazolam-Controlled Randomized Clinical Trial Article link for below:

Ketamine was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients, according to researchers at Columbia University Medical Center (CUMC). They also found that ketamine’s anti-suicidal effects occurred within hours after its administration.

The findings were published online last week in the American Journal of Psychiatry.

According to the Centers for Disease Control and Prevention, suicide rates in the U.S. increased by 26.5 percent between 1999 and 2015.

“There is a critical window in which depressed patients who are suicidal need rapid relief to prevent self-harm,” said Michael Grunebaum, MD, a research psychiatrist at CUMC, who led the study. “Currently available antidepressants can be effective in reducing suicidal thoughts in patients with depression, but they can take weeks to have an effect. Suicidal, depressed patients need treatments that are rapidly effective in reducing suicidal thoughts when they are at highest risk. Currently, there is no such treatment for rapid relief of suicidal thoughts in depressed patients.”

Most antidepressant trials have excluded patients with suicidal thoughts and behavior, limiting data on the effectiveness of antidepressants in this population. However, previous studies have shown that low doses of ketamine, an anesthetic drug, causes a rapid reduction in depression symptoms and may be accompanied by a decrease in suicidal thoughts.

The 80 depressed adults with clinically significant suicidal thoughts who enrolled in this study were randomly assigned to receive an infusion of low-dose ketamine or midazolam, a sedative. Within 24 hours, the ketamine group had a clinically significant reduction in suicidal thoughts that was greater than with the midazolam group. The improvement in suicidal thoughts and depression in the ketamine group appeared to persist for up to six weeks.

Those in the ketamine group also had greater improvement in overall mood, depression, and fatigue compared with the midazolam group. Ketamine’s effect on depression accounted for approximately one-third of its effect on suicidal thoughts, suggesting the treatment has a specific anti-suicidal effect.

Side effects, mainly dissociation (feeling spacey) and an increase in blood pressure during the infusion, were mild to moderate and typically resolved within minutes to hours after receiving ketamine.

“This study shows that ketamine offers promise as a rapidly acting treatment for reducing suicidal thoughts in patients with depression,” said Dr. Grunebaum. “Additional research to evaluate ketamine’s antidepressant and anti-suicidal effects may pave the way for the development of new antidepressant medications that are faster acting and have the potential to help individuals who do not respond to currently available treatments.”

Ketamine for Rapid Reduction of Suicidal Thoughts in major depression – A midazolam controlled trial PDF article

Ketamine for depression | PTSD | 703-844-0184 | NOVA Health Recovery | Fairfax, Virginia 22304
Ketamine for depression | PTSD | 703-844-0184 | NOVA Health Recovery | Fairfax, Virginia 22304

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Ketamine as a Potential Treatment for Suicidal Ideation A Systematic Review of the Literature 2015

Abstract
Objective To review the published literature on the efficacy
of ketamine for the treatment of suicidal ideation (SI).
Methods The PubMed and Cochrane databases were
searched up to January 2015 for clinical trials and case
reports describing therapeutic ketamine administration to
patients presenting with SI/suicidality. Searches were also
conducted for relevant background material regarding the
pharmacological function of ketamine.
Results Nine publications (six studies and three case
reports) met the search criteria for assessing SI after
administration of subanesthetic ketamine. There were no
studies examining the effect on suicide attempts or death
by suicide. Each study demonstrated a rapid and clinically
significant reduction in SI, with results similar to previously
described data on ketamine and treatment-resistant
depression. A total of 137 patients with SI have been
reported in the literature as receiving therapeutic ketamine.
Seven studies delivered a dose of 0.5 mg/kg intravenously
over 40 min, while one study administered a 0.2 mg/kg
intravenous bolus and another study administered a liquid
suspension. The earliest significant results were seen after
40 min, and the longest results were observed up to
10 days postinfusion.
Conclusion Consistent with clinical research on ketamine
as a rapid and effective treatment for depression, ketamine
has shown early preliminary evidence of a reduction in
depressive symptoms, as well as reducing SI, with minimal
short-term side effects. Additional studies are needed to
further investigate its mechanism of action, long-term
outcomes, and long-term adverse effects (including abuse)
and benefits. In addition, ketamine could potentially be
used as a prototype for further development of rapid-acting
antisuicidal medication with a practical route of administration
and the most favorable risk/benefit ratio.
Key Points
Preliminary data from randomized controlled trials
have demonstrated that ketamine may rapidly and
effectively control treatment-resistant depression,
though the effects are transient.
A small subset of studies has demonstrated similar
results in the effects of ketamine on suicidal ideation.
Ketamine has potential as a rapid treatment for
suicidal ideation and/or a possible model compound
for future drug development.

4 Discussion
With an estimated prevalence of mood disorders ranging
from 3.3 to 21.4 % and the substantially increased risk of
suicide among patients with mood disorders, treatment is
certainly warranted [19]. Current treatment options for
suicidality are limited. They include brain stimulation
therapeutics, such as ECT, and pharmacological intervention
(lithium, clozapine). The efficacy of lithium in treating
suicidality has been documented [20, 21] and has recently been reviewed and pooled in a recent meta-analysis of 48
studies [22]. Clozapine has also been shown to reduce
suicide risk in patients with schizophrenia [23, 24]. The
limitations of both lithium and clozapine include a longer
time to efficacy in this psychiatric emergency/urgency,
compared with the early response to ketamine [25]. Ketamine
seems to be gaining substantial evidence as a pharmacological
option for depression with a fast onset of
action, but its long-term effects need further investigation.
In addition, ketamine probably offers a faster onset of
action in terms of SI, but further work is certainly needed
in this area. Given the risk of suicide and even the
increasing rates of suicide in certain subgroups, such as
soldiers and veterans [26, 27], there is an urgent need for
faster therapeutics for SI and TRD. Importantly, suicidality
and suicide pose a high global burden of patient suffering
to families and society. Although several small-to-moderate
sized studies, in addition to several reviews, have been
published that have examined the efficacy of ketamine in
TRD, there are considerably fewer published data
specifically examining ketamine in patients presenting with
SI. Notably, only three studies have directly examined SI
as the primary outcome [11, 16, 17], while the rest
examined SI as the secondary outcome [4, 15, 18], not
including case reports. This review summarizes the current
published literature regarding ketamine as a treatment for
SI. The data so far show promising trends of ketamine
being an effective and rapid treatment with minimal side
effects.
Pharmacologically, ketamine is an N-methyl-D-aspartate
(NMDA) receptor antagonist. It has been used for anesthesia
in the USA since the 1970s. At subanesthetic doses,
ketamine has been shown to increase glutamate levels [3].
This mechanism is relevant, as glutamate regulation and
expression are altered in patients with major depressive
disorder (MDD). Studies have also demonstrated an
abnormal glutamate–glutamine–gamma-aminobutyric acid
cycle in patients with suicidality [28]. Furthermore, ketamine
has also been shown to work on nicotinic and opioid
receptors [29]. No other class of antidepressant medication
works to modulate the glutamatergic system, and research
continues into this, with the goal of characterizing the full
mechanism of action of ketamine and perhaps developing
other compounds that would have similar effects. Thus,
even if the approval and marketing of ketamine as a rapidacting
antisuicidal and antidepressant medication is not
realized, it could well be a prototype for development of
other medication(s) that retain the mechanism of action
with more favorable qualities and a lesser adverse effect
profile (such as a longer duration of action or less or no
addictive potential). Although the mechanisms explaining
the antisuicidal effect and the NMDA receptor antagonism
of ketamine are still unclear, some of the initial evidence
points to an anti-inflammatory action via the kynurenic
acid pathway. Strong suggestions as to the causal relationship
between inflammation and depression/suicidality
has come from studies demonstrating that cytokines [30,
31] and interferon-b [32] induce depression and suicidality.
Other recent studies have added to the notion of implicating
brain immune activation in the pathogenesis of suicidality.
For instance, one study showed microglial
activation of postmortem brain tissue in suicide victims
[33]. Another study found increased levels of the cytokine
interleukin-6 in cerebrospinal fluid from patients who had
attempted suicide [34]. Higher levels of inflammatory
markers have been shown in suicidal patients than in nonsuicidal
depressed patients [33, 35]. Inflammation leads to
production of both quinolinic acid (an NMDA agonist) and
kynurenic acid (a NMDA antagonist). An increased
quinolinic acid to kynurenic acid ratio leads to NMDA
receptor stimulation. The correlation between quinolinic
acid and Suicide Intent Scale scores indicates that changes
in glutamatergic neurotransmission could be specifically
linked to suicidality [36].
Small randomized controlled trials have demonstrated
the efficacy of ketamine in rapidly treating patients with
both TRD and/or bipolar depression [4, 8, 9, 11, 16–18].
Some studies have also examined suicide items as a secondary
measure in their depression rating scales [4, 7]. In
total, the studies examining ketamine and TRD have nearly
consistently demonstrated that ketamine provides relief
from depressive and suicidal symptoms, starting at 40 min
and lasting for as long as 5 days. Questions still remain as
to the long-term effects of this treatment, how much should
be administered and how often, any serious adverse effects,
and the mechanism of action.
Pharmacologically, ketamine has poor bioavailability
and is best administered via injection [37]. In their landmark
study, Berman et al. [4] found that a subanesthetic
dose (0.5 mg/kg) rapidly improved depressive symptoms.
Most of the subsequent studies have delivered ketamine as
a constant infusion for 40 min at a rate of 0.5 mg/kg.
Others have examined its efficacy after multiple infusions
and observed similar results [8, 13, 16, 38]. Currently, it is
recommended that ketamine be administered in a hospital
setting [39].

______________________________________

Characterizing the course of suicidal ideation response to ketamine

Characterizing the course of suicidal ideation response to ketamine PDF

2018 article from Carlos Zarate discussing the variable course outcomes with Ketamine for suicidality and correlations to serum markers and behavior and longevity of self-harm prior to treatment:

 

Background: : No pharmacological treatments exist for active suicidal ideation (SI), but the glutamatergic
modulator ketamine elicits rapid changes in SI. We developed data-driven subgroups of SI trajectories after
ketamine administration, then evaluated clinical, demographic, and neurobiological factors that might predict SI
response to ketamine.
Methods: : Data were pooled from five clinical ketamine trials. Treatment-resistant inpatients (n = 128) with
DSM-IV-TR-diagnosed major depressive disorder (MDD) or bipolar depression received one subanesthetic
(0.5 mg/kg) ketamine infusion over 40 min. Composite SI variable scores were analyzed using growth mixture
modeling to generate SI response classes, and class membership predictors were evaluated using multinomial
logistic regressions. Putative predictors included demographic variables and various peripheral plasma markers.
Results: : The best-fitting growth mixture model comprised three classes: Non-Responders (29%), Responders
(44%), and Remitters (27%). For Responders and Remitters, maximal improvements were achieved by Day 1.
Improvements in SI occurred independently of improvements in a composite Depressed Mood variable for
Responders, and partially independently for Remitters. Indicators of chronic SI and self-injury were associated
with belonging to the Non-Responder group. Higher levels of baseline plasma interleukin-5 (IL-5) were linked to
Remitters rather than Responders.
Limitations: : Subjects were not selected for active suicidal thoughts; findings only extend to Day 3; and plasma,
rather than CSF, markers were used.
Conclusion: : The results underscore the heterogeneity of SI response to ketamine and its potential independence
from changes in Depressed Mood. Individuals reporting symptoms suggesting a longstanding history of chronic
SI were less likely to respond or remit post-ketamine.

1. Introduction
Suicide poses a serious threat to public health. Worldwide, suicide
accounts for approximately 1 million deaths, and 10 million suicide
attempts are reported annually (World Health Organization, 2014). In
the United States, the national suicide rate has increased by approximately
28% over the last 15 years (Curtin et al., 2016). At the same
time, relatively few interventions for suicide risk exist. While treatments
such as clozapine and lithium have demonstrated effects on
suicidal behavior over weeks to months, these effects may be limited to
specific diagnoses (Cipriani et al., 2005; Griffiths et al., 2014). Currently,
no FDA-approved medications exist to treat suicidal ideation
(SI), leaving those who experience a suicidal crisis with limited options
for a reprieve of symptoms. Consequently, a critical need exists for
rapid-acting treatments that can be used in emergency settings.
A promising off-label agent for this purpose is the rapid-acting antidepressant
ketamine, which past studies have suggested reduces suicidal
thoughts (Diazgranados et al., 2010a; Murrough et al., 2015; Price
et al., 2009). A recent meta-analysis of 167 patients with a range of
mood disorder diagnoses found that ketamine reduced suicidal
thoughts compared to placebo as rapidly as within a few hours, with
effects lasting as long as seven days (Wilkinson et al., 2017). These
results are reinforced by newer findings of reduced active suicidal
ideation post-ketamine compared to a midazolam control(Grunebaum et al., 2018). As the efficacy literature develops in the era
of personalized medicine, two important issues must be addressed.
First, little is known about the acute course of SI following ketamine.
The speed with which antidepressant response occurs, and how much
improvement can be expected on average, has been documented for
single administrations of ketamine (Mathew et al., 2012; Sanacora
et al., 2017); in the limited available literature, researchers have
emulated previous studies examining antidepressant effect, where a
cutoff of 50% improvement demarcated response (Nierenberg and
DeCecco, 2001). Nevertheless, it remains unknown whether this categorization
accurately reflects the phenomenon of suicidal thoughts.
Empirically-derived approaches to the description of SI trajectory after
ketamine may be useful in operationalizing “response” in future clinical
trials.
Second, identifying demographic, clinical, or biological predictors
of SI response to ketamine would allow researchers and clinicians to
determine who is most likely to exhibit an SI response to ketamine. A
broad literature describes clinical and demographic predictors for suicide
risk (Franklin et al., 2017), and a smaller literature connects suicidal
thoughts and behaviors to plasma markers such as brain-derived
neurotrophic factor (BDNF) and cytokines (Bay-Richter et al., 2015;
Falcone et al., 2010; Isung et al., 2012; Serafini et al., 2017; Serafini
et al., 2013). However, no biomarkers have been shown to predict SI/
behavior response to intervention, a finding reinforced by the National
Action Alliance for Suicide Prevention’s Research Prioritization Task
Force’s Portfolio Analysis (National Action Alliance for Suicide
Prevention: Research Prioritization Task Force, 2015). Notably, predictor
analyses have the potential to reveal insights into personalized
treatments for suicidal individuals, as well as the neurobiology of SI
response. With respect to antidepressant response, for example, this
approach yielded the observation that individuals with a family history
of alcohol dependence may be more likely to exhibit an antidepressant
response to ketamine (Krystal et al., 2003; Niciu et al., 2014; PermodaOsip
et al., 2014).
The goals of this study were to elucidate trajectories of SI response
and identify predictors of that response, with the ultimate goal of
adding to the growing literature surrounding ketamine’s specific effects
on SI. In particular, we sought to determine whether the heterogeneous
patterns of change in SI after ketamine administration were better explained
by a model with two or more latent groups of trajectories rather
than a single average trajectory, using secondary analyses from previously
published clinical trials. These classes were then used to evaluate
potential clinical, demographic, and plasma biomarker predictors
of SI response to ketamine in order to generate hypotheses.. Discussion
This analysis used a data-driven approach to characterize SI response
to ketamine. The data were best explained by three trajectory
classes: one with severe average baseline SI and little to no response to
ketamine (Non-Responders), one with moderate average baseline levels
of SI and significant response to ketamine (Responders), and a third
with moderate average baseline levels of SI and complete remission of
SI by two days post-ketamine (Remitters). These findings suggest a
diversity of post-ketamine changes in SI that may not be captured under
traditional methods of categorizing response to treatment.
Furthermore, we found evidence that SI response and antidepressant
response could be distinguished from each other; one subset of participants
experienced improvement in SI that was partially explained by
improvements in Depressed Mood, while the other group’s improvements
in SI occurred independently of antidepressant response. With
regard to predictors of SI response trajectory, preliminary results suggest
the individuals least likely to experience improvement in SI postketamine
were those with the most severe SI and a history of self-injury.
Few plasma markers emerged as predictors of SI response in this study,
highlighting the limitations of connecting SI ratings of response with
biological markers.
The growth mixture modeling approach used here underscored the
heterogeneity of SI response to ketamine, which would not have been
captured by simply calculating the average trajectory. The class assignment
from this approach also differed from the definition of response
(50% reduction in symptoms) traditionally used in the antidepressant
literature, which often focuses on a specific timepoint rather
than the entire symptom trajectory. In comparing classification using a
50% response at Day 1 and Day 3 with the latent trajectory classes, we
found representation of almost every SI class across each responder
group, highlighting the potential limitations of the 50% response approach.
Further study is needed to determine which of these approaches
will prove more fruitful. Complete remission of SI has previously been
used as an outcome measure in clinical trials and in a meta-analysis of
ketamine’s efficacy (Grunebaum et al., 2017; Grunebaum et al., 2018;
Wilkinson et al., 2017), as well as in a study examining the relationship
between SI response to ketamine and changes in nocturnal wakefulness
(Vande Voort et al., 2017). One strength of the present study is that this
data-driven approach provides classifications that directly reflect the
phenomena under study as they are, as opposed to what they should be.
Especially when used in larger samples than the current study, this
approach is particularly promising in its ability to provide a more
nuanced understanding of the nature of SI response to ketamine.
Our results also support the idea that SI response in particular can target. First, it should be noted here that SI classes were not distinguishable
by baseline Depressed Mood scores; patients with the most
severe SI did not differ meaningfully in Depressed Mood scores from
those with the mildest SI. Second, while previous analyses of these data
documented that BMI and family history of alcohol dependence predicted
antidepressant response (Niciu et al., 2014), SI response was not
associated with these variables in the current analysis. Third, the antidepressant
response profiles of the SI classes suggest that SI response
and antidepressant response are not wholly redundant. This aligns with
previous clinical trials and meta-analytic reviews of the literature suggesting
that SI response to ketamine occurs partially independently of
antidepressant response (Grunebaum et al., 2018; Wilkinson et al.,
2017). Nevertheless, this independence did not hold true across both SI
response groups. Specifically, antidepressant and SI response were
clearly linked in Remitters, with depression accounting for half of the
changes in SI; however, in Responders, improvements in SI occurred
independently from improvements in Depressed Mood. These discrepancies
could be related to ketamine’s complex neurobiological
mechanisms or to the potentially low levels of clinical severity observed
in the Remitters.
Interestingly, the current analyses found no baseline demographic
variables that reliably distinguished Responders from Remitters. Some
phenotypic characteristics were uniquely associated with belonging to
the Non-Responder group, suggesting that a long-standing history of
self-injury or SI may indicate resistance to rapid changes in SI.
Relatedly, a recent, randomized clinical trial of repeat-dose ketamine
compared to placebo found that ketamine had no effect on SI in a
sample of patients selected for their longstanding, chronic history of SI
(Ionescu, 2017). These results highlight the importance of patient selection,
particularly for suicide risk. It should be stressed, however, that
SI does not necessarily translate to suicidal attempts or deaths; to our
knowledge, no study has yet linked ketamine with reduced risk of
suicidal behavior. Indeed, in the present study the SI Non-Responders
experienced limited antidepressant effects in response to ketamine, but
may nevertheless have improved on other, unmeasured symptoms that
could provide important benefit and relief. As the ketamine literature
develops, it will be important to identify which clinical symptom profiles
are most likely to have a robust anti-SI and anti-suicidal behavior
response to ketamine and which ones may benefit from other interventions.
While we evaluated a range of potential plasma markers previously
linked to suicidal ideation and behavior, in the present analysis only IL5
was associated with the SI Responder subgroup. Ketamine is known to
have anti-inflammatory effects (Zunszain et al., 2013), but the relationship
between antidepressant response and change in cytokine
levels remains unclear (Park et al., 2017). Cytokines have been linked
to suicidal behavior in the past; a recent meta-analysis found that lower
levels of IL-2 and IL-4, and higher levels of TGFbeta, were associated
with suicidal thoughts and behaviors (Serafini et al., 2013); however, toour knowledge IL-5 has not previously been linked to SI. Given the large
number of comparisons and lack of precedent in the literature, this
result may have been spurious and should be interpreted with caution.
A number of other results may reflect meaningful relationships, but the
high degree of variability—and the associated wide confidence intervals—suggests
that larger sample sizes are needed to better elucidate
the nature of any such relationships (e.g. baseline VEGF: χ2 = 6.13,
p = .05, but OR (95% CI) 13.33 (0.93–200.00)). Somewhat surprisingly,
plasma BDNF levels were not associated with responder class.
Previous studies of bipolar, but not MDD, samples found that plasma
BDNF levels were associated with SI response after ketamine
(Grunebaum, 2017; Grunebaum et al., 2017), suggesting that the mixed
diagnostic composition of this study may explain differences from
previous work. Studies exploring the relationship between BDNF and
antidepressant response to ketamine have also yielded mixed findings
(Haile et al., 2014; Machado-Vieira et al., 2009). Other data-driven
approaches have considered both biological and behavioral variables in
characterizing depression (Drysdale et al., 2017); a similar approach
might prove useful for predicting SI response.
The present study is associated with several strengths as well as
limitations. Strengths include the relatively large sample size of participants
who received ketamine, the use of composite SI scores from
previous exploratory factor analyses as opposed to individual items,
and the combination of clinical and biological markers as potential
predictors of class membership. Limitations include patient selection
methods, as these patients were part of an antidepressant trial and were
not selected for active suicidal thoughts, as well as the exploratory
nature of the analysis. As stated above, suicidal thoughts do not necessarily
equate to suicidal behavior, and class membership would thus
not necessarily correspond with an overall reduction in suicide risk.
Another limitation is that results were collapsed across several clinical
trials with slight variations in study design, and findings were thus only
extended to Day 3 rather than a week after ketamine administration. As
a result, only a subset of the sample could be used for predictive analyses.
In addition, plasma—rather than CSF—markers were used, and
the latter might better indicate underlying biology due to proximity to
the brain, though certain markers such as plasma BDNF may be related
to platelet storage, rather than the brain (Chacón-Fernández et al.,
2016). Comparison of results to trajectories of suicide-specific measures,
such as the Scale for Suicide Ideation (Beck et al., 1979), may also
give further insight into specific SI content. Finally, many clinical
predictors were collected upon hospital admission; future analyses
could use formal assessments, such as the Childhood Traumatic Questionnaire
(Bernstein et al., 1994), assessment of personality disorders,
or diagnoses such as post-traumatic stress disorder (PTSD) as potential
indicators of response.
Despite these limitations, the study demonstrates the utility of a
data-driven approach for characterizing the heterogeneity of SI response
to a rapid-acting intervention. This allows for a more finegrained
analysis of symptoms than would be permitted by traditionalapproaches, such as overall average response or dichotomization at
50% reduction in symptoms. This study identified several findings of
note. These included distinguishing at least three patterns of SI response
to ketamine and finding that subjects who exhibited more severe SI at
baseline were not likely to experience an SI response to ketamine.

 

____________________________________

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Ketamine | Rapid antidepressant | 703-844-0184 | Ketamine therapy in Fairfax, Va 22304

CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

Ketamine – NOVA Ketamine facebook page – ketamine treatment for depression

facebook Ketamine page

NOVA Health Recovery  << Ketamine clinic Fairfax, Va  – Call 703-844-0184 for an appointment – Fairfax, Virginia

Ketamine Consultants Blog

 

Ketamine for Depression | NOVA Health Recovery 703-844-0184 | Ketamine treatment for Bipolar, PTSD, Anxiety disorders

_________________________________________________________________________

Ketamine offers a rapid solution for many when their other treatments for depression have failed. Most patients studied for Ketamine treatment have failed standard therapies. Sanjay Gupta discusses this below in the link:

 

KETAMINE as a rapid antidepressant – CNN article Sanjay Gupta

Suicide in the United States

 

KETAMINE FOR DEPRESSION | NOVA HEALTH RECOVERY 703-844-0184 | KETAMINE TREATMENT FOR BIPOLAR, PTSD, ANXIETY DISORDERS | Drug addiction Treatment | Alcohol abuse treatment | Recovery

CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

Ketamine – NOVA Ketamine facebook page – ketamine treatment for depression

facebook Ketamine page

NOVA Health Recovery  << Ketamine clinic Fairfax, Va  – Call 703-844-0184 for an appointment – Fairfax, Virginia

Ketamine Consultants Blog

 

Ketamine for Depression | NOVA Health Recovery 703-844-0184 | Ketamine treatment for Bipolar, PTSD, Anxiety disorders

 

__________________________________________________________________________________________________________

Ketamine has been around for a long time and offers successful opportunities to treat individuals with very resistant depression, PTSD and anxiety. It is also rapid acting. Look at the following links below,

Useful in depression,anxiety, Bipolar, PTSD, pain, migraines, Bipolar, post partum depression, fibromyalgia, and multiple other hard-to-treat disorders. Here are some links and information below to popular press articles on Ketamine!

 

Ketamine For Severe Depression: ‘How Do You Not Offer This Drug To People?’

and

 

ketamine-a-miracle-drug-for-depression/   <<< Link to article

 

Ketamine Relieves Depression By Restoring Brain Connections

Chris Stephens, 28, has been battling depression all of his life. At times he wouldn’t get out of bed for weeks. In January, he said his depression hadn’t returned since he started taking ketamine.

Lianne Milton/For NPR

Scientists say they have figured out how an experimental drug called ketamine is able to relieve major depression in hours instead of weeks.

Researchers from Yale and the National Institute of Mental Health say ketamine seems to cause a burst of new connections to form between nerve cells in parts of the brain involved in emotion and mood.

The discovery, described in Science, should speed development of the first truly new depression drugs since the 1970s, the researchers say.

“It’s exciting,” says Ron Duman, a a psychiatarist and neurobiologist at Yale University. “The hope is that this new information about ketamine is really going to provide a whole array of new targets that can be developed that ultimately provide a much better way of treating depression.”

Ketamine is an FDA-approved anesthetic. It’s also a popular club drug that can produce out-of-body experiences. Not exactly the resume you’d expect for a depression drug.

But a few years ago, researchers discovered that ketamine could help people with major depression who hadn’t responded to other treatments. What’s more, the relief came almost instantly.

The discovery “represents maybe one of the biggest findings in the field over the last 50 years,” Duman says.

A rat neuron before (top) and after (bottom) ketamine treatment. The increased number of orange nodes are restored connections in the rat’s brain.

Ronald Duman/Yale University

Depression is associated with a loss of so-called synaptic connections between nerve cells, Duman says. So he and other scientists began to study mice exposed to stresses that produce symptoms a lot like those of human depression.

The stressed mice lost connections in certain parts of the brain. But a dose of ketamine was able to “rapidly increase these connections and also to rapidly reverse the deficits that are caused by stress,” Duman says.

A team at the National Institute of Mental Health also has found evidence that ketamine works by encouraging synaptic connections.

It’s possible to see the change just by studying rodent brain cells with a microscope, says Carlos Zarate from the Mood and Anxiety Disorders Program at NIMH.

A healthy neuron looks like a tree in spring, he says, with lots of branches and leaves extending toward synaptic connections with other neurons. “What happens in depression is there’s a shriveling of these branches and these leaves and It looks like a tree in winter. And a drug like ketamine does make the tree look like one back in spring.”

And there’s also indirect evidence that ketamine is restoring synaptic connections in people, Zarate says.

His team studied 30 depressed patients who got ketamine. And they found changes in brainwave activity that indicated the drug had strengthened connections between neurons in areas of the brain involved in depression.

All of this research is intended to produce drugs that will work like ketamine, but without the hallucinations. And several of these alternative drugs are already being tried in people.

Preliminary results suggest that “some of these compounds do have rapid antidepressant effects without the side effects that occur with ketamine,” Zarate says.

One of these drugs, called GLYX-13, has already been tested in two large groups of people — a key step toward FDA approval. The company that makes the drug, Naurex, says it will tell scientists how well GLYX-13 works at a meeting in December.

From Chaos To Calm: A Life Changed By Ketamine

 

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

 2018 Jan 1;225:545-551. doi: 10.1016/j.jad.2017.08.081. Epub 2017 Aug 30.

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

Abstract

OBJECTIVES:

Fear of Harm (FOH) is a pediatric onset phenotype of bipolar disorder (BD) characterized by BD plus treatment resistance, separation anxiety, aggressive obsessions, parasomnias, and thermal dysregulation. Intranasal ketamine (InK) in 12 youths with BD-FOH produced marked improvement during a two-week trial. Here we report on the open effectiveness and safety of InK in maintenance treatment of BD-FOH from the private practice of one author.

METHODS:

As part of a chart review, patients 18 years or older and parents of younger children responded to a clinical effectiveness and safety survey. Effectiveness was assessed from analysis of responses to 49 questions on symptomatology plus qualitative content analyses of written reports and chart review. Adverse events (AEs) were analyzed by frequency, duration and severity. Peak InK doses ranged from 20 to 360mg per administration.

RESULTS:

Surveys were completed on 45 patients treated with InK for 3 months to 6.5 years. Almost all patients were “much” to “very much” improved clinically and in ratings of social function and academic performance. Significant reductions were reported in all symptom categories. There were 13 reports of persistent AEs, none of which resulted in discontinuation. Acute emergence reactions were sporadically observed in up to 75%, but were mild and of brief duration.

LIMITATIONS:

Retrospective review from a single practice without placebo control with potential for response and recall bias.

CONCLUSIONS:

InK every 3-4 days at sub-anesthetic doses appeared to be a beneficial and well-tolerated treatment. Use of InK may be considered as a tertiary alternative in treatment refractory cases. Randomized control trials are warranted.

___________________________________________________________________________________

Low-dose ketamine for treatment resistant depression in an academic clinical practice setting. <<< ARTICLE link

BACKGROUND:

Recent studies demonstrating a rapid, robust improvement in treatment resistant depression (TRD) following a single sub-anesthetic infusion of ketamine have generated much excitement. However, these studies are limited in their generalizability to the broader TRD population due to their subject exclusion criteria which typically limit psychiatric comorbidity, concurrent medication, and level of suicide risk. This paper describes the safety and efficacy of sub-anesthetic ketamine infusions in a naturalistic TRD patient sample participating in a real-world TRD treatment program within a major university health system.

METHODS:

The effects of a sub-anesthetic dose (0.5mg/kg) of ketamine infused IV over forty minutes on TRD patients participating in a treatment program at the University of California, San Diego was investigated by retrospectively analyzing the medical charts of 41 adult TRD patients with a diagnosis of Major Depressive Disorder (MDD) or Bipolar Disorder (BD).

RESULTS:

Subjects were aged 48.6, 78% white, 36.6% female, and 82.9% had MDD. Significant psychiatric comorbidity existed in 73%. Average pre-infusion BDI score was 32.6 ± 8.4 (S.D) and dropped to 16.8 ± 3.1 at 24-h post-infusion (p < 0.001). The 24-h response (≥ 50% reduction from pre-infusion) and remission (BDI <13) rates were 53.7% and 41.5%, respectively. Three quarters of responders maintained responder status at 7-days. Ketamine infusions were well tolerated with occasional nausea or anxiety and mild hemodynamic effects during the infusion.

LIMITATIONS:

Retrospective nature of this study, lack of control group and use of self-report depression ratings scales.

CONCLUSIONS:

This is the first published study of sub-anesthetic ketamine infusions in a real-world TRD population. The results suggest that this treatment is effective and well tolerated in this population.

 

BACKGROUND:

Recent studies demonstrating a rapid, robust improvement in treatment resistant depression (TRD) following a single sub-anesthetic infusion of ketamine have generated much excitement. However, these studies are limited in their generalizability to the broader TRD population due to their subject exclusion criteria which typically limit psychiatric comorbidity, concurrent medication, and level of suicide risk. This paper describes the safety and efficacy of sub-anesthetic ketamine infusions in a naturalistic TRD patient sample participating in a real-world TRD treatment program within a major university health system.

METHODS:

The effects of a sub-anesthetic dose (0.5mg/kg) of ketamine infused IV over forty minutes on TRD patients participating in a treatment program at the University of California, San Diego was investigated by retrospectively analyzing the medical charts of 41 adult TRD patients with a diagnosis of Major Depressive Disorder (MDD) or Bipolar Disorder (BD).

RESULTS:

Subjects were aged 48.6, 78% white, 36.6% female, and 82.9% had MDD. Significant psychiatric comorbidity existed in 73%. Average pre-infusion BDI score was 32.6 ± 8.4 (S.D) and dropped to 16.8 ± 3.1 at 24-h post-infusion (p < 0.001). The 24-h response (≥ 50% reduction from pre-infusion) and remission (BDI <13) rates were 53.7% and 41.5%, respectively. Three quarters of responders maintained responder status at 7-days. Ketamine infusions were well tolerated with occasional nausea or anxiety and mild hemodynamic effects during the infusion.

LIMITATIONS:

Retrospective nature of this study, lack of control group and use of self-report depression ratings scales.

CONCLUSIONS:

This is the first published study of sub-anesthetic ketamine infusions in a real-world TRD population. The results suggest that this treatment is effective and well tolerated in this population.

 

NOVA Health Recovery

Call 703-844-0184 if you are interested in options for Ketamine treatment for Depression, Anxiety, PTSD, fibromyalgia, Lyme disease, CRPS, or other disorders.

Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications    << ARTICLE LINK

Population scale data reveals the antidepressant effects of Ketamine  << PDF copy

 

This article looked at the adverse event reporting system, evaluating the ‘side effects’ of Ketamine, which demonstrated LOWER depression rates in patients using Ketamine for pain. These same patients had fewer side effects from those pain medicines as well when they used Ketamine. In numerous settings, we have utilized Ketamine as an adjunct to control pain when opioids have failed (i.e.morphine) with excellent results.

Depression affects 8-12 % of the population at any one time and steals away quality of life as well as productivity. Depression is listed as the 4th leading cause of disease burden on the population by the World Health Organization.
Standard medications, such as SSRI antidepressants, may be ineffective or take several weeks to begin to have any effect. Ketamine has been shown to result in immediate (12-24 hours) improvement of depressive symptoms in a large percentage of patients. We see the same in many of our office infusions.

There is an inflammatory component to depression. This same article points out that Diclofenac, minocycline (an antibiotic), and Botox, also have some antidepressant effect as a result of their anti-inflammatory effects.

The bottom line is that Ketamine showed effectiveness for treatment-resistant depression in this article.

Has anyone had Botox with a Ketamine infusion? Just curious…

FACEBOOK NOVAKetamine LINK

Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications

  • Scientific Reportsvolume 7, Article number: 1450

Current therapeutic approaches to depression fail for millions of patients due to lag in clinical response and non-adherence. Here we provide new support for the antidepressant effect of an anesthetic drug, ketamine, by Inverse-Frequency Analysis of eight million reports from the FDA Adverse Effect Reporting System. The results of the examination of population scale data revealed that patients who received ketamine had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain. The analysis also revealed that patients who took ketamine had significantly lower frequency of reports of pain and opioid induced side effects, implying ketamine’s potential to act as a beneficial adjunct agent in pain management pharmacotherapy. Further, the Inverse-Frequency Analysis methodology provides robust statistical support for the antidepressant action of other currently approved therapeutics including diclofenac and minocycline.

 

The World Health Organization estimates depression as the 4th highest disease burden in the world1. In majority of the countries lifetime depression prevalence ranges 8–12%2,3,4. Current standard of practice of depression treatment consists of five main classes of antidepressants, serotonin reuptake inhibitors (SSRIs) being the most common. Nearly half of psychiatric and primary care patients discontinue their antidepressant therapy prematurely5. The main reasons for the discontinuation of therapy include late onset of beneficial outcomes, lack of efficacy for a fraction of patients, adverse reactions, fear of drug dependence, and lack of mechanisms to enforce adherence5. The initial therapeutic effect of antidepressants is delayed by 2–3 weeks after the first dose and the optimal effect is delayed by 6–10 weeks6. The long lag period renders the standard of care antidepressants ineffective for suicidal patients who can’t afford to wait 2–6 weeks. Aside from the lag in antidepressant effects, there is insufficient evidence that antidepressants prevent suicide during long-term treatment7, and in many cases the antidepressant increases the risk of suicidal thoughts and actions8. Efficacy is another issue affecting depression treatment. In the STAR*D protocol study depression remission is 67% after every drug class and drug class combination is tried9.

Because of these problems, some clinicians have been driven to utilize other drugs, such as ketamine, for treatment resistant depression (TRD) patients10,11,12. Ketamine is a drug used illicitly as a hallucinogen and clinically as an anesthetic since 1970’s. It is given intravenously, almost exclusively, due to a lack of an approved oral formulation. There have been some clinical trials where ketamine shows acute efficacy in treating TRD10,11, bipolar depression12 and major depressive disorder with suicidal ideation13, but the number of subjects in these trials ranges from 20 to 57 patients. There are financial and ethical obstacles for a larger scale clinical trial. Here we sought larger scale statistical evidence of ketamine antidepressant action in the FDA Adverse Event Reporting System (FAERS) postmarketing database containing over eight million patient records. Although FAERS was originally intended to track frequent adverse events, with sufficient amount of data, it can also be used to track the beneficial outcomes indirectly through monitoring reductions of related complaint frequencies. Here we apply Inverse-Frequency Analysis (IFA), which looks for statistically significant values of the negative log odds ratio (LogOR).

We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain (LogOR −0.67 ± 0.034) (Fig. 1c). This reduction in depression is specific to ketamine and is known to be much more rapid than current antidepressants, making this observed effect very promising for treatment of patients with acute depressive or suicidal episodes11. These patients cannot afford to wait up to six weeks for reductions in their depressive symptoms. Pain reports were also significantly lower for ketamine patients (LogOR −0.41 ± 0.019) (Fig. 1c)

Figure 1

Legend: (a) Frequencies of adverse events in patients on FAERS who took ketamine. Adverse events above 2.5% were reported. (b) Odds ratios were calculated comparing adverse event rates of ketamine patients (n = 41,337) and pain patients (n = 238,516). (c) LogOR of pain and depression event rates were calculated from the ketamine and pain patient cohorts. Negative values showing protective effect of ketamine. (d) LogOR of constipation, vomiting, and nausea were calculated from the ketamine and pain patient cohorts. Negative values showing protective effect of ketamine.

The analysis of the whole FAERS database revealed several other unintentional depression reducing drugs among antibiotics, cosmeceuticals and NSAIDS (Fig. 2). Our data supported previous studies that observed the psychiatric polypharmacology of minocycline, a tetracycline antibiotic14 (Fig. 2). The NSAID, diclofenac, was also observed to have some antidepressant properties (Fig. 2). It is theorized that both of these drugs may accomplish antidepressant effects through an anti-inflammatory mechanism15. Because of the antidepressant activity of several NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression event rates remained low (LogOR −0.56 ± 0.035) (Fig. 2).

Figure 2

LogOR of psychiatric events were calculated from FAERS patients who used botox, diclofenac or minocycline. FAERS patients who took any drugs for the indication of depression were used as the control cohort. Negative values showing protective effect

The reduction of depression rates in ketamine patient records makes a case for study of ketamine as a psychiatric drug. These results imply that ketamine may be further explored as a monotherapy or adjunct therapy for depression. It should also be noted that FAERS data revealed that ketamine use lead to renal side effects and awareness and caution in patients with renal or hepatic impairment may be warranted (Fig. 1a and b).

As an important side note, we also evaluated efficacy and side effects with the use of ketamine for pain management. We found that patients who were on ketamine had reduced opioid induced side effects including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) than patients who received any other combination of drugs for pain indications (Fig. 1d). Our data supports ketamine’s opioid-sparing properties and alludes to the fact that patients may receive benefits of improved pain, reduced requirement of opioids, and ultimately less opioid reduced side effects.

The results of this study support previous small scale studies’ conclusions that ketamine is a good monotherapy or adjunct therapy for depression. In clinical practice ketamine would be especially useful for depression because of the quick onset of its action compared to existing first line therapies10,11,12,13. Regardless of the causative mechanism ketamine appears to have therapeutic potential for TRD. Further, the potential to reduce many of the most complained side effects of opioid treatment makes ketamine adjunct therapy for pain seem desirable.

Overall, this study demonstrates that the therapeutic potential of ketamine can be derived from appropriate statistical analysis of existing population scale data. This study also outlines a methodology for discovering off label pharmacology of existing approved drugs. This method can be applied to other indications and may reveal new important uses of already approved drugs, providing reliable justification for new indications without large investments in additional clinical trials.

 

The rest of the article can be easily accessed from the above Link.

 

Botox and ketamine could help treat depression, study finds

Call 703-844-0184 to schedule a Ketamine evaluation or infusion.

 

The ketamine infusion for depression experience is not as scary as some people think. Read on to learn about what the ketamine infusion protocol feels like.
Ketamine Fairfax, Va |22308|703-844-0184 | Alexandria, Va | Ketamine for depression

Before getting ketamine infusions for depression, you’ll likely want to know what a ketamine infusion experience is like. While the ketamine infusion experience is different from person to person, the protocol for ketamine infusions for depression is similar for everyone. Read on to learn what it’s really like to receive intravenous ketamine infusions.

What Is a Ketamine Infusion?

A ketamine infusion is a dose of ketamine that is given via the intravenous (IV) route of administration. Ketamine infusions are typically used to treat major depression or depression in bipolar disorder but can be used to treat chronic pain conditions as well.

Before Getting a Ketamine Infusion

Before getting a ketamine infusion, you should expect thorough medical and psychiatric evaluations as well as medical tests to make sure you are healthy enough for the treatment. These assessments and tests are very important as ketamine infusions can be challenging both mentally and physically and only a doctor who is well-acquainted with your health can make good decisions for you.

Ketamine Infusion Procedure

You will likely be shown to a room with a comfortable reclining chair or bed. You will not need to disrobe or wear a hospital gown for treatment. The Ketamine Advocacy Network suggests that you always request a single-person room as a ketamine infusion is a very personal experience. A loved one is usually allowed to stay with you during the ketamine infusion treatment if you want. You’ll then be connected to vital sign monitors such as pulse and oxygen saturation monitors.

It is at this point that you’ll have an IV inserted. A tiny needle is used to insert a tube into a vein in your hand or arm and many find this to be painless. The tube will be connected to a bag held a couple of feet above you. The bag contains the specific dose of ketamine you will require and it will be delivered directly into your bloodstream at a controlled rate. The rate may be adjusted during your treatment to maximize its benefit. It takes approximately 45 minutes for a ketamine infusion and you may need to be under observation after that for an hour or occasionally more. You cannot drive yourself home after an infusion.

People, typically, initially receive six infusions over the course of two-three weeks.

What Does Getting an IV Ketamine Infusion for Depression Feel Like?

Once the ketamine enters your system, it will reach your brain within seconds and you will quickly be able to feel its effects. You won’t be able to stand or converse normally and you’ll feel extremely relaxed but you will still be awake. While others may view a person that seems almost asleep, your brain will still fully be engaged. While this sensation is often found to be “weird”, most people do find it pleasant.

Experience of Side Effects of the Ketamine Infusion

During the infusion, you may experience dissociation, where the mind and body seem to separate. This side effect of the ketamine infusion can often be minimized simply by opening your eyes.

As stated, your mind will be very active during the IV infusion so it may wander to thoughts of trauma or anxiety, but unlike your usual feelings around those thoughts, you will view it matter-of-factly. One patient described his ketamine infusion experience like this:

“. . . you start disassociating with everything, like you’re observing, not participating in anything. It’s really weird . . . As far as the mind goes, you start going through these weird levels, kind of like in the movies Inception or The Matrix, where you don’t know what’s real.

“You start thinking about all kinds of stuff. Whatever races through your mind—and usually when you’re depressed it’s negative sh*t—when you’re on ketamine, it’s just like: ‘Well, nothing I can do about that.’ You feel like, ‘I’m not in control, and that’s fine; you’re going to die someday and that’s just life.’ You kind of learn to just accept it, I guess.”

Although most patients do experience relaxation during a ketamine infusion, there can be moments of fright, particularly if you go into the experience with very high anxiety. Listening to calming music or watching a calming image may help with this, however.

Feeling Better After the Ketamine Infusion Procedure

It varies as to how long it will take for the ketamine to kick in. Some find relief within only an hour or two while others need multiple infusions to feel the benefit. Unfortunately, 20-40% of people do not experience a positive response to ketamine treatment (Reviews on Ketamine for Depression).

What’s important to remember is that no matter what you experience during a ketamine infusion, it’s the changes that the ketamine makes to your brain that relieve depression and not the infusion experience itself.

 

 

Ketamine treatment for depression reviews are scant but some are available. Read about ketamine for depression reviews from patients and doctors.

Ketamine is a relatively new treatment for depression so people are often looking for ketamine treatment for depression reviews to help guide their choices. This is understandable as ketamine treatment cost falls between $400-800 per intravenous (IV) infusion and more than six infusions may be needed. Read on for real patients’ ketamine for depression reviews.

Ketamine Treatment for Depression Reviews

It’s important to note that reviews for any type of treatment are personal and individual. This means that any one person may or may not have the same experience as you. This is why it’s important to work with your doctor to decide if ketamine is a good treatment option for your depression.

That being said, there are ketamine treatment for depression reviews available.

A site like PatientsLikeMe can be valuable as individual patients can report their experiences with a treatment. As of August 2017, four patients who took ketamine for major depressive disorder and two patients who took ketamine for bipolar depression have left reviews. Of the six, three indicated that ketamine had “major effectiveness” on their condition. Two patients noted moderate effectiveness and one noted no effectiveness. Side effects to ketamine included: dissociation, dizziness, nausea, memory problems, cognition problems and drowsiness. Two of the patients noted no side effects although one of those also reported no useful effect either.

When looking at these ketamine infusion reviews, most people were happy with the treatment, with one patient saying, “Very effective. I would do it again in a heartbeat.”

However, most patients noted the cost of ketamine infusions as being burdensome.

When looking at the reviews that all patients left, regardless as to the reason the ketamine was prescribed, two out of 24 noted severe side effects and nine out of 24 noted no side effects.

Ketamine Review Article

In 2015, Vice.com published a ketamine review article called, I Used Ketamine to Treat My Depression. In it, one person with bipolar depression discusses his experience with receiving ketamine infusion for depression. Brent Miles, a 41-year-old songwriter and journalist from Phoenix, Arizona, regularly got ketamine infusion treatments at a clinic in North Scottsdale in 2013 and shares his story.

Miles’ experiences are quite positive although he notes that he could not continue the ketamine depression treatment due to cost.

You can read Miles’ experience here.

 

Ketamine Treatment for Depression Reviews by Doctors

As with many treatments, some doctors are wary of this new depression treatment while others forge ahead with cautious optimism.

“A really important part of these recommendations is to make sure people fully understand what the risks and benefits are to treatment so that they are able to make an informed decision based on knowing what the risk-benefit ratio is,” said Gerard Sanacora, MD, PhD, professor of psychiatry and director of the Yale Depression Research Program.

Dr. Sanacora also added:

“The reality is that this is a unique situation where we have a tremendously promising treatment. We use it a lot, and I believe this really is a transformative change in the field, but we do have to appreciate the limits of the knowledge that we are working with right now.”

Ketamine side effects range from mild to severe. Get complete details on side effects of ketamine for depression on HealthyPlace.

The side effects of ketamine for depression are typically mild but can range in severity. Understanding the ketamine infusion therapy for depression side effects before starting treatment is a good idea so that you know what to look for and aren’t surprised by the more common ketamine side effects.

Side Effects of Ketamine

It’s important to remember that the doses of ketamine for depression treatment are far smaller than any dose that would be used recreationally or as an anesthetic (Can You Get Addicted to Ketamine?). Thus, if you read about the side effects of ketamine in general, you will likely see more severe and different side effects listed than those experienced by those being treated for depression.

Some of the common side effects experienced when larger dosages are used include:

  • High blood pressure
  • Increased cardiac output
  • Pressure inside the skull (intracranial pressure)
  • Irregular heart rhythm
  • Seizure-type movements (tonic-clonic movements)
  • Hallucinations
  • Vivid dreams

Side Effects of Ketamine for Depression

As mentioned, dosages of ketamine when used to treat depression are very small. However, ketamine infusion therapy side effects still exist.

According to a small 2012 study wherein patients received up to six ketamine infusion treatments for treatment-resistant depression, the following were the commonly-reported side effects:

  • The presence of psychotic symptoms (delusions and/or experiences of things that don’t exist such as hallucinations)
  • Dissociative symptoms (feeling “out of body,” disconnected, etc.)
  • Feeling “strange” or “unreal”
  • Abnormal sensations
  • Blurred vision
  • Feeling drowsy or sleepy
  • Elevated heart rate or blood pressure

Notably, only four people in the study (16.7%) reported any side effect that impaired functioning at any time.

That said, the majority of people who were given ketamine infusion therapy for depression did experience some side effects, most remitting within two hours after the infusion.

Those who responded positively to the ketamine treatment experienced the same level and type of side effects that those who did not respond experienced.

Positive Effects of Ketamine for Depression

In a small, recent study, it was found that within two hours of the first dose of ketamine, each individual item on a depression scale known as the Montgomery– Asberg Depression Rating Scale (MADRS), was reduced with the exception of appetite and sleep items which couldn’t be assessed at that time.

The following positive effects of ketamine for depression were seen as reductions in:

  • Suicidal thoughts
  • Pessimistic thoughts
  • Inability to feel
  • Feelings of weariness, diminished energy or listlessness (lassitude)
  • Concentration difficulties
  • Inner tension
  • Reported sadness
  • Apparent sadness

The largest positive changes were seen in lassitude, concentration difficulties, and apparent sadness.

It’s important to remember that while these positive ketamine health effects will be seen by many, not everyone responds to ketamine treatment in this way. In the above-mentioned study, 71% of people had a positive response to ketamine treatment for depression and it is known that those receiving more treatments have a better chance at a positive response.

Ketamine is both a legitimate medical treatment as well as a street drug. But can you get addicted to ketamine? Find out on HealthyPlace.

Ketamine isn’t just a drug used to treat depression, chronic pain or as an anesthesia, ketamine is also a street drug of abuse. Often called “special k,” ketamine is used in large doses by some in the party scene. It’s important to remember, however, that recreationally, people take much larger doses of ketamine than are used in depression treatment (How Does Ketamine Work for Depression?). This means that recreational users are more likely to experience increasing tolerance to the drug’s effects, seek greater doses and become addicted.

Ketamine Addiction

Ketamine is the number one drug of abuse in Asia, particularly Hong Kong. Some of the ketamine found on the street is diverted from pharmaceutical supplies but there is also increasing evidence of ketamine production specifically for street use, particularly in India and China. Ketamine may also be found in ecstasy in Asia.

Ketamine is also a drug of abuse in the United States. The reason why people abuse ketamine is its desirable acute effects on the person. If a person takes a street dose of ketamine, he or she may experience:

  • Reduced sensations in the body / a lack of pain
  • A floating or detached feeling
  • A feeling of being incapable of moving
  • A change in how the person sees and hears things, possibly causing hallucinations

Some people find these effects desirable. However, ketamine can also cause:

  • Confusion
  • Agitation
  • Panic attacks
  • Impairment in short- and long-term memory impairment
  • Attention problems
  • Difficulty in cognition
  • Impaired reaction time

Death from acute ketamine use is rare but does occur.

If a person continues to abuse ketamine, over time even worse effects can be felt. Someone who is addicted to ketamine or who consistently abuses ketamine may experience:

  • Depression
  • Very serious bladder problems possibly leading to the bladder needing removal
  • Serious damage to the urinary tract
  • Liver dysfunction
  • Impaired gallbladder activity
  • Kidney failure
  • Extreme pain, particularly during urination

You may not experience a physical addiction to ketamine but you can become addicted to ketamine psychologically. Being addicted to ketamine is no joke and anyone who abuses ketamine or who is addicted to ketamine needs to seek help immediately.

How to Get Off Ketamine

Getting off ketamine involves the same thing as getting off of other drugs: going through withdrawal. Withdrawal effects make it difficult for someone trying to get off ketamine to stay sober, but withdrawal effects can be managed.
If you’re trying to get off of ketamine, symptoms of withdrawal that you might experience include:

  • Double vision
  • Hearing loss
  • Increased heart beat
  • Rapid breathing
  • Loss of motor skills
  • Loss of coordination
  • Depression

These effects are not typically medically dangerous although if they get out of hand, medical intervention may be needed in the short-term. While these withdrawal effects may sound awful, it’s important to remember that these effects are short-lived and day-by-day, you will start to feel better.

 

I attached a youtube video on SAD – seasonal Affective Disorder

www.ubcsad.ca   <<  SAD website
https://youtu.be/pUYOxnuzRHU?t=1

 

 

 

https://www.healthyplace.com/depression/depression-treatment/can-you-get-addicted-to-ketamine/

Ketamine in the NEWS April 2018

http://sltbr.org/ Biological rhythms – depression  << Website

Medical Express Article regarding Ketamine for Depression <<<<

Ketamine, notorious club drug, shows promise as a treatment for depression, studies indicate

April 20, 2018 by John Keilman, Chicago Tribune

Sabrina Misra suffered from depression for most of her life, but last summer, it became almost too heavy to bear.

Despite years of therapy and many medications, Misra, 36, had become so despondent that she started planning her suicide. But then her psychiatrist introduced her to a new treatment with an unusual back story.

The treatment was ketamine, an anesthetic used to sedate both people and animals before surgery. It’s also a notorious street drug, abused by clubgoers seeking a trancelike, hallucinatory high.

But in recent years, numerous studies have found that ketamine can be an effective and speedy treatment for people with depression—particularly those who, like Misra, have found little relief from other medications.

“After the first couple of treatments it didn’t seem to work, but after I hit my fourth one, everything started to change,” said Misra, a therapist and college instructor who lives in Lisle, Ill. “I went from actively wanting to kill myself to being fine.”

Though some researchers have found that ketamine can be a valuable antidepressant, no one has performed the large-scale clinical trials necessary to get U.S. Food and Drug Administration approval to use it a psychiatric medication.

Consequently, most insurance plans won’t pay for it, leaving patients to pay thousands of dollars out of pocket for a series of intravenous infusions.

Some warn that questions remain about ketamine’s long-term safety and effectiveness. Dr. James Murrough, a psychiatrist at the Icahn School of Medicine at Mount Sinai in New York, said people who misuse the drug have developed cognitive problems, and high doses have proved toxic in rats.

And because ketamine has a history of abuse, he said, doctors and patients must consider the threat of addiction.

“We think the risk is low, but it’s probably not zero, particularly if it gets scaled up,” he said. “There’s excitement but also a justified caution.”

Nonetheless, demand for the drug is so great that dozens of specialty clinics are popping up around the country. The doctors who run them say ketamine has helped most of their patients.

“It’s much better than anything we’ve had before,” said Dr. Abid Nazeer, the psychiatrist who treated Misra at his Oak Brook clinic, Advanced Psychiatric Solutions. “I’ve seen it work so quickly that one infusion gets rid of suicidal thoughts that had been there for 20 years.”

Ketamine was created as an anesthetic, and doctors including veterinarians and battlefield medics embraced it for its fast-acting properties and relative safety. But because it produces strong out-of-body sensations in high doses, it became a club drug, potent enough to send hundreds of people to emergency rooms each year.

In the 1990s, researchers discovered another use for ketamine: A small dose, they found, limits the concentration of a neurotransmitter called glutamate in the brain, and with startling speed, lifts the mood of many depression sufferers who haven’t been helped by medications like Prozac or Lexapro.

“Our standard antidepressants can take six to eight weeks to be effective—ketamine can take just one hour,” said Dr. Carlos Zarate of the National Institute of Mental Health, whose studies in the 2000s accelerated interest in the drug.

Over the past few years, doctors have opened specialty clinics that offer ketamine to patients who have depression or, to a lesser extent, chronic pain. Though the FDA has not approved those uses, the agency allows doctors to dispense drugs for “off-label” purposes if they believe it is medically appropriate.

The basic regimen calls for the intravenous infusion of a small dose—0.5 mg per kilogram of body weight, far less than someone would use to get high—six times over two weeks. After that, patients return every few weeks or months for booster doses.

Clinic operators say they screen clients to focus on those who have not improved with standard antidepressants.

“This is a last resort for those that are treatment-resistant,” said Dr. June Lee of Lombard’s Optimum Ketamine Center. “Most of the patients we’ve seen here have tried everything.”

Zarate said research has shown ketamine to be effective for about 60 percent of people with treatment-resistant depression, though some local clinics say their results have been better.

“We’ve had about a 70 percent response rate, but it really works for them,” said Dr. Vikas Patel, an emergency room physician who runs the Midwest Ketamine Center in Arlington Heights. “For the 30 percent it doesn’t work for, there’s no benefit at all. I would say there isn’t a big in-between.”

He charges $500 per infusion. Insurance typically won’t cover ketamine treatments, though Patel said he expects that to change. A pharmaceutical company is seeking FDA approval for a nasal spray, he said, and other companies are testing their own versions.

But for now, the out-of-pocket cost limits the number of people who can afford the treatment. Misra said that while she put the infusions on her credit card, seeing them as a life-or-death investment, others aren’t so fortunate.

“I have patients who are struggling right now, and they actually can’t swing it,” she said. “I think that’s a horrible thing. No one should have to die because they can’t pay for treatment.”

Dominic Sisti, who directs the Scattergood Program for Applied Ethics of Behavioral Health Care at the University of Pennsylvania, co-wrote a paper three years ago warning about the possible risks of using for depression.

The research that has come out since then has persuaded him that it is appropriate for many people, he said, but he still believes doctors should share data on their results to further knowledge of the drug and improve the protocols for using it.

“In a sense, each patient they treat is an experiment of one,” he said. “It would be really helpful if all these clinics got together and figured out a way to report those outcomes. Without those data, I worry that someone’s going to get hurt.”

Antidepressant response within hours? Experts weigh evidence on ketamine as fast-acting treatment for depression

antidepressant-response-hours-experts-evidence << Article

Recent studies suggest that ketamine, a widely used anesthetic agent, could offer a wholly new approach to treating severe depression—producing an antidepressant response in hours rather than weeks. Two reviews of recent evidence on ketamine and related drugs for treating depression appear in the Harvard Review of Psychiatry.

Ketamine and related drugs may represent a “paradigm shift” in the treatment of  (MDD) and bipolar depression—especially in patients who do not respond to other treatments, according to a review by Carlos A. Zarate, Jr, MD and colleagues at the National Institute of Mental Health. A second article explores evidence on the mechanisms behind ‘s rapid antidepressant effects.

Growing Evidence, Clinical Caution about Ketamine for Severe Depression

Current treatments for MDD and bipolar depression have major limitations. Many patients with severe depressive symptoms don’t respond to available antidepressant drugs. Even for those who do respond, it may take several weeks before symptoms improve.

Ketamine, an anesthetic, is one of several glutamatergic drugs affecting neurotransmitters in the central nervous system. Over the past decade, several studies have reported “rapid, robust, and relatively sustained antidepressant response” to ketamine, injected intravenously at low, subanesthetic doses.

Dr. Zarate and colleagues review the research on ketamine and other glutamatergic drugs for depression. Ketamine, by far the best-studied of these medications, is notable for its very rapid antidepressant effects. In patients with treatment-resistant MDD, ketamine has produced initial reductions in depressive symptoms within two hours, with peak effects at 24 hours.

Ketamine may also rapidly reduce suicidal thoughts. Combined with other medications, ketamine has also produced rapid antidepressant effects in patients with treatment-resistant bipolar depression.

Prompted by these studies, some doctors are already using ketamine in patients with severe or treatment-resistant depression. However, since it is FDA-approved only as an anesthetic, use of ketamine in depressive disorders is “off-label,” unregulated, and not standardized. Many questions remain about its short- and long-term side effects and potential for abuse.

“Efforts are underway to bring ketamine to market, standardize its use, and determine its real-world effectiveness,” Dr. Zarate and coauthors write. They also present evidence on several other glutamatergic drugs. One , esketamine, has been given “breakthrough therapy” status by the FDA for  at imminent risk of suicide.

Cristina Cusin, MD of Massachusetts General Hospital and colleagues review neuroimaging studies evaluating ketamine’s effects in the brain. The studies show ketamine-induced changes in several brain areas involved in the development of depression. Ketamine may exert its antidepressant effects by “acutely disabl[ing] the emotional resources required to perpetuate the symptoms of depression,” as well as by increasing emotional blunting and increasing activity in reward processing.

Independent of how ketamine works or its ultimate role in clinical treatment, antidepressant response to glutamatergic drugs points to an exciting conclusion: “that rapid antidepressant effects are indeed achievable in humans,” Dr. Zarate and coauthors write. “This paradigm shift lends additional urgency to the development of novel treatments for MDD and bipolar , particularly for patient subgroups that do not respond to currently available therapies.”

Glutamatergic Modulators in Depression

Ketamine-Associated Brain Changes A Review of the Neuroimaging Literature bb

Brain-Derived Neurotrophic Factor and Major Depressive Disorder Evidence from Meta-Analyses

Suicidal thoughts rapidly reduced with ketamine, finds study

Suicidal thoughts rapidly reduced with ketamine, finds study

December 14, 2017, Columbia University Medical Center
Ketamine
3-D model of Ketamine. Credit: Wikipedia

Ketamine was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients, according to researchers at Columbia University Medical Center (CUMC). They also found that ketamine’s anti-suicidal effects occurred within hours after its administration.

The findings were published online last week in the American Journal of Psychiatry.

According to the Centers for Disease Control and Prevention, suicide rates in the U.S. increased by 26.5 percent between 1999 and 2015.

“There is a critical window in which  who are suicidal need rapid relief to prevent self-harm,” said Michael Grunebaum, MD, a research psychiatrist at CUMC, who led the study. “Currently available antidepressants can be effective in reducing  in with depression, but they can take weeks to have an effect. Suicidal, depressed patients need treatments that are rapidly effective in reducing suicidal thoughts when they are at highest risk. Currently, there is no such treatment for rapid relief of suicidal thoughts in depressed patients.”

Most antidepressant trials have excluded patients with suicidal thoughts and behavior, limiting data on the effectiveness of antidepressants in this population. However, previous studies have shown that low doses of ketamine, an anesthetic drug, causes a rapid reduction in depression symptoms and may be accompanied by a decrease in suicidal thoughts.

The 80 depressed adults with clinically significant suicidal thoughts who enrolled in this study were randomly assigned to receive an infusion of low-dose ketamine or midazolam, a sedative. Within 24 hours, the ketamine group had a clinically significant reduction in suicidal thoughts that was greater than with the midazolam group. The improvement in suicidal thoughts and depression in the ketamine group appeared to persist for up to six weeks.

Those in the ketamine group also had greater improvement in overall mood, depression, and fatigue compared with the midazolam group. Ketamine’s effect on depression accounted for approximately one-third of its effect on suicidal thoughts, suggesting the treatment has a specific anti-suicidal effect.

Side effects, mainly dissociation (feeling spacey) and an increase in blood pressure during the infusion, were mild to moderate and typically resolved within minutes to hours after receiving ketamine.

“This study shows that ketamine offers promise as a rapidly acting  for reducing suicidal thoughts in patients with ,” said Dr. Grunebaum. “Additional research to evaluate ‘s antidepressant and anti-suicidal effects may pave the way for the development of new antidepressant medications that are faster acting and have the potential to help individuals who do not respond to currently available treatments.”

The study is titled, “Ketamine for Rapid Reduction of Suicidal Thoughts in Major Depression: A Midazolam-Controlled Randomized Clinical Trial.”

https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2018.17060720

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients

Repeat intravenous treatment with low doses of the anesthetic drug ketamine quickly reduced suicidal thoughts in a small group of patients with treatment-resistant depression. In their report receiving Online First publication in the Journal of Clinical Psychiatry, a team of Massachusetts General Hospital (MGH) investigators report the results of their study in depressed outpatients who had been experiencing suicidal thought for three months or longer.

“Our finding that low doses of , when added on to current antidepressant medications, quickly decreased suicidal thinking in depressed patients is critically important because we don’t have many safe, effective, and easily available treatments for these patients,” says Dawn Ionescu, MD, of the Depression Clinical and Research Program in the MGH Department of Psychiatry, lead and corresponding author of the paper. “While several previous studies have shown that ketamine quickly decreases symptoms of depression in patients with treatment-resistant depression, many of them excluded patients with current suicidal thinking.”

It is well known that having suicidal thoughts increases the risk that patients will attempt suicide, and the risk for suicide attempts is 20 times higher in patients with depression than the general population. The medications currently used to treat patients with suicidal thinking—including lithium and clozapine—can have serious , requiring careful monitoring of blood levels; and while electroconvulsive therapy also can reduce suicidal thinking, its availability is limited and it can have significant side effects, including memory loss.

Primarily used as a general anesthetic, ketamine has been shown in several studies to provide rapid relief of symptoms of depression. In addition to excluding patients who reported current suicidal thinking, many of those studies involved only a single ketamine dose. The current study was designed not only to examine the antidepressant and antisuicidal effects of repeat, low-dose ketamine infusions in depressed outpatients with suicidal thinking that persisted in spite of antidepressant treatment, but also to examine the safety of increased ketamine dosage.

The study enrolled 14 patients with moderate to severe treatment-resistant depression who had suicidal thoughts for three months or longer. After meeting with the research team three times to insure that they met study criteria and were receiving stable antidepressant treatment, participants received two weekly ketamine infusions over a three-week period. The initial dosage administered was 0.5 mg/kg over a 45 minute period—about five times less than a typical anesthetic dose—and after the first three doses, it was increased to 0.75 mg/kg. During the three-month follow-up phase after the ketamine infusions, participants were assessed every other week.

The same assessment tools were used at each visit before, during and after the active treatment phase. At the treatment visits they were administered about 4 hours after the infusions were completed. The assessments included validated measures of suicidal thinking, in which patients were directly asked to rank whether they had specific suicide-related thoughts, their frequency and intensity.

While only 12 of the 14 enrolled participants completed all treatment visits—one dropped out because of ketamine side effects and one had a scheduling conflict—most of them experienced a decrease in suicidal thinking, and seven achieved complete remission of  at the end of the treatment period. Of those seven participants, two maintained remission from both suicidal thinking and depression symptoms throughout the follow-up period. While there were no serious adverse events at either dose and no major differences in side effects between the two dosage levels, additional studies in larger groups of patients are required before any conclusions can be drawn.

“In order to qualify for this study, patients had to have suicidal thinking for at least three months, along with persistent depression, so the fact that they experienced any reduction in suicidal thinking, let alone remission, is very exciting,” says Ionescu, who is an instructor in Psychiatry at Harvard Medical School. “We only studied intravenous ketamine, but this result opens the possibility for studying oral and intranasal doses, which may ease administration for  in suicidal crises.”

She adds, “One main limitation of our study was that all participants knew they were receiving ketamine. We are now finishing up a placebo-controlled study that we hope to have results for soon. Looking towards the future, studies that aim to understand the mechanism by which ketamine and its metabolites work for people with suicidal thinking and  may help us discover areas of the brain to target with new, even better therapeutic drugs.”

Dawn F. Ionescu et al, Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine, The Journal of Clinical Psychiatry (2016). DOI: 10.4088/JCP.15m10056

Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine: Secondary Analysis of an Open-Label Study

Background: Ketamine rapidly reduces thoughts of suicide in patients with treatment-resistant depression who are at low risk for suicide. However, the extent to which ketamine reduces thoughts of suicide in depressed patients with current suicidal ideation remains unknown.

Methods: Between April 2012 and October 2013, 14 outpatients with DSM-IV–diagnosed major depressive disorder were recruited for the presence of current, stable (≥ 3 months) suicidal thoughts. They received open-label ketamine infusions over 3 weeks (0.5 mg/kg over 45 minutes for the first 3 infusions; 0.75 mg/kg over 45 minutes for the last 3). In this secondary analysis, the primary outcome measures of suicidal ideation (Columbia-Suicide Severity Rating Scale [C-SSRS] and the Suicide Item of the 28-item Hamilton Depression Rating Scale [HDRS28-SI]) were assessed at 240 minutes postinfusion and for 3 months thereafter in a naturalistic follow-up.

Results: Over the course of the infusions (acute treatment phase), 7 of 14 patients (50%) showed remission of suicidal ideation on the C-SSRS Ideation scale (even among patients whose depression did not remit). There was a significant linear decrease in this score over time (P < .001), which approached significance even after controlling for severity of 6-item Hamilton Depression Rating Scale (HDRS6) core depression items (P = .05). Similarly, there were significant decreases in the C-SSRS Intensity (P < .01) and HDRS28-SI (P < .001) scores during the acute treatment phase. Two of the 7 patients who achieved remission during the acute treatment phase (29%) maintained their remission throughout a 3-month naturalistic follow-up.

Conclusions: In this preliminary study, repeated doses of open-label ketamine rapidly and robustly decreased suicidal ideation in pharmacologically treated outpatients with treatment-resistant depression with stable suicidal thoughts; this decrease was maintained for at least 3 months following the final ketamine infusion in 2 patients.

Ketamine improved bipolar depression within minutes

May 30, 2012, Elsevier

Bipolar disorder is a serious and debilitating condition where individuals experience severe swings in mood between mania and depression. The episodes of low or elevated mood can last days or months, and the risk of suicide is high.

Antidepressants are commonly prescribed to treat or prevent the , but they are not universally effective. Many patients still continue to experience periods of depression even while being treated, and many patients must try several different types of  before finding one that works for them. In addition, it may take several weeks of treatment before a patient begins to feel relief from the drug’s effects.

For these reasons, better treatments for depression are desperately needed. A new study in  this week confirms that scientists may have found one in a drug called ketamine.

A group of researchers at the National Institute of Mental Health, led by Dr. Carlos Zarate, previously found that a single dose of ketamine produced rapid antidepressant effects in  with . They have now replicated that finding in an independent group of depressed patients, also with bipolar disorder. Replication is an important component of the scientific method, as it helps ensure that the initial finding wasn’t accidental and can be repeated.

In this new study, they administered a single dose of ketamine and a single dose of placebo to a group of patients on two different days, two weeks apart. The patients were then carefully monitored and repeatedly completed ratings to ‘score’ their  and suicidal thoughts.

When the patients received ketamine, their  significantly improved within 40 minutes, and remained improved over 3 days. Overall, 79% of the patients improved with ketamine, but 0% reported improvement when they received placebo.

Importantly, and for the first time in a group of patients with bipolar depression, they also found that ketamine significantly reduced . These antisuicidal effects also occurred within one hour. Considering that bipolar disorder is one of the most lethal of all psychiatric disorders, these study findings could have a major impact on public health.

“Our finding that a single infusion of ketamine produces rapid antidepressant and antisuicidal effects within one hour and that is fairly sustained is truly exciting,” Dr. Zarate commented. “We think that these findings are of true importance given that we only have a few treatments approved for acute bipolar depression, and none of them have this rapid onset of action; they usually take weeks or longer to have comparable antidepressant effects as ketamine does.”

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, which means that it works by blocking the actions of NMDA. Dr. Zarate added, “Importantly, confirmation that blocking the NMDA receptor complex is involved in generating rapid antidepressant and antisuicidal effects offers an avenue for developing the next generation of treatments for depression that are radically different than existing ones.”

The article is “Replication of Ketamine’s Antidepressant Efficacy in Bipolar Depression: A Randomized Controlled Add-On Trial” by Carlos A. Zarate Jr., Nancy E. Brutsche, Lobna Ibrahim, Jose Franco-Chaves, Nancy Diazgranados, Anibal Cravchik, Jessica Selter, Craig A. Marquardt, Victoria Liberty, and David A. Luckenbaugh (doi: 10.1016/j.biopsych.2011.12.010). The article appears in Biological Psychiatry, Volume 71, Issue 11 (June 1, 2012)

Replication of Ketamine’s Antidepressant Efficacy in bipolar depression

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Areas served by NOVA Health Recovery:

Maryland (MD):
Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902

Washington DC:
Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016

Northern Virginia:
McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304 Fairfax – 20191 – Reston – 22009 – Springfield – 22152 22015 Lorton 22199
Fairfax, Va
2303 – 22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312
22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 – 20124
22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043
22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101
22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153
22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 – 22182
Woodbridge – 22191 – 22192 -22193 -22194 – 22195
Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161
Front Royal 22630
Warren County 22610 22630 22642 22649
Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412
Zip Code City County Zip Code Map 20101 Dulles Loudoun – 20102 Dulles Loudoun – 20103 Dulles Loudoun – 20104 Dulles Loudoun – 20105 Aldie Loudoun – 20106 Amissville Culpeper – 20107 Arcola Loudoun – 20108 Manassas Manassas City – 20109 Manassas Prince William – 20110 Manassas Manassas City – 20111 Manassas Prince William – 20112 Manassas Prince William – 20113 Manassas Manassas Park City – 20115 Marshall Fauquier – 20116 Marshall Fauquier – 20117 Middleburg Loudoun – 20118 Middleburg Loudoun – 20119 Catlett Fauquier View
Map 20120 Centreville Fairfax – 20121 Centreville Fairfax – 20122 Centreville Fairfax – 20124 Clifton Fairfax – 20128 Orlean Fauquier – 20129 Paeonian Springs Loudoun – 20130 Paris Clarke – 20131 Philomont Loudoun – 20132 Purcellville Loudoun – 20134 Purcellville Loudoun – 20135 Bluemont Clarke – 20136 Bristow Prince William – 20137 Broad Run Fauquier – 20138 Calverton Fauquier – 20139 Casanova Fauquier – 20140 Rectortown Fauquier – 20141 Round Hill Loudoun – 20142 Round Hill Loudoun – 20143 Catharpin Prince William View
Map 20144 Delaplane Fauquier – 20146 Ashburn Loudoun – 20147 Ashburn Loudoun – 20148 Ashburn Loudoun – 20149 Ashburn Loudoun – 20151 Chantilly Fairfax – 20152 Chantilly Loudoun – 20153 Chantilly Fairfax – 20155 Gainesville Prince William – 20156 Gainesville Prince William – 20158 Hamilton Loudoun – 20159 Hamilton Loudoun – 20160 Lincoln Loudoun – 20163 Sterling Loudoun – 20164 Sterling Loudoun – 20165 Sterling Loudoun – 20166 Sterling Loudoun – 20167 Sterling Loudoun – 20168 Haymarket Prince William View
Map 20169 Haymarket Prince William – 20170 Herndon Fairfax – 20171 Herndon Fairfax – 20172 Herndon Fairfax – 20175 Leesburg Loudoun – 20176 Leesburg Loudoun – 20177 Leesburg Loudoun – 20178 Leesburg Loudoun – 20180 Lovettsville Loudoun – 20181 Nokesville Prince William – 20182 Nokesville Prince William – 20184 Upperville Fauquier – 20185 Upperville Fauquier – 20186 Warrenton Fauquier – 20187 Warrenton Fauquier – 20188 Warrenton Fauquier – 20189 Dulles Loudoun – 20190 Reston Fairfax – 20191 Reston Fairfax View
Map 20192 Herndon Fairfax – 20193 Reston Fairfax – 20194 Reston Fairfax – 20195 Reston Fairfax – 20196 Reston Fairfax – 20197 Waterford Loudoun – 20198 The Plains Fauquier – 20199 Dulles Loudoun – 22003 Annandale Fairfax – 22009 Burke Fairfax – 22015 Burke Fairfax – 22025 Dumfries Prince William – 22026 Dumfries Prince William – 22027 Dunn Loring Fairfax – 22030 Fairfax Fairfax City – 22031 Fairfax Fairfax – 22032 Fairfax Fairfax – 22033 Fairfax Fairfax – 22034 Fairfax Fairfax View
Map 22035 Fairfax Fairfax – 22036 Fairfax Fairfax – 22037 Fairfax Fairfax – 22038 Fairfax Fairfax City – 22039 Fairfax Station Fairfax – 22040 Falls Church Falls Church City – 22041 Falls Church Fairfax – 22042 Falls Church Fairfax – 22043 Falls Church Fairfax – 22044 Falls Church Fairfax – 22046 Falls Church Falls Church City – 22047 Falls Church Fairfax – 22060 Fort Belvoir Fairfax – 22066 Great Falls Fairfax – 22067 Greenway Fairfax – 22079 Lorton Fairfax – 22081 Merrifield Fairfax – 22082 Merrifield Fairfax – 22092 Herndon Fairfax View
Map 22093 Ashburn Loudoun – 22095 Herndon Fairfax – 22096 Reston Fairfax – 22101 Mc Lean Fairfax – 22102 Mc Lean Fairfax – 22103 West Mclean Fairfax – 22106 Mc Lean Fairfax – 22107 Mc Lean Fairfax – 22108 Mc Lean Fairfax – 22109 Mc Lean Fairfax – 22116 Merrifield Fairfax – 22118 Merrifield Fairfax – 22119 Merrifield Fairfax – 22120 Merrifield Fairfax – 22121 Mount Vernon Fairfax – 22122 Newington Fairfax – 22124 Oakton Fairfax – 22125 Occoquan Prince William – 22134 Quantico Prince William View
Map 22135 Quantico Stafford – 22150 Springfield Fairfax – 22151 Springfield Fairfax – 22152 Springfield Fairfax – 22153 Springfield Fairfax – 22156 Springfield Fairfax – 22158 Springfield Fairfax – 22159 Springfield Fairfax – 22160 Springfield Fairfax – 22161 Springfield Fairfax – 22172 Triangle Prince William – 22180 Vienna Fairfax – 22181 Vienna Fairfax – 22182 Vienna Fairfax – 22183 Vienna Fairfax – 22184 Vienna Fairfax – 22185 Vienna Fairfax – 22191 Woodbridge Prince William – 22192 Woodbridge Prince William View
Map 22193 Woodbridge Prince William – 22194 Woodbridge Prince William – 22195 Woodbridge Prince William – 22199 Lorton Fairfax – 22201 Arlington Arlington – 22202 Arlington Arlington – 22203 Arlington Arlington – 22204 Arlington Arlington – 22205 Arlington Arlington – 22206 Arlington Arlington – 22207 Arlington Arlington – 22209 Arlington Arlington – 22210 Arlington Arlington – 22211 Ft Myer Arlington – 22212 Arlington Arlington – 22213 Arlington Arlington – 22214 Arlington Arlington – 22215 Arlington Arlington – 22216 Arlington Arlington View
Map 22217 Arlington Arlington – 22218 Arlington Arlington – 22219 Arlington Arlington – 22222 Arlington Arlington – 22223 Arlington Arlington – 22225 Arlington Arlington – 22226 Arlington Arlington – 22227 Arlington Arlington – 22229 Arlington Arlington – 22230 Arlington Arlington – 22234 Arlington Arlington – 22240 Arlington Arlington – 22241 Arlington Arlington – 22242 Arlington Arlington – 22243 Arlington Arlington – 22244 Arlington Arlington – 22245 Arlington Arlington – 22246 Arlington Arlington – 22301 Alexandria Alexandria City View
Map 22302 Alexandria Alexandria City – 22303 Alexandria Fairfax – 22304 Alexandria Alexandria City – 22305 Alexandria Alexandria City – 22306 Alexandria Fairfax – 22307 Alexandria Fairfax – 22308 Alexandria Fairfax – 22309 Alexandria Fairfax – 22310 Alexandria Fairfax – 22311 Alexandria Alexandria City – 22312 Alexandria Fairfax – 22313 Alexandria Alexandria City – 22314 Alexandria Alexandria City – 22315 Alexandria Fairfax – 22320 Alexandria Alexandria City – 22321 Alexandria Fairfax – 22331 Alexandria Alexandria City – 22332 Alexandria Alexandria City – 22333 Alexandria Alexandria City View
Map 22334 Alexandria Alexandria City – 22336 Alexandria Alexandria City – 22401 Fredericksburg Fredericksburg City – 22402 Fredericksburg Fredericksburg City – 22403 Fredericksburg Stafford – 22404 Fredericksburg Fredericksburg City – 22405 Fredericksburg Stafford – 22406 Fredericksburg Stafford – 22407 Fredericksburg Spotsylvania – 22408 Fredericksburg Spotsylvania – 22412 Fredericksburg Stafford – 22427 Bowling Green Caroline – 22428 Bowling Green Caroline – 22430 Brooke Stafford – 22432 Burgess Northumberland – 22433 Burr Hill Orange – 22435 Callao Northumberland – 22436 Caret Essex – 22437 Center Cross Essex View
Map 22438 Champlain Essex – 22442 Coles Point Westmoreland – 22443 Colonial Beach Westmoreland – 22446 Corbin Caroline – 22448 Dahlgren King George – 22451 Dogue King George – 22454 Dunnsville Essex – 22456 Edwardsville Northumberland – 22460 Farnham Richmond – 22463 Garrisonville Stafford – 22469 Hague Westmoreland – 22471 Hartwood Stafford – 22472 Haynesville Richmond – 22473 Heathsville Northumberland – 22476 Hustle Essex – 22480 Irvington Lancaster – 22481 Jersey King George – 22482 Kilmarnock Lancaster – 22485 King George King George View
Map 22488 Kinsale Westmoreland – 22501 Ladysmith Caroline – 22503 Lancaster Lancaster – 22504 Laneview Essex – 22507 Lively Lancaster – 22508 Locust Grove Orange – 22509 Loretto Essex – 22511 Lottsburg Northumberland – 22513 Merry Point Lancaster – 22514 Milford Caroline – 22517 Mollusk Lancaster – 22520 Montross Westmoreland – 22523 Morattico Lancaster – 22524 Mount Holly Westmoreland – 22526 Ninde King George – 22528 Nuttsville Lancaster – 22529 Oldhams Westmoreland – 22530 Ophelia Northumberland – 22534 Partlow Spotsylvania View
Map 22535 Port Royal Caroline – 22538 Rappahannock Academy Caroline – 22539 Reedville Northumberland – 22542 Rhoadesville Orange – 22544 Rollins Fork King George – 22545 Ruby Stafford – 22546 Ruther Glen Caroline – 22547 Sealston King George – 22548 Sharps Richmond – 22552 Sparta Caroline – 22553 Spotsylvania Spotsylvania – 22554 Stafford Stafford – 22555 Stafford Stafford – 22556 Stafford Stafford – 22558 Stratford Westmoreland – 22560 Tappahannock Essex – 22565 Thornburg Spotsylvania – 22567 Unionville Orange – 22570 Village Richmond View
Map 22572 Warsaw Richmond – 22576 Weems Lancaster – 22577 Sandy Point Westmoreland – 22578 White Stone Lancaster – 22579 Wicomico Church Northumberland – 22580 Woodford Caroline – 22581 Zacata Westmoreland – 22601 Winchester Winchester City – 22602 Winchester Frederick – 22603 Winchester Frederick – 22604 Winchester Winchester City – 22610 Bentonville Warren – 22611 Berryville Clarke – 22620 Boyce Clarke – 22622 Brucetown Frederick – 22623 Chester Gap Rappahannock – 22624 Clear Brook Frederick – 22625 Cross Junction Frederick – 22626 Fishers Hill Shenandoah View
Map 22627 Flint Hill Rappahannock – 22630 Front Royal Warren – 22637 Gore Frederick – 22638 Winchester Frederick – 22639 Hume Fauquier – 22640 Huntly Rappahannock – 22641 Strasburg Shenandoah – 22642 Linden Warren – 22643 Markham Fauquier – 22644 Maurertown Shenandoah – 22645 Middletown Frederick – 22646 Millwood Clarke – 22649 Middletown Warren – 22650 Rileyville Page – 22652 Fort Valley Shenandoah – 22654 Star Tannery Frederick – 22655 Stephens City Frederick – 22656 Stephenson Frederick – 22657 Strasburg Shenandoah View
Map 22660 Toms Brook Shenandoah – 22663 White Post Clarke – 22664 Woodstock Shenandoah – 22701 Culpeper Culpeper – 22709 Aroda Madison – 22711 Banco Madison – 22712 Bealeton Fauquier – 22713 Boston Culpeper – 22714 Brandy Station Culpeper – 22715 Brightwood Madison – 22716 Castleton Rappahannock – 22718 Elkwood Culpeper – 22719 Etlan Madison – 22720 Goldvein Fauquier – 22721 Graves Mill Madison – 22722 Haywood Madison – 22723 Hood Madison – 22724 Jeffersonton Culpeper – 22725 Leon Madison View
Map 22726 Lignum Culpeper – 22727 Madison Madison – 22728 Midland Fauquier – 22729 Mitchells Culpeper – 22730 Oakpark Madison – 22731 Pratts Madison – 22732 Radiant Madison – 22733 Rapidan Culpeper – 22734 Remington Fauquier – 22735 Reva Madison – 22736 Richardsville Culpeper – 22737 Rixeyville Culpeper – 22738 Rochelle Madison – 22739 Somerville Fauquier – 22740 Sperryville Rappahannock – 22741 Stevensburg Culpeper – 22742 Sumerduck Fauquier – 22743 Syria Madison – 22746 Viewtown Culpeper View
Map 22747 Washington Rappahannock – 22748 Wolftown Madison – 22749 Woodville Rappahannock – 22801 Harrisonburg Harrisonburg City – 22802 Harrisonburg Harrisonburg City – 22803 Harrisonburg Harrisonburg City – 22807 Harrisonburg Harrisonburg City – 22810 Basye Shenandoah – 22811 Bergton Rockingham – 22812 Bridgewater Rockingham – 22815 Broadway Rockingham – 22820 Criders Rockingham – 22821 Dayton Rockingham – 22824 Edinburg Shenandoah – 22827 Elkton Rockingham – 22830 Fulks Run Rockingham – 22831 Hinton Rockingham – 22832 Keezletown Rockingham – 22833 Lacey Spring Rockingham View
Map 22834 Linville Rockingham – 22835 Luray Page – 22840 Mc Gaheysville Rockingham – 22841 Mount Crawford Rockingham – 22842 Mount Jackson Shenandoah – 22843 Mount Solon Augusta – 22844 New Market Shenandoah – 22845 Orkney Springs Shenandoah – 22846 Penn Laird Rockingham – 22847 Quicksburg Shenandoah – 22848 Pleasant Valley Rockingham – 22849 Shenandoah Page – 22850 Singers Glen Rockingham – 22851 Stanley Page – 22853 Timberville Rockingham – 22901 Charlottesville Albemarle – 22902 Charlottesville Charlottesville City – 22903 Charlottesville Charlottesville City – 22904 Charlottesville Charlottesville City View
Map 22905 Charlottesville Charlottesville City – 22906 Charlottesville Charlottesville City – 22907 Charlottesville Charlottesville City – 22908 Charlottesville Charlottesville City – 22909 Charlottesville Albemarle – 22910 Charlottesville Charlottesville City – 22911 Charlottesville Albemarle – 22920 Afton Nelson – 22922 Arrington Nelson – 22923 Barboursville Orange – 22924 Batesville Albemarle – 22931 Covesville Albemarle – 22932 Crozet Albemarle – 22935 Dyke Greene – 22936 Earlysville Albemarle – 22937 Esmont Albemarle – 22938 Faber Nelson – 22939 Fishersville Augusta – 22940 Free Union Albemarle View
Map 22942 Gordonsville Orange – 22943 Greenwood Albemarle – 22945 Ivy Albemarle – 22946 Keene Albemarle – 22947 Keswick Albemarle – 22948 Locust Dale Madison – 22949 Lovingston Nelson – 22952 Lyndhurst Augusta – 22957 Montpelier Station Orange – 22958 Nellysford Nelson – 22959 North Garden Albemarle – 22960 Orange Orange – 22963 Palmyra Fluvanna – 22964 Piney River Nelson – 22965 Quinque Greene – 22967 Roseland Nelson – 22968 Ruckersville Greene – 22969 Schuyler Nelson – 22971 Shipman Nelson View
Map 22972 Somerset Orange – 22973 Stanardsville Greene – 22974 Troy Fluvanna – 22976 Tyro Nelson – 22980 Waynesboro Waynesboro City – 22987 White Hall Albemarle – 22989 Woodberry Forest Madison – 23001 Achilles Gloucester – 23002 Amelia Court House Amelia – 23003 Ark Gloucester – 23004 Arvonia Buckingham – 23005 Ashland Hanover – 23009 Aylett King William – 23011 Barhamsville New Kent – 23014 Beaumont Goochland – 23015 Beaverdam Hanover – 23018 Bena Gloucester – 23021 Bohannon Mathews – 23022 Bremo Bluff Fluvanna View
Map 23023 Bruington King And Queen – 23024 Bumpass Louisa – 23025 Cardinal Mathews – 23027 Cartersville Cumberland – 23030 Charles City Charles City – 23031 Christchurch Middlesex – 23032 Church View Middlesex – 23035 Cobbs Creek Mathews – 23038 Columbia Goochland – 23039 Crozier Goochland – 23040 Cumberland Cumberland – 23043 Deltaville Middlesex – 23045 Diggs Mathews – 23047 Doswell Hanover – 23050 Dutton Gloucester – 23055 Fork Union Fluvanna – 23056 Foster Mathews – 23058 Glen Allen Henrico – 23059 Glen Allen Henrico View
Map 23060 Glen Allen Henrico – 23061 Gloucester Gloucester – 23062 Gloucester Point Gloucester – 23063 Goochland Goochland – 23064 Grimstead Mathews – 23065 Gum Spring Goochland – 23066 Gwynn Mathews – 23067 Hadensville Goochland – 23068 Hallieford Mathews – 23069 Hanover Hanover – 23070 Hardyville Middlesex – 23071 Hartfield Middlesex – 23072 Hayes Gloucester – 23075 Highland Springs Henrico – 23076 Hudgins Mathews – 23079 Jamaica Middlesex – 23081 Jamestown James City – 23083 Jetersville Amelia – 23084 Kents Store Fluvanna View
Map 23085 King And Queen Court House King And Queen – 23086 King William King William – 23089 Lanexa New Kent – 23090 Lightfoot York – 23091 Little Plymouth King And Queen – 23092 Locust Hill Middlesex – 23093 Louisa Louisa – 23101 Macon Powhatan – 23102 Maidens Goochland – 23103 Manakin Sabot Goochland – 23105 Mannboro Amelia – 23106 Manquin King William – 23107 Maryus Gloucester – 23108 Mascot King And Queen – 23109 Mathews Mathews – 23110 Mattaponi King And Queen – 23111 Mechanicsville Hanover – 23112 Midlothian Chesterfield – 23113 Midlothian Chesterfield View
Map 23114 Midlothian Chesterfield – 23115 Millers Tavern Essex – 23116 Mechanicsville Hanover – 23117 Mineral Louisa – 23119 Moon Mathews – 23120 Moseley Chesterfield – 23123 New Canton Buckingham – 23124 New Kent New Kent – 23125 New Point Mathews – 23126 Newtown King And Queen – 23127 Norge James City – 23128 North Mathews – 23129 Oilville Goochland – 23130 Onemo Mathews – 23131 Ordinary Gloucester – 23138 Port Haywood Mathews – 23139 Powhatan Powhatan – 23140 Providence Forge New Kent – 23141 Quinton New Kent View
Map 23146 Rockville Hanover – 23147 Ruthville Charles City – 23148 Saint Stephens Church King And Queen – 23149 Saluda Middlesex – 23150 Sandston Henrico – 23153 Sandy Hook Goochland – 23154 Schley Gloucester – 23155 Severn Gloucester – 23156 Shacklefords King And Queen – 23160 State Farm Goochland – 23161 Stevensville King And Queen – 23162 Studley Hanover – 23163 Susan Mathews – 23168 Toano James City – 23169 Topping Middlesex – 23170 Trevilians Louisa – 23173 University Of Richmond Richmond City – 23175 Urbanna Middlesex – 23176 Wake Middlesex View
Map 23177 Walkerton King And Queen – 23178 Ware Neck Gloucester – 23180 Water View Middlesex – 23181 West Point King William – 23183 White Marsh Gloucester – 23184 Wicomico Gloucester – 23185 Williamsburg James City – 23186 Williamsburg Williamsburg City – 23187 Williamsburg Williamsburg City – 23188 Williamsburg James City – 23190 Woods Cross Roads Gloucester – 23192 Montpelier Hanover – 23218 Richmond Richmond City – 23219 Richmond Richmond City – 23220 Richmond Richmond City – 23221 Richmond Richmond City – 23222 Richmond Richmond City – 23223 Richmond Richmond City – 23224 Richmond Richmond City View
Map 23225 Richmond Richmond City – 23226 Richmond Henrico – 23227 Richmond Henrico – 23228 Richmond Henrico – 23229 Richmond Henrico – 23230 Richmond Henrico – 23231 Richmond Henrico – 23232 Richmond Richmond City – 23233 Richmond Henrico – 23234 Richmond Chesterfield – 23235 Richmond Chesterfield – 23236 Richmond Chesterfield – 23237 Richmond Chesterfield – 23238 Richmond Henrico – 23240 Richmond Richmond City – 23241 Richmond Richmond City – 23242 Richmond Henrico – 23249 Richmond Richmond City – 23250 Richmond Henrico View
Map 23255 Richmond Henrico – 23260 Richmond Richmond City – 23261 Richmond Richmond City – 23269 Richmond Richmond City – 23273 Richmond Richmond City – 23274 Richmond Richmond City – 23276 Richmond Richmond City – 23278 Richmond Richmond City – 23279 Richmond Richmond City – 23282 Richmond Richmond City – 23284 Richmond Richmond City – 23285 Richmond Richmond City – 23286 Richmond Richmond City – 23288 Richmond Henrico – 23289 Richmond Richmond City – 23290 Richmond Richmond City – 23291 Richmond Richmond City – 23292 Richmond Richmond City – 23293 Richmond Richmond City View
Map 23294 Richmond Henrico – 23295 Richmond Richmond City – 23297 Richmond Chesterfield – 23298 Richmond Richmond City – 23301 Accomac Accomack – 23302 Assawoman Accomack – 23303 Atlantic Accomack – 23304 Battery Park Isle Of Wight – 23306 Belle Haven Accomack – 23307 Birdsnest Northampton – 23308 Bloxom Accomack – 23310 Cape Charles Northampton – 23313 Capeville Northampton – 23314 Carrollton Isle Of Wight – 23315 Carrsville Isle Of Wight – 23316 Cheriton Northampton – 23320 Chesapeake Chesapeake City – 23321 Chesapeake Chesapeake City – 23322 Chesapeake Chesapeake City View
Map 23323 Chesapeake Chesapeake City – 23324 Chesapeake Chesapeake City – 23325 Chesapeake Chesapeake City – 23326 Chesapeake Chesapeake City – 23327 Chesapeake Chesapeake City – 23328 Chesapeake Chesapeake City – 23336 Chincoteague Island Accomack – 23337 Wallops Island Accomack – 23341 Craddockville Accomack – 23345 Davis Wharf Accomack – 23347 Eastville Northampton – 23350 Exmore Northampton – 23354 Franktown Northampton – 23356 Greenbackville Accomack – 23357 Greenbush Accomack – 23358 Hacksneck Accomack – 23359 Hallwood Accomack – 23389 Harborton Accomack – 23395 Horntown Accomack View
Map 23396 Oak Hall Accomack – 23397 Isle Of Wight Isle Of Wight – 23398 Jamesville Northampton – 23399 Jenkins Bridge Accomack – 23401 Keller Accomack – 23404 Locustville Accomack – 23405 Machipongo Northampton – 23407 Mappsville Accomack – 23408 Marionville Northampton – 23409 Mears Accomack – 23410 Melfa Accomack – 23412 Modest Town Accomack – 23413 Nassawadox Northampton – 23414 Nelsonia Accomack – 23415 New Church Accomack – 23416 Oak Hall Accomack – 23417 Onancock Accomack – 23418 Onley Accomack – 23419 Oyster Northampton View
Map 23420 Painter Accomack – 23421 Parksley Accomack – 23422 Pungoteague Accomack – 23423 Quinby Accomack – 23424 Rescue Isle Of Wight – 23426 Sanford Accomack – 23427 Saxis Accomack – 23429 Seaview Northampton – 23430 Smithfield Isle Of Wight – 23431 Smithfield Isle Of Wight – 23432 Suffolk Suffolk City – 23433 Suffolk Suffolk City – 23434 Suffolk Suffolk City – 23435 Suffolk Suffolk City – 23436 Suffolk Suffolk City – 23437 Suffolk Suffolk City – 23438 Suffolk Suffolk City – 23439 Suffolk Suffolk City – 23440 Tangier Accomack View
Map 23441 Tasley Accomack – 23442 Temperanceville Accomack – 23443 Townsend Northampton – 23450 Virginia Beach Virginia Beach City – 23451 Virginia Beach Virginia Beach City – 23452 Virginia Beach Virginia Beach City – 23453 Virginia Beach Virginia Beach City – 23454 Virginia Beach Virginia Beach City – 23455 Virginia Beach Virginia Beach City – 23456 Virginia Beach Virginia Beach City – 23457 Virginia Beach Virginia Beach City – 23458 Virginia Beach Virginia Beach City – 23459 Virginia Beach Virginia Beach City – 23460 Virginia Beach Virginia Beach City – 23461 Virginia Beach Virginia Beach City – 23462 Virginia Beach Virginia Beach City – 23463 Virginia Beach Virginia Beach City – 23464 Virginia Beach Virginia Beach City – 23465 Virginia Beach Virginia Beach City View
Map 23466 Virginia Beach Virginia Beach City – 23467 Virginia Beach Virginia Beach City – 23471 Virginia Beach Virginia Beach City – 23479 Virginia Beach Virginia Beach City – 23480 Wachapreague Accomack – 23482 Wardtown Northampton – 23483 Wattsville Accomack – 23486 Willis Wharf Northampton – 23487 Windsor Isle Of Wight – 23488 Withams Accomack – 23501 Norfolk Norfolk City – 23502 Norfolk Norfolk City – 23503 Norfolk Norfolk City – 23504 Norfolk Norfolk City – 23505 Norfolk Norfolk City – 23506 Norfolk Norfolk City – 23507 Norfolk Norfolk City – 23508 Norfolk Norfolk City – 23509 Norfolk Norfolk City View
Map 23510 Norfolk Norfolk City – 23511 Norfolk Norfolk City – 23512 Norfolk Norfolk City – 23513 Norfolk Norfolk City – 23514 Norfolk Norfolk City – 23515 Norfolk Norfolk City – 23517 Norfolk Norfolk City – 23518 Norfolk Norfolk City – 23519 Norfolk Norfolk City – 23520 Norfolk Norfolk City – 23521 Norfolk Norfolk City – 23523 Norfolk Norfolk City – 23529 Norfolk Norfolk City – 23541 Norfolk Norfolk City – 23551 Norfolk Norfolk City – 23601 Newport News Newport News City – 23602 Newport News Newport News City – 23603 Newport News Newport News City – 23604 Fort Eustis Newport News City View
Map 23605 Newport News Newport News City – 23606 Newport News Newport News City – 23607 Newport News Newport News City – 23608 Newport News Newport News City – 23609 Newport News Newport News City – 23612 Newport News Newport News City – 23628 Newport News Newport News City – 23630 Hampton Hampton City – 23651 Fort Monroe Hampton City – 23661 Hampton Hampton City – 23662 Poquoson Poquoson City – 23663 Hampton Hampton City – 23664 Hampton Hampton City – 23665 Hampton York – 23666 Hampton Hampton City – 23667 Hampton Hampton City – 23668 Hampton Hampton City – 23669 Hampton Hampton City – 23670 Hampton Hampton City View
Map 23681 Hampton Hampton City – 23690 Yorktown York – 23691 Yorktown York – 23692 Yorktown York – 23693 Yorktown York – 23694 Lackey York – 23696 Seaford York – 23701 Portsmouth Portsmouth City – 23702 Portsmouth Portsmouth City – 23703 Portsmouth Portsmouth City – 23704 Portsmouth Portsmouth City – 23705 Portsmouth Portsmouth City – 23707 Portsmouth Portsmouth City – 23708 Portsmouth Portsmouth City – 23709 Portsmouth Portsmouth City – 23801 Fort Lee Prince George – 23803 Petersburg Petersburg City – 23804 Petersburg Petersburg City – 23805 Petersburg Petersburg City View
Map 23806 Petersburg Petersburg City – 23821 Alberta Brunswick – 23822 Ammon Dinwiddie – 23824 Blackstone Nottoway – 23825 Blackstone Nottoway – 23827 Boykins Southampton – 23828 Branchville Southampton – 23829 Capron Southampton – 23830 Carson Dinwiddie – 23831 Chester Chesterfield – 23832 Chesterfield Chesterfield – 23833 Church Road Dinwiddie – 23834 Colonial Heights Colonial Heights City – 23836 Chester Chesterfield – 23837 Courtland Southampton – 23838 Chesterfield Chesterfield – 23839 Dendron Surry – 23840 Dewitt Dinwiddie – 23841 Dinwiddie Dinwiddie View
Map 23842 Disputanta Prince George – 23843 Dolphin Brunswick – 23844 Drewryville Southampton – 23845 Ebony Brunswick – 23846 Elberon Surry – 23847 Emporia Greensville – 23850 Ford Dinwiddie – 23851 Franklin Franklin City – 23856 Freeman Brunswick – 23857 Gasburg Brunswick – 23860 Hopewell Hopewell City – 23866 Ivor Southampton – 23867 Jarratt Greensville – 23868 Lawrenceville Brunswick – 23870 Jarratt Greensville – 23872 Mc Kenney Dinwiddie – 23873 Meredithville Brunswick – 23874 Newsoms Southampton – 23875 Prince George Prince George View
Map 23876 Rawlings Brunswick – 23878 Sedley Southampton – 23879 Skippers Greensville – 23881 Spring Grove Surry – 23882 Stony Creek Sussex – 23883 Surry Surry – 23884 Sussex Sussex – 23885 Sutherland Dinwiddie – 23887 Valentines Brunswick – 23888 Wakefield Sussex – 23889 Warfield Brunswick – 23890 Waverly Sussex – 23891 Waverly Sussex – 23893 White Plains Brunswick – 23894 Wilsons Dinwiddie – 23897 Yale Sussex – 23898 Zuni Isle Of Wight – 23899 Claremont Surry – 23901 Farmville Prince Edward View
Map 23909 Farmville Prince Edward – 23915 Baskerville Mecklenburg – 23917 Boydton Mecklenburg – 23919 Bracey Mecklenburg – 23920 Brodnax Brunswick – 23921 Buckingham Buckingham – 23922 Burkeville Nottoway – 23923 Charlotte Court House Charlotte – 23924 Chase City Mecklenburg – 23927 Clarksville Mecklenburg – 23930 Crewe Nottoway – 23934 Cullen Charlotte – 23936 Dillwyn Buckingham – 23937 Drakes Branch Charlotte – 23938 Dundas Lunenburg – 23939 Evergreen Appomattox – 23941 Fort Mitchell Lunenburg – 23942 Green Bay Prince Edward – 23943 Hampden Sydney Prince Edward View
Map 23944 Kenbridge Lunenburg – 23947 Keysville Charlotte – 23950 La Crosse Mecklenburg – 23952 Lunenburg Lunenburg – 23954 Meherrin Prince Edward – 23955 Nottoway Nottoway – 23958 Pamplin Appomattox – 23959 Phenix Charlotte – 23960 Prospect Prince Edward – 23962 Randolph Charlotte – 23963 Red House Charlotte – 23964 Red Oak Charlotte – 23966 Rice Prince Edward – 23967 Saxe Charlotte – 23968 Skipwith Mecklenburg – 23970 South Hill Mecklenburg – 23974 Victoria Lunenburg – 23976 Wylliesburg Charlotte – 24001 Roanoke Roanoke City View
Map 24002 Roanoke Roanoke City – 24003 Roanoke Roanoke City – 24004 Roanoke Roanoke City – 24005 Roanoke Roanoke City – 24006 Roanoke Roanoke City – 24007 Roanoke Roanoke City – 24008 Roanoke Roanoke City – 24009 Roanoke Roanoke City – 24010 Roanoke Roanoke City – 24011 Roanoke Roanoke City – 24012 Roanoke Roanoke City – 24013 Roanoke Roanoke City – 24014 Roanoke Roanoke City – 24015 Roanoke Roanoke City – 24016 Roanoke Roanoke City – 24017 Roanoke Roanoke City – 24018 Roanoke Roanoke – 24019 Roanoke Roanoke – 24020 Roanoke Roanoke View
Map 24022 Roanoke Roanoke City – 24023 Roanoke Roanoke City – 24024 Roanoke Roanoke City – 24025 Roanoke Roanoke City – 24026 Roanoke Roanoke City – 24027 Roanoke Roanoke City – 24028 Roanoke Roanoke City – 24029 Roanoke Roanoke City – 24030 Roanoke Roanoke City – 24031 Roanoke Roanoke City – 24032 Roanoke Roanoke City – 24033 Roanoke Roanoke City – 24034 Roanoke Roanoke City – 24035 Roanoke Roanoke City – 24036 Roanoke Roanoke City – 24037 Roanoke Roanoke City – 24038 Roanoke Roanoke City – 24040 Roanoke Roanoke City – 24042 Roanoke Roanoke City View
Map 24043 Roanoke Roanoke City – 24044 Roanoke Roanoke City – 24045 Roanoke Roanoke City – 24048 Roanoke Roanoke City – 24050 Roanoke Botetourt – 24053 Ararat Patrick – 24054 Axton Henry – 24055 Bassett Henry – 24058 Belspring Pulaski – 24059 Bent Mountain Roanoke – 24060 Blacksburg Montgomery – 24061 Blacksburg Montgomery – 24062 Blacksburg Montgomery – 24063 Blacksburg Montgomery – 24064 Blue Ridge Botetourt – 24065 Boones Mill Franklin – 24066 Buchanan Botetourt – 24067 Callaway Franklin – 24068 Christiansburg Montgomery View
Map 24069 Cascade Pittsylvania – 24070 Catawba Roanoke – 24072 Check Floyd – 24073 Christiansburg Montgomery – 24076 Claudville Patrick – 24077 Cloverdale Botetourt – 24078 Collinsville Henry – 24079 Copper Hill Floyd – 24082 Critz Patrick – 24083 Daleville Botetourt – 24084 Dublin Pulaski – 24085 Eagle Rock Botetourt – 24086 Eggleston Giles – 24087 Elliston Montgomery – 24088 Ferrum Franklin – 24089 Fieldale Henry – 24090 Fincastle Botetourt – 24091 Floyd Floyd – 24092 Glade Hill Franklin View
Map 24093 Glen Lyn Giles – 24095 Goodview Bedford – 24101 Hardy Franklin – 24102 Henry Franklin – 24104 Huddleston Bedford – 24105 Indian Valley Floyd – 24111 Mc Coy Montgomery – 24112 Martinsville Martinsville City – 24113 Martinsville Martinsville City – 24114 Martinsville Martinsville City – 24115 Martinsville Martinsville City – 24120 Meadows Of Dan Patrick – 24121 Moneta Bedford – 24122 Montvale Bedford – 24124 Narrows Giles – 24126 Newbern Pulaski – 24127 New Castle Craig – 24128 Newport Giles – 24129 New River Pulaski View
Map 24130 Oriskany Botetourt – 24131 Paint Bank Craig – 24132 Parrott Pulaski – 24133 Patrick Springs Patrick – 24134 Pearisburg Giles – 24136 Pembroke Giles – 24137 Penhook Franklin – 24138 Pilot Montgomery – 24139 Pittsville Pittsylvania – 24141 Radford Radford – 24142 Radford Radford – 24143 Radford Radford – 24146 Redwood Franklin – 24147 Rich Creek Giles – 24148 Ridgeway Henry – 24149 Riner Montgomery – 24150 Ripplemead Giles – 24151 Rocky Mount Franklin – 24153 Salem Salem View
Map 24155 Roanoke Salem – 24157 Roanoke Salem – 24161 Sandy Level Pittsylvania – 24162 Shawsville Montgomery – 24165 Spencer Henry – 24167 Staffordsville Giles – 24168 Stanleytown Henry – 24171 Stuart Patrick – 24174 Thaxton Bedford – 24175 Troutville Botetourt – 24176 Union Hall Franklin – 24177 Vesta Patrick – 24178 Villamont Bedford – 24179 Vinton Roanoke – 24184 Wirtz Franklin – 24185 Woolwine Patrick – 24201 Bristol Bristol – 24202 Bristol Washington – 24203 Bristol Bristol View
Map 24209 Bristol Bristol – 24210 Abingdon Washington – 24211 Abingdon Washington – 24212 Abingdon Washington – 24215 Andover Wise – 24216 Appalachia Wise – 24217 Bee Dickenson – 24218 Ben Hur Lee – 24219 Big Stone Gap Wise – 24220 Birchleaf Dickenson – 24221 Blackwater Lee – 24224 Castlewood Russell – 24225 Cleveland Russell – 24226 Clinchco Dickenson – 24228 Clintwood Dickenson – 24230 Coeburn Wise – 24236 Damascus Washington – 24237 Dante Russell – 24239 Davenport Buchanan View
Map 24243 Dryden Lee – 24244 Duffield Scott – 24245 Dungannon Scott – 24246 East Stone Gap Wise – 24248 Ewing Lee – 24250 Fort Blackmore Scott – 24251 Gate City Scott – 24256 Haysi Dickenson – 24258 Hiltons Scott – 24260 Honaker Russell – 24263 Jonesville Lee – 24265 Keokee Lee – 24266 Lebanon Russell – 24269 Mc Clure Dickenson – 24270 Mendota Washington – 24271 Nickelsville Scott – 24272 Nora Dickenson – 24273 Norton Norton City – 24277 Pennington Gap Lee View
Map 24279 Pound Wise – 24280 Rosedale Russell – 24281 Rose Hill Lee – 24282 Saint Charles Lee – 24283 Saint Paul Wise – 24290 Weber City Scott – 24292 Whitetop Grayson – 24293 Wise Wise – 24301 Pulaski Pulaski – 24311 Atkins Smyth – 24312 Austinville Wythe – 24313 Barren Springs Wythe – 24314 Bastian Bland – 24315 Bland Bland – 24316 Broadford Tazewell – 24317 Cana Carroll – 24318 Ceres Bland – 24319 Chilhowie Smyth – 24322 Cripple Creek Wythe View
Map 24323 Crockett Wythe – 24324 Draper Pulaski – 24325 Dugspur Carroll – 24326 Elk Creek Grayson – 24327 Emory Washington – 24328 Fancy Gap Carroll – 24330 Fries Grayson – 24333 Galax Galax City – 24340 Glade Spring Washington – 24343 Hillsville Carroll – 24347 Hiwassee Pulaski – 24348 Independence Grayson – 24350 Ivanhoe Wythe – 24351 Lambsburg Carroll – 24352 Laurel Fork Carroll – 24354 Marion Smyth – 24360 Max Meadows Wythe – 24361 Meadowview Washington – 24363 Mouth Of Wilson Grayson View
Map 24366 Rocky Gap Bland – 24368 Rural Retreat Wythe – 24370 Saltville Smyth – 24374 Speedwell Wythe – 24375 Sugar Grove Smyth – 24377 Tannersville Tazewell – 24378 Troutdale Grayson – 24380 Willis Floyd – 24381 Woodlawn Carroll – 24382 Wytheville Wythe – 24401 Staunton Staunton City – 24402 Staunton Staunton City – 24411 Augusta Springs Augusta – 24412 Bacova Bath – 24413 Blue Grass Highland – 24415 Brownsburg Rockbridge – 24416 Buena Vista Buena Vista City – 24421 Churchville Augusta – 24422 Clifton Forge Alleghany View
Map 24426 Covington Covington City – 24430 Craigsville Augusta – 24431 Crimora Augusta – 24432 Deerfield Augusta – 24433 Doe Hill Highland – 24435 Fairfield Rockbridge – 24437 Fort Defiance Augusta – 24438 Glen Wilton Botetourt – 24439 Goshen Rockbridge – 24440 Greenville Augusta – 24441 Grottoes Rockingham – 24442 Head Waters Highland – 24445 Hot Springs Bath – 24448 Iron Gate Alleghany – 24450 Lexington Lexington City – 24457 Low Moor Alleghany – 24458 Mc Dowell Highland – 24459 Middlebrook Augusta – 24460 Millboro Bath View
Map 24463 Mint Spring Augusta – 24464 Montebello Nelson – 24465 Monterey Highland – 24467 Mount Sidney Augusta – 24468 Mustoe Highland – 24469 New Hope Augusta – 24471 Port Republic Rockingham – 24472 Raphine Rockbridge – 24473 Rockbridge Baths Rockbridge – 24474 Selma Alleghany – 24476 Steeles Tavern Augusta – 24477 Stuarts Draft Augusta – 24479 Swoope Augusta – 24482 Verona Augusta – 24483 Vesuvius Rockbridge – 24484 Warm Springs Bath – 24485 West Augusta Augusta – 24486 Weyers Cave Augusta – 24487 Williamsville Bath View
Map 24501 Lynchburg Lynchburg City – 24502 Lynchburg Lynchburg City – 24503 Lynchburg Lynchburg City – 24504 Lynchburg Lynchburg City – 24505 Lynchburg Lynchburg City – 24506 Lynchburg Lynchburg City – 24512 Lynchburg Lynchburg City – 24513 Lynchburg Lynchburg City – 24514 Lynchburg Lynchburg City – 24515 Lynchburg Lynchburg City – 24517 Altavista Campbell – 24520 Alton Halifax – 24521 Amherst Amherst – 24522 Appomattox Appomattox – 24523 Bedford Bedford – 24526 Big Island Bedford – 24527 Blairs Pittsylvania – 24528 Brookneal Campbell – 24529 Buffalo Junction Mecklenburg View
Map 24530 Callands Pittsylvania – 24531 Chatham Pittsylvania – 24533 Clifford Amherst – 24534 Clover Halifax – 24535 Cluster Springs Halifax – 24536 Coleman Falls Bedford – 24538 Concord Campbell – 24539 Crystal Hill Halifax – 24540 Danville Danville City – 24541 Danville Danville City – 24543 Danville Danville City – 24544 Danville Danville City – 24549 Dry Fork Pittsylvania – 24550 Evington Campbell – 24551 Forest Bedford – 24553 Gladstone Nelson – 24554 Gladys Campbell – 24555 Glasgow Rockbridge – 24556 Goode Bedford View
Map 24557 Gretna Pittsylvania – 24558 Halifax Halifax – 24562 Howardsville Buckingham – 24563 Hurt Pittsylvania – 24565 Java Pittsylvania – 24566 Keeling Pittsylvania – 24569 Long Island Pittsylvania – 24570 Lowry Bedford – 24571 Lynch Station Campbell – 24572 Madison Heights Amherst – 24574 Monroe Amherst – 24576 Naruna Campbell – 24577 Nathalie Halifax – 24578 Natural Bridge Rockbridge – 24579 Natural Bridge Station Rockbridge – 24580 Nelson Mecklenburg – 24581 Norwood Nelson – 24586 Ringgold Pittsylvania – 24588 Rustburg Campbell View
Map 24589 Scottsburg Halifax – 24590 Scottsville Albemarle – 24592 South Boston Halifax – 24593 Spout Spring Appomattox – 24594 Sutherlin Pittsylvania – 24595 Sweet Briar Amherst – 24597 Vernon Hill Halifax – 24598 Virgilina Halifax – 24599 Wingina Buckingham – 24601 Amonate Tazewell – 24602 Bandy Tazewell – 24603 Big Rock Buchanan – 24604 Bishop Tazewell – 24605 Bluefield Tazewell – 24606 Boissevain Tazewell – 24607 Breaks Dickenson – 24608 Burkes Garden Tazewell – 24609 Cedar Bluff Tazewell – 24612 Doran Tazewell View
Map 24613 Falls Mills Tazewell – 24614 Grundy Buchanan – 24619 Horsepen Tazewell – 24620 Hurley Buchanan – 24622 Jewell Ridge Tazewell – 24624 Keen Mountain Buchanan – 24627 Mavisdale Buchanan – 24628 Maxie Buchanan – 24630 North Tazewell Tazewell – 24631 Oakwood Buchanan – 24634 Pilgrims Knob Buchanan – 24635 Pocahontas Tazewell – 24637 Pounding Mill Tazewell – 24639 Raven Buchanan – 24640 Red Ash Tazewell – 24641 Richlands Tazewell – 24646 Rowe Buchanan – 24647 Shortt Gap Buchanan – 24649 Swords Creek Russell View
Map 24651 Tazewell Tazewell – 24656 Vansant Buchanan – 24657 Whitewood Buchanan – 24658 Wolford Buchanan – 24701 Bluefield Mercer – 24712 Athens Mercer – 24714 Beeson Mercer – 24715 Bramwell Mercer – 24716 Bud Wyoming – 24719 Covel Wyoming – 24724 Freeman Mercer – 24726 Herndon Wyoming – 24729 Hiawatha Mercer – 24731 Kegley Mercer – 24732 Kellysville Mercer – 24733 Lashmeet Mercer – 24736 Matoaka Mercer – 24737 Montcalm Mercer – 24738 Nemours Mercer View
Map 24739 Oakvale Mercer – 24740 Princeton Mercer – 24747 Rock Mercer – 24751 Wolfe Mercer – 24801 Welch Mcdowell – 24808 Anawalt Mcdowell – 24811 Avondale Mcdowell – 24813 Bartley Mcdowell – 24815 Berwind Mcdowell – 24816 Big Sandy Mcdowell – 24817 Bradshaw Mcdowell – 24818 Brenton Wyoming – 24822 Clear Fork Wyoming – 24823 Coal Mountain Wyoming – 24824 Coalwood Mcdowell – 24826 Cucumber Mcdowell – 24827 Cyclone Wyoming – 24828 Davy Mcdowell – 24829 Eckman Mcdowell View
Map 24830 Elbert Mcdowell – 24831 Elkhorn Mcdowell – 24834 Fanrock Wyoming – 24836 Gary Mcdowell – 24839 Hanover Wyoming – 24842 Hemphill Mcdowell – 24843 Hensley Mcdowell – 24844 Iaeger Mcdowell – 24845 Ikes Fork Wyoming – 24846 Isaban Mcdowell – 24847 Itmann Wyoming – 24848 Jenkinjones Mcdowell – 24849 Jesse Wyoming – 24850 Jolo Mcdowell – 24851 Justice Mingo – 24853 Kimball Mcdowell – 24854 Kopperston Wyoming – 24855 Kyle Mcdowell – 24857 Lynco Wyoming View
Map 24859 Marianna Wyoming – 24860 Matheny Wyoming – 24861 Maybeury Mcdowell – 24862 Mohawk Mcdowell – 24866 Newhall Mcdowell – 24867 New Richmond Wyoming – 24868 Northfork Mcdowell – 24869 North Spring Wyoming – 24870 Oceana Wyoming – 24871 Pageton Mcdowell – 24872 Panther Mcdowell – 24873 Paynesville Mcdowell – 24874 Pineville Wyoming – 24878 Premier Mcdowell – 24879 Raysal Mcdowell – 24880 Rock View Wyoming – 24881 Roderfield Mcdowell – 24882 Simon Wyoming – 24884 Squire Mcdowell View
Map 24887 Switchback Mcdowell – 24888 Thorpe Mcdowell – 24892 War Mcdowell – 24894 Warriormine Mcdowell – 24895 Wilcoe Mcdowell – 24898 Wyoming Wyoming – 24901 Lewisburg Greenbrier – 24902 Fairlea Greenbrier – 24910 Alderson Greenbrier – 24915 Arbovale Pocahontas – 24916 Asbury Greenbrier – 24918 Ballard Monroe – 24920 Bartow Pocahontas – 24924 Buckeye Pocahontas – 24925 Caldwell Greenbrier – 24927 Cass Pocahontas – 24931 Crawley Greenbrier – 24934 Dunmore Pocahontas – 24935 Forest Hill Summers View
Map 24938 Frankford Greenbrier – 24941 Gap Mills Monroe – 24943 Grassy Meadows Greenbrier – 24944 Green Bank Pocahontas – 24945 Greenville Monroe – 24946 Hillsboro Pocahontas – 24951 Lindside Monroe – 24954 Marlinton Pocahontas – 24957 Maxwelton Greenbrier – 24961 Neola Greenbrier – 24962 Pence Springs Summers – 24963 Peterstown Monroe – 24966 Renick Greenbrier – 24970 Ronceverte Greenbrier – 24974 Secondcreek Monroe – 24976 Sinks Grove Monroe – 24977 Smoot Greenbrier – 24981 Talcott Summers – 24983 Union Monroe View
Map 24984 Waiteville Monroe – 24985 Wayside Monroe – 24986 White Sulphur Springs Greenbrier – 24991 Williamsburg Greenbrier – 24993 Wolfcreek Monroe – 25002 Alloy Fayette – 25003 Alum Creek Kanawha – 25005 Amma Roane – 25007 Arnett Raleigh – 25008 Artie Raleigh – 25009 Ashford Boone – 25011 Bancroft Putnam – 25015 Belle Kanawha – 25019 Bickmore Clay – 25021 Bim Boone – 25022 Blair Logan – 25024 Bloomingrose Boone – 25025 Blount Kanawha – 25026 Blue Creek Kanawha View
Map 25028 Bob White Boone – 25030 Bomont Clay – 25031 Boomer Fayette – 25033 Buffalo Putnam – 25035 Cabin Creek Kanawha – 25036 Cannelton Fayette – 25039 Cedar Grove Kanawha – 25040 Charlton Heights Fayette – 25043 Clay Clay – 25044 Clear Creek Raleigh – 25045 Clendenin Kanawha – 25047 Clothier Logan – 25048 Colcord Raleigh – 25049 Comfort Boone – 25051 Costa Boone – 25053 Danville Boone – 25054 Dawes Kanawha – 25057 Deep Water Fayette – 25059 Dixie Nicholas View
Map 25060 Dorothy Raleigh – 25061 Drybranch Kanawha – 25062 Dry Creek Raleigh – 25063 Duck Clay – 25064 Dunbar Kanawha – 25067 East Bank Kanawha – 25070 Eleanor Putnam – 25071 Elkview Kanawha – 25075 Eskdale Kanawha – 25076 Ethel Logan – 25079 Falling Rock Kanawha – 25081 Foster Boone – 25082 Fraziers Bottom Putnam – 25083 Gallagher Kanawha – 25085 Gauley Bridge Fayette – 25086 Glasgow Kanawha – 25088 Glen Clay – 25090 Glen Ferris Fayette – 25093 Gordon Boone View
Map 25102 Handley Kanawha – 25103 Hansford Kanawha – 25106 Henderson Mason – 25107 Hernshaw Kanawha – 25108 Hewett Boone – 25109 Hometown Putnam – 25110 Hugheston Kanawha – 25111 Indore Clay – 25112 Institute Kanawha – 25113 Ivydale Clay – 25114 Jeffrey Boone – 25115 Kanawha Falls Fayette – 25118 Kimberly Fayette – 25119 Kincaid Fayette – 25121 Lake Logan – 25123 Leon Mason – 25124 Liberty Putnam – 25125 Lizemores Clay – 25126 London Kanawha View
Map 25130 Madison Boone – 25132 Mammoth Kanawha – 25133 Maysel Clay – 25134 Miami Kanawha – 25136 Montgomery Fayette – 25139 Mount Carbon Fayette – 25140 Naoma Raleigh – 25141 Nebo Clay – 25142 Nellis Boone – 25143 Nitro Kanawha – 25148 Orgas Boone – 25149 Ottawa Boone – 25152 Page Fayette – 25154 Peytona Boone – 25156 Pinch Kanawha – 25159 Poca Putnam – 25160 Pond Gap Kanawha – 25161 Powellton Fayette – 25162 Pratt Kanawha View
Map 25164 Procious Clay – 25165 Racine Boone – 25168 Red House Putnam – 25169 Ridgeview Boone – 25173 Robson Fayette – 25174 Rock Creek Raleigh – 25177 Saint Albans Kanawha – 25180 Saxon Boone – 25181 Seth Boone – 25183 Sharples Logan – 25185 Mount Olive Fayette – 25186 Smithers Fayette – 25187 Southside Mason – 25193 Sylvester Boone – 25201 Tad Kanawha – 25202 Tornado Kanawha – 25203 Turtle Creek Boone – 25204 Twilight Boone – 25205 Uneeda Boone View
Map 25206 Van Boone – 25208 Wharton Boone – 25209 Whitesville Boone – 25211 Widen Clay – 25213 Winfield Putnam – 25214 Winifrede Kanawha – 25231 Advent Jackson – 25234 Arnoldsburg Calhoun – 25235 Chloe Calhoun – 25239 Cottageville Jackson – 25241 Evans Jackson – 25243 Gandeeville Roane – 25244 Gay Jackson – 25245 Given Jackson – 25247 Hartford Mason – 25248 Kenna Jackson – 25251 Left Hand Roane – 25252 Le Roy Jackson – 25253 Letart Mason View
Map 25259 Looneyville Roane – 25260 Mason Mason – 25261 Millstone Calhoun – 25262 Millwood Jackson – 25264 Mount Alto Mason – 25265 New Haven Mason – 25266 Newton Roane – 25267 Normantown Gilmer – 25268 Orma Calhoun – 25270 Reedy Roane – 25271 Ripley Jackson – 25275 Sandyville Jackson – 25276 Spencer Roane – 25285 Wallback Clay – 25286 Walton Roane – 25287 West Columbia Mason – 25301 Charleston Kanawha – 25302 Charleston Kanawha – 25303 Charleston Kanawha View
Map 25304 Charleston Kanawha – 25305 Charleston Kanawha – 25306 Charleston Kanawha – 25309 Charleston Kanawha – 25311 Charleston Kanawha – 25312 Charleston Kanawha – 25313 Charleston Kanawha – 25314 Charleston Kanawha – 25315 Charleston Kanawha – 25317 Charleston Kanawha – 25320 Charleston Kanawha – 25321 Charleston Kanawha – 25322 Charleston Kanawha – 25323 Charleston Kanawha – 25324 Charleston Kanawha – 25325 Charleston Kanawha – 25326 Charleston Kanawha – 25327 Charleston Kanawha – 25328 Charleston Kanawha View
Map 25329 Charleston Kanawha – 25330 Charleston Kanawha – 25331 Charleston Kanawha – 25332 Charleston Kanawha – 25333 Charleston Kanawha – 25334 Charleston Kanawha – 25335 Charleston Kanawha – 25336 Charleston Kanawha – 25337 Charleston Kanawha – 25338 Charleston Kanawha – 25339 Charleston Kanawha – 25350 Charleston Kanawha – 25356 Charleston Kanawha – 25357 Charleston Kanawha – 25358 Charleston Kanawha – 25360 Charleston Kanawha – 25361 Charleston Kanawha – 25362 Charleston Kanawha – 25364 Charleston Kanawha View
Map 25365 Charleston Kanawha – 25375 Charleston Kanawha – 25387 Charleston Kanawha – 25389 Charleston Kanawha – 25392 Charleston Kanawha – 25396 Charleston Kanawha – 25401 Martinsburg Berkeley – 25402 Martinsburg Berkeley – 25403 Martinsburg Berkeley – 25404 Martinsburg Berkeley – 25405 Martinsburg Berkeley – 25410 Bakerton Jefferson – 25411 Berkeley Springs Morgan – 25413 Bunker Hill Berkeley – 25414 Charles Town Jefferson – 25419 Falling Waters Berkeley – 25420 Gerrardstown Berkeley – 25421 Glengary Berkeley – 25422 Great Cacapon Morgan View
Map 25423 Halltown Jefferson – 25425 Harpers Ferry Jefferson – 25427 Hedgesville Berkeley – 25428 Inwood Berkeley – 25429 Martinsburg Berkeley – 25430 Kearneysville Jefferson – 25431 Levels Hampshire – 25432 Millville Jefferson – 25434 Paw Paw Morgan – 25437 Points Hampshire – 25438 Ranson Jefferson – 25440 Ridgeway Berkeley – 25441 Rippon Jefferson – 25442 Shenandoah Junction Jefferson – 25443 Shepherdstown Jefferson – 25444 Slanesville Hampshire – 25446 Summit Point Jefferson – 25501 Alkol Lincoln – 25502 Apple Grove Mason View
Map 25503 Ashton Mason – 25504 Barboursville Cabell – 25505 Big Creek Logan – 25506 Branchland Lincoln – 25507 Ceredo Wayne – 25508 Chapmanville Logan – 25510 Culloden Cabell – 25511 Dunlow Wayne – 25512 East Lynn Wayne – 25514 Fort Gay Wayne – 25515 Gallipolis Ferry Mason – 25517 Genoa Wayne – 25520 Glenwood Mason – 25521 Griffithsville Lincoln – 25523 Hamlin Lincoln – 25524 Harts Lincoln – 25526 Hurricane Putnam – 25529 Julian Boone – 25530 Kenova Wayne View
Map 25534 Kiahsville Wayne – 25535 Lavalette Wayne – 25537 Lesage Cabell – 25540 Midkiff Lincoln – 25541 Milton Cabell – 25544 Myra Lincoln – 25545 Ona Cabell – 25547 Pecks Mill Logan – 25550 Point Pleasant Mason – 25555 Prichard Wayne – 25557 Ranger Lincoln – 25559 Salt Rock Cabell – 25560 Scott Depot Putnam – 25562 Shoals Wayne – 25564 Sod Lincoln – 25565 Spurlockville Lincoln – 25567 Sumerco Lincoln – 25569 Teays Putnam – 25570 Wayne Wayne View
Map 25571 West Hamlin Lincoln – 25572 Woodville Boone – 25573 Yawkey Lincoln – 25601 Logan Logan – 25606 Accoville Logan – 25607 Amherstdale Logan – 25608 Baisden Mingo – 25611 Bruno Logan – 25612 Chauncey Logan – 25614 Cora Logan – 25617 Davin Logan – 25621 Gilbert Mingo – 25624 Henlawson Logan – 25625 Holden Logan – 25628 Kistler Logan – 25630 Lorado Logan – 25632 Lyburn Logan – 25634 Mallory Logan – 25635 Man Logan View
Map 25637 Mount Gay Logan – 25638 Omar Logan – 25639 Peach Creek Logan – 25644 Sarah Ann Logan – 25646 Stollings Logan – 25647 Switzer Logan – 25649 Verdunville Logan – 25650 Verner Mingo – 25651 Wharncliffe Mingo – 25652 Whitman Logan – 25653 Wilkinson Logan – 25654 Yolyn Logan – 25661 Williamson Mingo – 25665 Borderland Mingo – 25666 Breeden Mingo – 25667 Chattaroy Mingo – 25669 Crum Wayne – 25670 Delbarton Mingo – 25671 Dingess Mingo View
Map 25672 Edgarton Mingo – 25674 Kermit Mingo – 25676 Lenore Mingo – 25678 Matewan Mingo – 25685 Naugatuck Mingo – 25686 Newtown Mingo – 25688 North Matewan Mingo – 25690 Ragland Mingo – 25691 Rawl Mingo – 25692 Red Jacket Mingo – 25696 Varney Mingo – 25697 Vulcan Mingo – 25699 Wilsondale Wayne – 25701 Huntington Cabell – 25702 Huntington Cabell – 25703 Huntington Cabell – 25704 Huntington Wayne – 25705 Huntington Cabell – 25706 Huntington Cabell View
Map 25707 Huntington Cabell – 25708 Huntington Cabell – 25709 Huntington Cabell – 25710 Huntington Cabell – 25711 Huntington Cabell – 25712 Huntington Cabell – 25713 Huntington Cabell – 25714 Huntington Cabell – 25715 Huntington Cabell – 25716 Huntington Cabell – 25717 Huntington Cabell – 25718 Huntington Cabell – 25719 Huntington Cabell – 25720 Huntington Cabell – 25721 Huntington Cabell – 25722 Huntington Cabell – 25723 Huntington Cabell – 25724 Huntington Cabell – 25725 Huntington Cabell View
Map 25726 Huntington Cabell – 25727 Huntington Cabell – 25728 Huntington Cabell – 25729 Huntington Cabell – 25755 Huntington Cabell – 25770 Huntington Cabell – 25771 Huntington Cabell – 25772 Huntington Cabell – 25773 Huntington Cabell – 25774 Huntington Cabell – 25775 Huntington Cabell – 25776 Huntington Cabell – 25777 Huntington Cabell – 25778 Huntington Cabell – 25779 Huntington Cabell – 25801 Beckley Raleigh – 25802 Beckley Raleigh – 25810 Allen Junction Wyoming – 25811 Amigo Wyoming View
Map 25812 Ansted Fayette – 25813 Beaver Raleigh – 25816 Blue Jay Raleigh – 25817 Bolt Raleigh – 25818 Bradley Raleigh – 25820 Camp Creek Mercer – 25823 Coal City Raleigh – 25825 Cool Ridge Raleigh – 25826 Corinne Wyoming – 25827 Crab Orchard Raleigh – 25831 Danese Fayette – 25832 Daniels Raleigh – 25833 Dothan Fayette – 25836 Eccles Raleigh – 25837 Edmond Fayette – 25839 Fairdale Raleigh – 25840 Fayetteville Fayette – 25841 Flat Top Mercer – 25843 Ghent Raleigh View
Map 25844 Glen Daniel Raleigh – 25845 Glen Fork Wyoming – 25846 Glen Jean Fayette – 25848 Glen Rogers Wyoming – 25849 Glen White Raleigh – 25851 Harper Raleigh – 25853 Helen Raleigh – 25854 Hico Fayette – 25855 Hilltop Fayette – 25857 Josephine Raleigh – 25860 Lanark Raleigh – 25862 Lansing Fayette – 25864 Layland Fayette – 25865 Lester Raleigh – 25866 Lochgelly Fayette – 25868 Lookout Fayette – 25870 Maben Wyoming – 25871 Mabscott Raleigh – 25873 Mac Arthur Raleigh View
Map 25875 Mc Graws Wyoming – 25876 Saulsville Wyoming – 25878 Midway Raleigh – 25879 Minden Fayette – 25880 Mount Hope Fayette – 25882 Mullens Wyoming – 25901 Oak Hill Fayette – 25902 Odd Raleigh – 25904 Pax Fayette – 25906 Piney View Raleigh – 25907 Prince Fayette – 25908 Princewick Raleigh – 25909 Prosperity Raleigh – 25911 Raleigh Raleigh – 25913 Ravencliff Wyoming – 25914 Redstar Fayette – 25915 Rhodell Raleigh – 25916 Sabine Wyoming – 25917 Scarbro Fayette View
Map 25918 Shady Spring Raleigh – 25919 Skelton Raleigh – 25920 Slab Fork Raleigh – 25921 Sophia Raleigh – 25922 Spanishburg Mercer – 25926 Sprague Raleigh – 25927 Stanaford Raleigh – 25928 Stephenson Wyoming – 25932 Surveyor Raleigh – 25936 Thurmond Fayette – 25938 Victor Fayette – 25942 Winona Fayette – 25943 Wyco Wyoming – 25951 Hinton Summers – 25958 Charmco Greenbrier – 25962 Rainelle Greenbrier – 25965 Elton Summers – 25966 Green Sulphur Springs Summers – 25969 Jumping Branch Summers View
Map 25971 Lerona Mercer – 25972 Leslie Greenbrier – 25976 Meadow Bridge Fayette – 25977 Meadow Creek Summers – 25978 Nimitz Summers – 25979 Pipestem Summers – 25981 Quinwood Greenbrier – 25984 Rupert Greenbrier – 25985 Sandstone Summers – 25986 Spring Dale Fayette – 25989 White Oak Raleigh – 26003 Wheeling Ohio – 26030 Beech Bottom Brooke – 26031 Benwood Marshall – 26032 Bethany Brooke – 26033 Cameron Marshall – 26034 Chester Hancock – 26035 Colliers Brooke – 26036 Dallas Marshall View
Map 26037 Follansbee Brooke – 26038 Glen Dale Marshall – 26039 Glen Easton Marshall – 26040 Mcmechen Marshall – 26041 Moundsville Marshall – 26047 New Cumberland Hancock – 26050 Newell Hancock – 26055 Proctor Marshall – 26056 New Manchester Hancock – 26058 Short Creek Brooke – 26059 Triadelphia Ohio – 26060 Valley Grove Ohio – 26062 Weirton Hancock – 26070 Wellsburg Brooke – 26074 West Liberty Ohio – 26075 Windsor Heights Brooke – 26101 Parkersburg Wood – 26102 Parkersburg Wood – 26103 Parkersburg Wood View
Map 26104 Parkersburg Wood – 26105 Vienna Wood – 26106 Parkersburg Wood – 26120 Mineral Wells Wood – 26121 Mineral Wells Wood – 26133 Belleville Wood – 26134 Belmont Pleasants – 26136 Big Bend Calhoun – 26137 Big Springs Calhoun – 26138 Brohard Wirt – 26141 Creston Wirt – 26142 Davisville Wood – 26143 Elizabeth Wirt – 26146 Friendly Tyler – 26147 Grantsville Calhoun – 26148 Macfarlan Ritchie – 26149 Middlebourne Tyler – 26150 Mineral Wells Wood – 26151 Mount Zion Calhoun View
Map 26152 Munday Calhoun – 26155 New Martinsville Wetzel – 26159 Paden City Wetzel – 26160 Palestine Wirt – 26161 Petroleum Ritchie – 26162 Porters Falls Wetzel – 26164 Ravenswood Jackson – 26167 Reader Wetzel – 26169 Rockport Wood – 26170 Saint Marys Pleasants – 26175 Sistersville Tyler – 26178 Smithville Ritchie – 26180 Walker Wood – 26181 Washington Wood – 26184 Waverly Wood – 26186 Wileyville Wetzel – 26187 Williamstown Wood – 26201 Buckhannon Upshur – 26202 Fenwick Nicholas View
Map 26203 Erbacon Webster – 26205 Craigsville Nicholas – 26206 Cowen Webster – 26208 Camden On Gauley Webster – 26209 Snowshoe Pocahontas – 26210 Adrian Upshur – 26215 Cleveland Upshur – 26217 Diana Webster – 26218 French Creek Upshur – 26219 Frenchton Upshur – 26222 Hacker Valley Webster – 26224 Helvetia Randolph – 26228 Kanawha Head Upshur – 26229 Lorentz Upshur – 26230 Pickens Randolph – 26234 Rock Cave Upshur – 26236 Selbyville Upshur – 26237 Tallmansville Upshur – 26238 Volga Barbour View
Map 26241 Elkins Randolph – 26250 Belington Barbour – 26253 Beverly Randolph – 26254 Bowden Tucker – 26257 Coalton Randolph – 26259 Dailey Randolph – 26260 Davis Tucker – 26261 Richwood Nicholas – 26263 Dryfork Randolph – 26264 Durbin Pocahontas – 26266 Upperglade Webster – 26267 Ellamore Randolph – 26268 Glady Randolph – 26269 Hambleton Tucker – 26270 Harman Randolph – 26271 Hendricks Tucker – 26273 Huttonsville Randolph – 26275 Junior Barbour – 26276 Kerens Randolph View
Map 26278 Mabie Randolph – 26280 Mill Creek Randolph – 26282 Monterville Randolph – 26283 Montrose Randolph – 26285 Norton Randolph – 26287 Parsons Tucker – 26288 Webster Springs Webster – 26289 Red Creek Tucker – 26291 Slatyfork Pocahontas – 26292 Thomas Tucker – 26293 Valley Bend Randolph – 26294 Valley Head Randolph – 26296 Whitmer Randolph – 26298 Bergoo Webster – 26301 Clarksburg Harrison – 26302 Clarksburg Harrison – 26306 Clarksburg Harrison – 26320 Alma Tyler – 26321 Alum Bridge Lewis View
Map 26323 Anmoore Harrison – 26325 Auburn Ritchie – 26327 Berea Ritchie – 26330 Bridgeport Harrison – 26335 Burnsville Braxton – 26337 Cairo Ritchie – 26338 Camden Lewis – 26339 Center Point Doddridge – 26342 Coxs Mills Gilmer – 26343 Crawford Lewis – 26346 Ellenboro Ritchie – 26347 Flemington Taylor – 26348 Folsom Wetzel – 26349 Galloway Barbour – 26351 Glenville Gilmer – 26354 Grafton Taylor – 26361 Gypsy Harrison – 26362 Harrisville Ritchie – 26366 Haywood Harrison View
Map 26369 Hepzibah Harrison – 26372 Horner Lewis – 26374 Independence Preston – 26376 Ireland Lewis – 26377 Jacksonburg Wetzel – 26378 Jane Lew Lewis – 26384 Linn Gilmer – 26385 Lost Creek Harrison – 26386 Lumberport Harrison – 26404 Meadowbrook Harrison – 26405 Moatsville Barbour – 26408 Mount Clare Harrison – 26410 Newburg Preston – 26411 New Milton Doddridge – 26412 Orlando Lewis – 26415 Pennsboro Ritchie – 26416 Philippi Barbour – 26419 Pine Grove Wetzel – 26421 Pullman Ritchie View
Map 26422 Reynoldsville Harrison – 26424 Rosemont Taylor – 26425 Rowlesburg Preston – 26426 Salem Harrison – 26430 Sand Fork Gilmer – 26431 Shinnston Harrison – 26434 Shirley Tyler – 26435 Simpson Taylor – 26436 Smithburg Doddridge – 26437 Smithfield Wetzel – 26438 Spelter Harrison – 26440 Thornton Taylor – 26443 Troy Gilmer – 26444 Tunnelton Preston – 26447 Walkersville Lewis – 26448 Wallace Harrison – 26451 West Milford Harrison – 26452 Weston Lewis – 26456 West Union Doddridge View
Map 26461 Wilsonburg Harrison – 26463 Wyatt Harrison – 26501 Morgantown Monongalia – 26502 Morgantown Monongalia – 26504 Morgantown Monongalia – 26505 Morgantown Monongalia – 26506 Morgantown Monongalia – 26507 Morgantown Monongalia – 26508 Morgantown Monongalia – 26519 Albright Preston – 26520 Arthurdale Preston – 26521 Blacksville Monongalia – 26524 Bretz Preston – 26525 Bruceton Mills Preston – 26527 Cassville Monongalia – 26531 Dellslow Monongalia – 26534 Granville Monongalia – 26537 Kingwood Preston – 26541 Maidsville Monongalia View
Map 26542 Masontown Preston – 26543 Osage Monongalia – 26544 Pentress Monongalia – 26546 Pursglove Monongalia – 26547 Reedsville Preston – 26554 Fairmont Marion – 26555 Fairmont Marion – 26559 Barrackville Marion – 26560 Baxter Marion – 26561 Big Run Wetzel – 26562 Burton Wetzel – 26563 Carolina Marion – 26566 Colfax Marion – 26568 Enterprise Harrison – 26570 Fairview Marion – 26571 Farmington Marion – 26572 Four States Marion – 26574 Grant Town Marion – 26575 Hundred Wetzel View
Map 26576 Idamay Marion – 26578 Kingmont Marion – 26581 Littleton Wetzel – 26582 Mannington Marion – 26585 Metz Marion – 26586 Montana Mines Marion – 26587 Rachel Marion – 26588 Rivesville Marion – 26590 Wana Monongalia – 26591 Worthington Marion – 26601 Sutton Braxton – 26610 Birch River Nicholas – 26611 Cedarville Gilmer – 26615 Copen Braxton – 26617 Dille Clay – 26619 Exchange Braxton – 26621 Flatwoods Braxton – 26623 Frametown Braxton – 26624 Gassaway Braxton View
Map 26627 Heaters Braxton – 26629 Little Birch Braxton – 26631 Napier Braxton – 26636 Rosedale Gilmer – 26638 Shock Gilmer – 26651 Summersville Nicholas – 26656 Belva Nicholas – 26660 Calvin Nicholas – 26662 Canvas Nicholas – 26667 Drennen Nicholas – 26671 Gilboa Nicholas – 26675 Keslers Cross Lanes Nicholas – 26676 Leivasy Nicholas – 26678 Mount Lookout Nicholas – 26679 Mount Nebo Nicholas – 26680 Nallen Fayette – 26681 Nettie Nicholas – 26684 Pool Nicholas – 26690 Swiss Nicholas View
Map 26691 Tioga Nicholas – 26704 Augusta Hampshire – 26705 Aurora Preston – 26707 Bayard Grant – 26710 Burlington Mineral – 26711 Capon Bridge Hampshire – 26714 Delray Hampshire – 26716 Eglon Preston – 26717 Elk Garden Mineral – 26719 Fort Ashby Mineral – 26720 Gormania Grant – 26722 Green Spring Hampshire – 26726 Keyser Mineral – 26731 Lahmansville Grant – 26739 Mount Storm Grant – 26743 New Creek Mineral – 26750 Piedmont Mineral – 26753 Ridgeley Mineral – 26755 Rio Hampshire View
Map 26757 Romney Hampshire – 26761 Shanks Hampshire – 26763 Springfield Hampshire – 26764 Terra Alta Preston – 26767 Wiley Ford Mineral – 26801 Baker Hardy – 26802 Brandywine Pendleton – 26804 Circleville Pendleton – 26807 Franklin Pendleton – 26808 High View Hampshire – 26810 Lost City Hardy – 26812 Mathias Hardy – 26814 Riverton Pendleton – 26815 Sugar Grove Pendleton – 26817 Bloomery Hampshire – 26818 Fisher Hardy – 26823 Capon Springs Hampshire – 26833 Maysville Grant – 26836 Moorefield Hardy View
Map 26838 Milam Hardy – 26845 Old Fields Hardy – 26847 Petersburg Grant – 26851 Wardensville Hardy – 26852 Purgitsville Hampshire – 26855 Cabins Grant – 26865 Yellow Spring Hampshire – 26866 Upper Tract Pendleton – 26884 Seneca Rocks Pendleton – 26886 Onego Pendleton

Areas served by NOVA Health Recovery:

Maryland (MD):
Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902

Washington DC:
Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016

Northern Virginia:
McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304 Fairfax – 20191 – Reston – 22009 – Springfield – 22152 22015 Lorton 22199
Fairfax, Va
2303 – 22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312
22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 – 20124
22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043
22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101
22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153
22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 – 22182
Woodbridge – 22191 – 22192 -22193 -22194 – 22195
Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161
Front Royal 22630
Warren County 22610 22630 22642 22649
Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412
Zip Code City County Zip Code Map 20101 Dulles Loudoun – 20102 Dulles Loudoun – 20103 Dulles Loudoun – 20104 Dulles Loudoun – 20105 Aldie Loudoun – 20106 Amissville Culpeper – 20107 Arcola Loudoun – 20108 Manassas Manassas City – 20109 Manassas Prince William – 20110 Manassas Manassas City – 20111 Manassas Prince William – 20112 Manassas Prince William – 20113 Manassas Manassas Park City – 20115 Marshall Fauquier – 20116 Marshall Fauquier – 20117 Middleburg Loudoun – 20118 Middleburg Loudoun – 20119 Catlett Fauquier View
Map 20120 Centreville Fairfax – 20121 Centreville Fairfax – 20122 Centreville Fairfax – 20124 Clifton Fairfax – 20128 Orlean Fauquier – 20129 Paeonian Springs Loudoun – 20130 Paris Clarke – 20131 Philomont Loudoun – 20132 Purcellville Loudoun – 20134 Purcellville Loudoun – 20135 Bluemont Clarke – 20136 Bristow Prince William – 20137 Broad Run Fauquier – 20138 Calverton Fauquier – 20139 Casanova Fauquier – 20140 Rectortown Fauquier – 20141 Round Hill Loudoun – 20142 Round Hill Loudoun – 20143 Catharpin Prince William View
Map 20144 Delaplane Fauquier – 20146 Ashburn Loudoun – 20147 Ashburn Loudoun – 20148 Ashburn Loudoun – 20149 Ashburn Loudoun – 20151 Chantilly Fairfax – 20152 Chantilly Loudoun – 20153 Chantilly Fairfax – 20155 Gainesville Prince William – 20156 Gainesville Prince William – 20158 Hamilton Loudoun – 20159 Hamilton Loudoun – 20160 Lincoln Loudoun – 20163 Sterling Loudoun – 20164 Sterling Loudoun – 20165 Sterling Loudoun – 20166 Sterling Loudoun – 20167 Sterling Loudoun – 20168 Haymarket Prince William View
Map 20169 Haymarket Prince William – 20170 Herndon Fairfax – 20171 Herndon Fairfax – 20172 Herndon Fairfax – 20175 Leesburg Loudoun – 20176 Leesburg Loudoun – 20177 Leesburg Loudoun – 20178 Leesburg Loudoun – 20180 Lovettsville Loudoun – 20181 Nokesville Prince William – 20182 Nokesville Prince William – 20184 Upperville Fauquier – 20185 Upperville Fauquier – 20186 Warrenton Fauquier – 20187 Warrenton Fauquier – 20188 Warrenton Fauquier – 20189 Dulles Loudoun – 20190 Reston Fairfax – 20191 Reston Fairfax View
Map 20192 Herndon Fairfax – 20193 Reston Fairfax – 20194 Reston Fairfax – 20195 Reston Fairfax – 20196 Reston Fairfax – 20197 Waterford Loudoun – 20198 The Plains Fauquier – 20199 Dulles Loudoun – 22003 Annandale Fairfax – 22009 Burke Fairfax – 22015 Burke Fairfax – 22025 Dumfries Prince William – 22026 Dumfries Prince William – 22027 Dunn Loring Fairfax – 22030 Fairfax Fairfax City – 22031 Fairfax Fairfax – 22032 Fairfax Fairfax – 22033 Fairfax Fairfax – 22034 Fairfax Fairfax View
Map 22035 Fairfax Fairfax – 22036 Fairfax Fairfax – 22037 Fairfax Fairfax – 22038 Fairfax Fairfax City – 22039 Fairfax Station Fairfax – 22040 Falls Church Falls Church City – 22041 Falls Church Fairfax – 22042 Falls Church Fairfax – 22043 Falls Church Fairfax – 22044 Falls Church Fairfax – 22046 Falls Church Falls Church City – 22047 Falls Church Fairfax – 22060 Fort Belvoir Fairfax – 22066 Great Falls Fairfax – 22067 Greenway Fairfax – 22079 Lorton Fairfax – 22081 Merrifield Fairfax – 22082 Merrifield Fairfax – 22092 Herndon Fairfax View
Map 22093 Ashburn Loudoun – 22095 Herndon Fairfax – 22096 Reston Fairfax – 22101 Mc Lean Fairfax – 22102 Mc Lean Fairfax – 22103 West Mclean Fairfax – 22106 Mc Lean Fairfax – 22107 Mc Lean Fairfax – 22108 Mc Lean Fairfax – 22109 Mc Lean Fairfax – 22116 Merrifield Fairfax – 22118 Merrifield Fairfax – 22119 Merrifield Fairfax – 22120 Merrifield Fairfax – 22121 Mount Vernon Fairfax – 22122 Newington Fairfax – 22124 Oakton Fairfax – 22125 Occoquan Prince William – 22134 Quantico Prince William View
Map 22135 Quantico Stafford – 22150 Springfield Fairfax – 22151 Springfield Fairfax – 22152 Springfield Fairfax – 22153 Springfield Fairfax – 22156 Springfield Fairfax – 22158 Springfield Fairfax – 22159 Springfield Fairfax – 22160 Springfield Fairfax – 22161 Springfield Fairfax – 22172 Triangle Prince William – 22180 Vienna Fairfax – 22181 Vienna Fairfax – 22182 Vienna Fairfax – 22183 Vienna Fairfax – 22184 Vienna Fairfax – 22185 Vienna Fairfax – 22191 Woodbridge Prince William – 22192 Woodbridge Prince William View
Map 22193 Woodbridge Prince William – 22194 Woodbridge Prince William – 22195 Woodbridge Prince William – 22199 Lorton Fairfax – 22201 Arlington Arlington – 22202 Arlington Arlington – 22203 Arlington Arlington – 22204 Arlington Arlington – 22205 Arlington Arlington – 22206 Arlington Arlington – 22207 Arlington Arlington – 22209 Arlington Arlington – 22210 Arlington Arlington – 22211 Ft Myer Arlington – 22212 Arlington Arlington – 22213 Arlington Arlington – 22214 Arlington Arlington – 22215 Arlington Arlington – 22216 Arlington Arlington View
Map 22217 Arlington Arlington – 22218 Arlington Arlington – 22219 Arlington Arlington – 22222 Arlington Arlington – 22223 Arlington Arlington – 22225 Arlington Arlington – 22226 Arlington Arlington – 22227 Arlington Arlington – 22229 Arlington Arlington – 22230 Arlington Arlington – 22234 Arlington Arlington – 22240 Arlington Arlington – 22241 Arlington Arlington – 22242 Arlington Arlington – 22243 Arlington Arlington – 22244 Arlington Arlington – 22245 Arlington Arlington – 22246 Arlington Arlington – 22301 Alexandria Alexandria City View
Map 22302 Alexandria Alexandria City – 22303 Alexandria Fairfax – 22304 Alexandria Alexandria City – 22305 Alexandria Alexandria City – 22306 Alexandria Fairfax – 22307 Alexandria Fairfax – 22308 Alexandria Fairfax – 22309 Alexandria Fairfax – 22310 Alexandria Fairfax – 22311 Alexandria Alexandria City – 22312 Alexandria Fairfax – 22313 Alexandria Alexandria City – 22314 Alexandria Alexandria City – 22315 Alexandria Fairfax – 22320 Alexandria Alexandria City – 22321 Alexandria Fairfax – 22331 Alexandria Alexandria City – 22332 Alexandria Alexandria City – 22333 Alexandria Alexandria City View
Map 22334 Alexandria Alexandria City – 22336 Alexandria Alexandria City – 22401 Fredericksburg Fredericksburg City – 22402 Fredericksburg Fredericksburg City – 22403 Fredericksburg Stafford – 22404 Fredericksburg Fredericksburg City – 22405 Fredericksburg Stafford – 22406 Fredericksburg Stafford – 22407 Fredericksburg Spotsylvania – 22408 Fredericksburg Spotsylvania – 22412 Fredericksburg Stafford – 22427 Bowling Green Caroline – 22428 Bowling Green Caroline – 22430 Brooke Stafford – 22432 Burgess Northumberland – 22433 Burr Hill Orange – 22435 Callao Northumberland – 22436 Caret Essex – 22437 Center Cross Essex View
Map 22438 Champlain Essex – 22442 Coles Point Westmoreland – 22443 Colonial Beach Westmoreland – 22446 Corbin Caroline – 22448 Dahlgren King George – 22451 Dogue King George – 22454 Dunnsville Essex – 22456 Edwardsville Northumberland – 22460 Farnham Richmond – 22463 Garrisonville Stafford – 22469 Hague Westmoreland – 22471 Hartwood Stafford – 22472 Haynesville Richmond – 22473 Heathsville Northumberland – 22476 Hustle Essex – 22480 Irvington Lancaster – 22481 Jersey King George – 22482 Kilmarnock Lancaster – 22485 King George King George View
Map 22488 Kinsale Westmoreland – 22501 Ladysmith Caroline – 22503 Lancaster Lancaster – 22504 Laneview Essex – 22507 Lively Lancaster – 22508 Locust Grove Orange – 22509 Loretto Essex – 22511 Lottsburg Northumberland – 22513 Merry Point Lancaster – 22514 Milford Caroline – 22517 Mollusk Lancaster – 22520 Montross Westmoreland – 22523 Morattico Lancaster – 22524 Mount Holly Westmoreland – 22526 Ninde King George – 22528 Nuttsville Lancaster – 22529 Oldhams Westmoreland – 22530 Ophelia Northumberland – 22534 Partlow Spotsylvania View
Map 22535 Port Royal Caroline – 22538 Rappahannock Academy Caroline – 22539 Reedville Northumberland – 22542 Rhoadesville Orange – 22544 Rollins Fork King George – 22545 Ruby Stafford – 22546 Ruther Glen Caroline – 22547 Sealston King George – 22548 Sharps Richmond – 22552 Sparta Caroline – 22553 Spotsylvania Spotsylvania – 22554 Stafford Stafford – 22555 Stafford Stafford – 22556 Stafford Stafford – 22558 Stratford Westmoreland – 22560 Tappahannock Essex – 22565 Thornburg Spotsylvania – 22567 Unionville Orange – 22570 Village Richmond View
Map 22572 Warsaw Richmond – 22576 Weems Lancaster – 22577 Sandy Point Westmoreland – 22578 White Stone Lancaster – 22579 Wicomico Church Northumberland – 22580 Woodford Caroline – 22581 Zacata Westmoreland – 22601 Winchester Winchester City – 22602 Winchester Frederick – 22603 Winchester Frederick – 22604 Winchester Winchester City – 22610 Bentonville Warren – 22611 Berryville Clarke – 22620 Boyce Clarke – 22622 Brucetown Frederick – 22623 Chester Gap Rappahannock – 22624 Clear Brook Frederick – 22625 Cross Junction Frederick – 22626 Fishers Hill Shenandoah View
Map 22627 Flint Hill Rappahannock – 22630 Front Royal Warren – 22637 Gore Frederick – 22638 Winchester Frederick – 22639 Hume Fauquier – 22640 Huntly Rappahannock – 22641 Strasburg Shenandoah – 22642 Linden Warren – 22643 Markham Fauquier – 22644 Maurertown Shenandoah – 22645 Middletown Frederick – 22646 Millwood Clarke – 22649 Middletown Warren – 22650 Rileyville Page – 22652 Fort Valley Shenandoah – 22654 Star Tannery Frederick – 22655 Stephens City Frederick – 22656 Stephenson Frederick – 22657 Strasburg Shenandoah View
Map 22660 Toms Brook Shenandoah – 22663 White Post Clarke – 22664 Woodstock Shenandoah – 22701 Culpeper Culpeper – 22709 Aroda Madison – 22711 Banco Madison – 22712 Bealeton Fauquier – 22713 Boston Culpeper – 22714 Brandy Station Culpeper – 22715 Brightwood Madison – 22716 Castleton Rappahannock – 22718 Elkwood Culpeper – 22719 Etlan Madison – 22720 Goldvein Fauquier – 22721 Graves Mill Madison – 22722 Haywood Madison – 22723 Hood Madison – 22724 Jeffersonton Culpeper – 22725 Leon Madison View
Map 22726 Lignum Culpeper – 22727 Madison Madison – 22728 Midland Fauquier – 22729 Mitchells Culpeper – 22730 Oakpark Madison – 22731 Pratts Madison – 22732 Radiant Madison – 22733 Rapidan Culpeper – 22734 Remington Fauquier – 22735 Reva Madison – 22736 Richardsville Culpeper – 22737 Rixeyville Culpeper – 22738 Rochelle Madison – 22739 Somerville Fauquier – 22740 Sperryville Rappahannock – 22741 Stevensburg Culpeper – 22742 Sumerduck Fauquier – 22743 Syria Madison – 22746 Viewtown Culpeper View
Map 22747 Washington Rappahannock – 22748 Wolftown Madison – 22749 Woodville Rappahannock – 22801 Harrisonburg Harrisonburg City – 22802 Harrisonburg Harrisonburg City – 22803 Harrisonburg Harrisonburg City – 22807 Harrisonburg Harrisonburg City – 22810 Basye Shenandoah – 22811 Bergton Rockingham – 22812 Bridgewater Rockingham – 22815 Broadway Rockingham – 22820 Criders Rockingham – 22821 Dayton Rockingham – 22824 Edinburg Shenandoah – 22827 Elkton Rockingham – 22830 Fulks Run Rockingham – 22831 Hinton Rockingham – 22832 Keezletown Rockingham – 22833 Lacey Spring Rockingham View
Map 22834 Linville Rockingham – 22835 Luray Page – 22840 Mc Gaheysville Rockingham – 22841 Mount Crawford Rockingham – 22842 Mount Jackson Shenandoah – 22843 Mount Solon Augusta – 22844 New Market Shenandoah – 22845 Orkney Springs Shenandoah – 22846 Penn Laird Rockingham – 22847 Quicksburg Shenandoah – 22848 Pleasant Valley Rockingham – 22849 Shenandoah Page – 22850 Singers Glen Rockingham – 22851 Stanley Page – 22853 Timberville Rockingham – 22901 Charlottesville Albemarle – 22902 Charlottesville Charlottesville City – 22903 Charlottesville Charlottesville City – 22904 Charlottesville Charlottesville City View
Map 22905 Charlottesville Charlottesville City – 22906 Charlottesville Charlottesville City – 22907 Charlottesville Charlottesville City – 22908 Charlottesville Charlottesville City – 22909 Charlottesville Albemarle – 22910 Charlottesville Charlottesville City – 22911 Charlottesville Albemarle – 22920 Afton Nelson – 22922 Arrington Nelson – 22923 Barboursville Orange – 22924 Batesville Albemarle – 22931 Covesville Albemarle – 22932 Crozet Albemarle – 22935 Dyke Greene – 22936 Earlysville Albemarle – 22937 Esmont Albemarle – 22938 Faber Nelson – 22939 Fishersville Augusta – 22940 Free Union Albemarle View
Map 22942 Gordonsville Orange – 22943 Greenwood Albemarle – 22945 Ivy Albemarle – 22946 Keene Albemarle – 22947 Keswick Albemarle – 22948 Locust Dale Madison – 22949 Lovingston Nelson – 22952 Lyndhurst Augusta – 22957 Montpelier Station Orange – 22958 Nellysford Nelson – 22959 North Garden Albemarle – 22960 Orange Orange – 22963 Palmyra Fluvanna – 22964 Piney River Nelson – 22965 Quinque Greene – 22967 Roseland Nelson – 22968 Ruckersville Greene – 22969 Schuyler Nelson – 22971 Shipman Nelson View
Map 22972 Somerset Orange – 22973 Stanardsville Greene – 22974 Troy Fluvanna – 22976 Tyro Nelson – 22980 Waynesboro Waynesboro City – 22987 White Hall Albemarle – 22989 Woodberry Forest Madison – 23001 Achilles Gloucester – 23002 Amelia Court House Amelia – 23003 Ark Gloucester – 23004 Arvonia Buckingham – 23005 Ashland Hanover – 23009 Aylett King William – 23011 Barhamsville New Kent – 23014 Beaumont Goochland – 23015 Beaverdam Hanover – 23018 Bena Gloucester – 23021 Bohannon Mathews – 23022 Bremo Bluff Fluvanna View
Map 23023 Bruington King And Queen – 23024 Bumpass Louisa – 23025 Cardinal Mathews – 23027 Cartersville Cumberland – 23030 Charles City Charles City – 23031 Christchurch Middlesex – 23032 Church View Middlesex – 23035 Cobbs Creek Mathews – 23038 Columbia Goochland – 23039 Crozier Goochland – 23040 Cumberland Cumberland – 23043 Deltaville Middlesex – 23045 Diggs Mathews – 23047 Doswell Hanover – 23050 Dutton Gloucester – 23055 Fork Union Fluvanna – 23056 Foster Mathews – 23058 Glen Allen Henrico – 23059 Glen Allen Henrico View
Map 23060 Glen Allen Henrico – 23061 Gloucester Gloucester – 23062 Gloucester Point Gloucester – 23063 Goochland Goochland – 23064 Grimstead Mathews – 23065 Gum Spring Goochland – 23066 Gwynn Mathews – 23067 Hadensville Goochland – 23068 Hallieford Mathews – 23069 Hanover Hanover – 23070 Hardyville Middlesex – 23071 Hartfield Middlesex – 23072 Hayes Gloucester – 23075 Highland Springs Henrico – 23076 Hudgins Mathews – 23079 Jamaica Middlesex – 23081 Jamestown James City – 23083 Jetersville Amelia – 23084 Kents Store Fluvanna View
Map 23085 King And Queen Court House King And Queen – 23086 King William King William – 23089 Lanexa New Kent – 23090 Lightfoot York – 23091 Little Plymouth King And Queen – 23092 Locust Hill Middlesex – 23093 Louisa Louisa – 23101 Macon Powhatan – 23102 Maidens Goochland – 23103 Manakin Sabot Goochland – 23105 Mannboro Amelia – 23106 Manquin King William – 23107 Maryus Gloucester – 23108 Mascot King And Queen – 23109 Mathews Mathews – 23110 Mattaponi King And Queen – 23111 Mechanicsville Hanover – 23112 Midlothian Chesterfield – 23113 Midlothian Chesterfield View
Map 23114 Midlothian Chesterfield – 23115 Millers Tavern Essex – 23116 Mechanicsville Hanover – 23117 Mineral Louisa – 23119 Moon Mathews – 23120 Moseley Chesterfield – 23123 New Canton Buckingham – 23124 New Kent New Kent – 23125 New Point Mathews – 23126 Newtown King And Queen – 23127 Norge James City – 23128 North Mathews – 23129 Oilville Goochland – 23130 Onemo Mathews – 23131 Ordinary Gloucester – 23138 Port Haywood Mathews – 23139 Powhatan Powhatan – 23140 Providence Forge New Kent – 23141 Quinton New Kent View
Map 23146 Rockville Hanover – 23147 Ruthville Charles City – 23148 Saint Stephens Church King And Queen – 23149 Saluda Middlesex – 23150 Sandston Henrico – 23153 Sandy Hook Goochland – 23154 Schley Gloucester – 23155 Severn Gloucester – 23156 Shacklefords King And Queen – 23160 State Farm Goochland – 23161 Stevensville King And Queen – 23162 Studley Hanover – 23163 Susan Mathews – 23168 Toano James City – 23169 Topping Middlesex – 23170 Trevilians Louisa – 23173 University Of Richmond Richmond City – 23175 Urbanna Middlesex – 23176 Wake Middlesex View
Map 23177 Walkerton King And Queen – 23178 Ware Neck Gloucester – 23180 Water View Middlesex – 23181 West Point King William – 23183 White Marsh Gloucester – 23184 Wicomico Gloucester – 23185 Williamsburg James City – 23186 Williamsburg Williamsburg City – 23187 Williamsburg Williamsburg City – 23188 Williamsburg James City – 23190 Woods Cross Roads Gloucester – 23192 Montpelier Hanover – 23218 Richmond Richmond City – 23219 Richmond Richmond City – 23220 Richmond Richmond City – 23221 Richmond Richmond City – 23222 Richmond Richmond City – 23223 Richmond Richmond City – 23224 Richmond Richmond City View
Map 23225 Richmond Richmond City – 23226 Richmond Henrico – 23227 Richmond Henrico – 23228 Richmond Henrico – 23229 Richmond Henrico – 23230 Richmond Henrico – 23231 Richmond Henrico – 23232 Richmond Richmond City – 23233 Richmond Henrico – 23234 Richmond Chesterfield – 23235 Richmond Chesterfield – 23236 Richmond Chesterfield – 23237 Richmond Chesterfield – 23238 Richmond Henrico – 23240 Richmond Richmond City – 23241 Richmond Richmond City – 23242 Richmond Henrico – 23249 Richmond Richmond City – 23250 Richmond Henrico View
Map 23255 Richmond Henrico – 23260 Richmond Richmond City – 23261 Richmond Richmond City – 23269 Richmond Richmond City – 23273 Richmond Richmond City – 23274 Richmond Richmond City – 23276 Richmond Richmond City – 23278 Richmond Richmond City – 23279 Richmond Richmond City – 23282 Richmond Richmond City – 23284 Richmond Richmond City – 23285 Richmond Richmond City – 23286 Richmond Richmond City – 23288 Richmond Henrico – 23289 Richmond Richmond City – 23290 Richmond Richmond City – 23291 Richmond Richmond City – 23292 Richmond Richmond City – 23293 Richmond Richmond City View
Map 23294 Richmond Henrico – 23295 Richmond Richmond City – 23297 Richmond Chesterfield – 23298 Richmond Richmond City – 23301 Accomac Accomack – 23302 Assawoman Accomack – 23303 Atlantic Accomack – 23304 Battery Park Isle Of Wight – 23306 Belle Haven Accomack – 23307 Birdsnest Northampton – 23308 Bloxom Accomack – 23310 Cape Charles Northampton – 23313 Capeville Northampton – 23314 Carrollton Isle Of Wight – 23315 Carrsville Isle Of Wight – 23316 Cheriton Northampton – 23320 Chesapeake Chesapeake City – 23321 Chesapeake Chesapeake City – 23322 Chesapeake Chesapeake City View
Map 23323 Chesapeake Chesapeake City – 23324 Chesapeake Chesapeake City – 23325 Chesapeake Chesapeake City – 23326 Chesapeake Chesapeake City – 23327 Chesapeake Chesapeake City – 23328 Chesapeake Chesapeake City – 23336 Chincoteague Island Accomack – 23337 Wallops Island Accomack – 23341 Craddockville Accomack – 23345 Davis Wharf Accomack – 23347 Eastville Northampton – 23350 Exmore Northampton – 23354 Franktown Northampton – 23356 Greenbackville Accomack – 23357 Greenbush Accomack – 23358 Hacksneck Accomack – 23359 Hallwood Accomack – 23389 Harborton Accomack – 23395 Horntown Accomack View
Map 23396 Oak Hall Accomack – 23397 Isle Of Wight Isle Of Wight – 23398 Jamesville Northampton – 23399 Jenkins Bridge Accomack – 23401 Keller Accomack – 23404 Locustville Accomack – 23405 Machipongo Northampton – 23407 Mappsville Accomack – 23408 Marionville Northampton – 23409 Mears Accomack – 23410 Melfa Accomack – 23412 Modest Town Accomack – 23413 Nassawadox Northampton – 23414 Nelsonia Accomack – 23415 New Church Accomack – 23416 Oak Hall Accomack – 23417 Onancock Accomack – 23418 Onley Accomack – 23419 Oyster Northampton View
Map 23420 Painter Accomack – 23421 Parksley Accomack – 23422 Pungoteague Accomack – 23423 Quinby Accomack – 23424 Rescue Isle Of Wight – 23426 Sanford Accomack – 23427 Saxis Accomack – 23429 Seaview Northampton – 23430 Smithfield Isle Of Wight – 23431 Smithfield Isle Of Wight – 23432 Suffolk Suffolk City – 23433 Suffolk Suffolk City – 23434 Suffolk Suffolk City – 23435 Suffolk Suffolk City – 23436 Suffolk Suffolk City – 23437 Suffolk Suffolk City – 23438 Suffolk Suffolk City – 23439 Suffolk Suffolk City – 23440 Tangier Accomack View
Map 23441 Tasley Accomack – 23442 Temperanceville Accomack – 23443 Townsend Northampton – 23450 Virginia Beach Virginia Beach City – 23451 Virginia Beach Virginia Beach City – 23452 Virginia Beach Virginia Beach City – 23453 Virginia Beach Virginia Beach City – 23454 Virginia Beach Virginia Beach City – 23455 Virginia Beach Virginia Beach City – 23456 Virginia Beach Virginia Beach City – 23457 Virginia Beach Virginia Beach City – 23458 Virginia Beach Virginia Beach City – 23459 Virginia Beach Virginia Beach City – 23460 Virginia Beach Virginia Beach City – 23461 Virginia Beach Virginia Beach City – 23462 Virginia Beach Virginia Beach City – 23463 Virginia Beach Virginia Beach City – 23464 Virginia Beach Virginia Beach City – 23465 Virginia Beach Virginia Beach City View
Map 23466 Virginia Beach Virginia Beach City – 23467 Virginia Beach Virginia Beach City – 23471 Virginia Beach Virginia Beach City – 23479 Virginia Beach Virginia Beach City – 23480 Wachapreague Accomack – 23482 Wardtown Northampton – 23483 Wattsville Accomack – 23486 Willis Wharf Northampton – 23487 Windsor Isle Of Wight – 23488 Withams Accomack – 23501 Norfolk Norfolk City – 23502 Norfolk Norfolk City – 23503 Norfolk Norfolk City – 23504 Norfolk Norfolk City – 23505 Norfolk Norfolk City – 23506 Norfolk Norfolk City – 23507 Norfolk Norfolk City – 23508 Norfolk Norfolk City – 23509 Norfolk Norfolk City View
Map 23510 Norfolk Norfolk City – 23511 Norfolk Norfolk City – 23512 Norfolk Norfolk City – 23513 Norfolk Norfolk City – 23514 Norfolk Norfolk City – 23515 Norfolk Norfolk City – 23517 Norfolk Norfolk City – 23518 Norfolk Norfolk City – 23519 Norfolk Norfolk City – 23520 Norfolk Norfolk City – 23521 Norfolk Norfolk City – 23523 Norfolk Norfolk City – 23529 Norfolk Norfolk City – 23541 Norfolk Norfolk City – 23551 Norfolk Norfolk City – 23601 Newport News Newport News City – 23602 Newport News Newport News City – 23603 Newport News Newport News City – 23604 Fort Eustis Newport News City View
Map 23605 Newport News Newport News City – 23606 Newport News Newport News City – 23607 Newport News Newport News City – 23608 Newport News Newport News City – 23609 Newport News Newport News City – 23612 Newport News Newport News City – 23628 Newport News Newport News City – 23630 Hampton Hampton City – 23651 Fort Monroe Hampton City – 23661 Hampton Hampton City – 23662 Poquoson Poquoson City – 23663 Hampton Hampton City – 23664 Hampton Hampton City – 23665 Hampton York – 23666 Hampton Hampton City – 23667 Hampton Hampton City – 23668 Hampton Hampton City – 23669 Hampton Hampton City – 23670 Hampton Hampton City View
Map 23681 Hampton Hampton City – 23690 Yorktown York – 23691 Yorktown York – 23692 Yorktown York – 23693 Yorktown York – 23694 Lackey York – 23696 Seaford York – 23701 Portsmouth Portsmouth City – 23702 Portsmouth Portsmouth City – 23703 Portsmouth Portsmouth City – 23704 Portsmouth Portsmouth City – 23705 Portsmouth Portsmouth City – 23707 Portsmouth Portsmouth City – 23708 Portsmouth Portsmouth City – 23709 Portsmouth Portsmouth City – 23801 Fort Lee Prince George – 23803 Petersburg Petersburg City – 23804 Petersburg Petersburg City – 23805 Petersburg Petersburg City View
Map 23806 Petersburg Petersburg City – 23821 Alberta Brunswick – 23822 Ammon Dinwiddie – 23824 Blackstone Nottoway – 23825 Blackstone Nottoway – 23827 Boykins Southampton – 23828 Branchville Southampton – 23829 Capron Southampton – 23830 Carson Dinwiddie – 23831 Chester Chesterfield – 23832 Chesterfield Chesterfield – 23833 Church Road Dinwiddie – 23834 Colonial Heights Colonial Heights City – 23836 Chester Chesterfield – 23837 Courtland Southampton – 23838 Chesterfield Chesterfield – 23839 Dendron Surry – 23840 Dewitt Dinwiddie – 23841 Dinwiddie Dinwiddie View
Map 23842 Disputanta Prince George – 23843 Dolphin Brunswick – 23844 Drewryville Southampton – 23845 Ebony Brunswick – 23846 Elberon Surry – 23847 Emporia Greensville – 23850 Ford Dinwiddie – 23851 Franklin Franklin City – 23856 Freeman Brunswick – 23857 Gasburg Brunswick – 23860 Hopewell Hopewell City – 23866 Ivor Southampton – 23867 Jarratt Greensville – 23868 Lawrenceville Brunswick – 23870 Jarratt Greensville – 23872 Mc Kenney Dinwiddie – 23873 Meredithville Brunswick – 23874 Newsoms Southampton – 23875 Prince George Prince George View
Map 23876 Rawlings Brunswick – 23878 Sedley Southampton – 23879 Skippers Greensville – 23881 Spring Grove Surry – 23882 Stony Creek Sussex – 23883 Surry Surry – 23884 Sussex Sussex – 23885 Sutherland Dinwiddie – 23887 Valentines Brunswick – 23888 Wakefield Sussex – 23889 Warfield Brunswick – 23890 Waverly Sussex – 23891 Waverly Sussex – 23893 White Plains Brunswick – 23894 Wilsons Dinwiddie – 23897 Yale Sussex – 23898 Zuni Isle Of Wight – 23899 Claremont Surry – 23901 Farmville Prince Edward View
Map 23909 Farmville Prince Edward – 23915 Baskerville Mecklenburg – 23917 Boydton Mecklenburg – 23919 Bracey Mecklenburg – 23920 Brodnax Brunswick – 23921 Buckingham Buckingham – 23922 Burkeville Nottoway – 23923 Charlotte Court House Charlotte – 23924 Chase City Mecklenburg – 23927 Clarksville Mecklenburg – 23930 Crewe Nottoway – 23934 Cullen Charlotte – 23936 Dillwyn Buckingham – 23937 Drakes Branch Charlotte – 23938 Dundas Lunenburg – 23939 Evergreen Appomattox – 23941 Fort Mitchell Lunenburg – 23942 Green Bay Prince Edward – 23943 Hampden Sydney Prince Edward View
Map 23944 Kenbridge Lunenburg – 23947 Keysville Charlotte – 23950 La Crosse Mecklenburg – 23952 Lunenburg Lunenburg – 23954 Meherrin Prince Edward – 23955 Nottoway Nottoway – 23958 Pamplin Appomattox – 23959 Phenix Charlotte – 23960 Prospect Prince Edward – 23962 Randolph Charlotte – 23963 Red House Charlotte – 23964 Red Oak Charlotte – 23966 Rice Prince Edward – 23967 Saxe Charlotte – 23968 Skipwith Mecklenburg – 23970 South Hill Mecklenburg – 23974 Victoria Lunenburg – 23976 Wylliesburg Charlotte – 24001 Roanoke Roanoke City View
Map 24002 Roanoke Roanoke City – 24003 Roanoke Roanoke City – 24004 Roanoke Roanoke City – 24005 Roanoke Roanoke City – 24006 Roanoke Roanoke City – 24007 Roanoke Roanoke City – 24008 Roanoke Roanoke City – 24009 Roanoke Roanoke City – 24010 Roanoke Roanoke City – 24011 Roanoke Roanoke City – 24012 Roanoke Roanoke City – 24013 Roanoke Roanoke City – 24014 Roanoke Roanoke City – 24015 Roanoke Roanoke City – 24016 Roanoke Roanoke City – 24017 Roanoke Roanoke City – 24018 Roanoke Roanoke – 24019 Roanoke Roanoke – 24020 Roanoke Roanoke View
Map 24022 Roanoke Roanoke City – 24023 Roanoke Roanoke City – 24024 Roanoke Roanoke City – 24025 Roanoke Roanoke City – 24026 Roanoke Roanoke City – 24027 Roanoke Roanoke City – 24028 Roanoke Roanoke City – 24029 Roanoke Roanoke City – 24030 Roanoke Roanoke City – 24031 Roanoke Roanoke City – 24032 Roanoke Roanoke City – 24033 Roanoke Roanoke City – 24034 Roanoke Roanoke City – 24035 Roanoke Roanoke City – 24036 Roanoke Roanoke City – 24037 Roanoke Roanoke City – 24038 Roanoke Roanoke City – 24040 Roanoke Roanoke City – 24042 Roanoke Roanoke City View
Map 24043 Roanoke Roanoke City – 24044 Roanoke Roanoke City – 24045 Roanoke Roanoke City – 24048 Roanoke Roanoke City – 24050 Roanoke Botetourt – 24053 Ararat Patrick – 24054 Axton Henry – 24055 Bassett Henry – 24058 Belspring Pulaski – 24059 Bent Mountain Roanoke – 24060 Blacksburg Montgomery – 24061 Blacksburg Montgomery – 24062 Blacksburg Montgomery – 24063 Blacksburg Montgomery – 24064 Blue Ridge Botetourt – 24065 Boones Mill Franklin – 24066 Buchanan Botetourt – 24067 Callaway Franklin – 24068 Christiansburg Montgomery View
Map 24069 Cascade Pittsylvania – 24070 Catawba Roanoke – 24072 Check Floyd – 24073 Christiansburg Montgomery – 24076 Claudville Patrick – 24077 Cloverdale Botetourt – 24078 Collinsville Henry – 24079 Copper Hill Floyd – 24082 Critz Patrick – 24083 Daleville Botetourt – 24084 Dublin Pulaski – 24085 Eagle Rock Botetourt – 24086 Eggleston Giles – 24087 Elliston Montgomery – 24088 Ferrum Franklin – 24089 Fieldale Henry – 24090 Fincastle Botetourt – 24091 Floyd Floyd – 24092 Glade Hill Franklin View
Map 24093 Glen Lyn Giles – 24095 Goodview Bedford – 24101 Hardy Franklin – 24102 Henry Franklin – 24104 Huddleston Bedford – 24105 Indian Valley Floyd – 24111 Mc Coy Montgomery – 24112 Martinsville Martinsville City – 24113 Martinsville Martinsville City – 24114 Martinsville Martinsville City – 24115 Martinsville Martinsville City – 24120 Meadows Of Dan Patrick – 24121 Moneta Bedford – 24122 Montvale Bedford – 24124 Narrows Giles – 24126 Newbern Pulaski – 24127 New Castle Craig – 24128 Newport Giles – 24129 New River Pulaski View
Map 24130 Oriskany Botetourt – 24131 Paint Bank Craig – 24132 Parrott Pulaski – 24133 Patrick Springs Patrick – 24134 Pearisburg Giles – 24136 Pembroke Giles – 24137 Penhook Franklin – 24138 Pilot Montgomery – 24139 Pittsville Pittsylvania – 24141 Radford Radford – 24142 Radford Radford – 24143 Radford Radford – 24146 Redwood Franklin – 24147 Rich Creek Giles – 24148 Ridgeway Henry – 24149 Riner Montgomery – 24150 Ripplemead Giles – 24151 Rocky Mount Franklin – 24153 Salem Salem View
Map 24155 Roanoke Salem – 24157 Roanoke Salem – 24161 Sandy Level Pittsylvania – 24162 Shawsville Montgomery – 24165 Spencer Henry – 24167 Staffordsville Giles – 24168 Stanleytown Henry – 24171 Stuart Patrick – 24174 Thaxton Bedford – 24175 Troutville Botetourt – 24176 Union Hall Franklin – 24177 Vesta Patrick – 24178 Villamont Bedford – 24179 Vinton Roanoke – 24184 Wirtz Franklin – 24185 Woolwine Patrick – 24201 Bristol Bristol – 24202 Bristol Washington – 24203 Bristol Bristol View
Map 24209 Bristol Bristol – 24210 Abingdon Washington – 24211 Abingdon Washington – 24212 Abingdon Washington – 24215 Andover Wise – 24216 Appalachia Wise – 24217 Bee Dickenson – 24218 Ben Hur Lee – 24219 Big Stone Gap Wise – 24220 Birchleaf Dickenson – 24221 Blackwater Lee – 24224 Castlewood Russell – 24225 Cleveland Russell – 24226 Clinchco Dickenson – 24228 Clintwood Dickenson – 24230 Coeburn Wise – 24236 Damascus Washington – 24237 Dante Russell – 24239 Davenport Buchanan View
Map 24243 Dryden Lee – 24244 Duffield Scott – 24245 Dungannon Scott – 24246 East Stone Gap Wise – 24248 Ewing Lee – 24250 Fort Blackmore Scott – 24251 Gate City Scott – 24256 Haysi Dickenson – 24258 Hiltons Scott – 24260 Honaker Russell – 24263 Jonesville Lee – 24265 Keokee Lee – 24266 Lebanon Russell – 24269 Mc Clure Dickenson – 24270 Mendota Washington – 24271 Nickelsville Scott – 24272 Nora Dickenson – 24273 Norton Norton City – 24277 Pennington Gap Lee View
Map 24279 Pound Wise – 24280 Rosedale Russell – 24281 Rose Hill Lee – 24282 Saint Charles Lee – 24283 Saint Paul Wise – 24290 Weber City Scott – 24292 Whitetop Grayson – 24293 Wise Wise – 24301 Pulaski Pulaski – 24311 Atkins Smyth – 24312 Austinville Wythe – 24313 Barren Springs Wythe – 24314 Bastian Bland – 24315 Bland Bland – 24316 Broadford Tazewell – 24317 Cana Carroll – 24318 Ceres Bland – 24319 Chilhowie Smyth – 24322 Cripple Creek Wythe View
Map 24323 Crockett Wythe – 24324 Draper Pulaski – 24325 Dugspur Carroll – 24326 Elk Creek Grayson – 24327 Emory Washington – 24328 Fancy Gap Carroll – 24330 Fries Grayson – 24333 Galax Galax City – 24340 Glade Spring Washington – 24343 Hillsville Carroll – 24347 Hiwassee Pulaski – 24348 Independence Grayson – 24350 Ivanhoe Wythe – 24351 Lambsburg Carroll – 24352 Laurel Fork Carroll – 24354 Marion Smyth – 24360 Max Meadows Wythe – 24361 Meadowview Washington – 24363 Mouth Of Wilson Grayson View
Map 24366 Rocky Gap Bland – 24368 Rural Retreat Wythe – 24370 Saltville Smyth – 24374 Speedwell Wythe – 24375 Sugar Grove Smyth – 24377 Tannersville Tazewell – 24378 Troutdale Grayson – 24380 Willis Floyd – 24381 Woodlawn Carroll – 24382 Wytheville Wythe – 24401 Staunton Staunton City – 24402 Staunton Staunton City – 24411 Augusta Springs Augusta – 24412 Bacova Bath – 24413 Blue Grass Highland – 24415 Brownsburg Rockbridge – 24416 Buena Vista Buena Vista City – 24421 Churchville Augusta – 24422 Clifton Forge Alleghany View
Map 24426 Covington Covington City – 24430 Craigsville Augusta – 24431 Crimora Augusta – 24432 Deerfield Augusta – 24433 Doe Hill Highland – 24435 Fairfield Rockbridge – 24437 Fort Defiance Augusta – 24438 Glen Wilton Botetourt – 24439 Goshen Rockbridge – 24440 Greenville Augusta – 24441 Grottoes Rockingham – 24442 Head Waters Highland – 24445 Hot Springs Bath – 24448 Iron Gate Alleghany – 24450 Lexington Lexington City – 24457 Low Moor Alleghany – 24458 Mc Dowell Highland – 24459 Middlebrook Augusta – 24460 Millboro Bath View
Map 24463 Mint Spring Augusta – 24464 Montebello Nelson – 24465 Monterey Highland – 24467 Mount Sidney Augusta – 24468 Mustoe Highland – 24469 New Hope Augusta – 24471 Port Republic Rockingham – 24472 Raphine Rockbridge – 24473 Rockbridge Baths Rockbridge – 24474 Selma Alleghany – 24476 Steeles Tavern Augusta – 24477 Stuarts Draft Augusta – 24479 Swoope Augusta – 24482 Verona Augusta – 24483 Vesuvius Rockbridge – 24484 Warm Springs Bath – 24485 West Augusta Augusta – 24486 Weyers Cave Augusta – 24487 Williamsville Bath View
Map 24501 Lynchburg Lynchburg City – 24502 Lynchburg Lynchburg City – 24503 Lynchburg Lynchburg City – 24504 Lynchburg Lynchburg City – 24505 Lynchburg Lynchburg City – 24506 Lynchburg Lynchburg City – 24512 Lynchburg Lynchburg City – 24513 Lynchburg Lynchburg City – 24514 Lynchburg Lynchburg City – 24515 Lynchburg Lynchburg City – 24517 Altavista Campbell – 24520 Alton Halifax – 24521 Amherst Amherst – 24522 Appomattox Appomattox – 24523 Bedford Bedford – 24526 Big Island Bedford – 24527 Blairs Pittsylvania – 24528 Brookneal Campbell – 24529 Buffalo Junction Mecklenburg View
Map 24530 Callands Pittsylvania – 24531 Chatham Pittsylvania – 24533 Clifford Amherst – 24534 Clover Halifax – 24535 Cluster Springs Halifax – 24536 Coleman Falls Bedford – 24538 Concord Campbell – 24539 Crystal Hill Halifax – 24540 Danville Danville City – 24541 Danville Danville City – 24543 Danville Danville City – 24544 Danville Danville City – 24549 Dry Fork Pittsylvania – 24550 Evington Campbell – 24551 Forest Bedford – 24553 Gladstone Nelson – 24554 Gladys Campbell – 24555 Glasgow Rockbridge – 24556 Goode Bedford View
Map 24557 Gretna Pittsylvania – 24558 Halifax Halifax – 24562 Howardsville Buckingham – 24563 Hurt Pittsylvania – 24565 Java Pittsylvania – 24566 Keeling Pittsylvania – 24569 Long Island Pittsylvania – 24570 Lowry Bedford – 24571 Lynch Station Campbell – 24572 Madison Heights Amherst – 24574 Monroe Amherst – 24576 Naruna Campbell – 24577 Nathalie Halifax – 24578 Natural Bridge Rockbridge – 24579 Natural Bridge Station Rockbridge – 24580 Nelson Mecklenburg – 24581 Norwood Nelson – 24586 Ringgold Pittsylvania – 24588 Rustburg Campbell View
Map 24589 Scottsburg Halifax – 24590 Scottsville Albemarle – 24592 South Boston Halifax – 24593 Spout Spring Appomattox – 24594 Sutherlin Pittsylvania – 24595 Sweet Briar Amherst – 24597 Vernon Hill Halifax – 24598 Virgilina Halifax – 24599 Wingina Buckingham – 24601 Amonate Tazewell – 24602 Bandy Tazewell – 24603 Big Rock Buchanan – 24604 Bishop Tazewell – 24605 Bluefield Tazewell – 24606 Boissevain Tazewell – 24607 Breaks Dickenson – 24608 Burkes Garden Tazewell – 24609 Cedar Bluff Tazewell – 24612 Doran Tazewell View
Map 24613 Falls Mills Tazewell – 24614 Grundy Buchanan – 24619 Horsepen Tazewell – 24620 Hurley Buchanan – 24622 Jewell Ridge Tazewell – 24624 Keen Mountain Buchanan – 24627 Mavisdale Buchanan – 24628 Maxie Buchanan – 24630 North Tazewell Tazewell – 24631 Oakwood Buchanan – 24634 Pilgrims Knob Buchanan – 24635 Pocahontas Tazewell – 24637 Pounding Mill Tazewell – 24639 Raven Buchanan – 24640 Red Ash Tazewell – 24641 Richlands Tazewell – 24646 Rowe Buchanan – 24647 Shortt Gap Buchanan – 24649 Swords Creek Russell View
Map 24651 Tazewell Tazewell – 24656 Vansant Buchanan – 24657 Whitewood Buchanan – 24658 Wolford Buchanan – 24701 Bluefield Mercer – 24712 Athens Mercer – 24714 Beeson Mercer – 24715 Bramwell Mercer – 24716 Bud Wyoming – 24719 Covel Wyoming – 24724 Freeman Mercer – 24726 Herndon Wyoming – 24729 Hiawatha Mercer – 24731 Kegley Mercer – 24732 Kellysville Mercer – 24733 Lashmeet Mercer – 24736 Matoaka Mercer – 24737 Montcalm Mercer – 24738 Nemours Mercer View
Map 24739 Oakvale Mercer – 24740 Princeton Mercer – 24747 Rock Mercer – 24751 Wolfe Mercer – 24801 Welch Mcdowell – 24808 Anawalt Mcdowell – 24811 Avondale Mcdowell – 24813 Bartley Mcdowell – 24815 Berwind Mcdowell – 24816 Big Sandy Mcdowell – 24817 Bradshaw Mcdowell – 24818 Brenton Wyoming – 24822 Clear Fork Wyoming – 24823 Coal Mountain Wyoming – 24824 Coalwood Mcdowell – 24826 Cucumber Mcdowell – 24827 Cyclone Wyoming – 24828 Davy Mcdowell – 24829 Eckman Mcdowell View
Map 24830 Elbert Mcdowell – 24831 Elkhorn Mcdowell – 24834 Fanrock Wyoming – 24836 Gary Mcdowell – 24839 Hanover Wyoming – 24842 Hemphill Mcdowell – 24843 Hensley Mcdowell – 24844 Iaeger Mcdowell – 24845 Ikes Fork Wyoming – 24846 Isaban Mcdowell – 24847 Itmann Wyoming – 24848 Jenkinjones Mcdowell – 24849 Jesse Wyoming – 24850 Jolo Mcdowell – 24851 Justice Mingo – 24853 Kimball Mcdowell – 24854 Kopperston Wyoming – 24855 Kyle Mcdowell – 24857 Lynco Wyoming View
Map 24859 Marianna Wyoming – 24860 Matheny Wyoming – 24861 Maybeury Mcdowell – 24862 Mohawk Mcdowell – 24866 Newhall Mcdowell – 24867 New Richmond Wyoming – 24868 Northfork Mcdowell – 24869 North Spring Wyoming – 24870 Oceana Wyoming – 24871 Pageton Mcdowell – 24872 Panther Mcdowell – 24873 Paynesville Mcdowell – 24874 Pineville Wyoming – 24878 Premier Mcdowell – 24879 Raysal Mcdowell – 24880 Rock View Wyoming – 24881 Roderfield Mcdowell – 24882 Simon Wyoming – 24884 Squire Mcdowell View
Map 24887 Switchback Mcdowell – 24888 Thorpe Mcdowell – 24892 War Mcdowell – 24894 Warriormine Mcdowell – 24895 Wilcoe Mcdowell – 24898 Wyoming Wyoming – 24901 Lewisburg Greenbrier – 24902 Fairlea Greenbrier – 24910 Alderson Greenbrier – 24915 Arbovale Pocahontas – 24916 Asbury Greenbrier – 24918 Ballard Monroe – 24920 Bartow Pocahontas – 24924 Buckeye Pocahontas – 24925 Caldwell Greenbrier – 24927 Cass Pocahontas – 24931 Crawley Greenbrier – 24934 Dunmore Pocahontas – 24935 Forest Hill Summers View
Map 24938 Frankford Greenbrier – 24941 Gap Mills Monroe – 24943 Grassy Meadows Greenbrier – 24944 Green Bank Pocahontas – 24945 Greenville Monroe – 24946 Hillsboro Pocahontas – 24951 Lindside Monroe – 24954 Marlinton Pocahontas – 24957 Maxwelton Greenbrier – 24961 Neola Greenbrier – 24962 Pence Springs Summers – 24963 Peterstown Monroe – 24966 Renick Greenbrier – 24970 Ronceverte Greenbrier – 24974 Secondcreek Monroe – 24976 Sinks Grove Monroe – 24977 Smoot Greenbrier – 24981 Talcott Summers – 24983 Union Monroe View
Map 24984 Waiteville Monroe – 24985 Wayside Monroe – 24986 White Sulphur Springs Greenbrier – 24991 Williamsburg Greenbrier – 24993 Wolfcreek Monroe – 25002 Alloy Fayette – 25003 Alum Creek Kanawha – 25005 Amma Roane – 25007 Arnett Raleigh – 25008 Artie Raleigh – 25009 Ashford Boone – 25011 Bancroft Putnam – 25015 Belle Kanawha – 25019 Bickmore Clay – 25021 Bim Boone – 25022 Blair Logan – 25024 Bloomingrose Boone – 25025 Blount Kanawha – 25026 Blue Creek Kanawha View
Map 25028 Bob White Boone – 25030 Bomont Clay – 25031 Boomer Fayette – 25033 Buffalo Putnam – 25035 Cabin Creek Kanawha – 25036 Cannelton Fayette – 25039 Cedar Grove Kanawha – 25040 Charlton Heights Fayette – 25043 Clay Clay – 25044 Clear Creek Raleigh – 25045 Clendenin Kanawha – 25047 Clothier Logan – 25048 Colcord Raleigh – 25049 Comfort Boone – 25051 Costa Boone – 25053 Danville Boone – 25054 Dawes Kanawha – 25057 Deep Water Fayette – 25059 Dixie Nicholas View
Map 25060 Dorothy Raleigh – 25061 Drybranch Kanawha – 25062 Dry Creek Raleigh – 25063 Duck Clay – 25064 Dunbar Kanawha – 25067 East Bank Kanawha – 25070 Eleanor Putnam – 25071 Elkview Kanawha – 25075 Eskdale Kanawha – 25076 Ethel Logan – 25079 Falling Rock Kanawha – 25081 Foster Boone – 25082 Fraziers Bottom Putnam – 25083 Gallagher Kanawha – 25085 Gauley Bridge Fayette – 25086 Glasgow Kanawha – 25088 Glen Clay – 25090 Glen Ferris Fayette – 25093 Gordon Boone View
Map 25102 Handley Kanawha – 25103 Hansford Kanawha – 25106 Henderson Mason – 25107 Hernshaw Kanawha – 25108 Hewett Boone – 25109 Hometown Putnam – 25110 Hugheston Kanawha – 25111 Indore Clay – 25112 Institute Kanawha – 25113 Ivydale Clay – 25114 Jeffrey Boone – 25115 Kanawha Falls Fayette – 25118 Kimberly Fayette – 25119 Kincaid Fayette – 25121 Lake Logan – 25123 Leon Mason – 25124 Liberty Putnam – 25125 Lizemores Clay – 25126 London Kanawha View
Map 25130 Madison Boone – 25132 Mammoth Kanawha – 25133 Maysel Clay – 25134 Miami Kanawha – 25136 Montgomery Fayette – 25139 Mount Carbon Fayette – 25140 Naoma Raleigh – 25141 Nebo Clay – 25142 Nellis Boone – 25143 Nitro Kanawha – 25148 Orgas Boone – 25149 Ottawa Boone – 25152 Page Fayette – 25154 Peytona Boone – 25156 Pinch Kanawha – 25159 Poca Putnam – 25160 Pond Gap Kanawha – 25161 Powellton Fayette – 25162 Pratt Kanawha View
Map 25164 Procious Clay – 25165 Racine Boone – 25168 Red House Putnam – 25169 Ridgeview Boone – 25173 Robson Fayette – 25174 Rock Creek Raleigh – 25177 Saint Albans Kanawha – 25180 Saxon Boone – 25181 Seth Boone – 25183 Sharples Logan – 25185 Mount Olive Fayette – 25186 Smithers Fayette – 25187 Southside Mason – 25193 Sylvester Boone – 25201 Tad Kanawha – 25202 Tornado Kanawha – 25203 Turtle Creek Boone – 25204 Twilight Boone – 25205 Uneeda Boone View
Map 25206 Van Boone – 25208 Wharton Boone – 25209 Whitesville Boone – 25211 Widen Clay – 25213 Winfield Putnam – 25214 Winifrede Kanawha – 25231 Advent Jackson – 25234 Arnoldsburg Calhoun – 25235 Chloe Calhoun – 25239 Cottageville Jackson – 25241 Evans Jackson – 25243 Gandeeville Roane – 25244 Gay Jackson – 25245 Given Jackson – 25247 Hartford Mason – 25248 Kenna Jackson – 25251 Left Hand Roane – 25252 Le Roy Jackson – 25253 Letart Mason View
Map 25259 Looneyville Roane – 25260 Mason Mason – 25261 Millstone Calhoun – 25262 Millwood Jackson – 25264 Mount Alto Mason – 25265 New Haven Mason – 25266 Newton Roane – 25267 Normantown Gilmer – 25268 Orma Calhoun – 25270 Reedy Roane – 25271 Ripley Jackson – 25275 Sandyville Jackson – 25276 Spencer Roane – 25285 Wallback Clay – 25286 Walton Roane – 25287 West Columbia Mason – 25301 Charleston Kanawha – 25302 Charleston Kanawha – 25303 Charleston Kanawha View
Map 25304 Charleston Kanawha – 25305 Charleston Kanawha – 25306 Charleston Kanawha – 25309 Charleston Kanawha – 25311 Charleston Kanawha – 25312 Charleston Kanawha – 25313 Charleston Kanawha – 25314 Charleston Kanawha – 25315 Charleston Kanawha – 25317 Charleston Kanawha – 25320 Charleston Kanawha – 25321 Charleston Kanawha – 25322 Charleston Kanawha – 25323 Charleston Kanawha – 25324 Charleston Kanawha – 25325 Charleston Kanawha – 25326 Charleston Kanawha – 25327 Charleston Kanawha – 25328 Charleston Kanawha View
Map 25329 Charleston Kanawha – 25330 Charleston Kanawha – 25331 Charleston Kanawha – 25332 Charleston Kanawha – 25333 Charleston Kanawha – 25334 Charleston Kanawha – 25335 Charleston Kanawha – 25336 Charleston Kanawha – 25337 Charleston Kanawha – 25338 Charleston Kanawha – 25339 Charleston Kanawha – 25350 Charleston Kanawha – 25356 Charleston Kanawha – 25357 Charleston Kanawha – 25358 Charleston Kanawha – 25360 Charleston Kanawha – 25361 Charleston Kanawha – 25362 Charleston Kanawha – 25364 Charleston Kanawha View
Map 25365 Charleston Kanawha – 25375 Charleston Kanawha – 25387 Charleston Kanawha – 25389 Charleston Kanawha – 25392 Charleston Kanawha – 25396 Charleston Kanawha – 25401 Martinsburg Berkeley – 25402 Martinsburg Berkeley – 25403 Martinsburg Berkeley – 25404 Martinsburg Berkeley – 25405 Martinsburg Berkeley – 25410 Bakerton Jefferson – 25411 Berkeley Springs Morgan – 25413 Bunker Hill Berkeley – 25414 Charles Town Jefferson – 25419 Falling Waters Berkeley – 25420 Gerrardstown Berkeley – 25421 Glengary Berkeley – 25422 Great Cacapon Morgan View
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Ketamine: Key Predictor of Treatment Response for MDD Identified

 

 

I am going to link into a few articles that discuss a phenomena that I have observed in the office setting at NOVA Health Recovery (Alexandria, Va 703-844-0184) for our Ketamine infusions in depressed and PTSD patients. The best long term results seem to occur when the individual has a slightly more dissociative experience during the infusion.  A lot of times I will give an initial boost to the medication at the start to get that state of mind going. Studies below have hinted that the slight dissociation actually improves outcomes:

Ketamine: Key Predictor of Treatment Response for MDD Identified  < Medscape article

 

Ketamine: Key Predictor of Treatment Response for MDD Identified

Nancy A. Melville

April 12, 2018

WASHINGTON — More intense dissociative symptoms exhibited during ketamine infusion for severe depression, particularly depersonalization, may be key predictors of treatment response. In addition, new safety and efficacy data for off-label use of the drug are encouraging.

Mark Niciu, MD, PhD, of the National Institute of Mental Health (NIMH), and colleagues analyzed three studies involving 126 patients with treatment-resistant depression. They found a significant association between dissociative symptoms experienced during infusion and reductions in depressive symptoms, as reflected in some, but not all, dissociation subscale measures.

“The findings suggest that mechanistic similarities may exist between ketamine-induced depersonalization and antidepressant response, although off-target effects cannot be excluded,” Niciu told delegates attending the Anxiety and Depression Association of America (ADAA) Conference 2018.

The results were also published in the May issue of the Journal of Affective Disorders.

In another presentation at the ADAA conference, Samuel Wilkinson, MD, assistant director of the Depression Research Program at Yale University, New Haven, Connecticut, reported details from his institution’s experience with the use of ketamine during a period of more than 30 months in patients with severe and treatment-resistant mood disorders.

Among 50 patients who received one to four treatments, the response rate, defined as a 50% improvement in symptoms, was approximately 50%; the remission rate was 27.3%.

In a subset of 14 patients who received 12 to 45 total treatments during a period of 14 to 126 weeks, there was no evidence of cognitive decline or delusions, as measured with the CogState cognitive assessment tool, Wilkinson reported.

Soaring Interest

Because conventional antidepressants can take weeks if not months to reach full effect and are completely ineffective in many patients, interest in ketamine, an N-methyl-d-aspartate receptor antagonist, as a rapid-acting treatment for severe mood disorders has soared in recent years, noted Niciu.

Previous studies have reported significant improvements in depression following a single ketamine infusion, with improvements lasting from several days to a week. However, not everyone responds to ketamine.

In the new study, 84 of the 126 participants had major depressive disorder, and 42 had bipolar depression. All were treated with the standard ketamine treatment for depression, consisting of a single subanesthetic dose (0.5 mg/kg) delivered by infusion over 40 minutes.

Patients were followed for at least 1 week post infusion and, in one of the three studies that were assessed, for up to 28 days.

In one of the studies, dissociative effects, measured using the Clinician-Administered Dissociative States Scale (CADSS) at baseline and at the end of infusion, were associated with symptoms of depression, as measured with the Hamilton Depression Rating Scale (HDRS-17), at day 7 following the infusion (P = .04).

Scores on the depersonalization subscale of the CADSS were related to percentage change in HDRS-17 score in all three studies and at all time points (P = .04).

Scores on the subscale of derealization were associated with percentage change in HDRS score on day 7 post infusion in one study (P = .01).

No association was observed between amnesia symptoms during infusion and reduction in depression, as reflected in percentage change in HDRS score.

Mechanistic Similarities

“What really jumped out at us was the depersonalization subscale,” Niciu said.

He speculated that depersonalization in particular may relate to some of the deeper aspects of depression, more so than derealization, which involves detachment from reality, or amnesia.

“There might be mechanistic similarities between depersonalization and an antidepressant response,” Niciu explained.

“These are people with a highly introspective disorder and are often focused on their inner self. If you can detach them from that for a period of time and disconnect them from the subjective sensations, then that may result in a better antidepressant response, but that’s a hypothesis,” he said.

The findings suggest that the use of the depersonalization scale could represent a relatively easy way to assess the possibility of the patient’s responding to ketamine.

“In the clinical setting, if someone is administering ketamine and doesn’t have much time and just wants to get a sense of how a patient might respond, the CADSS depersonalization subscale is something they might want to administer,” Niciu said.

“It is easy to administer — it’s only five items, and those who tend to score higher on that subscale may be more likely to be responders,” he added.

Relevance Questioned

The study was an extension of earlier research from the investigators linking the degree of dissociative symptoms with ketamine’s antidepressant effects.

On the basis of those findings, some clinicians already try to achieve the effects in order to evoke a better response, said Sanjay Mathew, MD, professor of psychiatry and behavioral sciences, Baylor College of Medicine and the Michael E. Debakey VA Medical Center, Houston, Texas, while commenting on the study at the meeting.

“Often, anesthesiologists and psychiatrists at ketamine clinics will start at 0.5 mg/kg and titrate the dose to mild dissociation,” said Matthew. “They often want the patient to feel buzzed, because that’s when they feel confident that they’ve hit the ‘sweet spot’ of NMDA modulation.”

He noted that another NIMH study of 99 patients, which is currently under review, showed that the best outcomes, as reflected in scores on depression scales, were achieved with the standard 0.5 mg/kg dose in comparison with the 1.0 mg/kg dose and the very low dose of 0.1 mg/kg, which were associated with a high degree of dissociation.

“Clearly, the message from that study is that you don’t need to dissociate to get better,” he said.

Nevertheless, “the issue is fascinating, with high clinical relevance in terms of how clinicians are using ketamine in the community,” Mathew said.

However, Wilkinson noted that he has not seen similar patterns in his patients who were treated with ketamine, and he questioned the use of the CADSS tool for determining dissociation symptoms in the study.

“We have not observed that the level of dissociation and depersonalization predict response,” he told Medscape Medical News.

“I am skeptical of this finding, as the CADSS instrument was not designed for use in ketamine studies and in my opinion does not do a great job at capturing this phenomenon related to ketamine,” he added.

Wilkinson noted that the dissociative symptoms that can occur with ketamine treatment do not appear to subside after multiple infusion sessions.

“In my experience treating patients, there seem to be a group of patients who always develop fairly significant symptoms, even though they have been treated 20 times or more with ketamine,” he said.

Longer-term Outcomes

During the presentation of his own study, Wilkinson reported that 21 participants (38%) were men and 96% were being treated with concomitant medications during the acute course. These medications included antidepressants (72.2%), antipsychotics (53.7%), mood stabilizers (37%), lithium (18.5%), and sedatives/hypnotics (50%).

Patients were initially treated intravenously with a single or double infusion of 0.5 mg/kg over 40 minutes. However, patients were later transitioned to a four-dose protocol administered twice per week over 2 weeks.

The response rate was about 50%, and the remission rate was 27.3% among 50 patients who received one to four treatments.

Although there was no evidence of cognitive decline or delusions, one person discontinued infusion because of intolerability, one discontinued because of hypertension, one experienced relapse of cannabis use disorder, and three required rehospitalization for suicidal ideation or suicide attempts.

There were two completed suicides, one occurring 10 months after last contact with the program, and one 4 months after last contact.

Wilkinson noted that the 50% response rate is somewhat lower than rates reported in clinical trials, which may reflect a real-world setting.

“This is sometimes called the ‘efficacy-effectiveness gap’ and is not really surprising, because clinical trials are usually done in ideal conditions, whereas community practice represents real-world conditions and the patients are generally sicker and have comorbidities,” he told Medscape Medical News.

He added that once patients have responded to several weeks of ketamine treatments, efforts are made to help them shift to other forms of management.

 

“For those patients who do well following a series of four to six ketamine infusions, we initially try and keep them well using a strategy that does not involve repeated use of ketamine,” said Wilkinson.

 

Concerns Remain

Despite the encouraging improvements in depression that have been reported, the increased popularity of ketamine without long-term safety or efficacy data has raised considerable concerns, as reflected in aconsensus statement issued by an American Psychiatric Association Task Force in 2017.

Wilkinson said he shares the task force’s concerns.

“Ketamine has tremendous potential, but this needs to be tempered with the potential risks. There needs to be a higher level of regulation than currently exists,” he said.

“Ketamine is very safe in the short term, but we need better long-term data, because the risks of long-term adverse effects with repeated use are not theoretical,” Wilkinson added.

“We know that too much ketamine is not good for the brain or bladder. We just don’t know how much is too much,” he said.

Dr Niciu has disclosed no relevant financial relationships. The senior author of the study is a coinventor on a patent for the use of ketamine and its metabolites in the treatment of major depression. Although he assigned his rights in the patent to the US Government, he will share a percentage of any royalties that may be received. Wilkinson has received funding, administered through Yale University, from Janssen to conduct clinical trials with esketamine. He has also received consulting fees of less than $5000 from Janssen.

Anxiety and Depression Association of America (ADAA) Conference 2018. Session 341R, presented April 7, 2018.

 

CADSS-test-for-PTSD  <<Clinician-Administered Dissociative States Scale (CADSS)  A test to see how dissociated an individual is – the more the better!

 

Do the dissociative side effects of ketamine mediate its antidepressant effects?

Abstract

Background

The N-methyl-d-aspartate receptor antagonist ketamine has rapid antidepressant effects in major depression. Psychotomimetic symptoms, dissociation and hemodynamic changes are known side effects of ketamine, but it is unclear if these side effects relate to its antidepressant efficacy.

Methods

Data from 108 treatment-resistant inpatients meeting criteria for major depressive disorder and bipolar disorder who received a single subanesthetic ketamine infusion were analyzed. Pearson correlations were performed to examine potential associations between rapid changes in dissociation and psychotomimesis with the Clinician-Administered Dissociative States Scale (CADSS) and Brief Psychiatric Rating Scale (BPRS), respectively, manic symptoms with Young Mania Rating Scale (YMRS), and vital sign changes, with percent change in the 17-item Hamilton Depression Rating scale (HDRS) at 40 and 230 min and Days 1 and 7.

Results

Pearson correlations showed significant association between increased CADSS score at 40 min and percent improvement with ketamine in HDRS at 230 min (r=−0.35, p=0.007) and Day 7 (r=−0.41, p=0.01). Changes in YMRS or BPRS Positive Symptom score at 40 min were not significantly correlated with percent HDRS improvement at any time point with ketamine. Changes in systolic blood pressure, diastolic blood pressure, and pulse were also not significantly related to HDRS change.

Limitations

Secondary data analysis, combined diagnostic groups, potential unblinding.

Conclusions

Among the examined mediators of ketamine׳s antidepressant response, only dissociative side effects predicted a more robust and sustained antidepressant. Prospective, mechanistic investigations are critically needed to understand why intra-infusion dissociation correlates with a more robust antidepressant efficacy of ketamine.

Features of dissociation differentially predict antidepressant response to ketamine in treatment-resistant depression

Highlights

  • Intra-infusion dissociation is associated with antidepressant response to ketamine.
  • Antidepressant response may be uniquely related to dissociative symptom clusters.
  • Depersonalization was globally associated with antidepressant response.
  • Derealization was discriminately associated with antidepressant response.

Abstract

Background

Ketamine induces rapid and robust antidepressant effects, and many patients also describe dissociation, which is associated with antidepressant response. This follow-up study investigated whether antidepressant efficacy is uniquely related to dissociative symptom clusters.

Methods

Treatment-resistant patients with major depressive disorder (MDD) or bipolar disorder (BD) (n = 126) drawn from three studies received a single subanesthetic (0.5 mg/kg) ketamine infusion. Dissociative effects were measured using the Clinician-Administered Dissociative States Scale (CADSS). Antidepressant response was measured using the 17-item Hamilton Depression Rating Scale (HAM-D). A confirmatory factor analysis established the validity of CADSS subscales (derealization, depersonalization, amnesia), and a general linear model with repeated measures was fitted to test whether subscale scores were associated with antidepressant response.

Results

Factor validity was supported, with a root mean square error of approximation of .06, a comparative fit index of .97, and a Tucker-Lewis index of .96. Across all studies and timepoints, the depersonalization subscale was positively related to HAM-D percent change. A significant effect of derealization on HAM-D percent change was observed at one timepoint (Day 7) in one study. The amnesia subscale was unrelated to HAM-D percent change.

Limitations

Possible inadequate blinding; combined MDD/BD datasets might have underrepresented ketamine’s antidepressant efficacy; the possibility of Type I errors in secondary analyses.

Conclusions

From a psychometric perspective, researchers may elect to administer only the CADSS depersonalization subscale, given that it was most closely related to antidepressant response. From a neurobiological perspective, mechanistic similarities may exist between ketamine-induced depersonalization and antidepressant response, although off-target effects cannot be excluded.

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I sifted through the article and took out several points in the discussion of the article below.:

By taking the focus off “oneself” and placing it on other stimuli,
it is possible that ketamine decreases awareness of negative
experiences and consequently improves mood.

The transient dissociation experienced by depressed patients
during a ketamine infusion may have the effect of dampening
what the hyperactive self-monitoring associated with
depressive illness.

Radiology findings may reflect ketamine’s ability to reclaim frontal control over deeper limbic structures, thus strengthening the cognitive control of emotions and decreasing depressive symptoms.

Ketamine may cause a “disconnect”
in several circuits related to affective processing, perhaps
by shifting focus of attention away from the internal
states of anxiety, depression, and somatization, and more toward
the perceptual changes (e.g., hallucinations, visual distortions,
derealization) induced by ketamine. Similarly,
during an emotion task, ketamine attenuated responses to
negative pictures, suggesting that the processing of negative
information is specifically altered in response to ketamine.57
By taking the focus off “oneself” and placing it on other stimuli,
it is possible that ketamine decreases awareness of negative
experiences and consequently improves mood

Ketamine-Associated Brain Changes A Review of the Neuroimaging Literature

Abstract
Major depressive disorder (MDD) is one of the most prevalent conditions in psychiatry. Patients who do not respond to traditional monoaminergic antidepressant treatments have an especially difficult-to-treat type of MDD termed treatment-resistant depression. Subanesthetic doses of ketamine-a glutamatergic modulator-have shown great promise for rapidly treating patients with the most severe forms of depression. As such, ketamine represents a promising probe for understanding the pathophysiology of depression and treatment response. Through neuroimaging, ketamine’s mechanism may be elucidated in humans. Here, we review 47 articles of ketamine’s effects as revealed by neuroimaging studies. Some important brain areas emerge, especially the subgenual anterior cingulate cortex.

Ketamine-Associated Brain Changes: A Review of the…. Available from: https://www.researchgate.net/publication/323324257_Ketamine-Associated_Brain_Changes_A_Review_of_the_Neuroimaging_Literature [accessed Mar 31 2018].

 

Newsweek article showing that ketamine can help in Depression – 2018

This is the article in Newsweek below:

Ketamine could offer a fast and effective treatment for people with depression, even those who have failed to respond to current therapy options. A new medical reviewpublished this month adds to the growing evidence that the drug could be used in a clinical setting.

The review, published in the Harvard Review of Psychiatry, analyzed 47 studies on ketamine as a treatment for depression. The paper outlined specific ways in which ketamine affected the brains of depression patients.

Ketamine is a drug that can relieve pain and cause feelings of relaxation. It is generally used as an anesthetic in medical setting, but it is also abused as a party drug. Recreational users typically seek a sensation described as being similar to an out-of-body experience. 

A New Drug for Depression

03_05_ketamineKetamine could double as a depression treatment.

Despite its popularity at parties, ketamine has been the subject of numerous clinical studies for its potential to treat depression. Data have been mounting in its favor, and now a team at Harvard Medical School has reviewed the evidence thus far. 

The authors found that many patients given ketamine displayed measurable positive changes in brain activity in areas associated with the ability to process and control emotions, Business Insider reported.

Those changes include activation of the subgenual anterior cingulate cortex—connected to both emotions and cognition—as observed by neuroimaging. The activation was directly associated with improvement of depression symptoms in as little as 24 hours after patients received a single intravenous subanesthetic ketamine dose.

The drug also enhanced how the brain responded to positive emotions, a change indicated by increased connectivity in the right-hemisphere caudate. That enhancement helped relieve symptoms of depression, possibly because of this region’s connection to the brain’s reward system. 

Related: Perfectionists Are More Likely to Be Depressed—But One Thing Might Help Them

Ketamine also appears to decrease the ability to self-monitor, the report noted. This decrease may cause “emotional blunting,” which could help increase reward processing—and, in turn, happiness.

How Does Ketamine Work? 

Although the review did not describe exactly how ketamine produces its antidepressant effect, the authors noted that the effect may be indirect. Past research found that ketamine affects several receptors in the brain, such as opioid receptors, adrenegic receptors and serotinin receptors. The review concluded that the side effects of ketamine’s effect on those receptors may be the root cause of its antidepressant response. However, more research is needed to confirm this. 

Related: Are Nice People More Likely to Be Depressed?

The recent review is the latest scientific publication to suggest that this commonly used (and abused) drug could be an extremely helpful depression treatment.