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Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid

  • Ketamine is emerging as a way to treat depression, but it appears to act like an opioid, Stanford researchers found.
  • Clinics are cropping up around the country where people receive ketamine infusions.
  • A handful of pharmaceutical companies, including Johnson & Johnson and Allergan, are using ketamine as inspiration for new prescription drugs to treat depression.
This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as "Special K."
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This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as “Special K.”

Ketamine is emerging as a way to treat depression, but it appears to act like an opioid — and it may carry similar risks, Stanford researchers found.

Clinics are cropping up around the country where people receive ketamine infusions. A handful of pharmaceutical companies are using ketamine as inspiration for new prescription drugs to treat depression. Yet the new research questions whether scientists know enough about chronic ketamine use to introduce it broadly.

The drug blocks NMDA receptors, which scientists think may treat depressive symptoms. Researchers wanted to test whether it was possible to elicit this reaction without activating the brain’s opioid receptors.

To block an opioid response, they gave participants naltrexone then infused them with ketamine. To compare that response with the normal response, they also gave participants a placebo before giving them the treatment.

Naltrexone so successfully blocked the anti-depressant effects of ketamine that researchers cancelled the study after the first interval because they felt it wasn’t ethical to continue it, said Dr. Nolan Williams, one of the study’s authors and a clinical assistant professor of psychiatry and behavioral sciences at Stanford University.

When patients took naltrexone, the opioid blocker, their symptoms did not improve, suggesting ketamine must first activate opioid receptors in order to treat depression, according to the study, published Wednesday in the American Journal of Psychiatry.

That’s not to say ketamine cannot be used occasionally, but it does raise questions about using it repeatedly over time, said Dr. Alan F. Schatzberg, co-author of the study and Stanford’s Kenneth T. Norris, Jr., professor of psychiatry and behavioral sciences. He likens it to opioid painkillers being an appropriate pain treatment when used once in the emergency room but posing problems, such as the risk of dependence, when used chronically.

“More studies need to be done to fully understand ketamine before it’s widely rolled out for long-term chronic use,” Schatzberg said.

Researchers planned on studying 30 adults but stopped enrolling patients once they decided combining ketamine and naltrexone was not only ineffective but also “noxious” for many participants. They tested a total of 12 people with both naltrexone and the placebo.

Of those 12, seven who received naltrexone experienced nausea after the ketamine infusion, compared to three in the placebo group. Two participants in each group also experienced vomiting.

Participants who received the placebo and ketamine treatment reported reduced depression symptoms. But those same participants did not see a decrease in depression symptoms after receiving ketamine and opioid-blocker naltrexone.

“We essentially blocked the mechanism for producing the anti-depressant effect, which were opioids,” said Williams.

The findings may have implications for clinics offering ketamine infusions and drug manufacturers trying to commercialize ketamine-like drugs.

Ketamine is meant to be used as an anesthetic. Since ketamine is currently not indicated to treat depression, insurance typically doesn’t cover the cost of infusions, so people tend to pay out of their own pocket. One session can run more than $500.

Meanwhile, drug giant Johnson & Johnson plans to seek approval from the Food and Drug Administration for its nasal spray esketamine this year after reporting positive results from a Phase 3 trial. Allergan plans to file its drug Rapastinel, which targets the NMDA receptors like ketamine, within the next two years. VistaGen Therapeutics is working on a similar drug.

In a statement, J&J said while the study reviewed ketamine and not esketamine, the findings “are difficult to interpret because of the study’s design.”

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Revisiting the Hallucinogenic Potential of Ketamine

 

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A Case Built on Current Research Findings

Ketamine has caused quite a stir in psychiatric practice. Sub-anesthetic administrations of ketamine have been shown to markedly improve symptoms of depression and anxiety.1 While the growing off-label use of ketamine speaks to the need for novel approaches to psychiatric care and treatment-resistant illness, it also presents an ethical dilemma, wherein widespread adoption has once again leaped ahead of scientific understanding.

The current literature suggests that therapeutic effects of ketamine involve modulation of glutamate neurotransmission, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor potentiation, downstream influences on neurotrophic signaling cascades and neuroplasticity, and functional changes in assorted neural networks. Additional work is necessary to clarify the importance and reliability of these biological findings.

Another arc to the ketamine story dates back to a decades-old era of psychedelic research and search for medications with transformative power. Indeed, although primarily conceptualized today as a dissociative anesthetic, ketamine has also been classified more broadly as a hallucinogen. Hallucinogens function by various pharmacological mechanisms of action but exhibit similarities in their ability to occasion temporary but profound alterations of consciousness, involving acute changes in somatic, perceptual, cognitive, and affective processes.

Current biological theories involving ketamine’s antidepressant effect may be inseparable from these non-ordinary experiences of consciousness, but we can only know the answers to questions we ask. Here we examine findings from contemporary research that hint at the unexplored hallucinogenic potential of ketamine and considerations for future investigation.

There has been a resurgence of interest in hallucinogenic psychedelics (eg, psilocybin, lysergic acid diethylamide (LSD), mescaline, N,N-Dimethyltryptamine (DMT)) and entactogens (eg, 3, 4-methylenedioxymethamphetamine [MDMA]) in psychiatric research, which are hypothesized to achieve clinical benefit due to, in part, experiences of altered consciousness and fundamental shifts in mental frameworks.2

These drugs have been associated with cognitive states of enduring personal importance and have been compared with mystical experiences that might emerge over the ordinary course of life and carry sacred or spiritual meaning. Furthermore, these experiences may powerfully influence existential concepts of self, including moral values, self-identity, and purpose. There is converging evidence that these psychedelic effects are mediated in part by activity at 5HT-2A receptors. Ketamine may induce alterations in consciousness and personal frameworks similar to those achieved by serotonergic psychedelics while also sharing a common glutamatergic pathway of drug effect.3,4 However, there has been little investigation into how such changes might mediate the therapeutic potential of ketamine.

Preliminary data suggest that ketamine produces meaningful, transformative experiences that may help patients accept healthier values, behaviors, and beliefs related to abstinence from drugs and alcohol.5,6 Other evidence suggests that dose-related mystical-type experiences mediate the effects of ketamine on motivation to quit in cocaine-dependent research volunteers.7Few recent studies have examined whether ketamine’s hallucinogenic properties are implicated in antidepressant effects; however, psychiatric vulnerabilities to depression plausibly involve an existential dimension. This dimension includes depressive symptoms of hopelessness, guilt, and suicidality, which appear to be ketamine-sensitive.8

viagra for women The evidence

Given the paucity of modern literature exploring the psychedelic and mystical properties of ketamine in depression, more widespread data on psychotomimetic and dissociative effects of ketamine provide some initial groundwork. Berman and collegeagues9 and Zarate and colleagues10 suggested that the antidepressant effects of ketamine (0.5 mg/kg over 40 min) were disconnected from ketamine-induced psychotomimetic symptoms. The antidepressant effects, measured by the Hamilton Depression Rating Scale (HDRS), were significant even after positive symptoms on the Brief Psychiatric Rating Scale (BPRS) returned to baseline. However, it was also noted that initial changes in BPRS positive symptom scales from baseline trended to predict a greater decrease in HDRS scores within a day of treatment with ketamine.

A small study further demonstrated a substantial relationship between psychotomimetic effects 30 minutes after ketamine administration (0.54mg/kg over 30 min) as measured by BPRS and antidepressant effects in the following week.11 A larger study involving 108 patients found that dissociation measured by the Clinician Administered Dissociative States Scale (CADDS) at 40 minutes was associated with HDRS score improvement at 230 minutes and 7 days after infusion.12 Although no relationship between initial BPRS positive subscale scores and antidepressant effect was found, a correlation between CADSS and BPRS scores was found at 40 minutes postinfusion.

In a small study by Valentine and colleagues,13 the proposed correlation between ketamine-induced dissociation and antidepressant efficacy was not observed. However, a larger analysis found that greater intra-infusion dissociation as measured by CADDS was one of the strongest predictors of extended antidepressant response.14 Both of these studies utilized a single 0.5 mg/kg ketamine infusion delivered over 40 minutes.

Further investigation is needed, but there is an emerging rationale for a connection between the psychotomimetic or dissociative effects of ketamine and its antidepressant efficacy. Perhaps the experience of these effects simply un-blinds patients as to whether they are receiving ketamine or placebo in randomized trials; it may also be that such symptoms are only a “side effect” of ketamine’s mechanism of action. However, it is also worth considering that the psychotomimetic or dissociative effects associated with ketamine treatment are markers or mediators of subjective experiences of potential therapeutic value seen with other hallucinogenic agents.

purchase cialis super active buy online Recommended dosing

The recommended doses of ketamine for anesthetic induction are typically 1 to 4.5mg/kg IV and 6.5 to 13 mg/kg IM, with alternate, off-label recommendations for 0.5 to 2 mg/kg IV and 4 to 10 mg/kg IM, primarily in the context of adjuvant drug use. For use in depression, ketamine is most commonly administered at a sub-anesthetic dose of 0.5mg/kg IV across 40 minutes.

Interestingly, in a study of electroconvulsive therapy (ECT) and anesthetic induction with either a near-anesthetic dose of IV ketamine (0.8mg/kg) alone, sub-anesthetic ketamine (0.5mg/kg) plus propofol (0.8mg/kg), or propofol alone (0.8mg/kg), predicted a more rapid antidepressant effect and a higher remission rate than propofol use. The near-anesthetic dose of ketamine was associated with superior antidepressant effects than the mixed, sub-anesthetic dose.15

In a study of ketamine alongside psychotherapy for heroin addiction, Krupitsky and colleagues6compared the effects of 2 doses of ketamine (0.2 and 2.0 mg/kg IM) and found that only the higher dose was associated with a “full psychedelic experience” as measured by the Hallucinogen Rating Scale (HRS). The lower dose was considered a “sub-psychedelic” active placebo, but was nonetheless associated with some positive drug effects: patients were still affected by their experiences and considered them useful and therapeutic. The high dose group ultimately experienced higher rates of abstinence, greater effect on emotional attitudes related to abstinence, and lower rates of relapse and drug craving than the low dose group. Both doses resulted in post-treatment reductions in measures of depression and anxiety; there were no significant differences between the groups.

Similarly, Dakwar and colleagues7 compared the effects of 0.41 mg/kg and 0.71 mg/kg doses of IV ketamine given to cocaine-dependent patients. Dose-dependent mystical-type effects as measured by Hood’s Mysticism Scale (HMS) were seen as well as a relationship between HMS scores and the motivation to quit cocaine 24 hours post-infusion.

A different study involving a lower dose of intramuscular (IM) ketamine did not generate the same mystical-type phenomena.16 Perhaps these results highlight the importance of calibrating dosing and delivery. Clements and colleagues17 demonstrated that ketamine had reduced bioavailability with IM administration compared with IV administration. Taken together, these findings support the idea that positive treatment outcomes for ketamine may be dose-dependent and its psychoactive effects are based on delivery parameters.

go to site Limitation

One criticism of ketamine has been its short duration of antidepressant effect, with benefits peaking at 24 hours post-infusion and generally subsiding by 72 hours. The most promising approach to this challenge thus far seems to be the strategy of repeated-dose ketamine infusions, which have observed extended time-to-relapse and increased rates of antidepressant response.18

If ketamine’s therapeutic effect is indeed mediated by psychoactive experience, it may be that repeated dosing of ketamine improves outcomes by increasing opportunities for personally meaningful events to occur. One caveat is that some studies have shown repeated dosing to be associated with fewer dissociative symptoms over time—at first glance this suggests that the antidepressant value of serial ketamine administration might be independent of hallucinogenic effects.

While this requires further investigation, it is also important to consider other interpretations of that evidence: that acclimation to altered states of consciousness may contribute to recall bias, that experimental protocols that frame dissociative symptoms as a “side effect” or “adverse event” may lead to underreporting if overall patient experiences of ketamine are positive, or even that the benefit of repeated dosing may be less related to cumulative drug effect than other factors, such as repeated interactions with care providers or increased opportunities for reflection and synthesis.

One study of repeated infusions demonstrated that antidepressant response very early in the course of treatment strongly predicted subsequent response; conversely, a lack of rapid response was a poor prognostic indicator for improvement after additional infusions. Whether positive early responses to ketamine are mediated by psychological factors, biological susceptibility, or both: it is necessary to clarify these factors in shaping sustainable strategies for treatment.

A cautious approach also seems imperative given evidence that ketamine demonstrates agonist activity at μ-opioid receptors and dopaminergic effects that may confer acute relief of depressive symptoms but also greater risk for positive drug reinforcement and dependence. With further insight into psychological responses mediated by ketamine, it may be that a therapy-based framework for ketamine administration optimizes treatment efficacy and sustainability, while also minimizing unnecessary drug exposure, adverse effects of chronic use, and dependency risk.

Further study needed

In one study, long-term abstinence in persons who were substance dependent was achieved with Ketamine Psychedelic Therapy (KPT), which incorporates 1 or 2 sessions of ketamine-facilitated existential reappraisal into an existential psychotherapy.6 Additional exploration would be needed to determine which therapeutic approaches most beneficially augment ketamine treatment and minimize risks for harm. Nevertheless, a more holistic approach to ketamine as a treatment modality may be better suited to recreate the marked, persistent effects of MDMA in patients with PTSD. For example, in one study sustained symptom reductions were achieved with 12 weeks of psychotherapy but with limited MDMA exposures of only three 8-hour sessions.19

Another area that requires further investigation is how a patient’s past history might shape psychoactive responses. These personal and quite variable histories have been explored for some hallucinogenic agents but minimally for ketamine. The expectations and personal experiences of the individual user along with the external environment of use have been identified as critical factors in influencing subjective drug effects—coined “set” and “setting,” respectively—and are now considered well-established elements of human hallucinogen research.20

Therapies aimed at the pharmacological production of a transformative experience may depend on factors such as patient personality structure, preparation for treatment, emotional activation before drug intake, treatment context, and perceived quality of the experience. Given the unique psychological risks of hallucinogen administration, it is recommended that clinicians screen for personal or family histories of psychotic or other severe psychiatric disorders prior to treatment. Clinicians are also encouraged to facilitate careful patient preparation for sessions, provide a safe physical environment for treatment administration, and allow for interpersonal support during sessions. These and other insights from hallucinogenic research might valuably inform treatment protocols for ketamine administration.

Ketamine is uniquely poised to make a tremendous impact on psychiatric care, even redefining boundaries for patients with variations in depressive disorders that were once thought to be “treatment resistant.” Our synthesis of this emerging and old literature points to the unexplored hallucinogenic potential of ketamine. By further understanding the desirable psychoactive effects of ketamine, clinicians can build on initial treatment successes and maximize patient successes.

Future directions for research include:

• Further investigating the relationship between ketamine-induced psychotomimetic and dissociative effects and treatment efficacy

• Clarifying the connection between these effects and potentially desirable hallucinogenic experiences

• Exploring the therapeutic value of such elicited experiences

• Revisiting dosing strategies that account for existential phenomena and looking beyond dissociation as simply being an “adverse event”

• Incorporating psychotherapy-based frameworks into ongoing investigation

• Assessing set and setting factors that may shape treatment responses

Some answers and clues are likely to be found in the forgotten works of older psychedelic research. Agents like ketamine can exert their greatest therapeutic effect in the afterglow of profound alterations of consciousness, revealing a propensity for growth and healing that has not been evident to the suffering, depressed patient. Wherever the journey takes us, it is exactly the right time to bring together all the strands—brain and mind, old and new, caution and thrill—in assembling the unfinished story of ketamine.

 

References:

1. Feifel D. Breaking sad: unleashing the breakthrough potential of ketamine’s rapid antidepressant effects. Drug Dev Res. 2016;77;489-494.

2. Griffiths RR, Richards WA, McCann U, Jesse R. Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance. Psychopharmacol (Berl). 2006;187:268-283, 292.

3. Perry EB, Cramer JA, Cho HS, et al. Psychiatric safety of ketamine in psychopharmacology research. Psychopharmacol (Berl). 2007;192:253-260.

4. Vollenweider FX, Kometer M. The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nat Rev Neurosci. 2010;11:642-651.

5. Jansen KLR. Ketamine: Dreams and Realities. Sarasota, FL: Multidisciplinary Association for Psychedelic Studies; 2001.

6. Krupitsky E, Burakov A, Romanova T, et al. Ketamine psychotherapy for heroin addiction: immediate effects and two-year follow-up. J Subst Abuse Treat. 2002;23:273-283.

7. Dakwar E, Levin F, Foltin RW, et al. The effects of sub-anesthetic ketamine infusions on motivation to quit and cue-induced craving in cocaine dependent research volunteers. Biol Psychiatry. 2014;76:40-46.

8. Mathew SJ, Shah A, Lapidus K, et al. Ketamine for treatment-resistant unipolar depression: current evidence. CNS Drugs. 2012;26:189-204.

9. Berman RM, Cappiello A, Anand A, et al. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry. 2000;47:351-354.

10. Zarate CA, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006;63:856-864.

11. Sos P, Kirova M, Novak T, et al. Relationship of ketamine’s antidepressant and psychotomimetic effects in unipolar depression. Neuro Endocrinol Lett. 2013;34:287-293.

12. Luckenbaugh DA, Niciu MJ, Ionescu DF, et al. Do the dissociative side effects of ketamine mediate its antidepressant effects? J Affect Disord. 2014;159:56-61.

13. Valentine GW, Mason GF, Gomez R, et al. The antidepressant effect of ketamine is not associated with changes in occipital amino acid neurotransmitter content as measured by [(1)H]-MRS. Psychiatry Res. 2011;191:122-127.

14. Pennybaker SJ, Niciu MJ, Luckenbaugh DA, Zarate CA. Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion. J Affect Disord. 2017;208:560-566.

15. Zhong X, He H, Zhang C, et al. Mood and neuropsychological effects of different doses of ketamine in electroconvulsive therapy for treatment-resistant depression. J Affect Disord. 2016;201:124-130.

16. Lofwall MR, Griffiths RR, Mintzer MZ. Cognitive and subjective acute dose effects of intramuscular ketamine in healthy adults. Exp Clin Psychopharmacol. 2006;14:439-449.

17. Clements JA, Nimmo WS, Grant IS. Bioavailability, pharmacokinetics, and analgesic activity of ketamine in humans. J Pharma Sci. 1982;71:539-542.

18. Murrough JW, Perez AM, Pillemer S, et al. Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression. Biol Psychiatry. 2013;74:250-256.

19. Mithoefer, M. C. et al. Durability of improvement in post-traumatic stress disorder symptoms and absence of harmful effects or drug dependency after 3,4-methylenedioxymethamphetamine-assisted psychotherapy: a prospective long-term follow-up study. J Psychopharmacol. 2013;27:28-39.

20. Leary T, Litwin GH, Metzner R. Reactions to psilocybin administered in a supportive environment. J Nerv Ment Dis. 1963;137:561-573.

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Ketamine

The drug Ketamine is considered a breakthrough treatment for depression and some other neuropsychiatric conditions. Below are excerpts from recent articles discussing this revolutionary treatment and the links to the full articles.

Ketamine For Depression: the Highs and Lows.

The Lancet Psychiatry. VOLUME 2, ISSUE 9, P783–784, SEPTEMBER 2015

Long used as an anaesthetic and analgesic, most people familiar with ketamine know of it for this purpose. Others know it as a party drug that can give users an out-of-body experience, leaving them completely disconnected from reality. Less well known is its growing off-label use in the USA for depression, in many cases when other options have been exhausted.

David Feifel, a professor of psychiatry at the University of California, San Diego, was one of the first clinicians to use ketamine off-label to treat depression at UCDS’s Center for Advanced Treatment of Mood and Anxiety Disorders, which he recently founded. “Currently approved medications for depression all have about the same, very limited efficacy. A large percentage of patients with depression do not get an adequate level of relief from these antidepressants even when they have tried several different ones and even when other drugs known to augment their effects are added to them”, Feifel tells The Lancet Psychiatry. “The stagnation in current antidepressant medication on the one hand, and the tremendous number of treatment-resistant patients, has propelled me to explore truly novel treatments like ketamine.”

Compelling published study results and case reports exist of patients’ depression—in some cases deeply entrenched depression that has lasted months or even years—alleviating within hours of use of ketamine. However, critics have warned that the drug has not been studied sufficiently (at least outside clinical trials), and also emphasized the cost. Patients can pay more than $1000 per session for treatment that must usually be repeated several times. That cost is rarely covered by the patient’s medical insurance.

Advocates of ketamine use in depression are excited because it has a different mechanism of action to standard antidepressants, which affect signalling by monoamine neurotransmitters such as serotonin, noradrenaline, or dopamine. Ketamine is thought to act by blocking N-methyl-d-aspartate (NMDA) receptors in the brain, which interact with the amino acid neurotransmitter glutamate.

Feifel states that he has patients who have been receiving ketamine treatments every 2–4 weeks for long periods, some for around 3 years, and has not yet seen any safety issues arise.

Pharmaceutical companies are entering this exciting arena by attempting to develop new drugs based on ketamine without similar side-effects. Feifel dismisses the notion that the dissociative so-called trip induced by ketamine is actually an important negative side-effect. “Although I have had a couple patients have unpleasant ‘trips’, it’s exceedingly rare, usually dose related, and very transitory due to ketamine’s rapid metabolism.” Feifel says that, more often than not, patients find the trip to be positive, or even spiritual, and believe it is an important component of the antidepressant effect they experience afterwards. “There is no doubt the dissociative effect represents a logistical issue, requiring monitoring—and this should be addressed in any approval given for ketamine”, he adds.

Feifel says that it is not for him, but for his patients to decide where the balance of risks and benefits lies in trying ketamine to treat their depression”One could make a compelling argument that it’s unethical to withhold ketamine treatments from someone who has chronic, severe treatment resistant depression. But I know this from the patients who tell me they would not be in this world right now if it were not for the ketamine.”

Feifel concludes that it is straightforward to talk to TRD patients about ketamine. “I tell them all the relevant information. The efficacy rates, time to onset of benefits, duration limitations, alternatives, lack of insurance coverage, and other information. My job is to make sure they understand the parameters of the treatment, not to decide whether they should do it.”

Full article: The Lancet

Ketamine for depression the highs and lows b

Onetime Party Drug Hailed as Miracle for Treating Severe Depression

Washington Post, Feb 2, 2016

Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile. Since 2006, dozens of studies have reported that it can also reverse the kind of severe depression that traditional antidepressants often don’t touch.

Experts are calling it the most significant advance in mental health in more than half a century. They point to studies showing ketamine not only produces a rapid and robust antidepressant effect; it also puts a quick end to suicidal thinking.  “This is the next big thing in psychiatry,” says L. Alison McInnes, a San Francisco psychiatrist who over the past year has enrolled 58 severely depressed patients in Kaiser’s San Francisco clinic. The excitement stems from the fact that it’s working for patients who have spent years cycling through antidepressants, mood stabilizers and various therapies. “Psychiatry has run out of gas” in trying to help depressed patients for whom nothing has worked, she says. “There is a significant number of people who don’t respond to antidepressants, and we’ve had nothing to offer them other than cognitive behavior therapy, electroshock therapy and transcranial stimulation.”

Ketamine does, however, have one major limitation: Its relief is temporary. Clinical trials at NIMH have found that relapse usually occurs about a week after a single infusion.

A study published in the journal Science in 2010 suggested that ketamine restores brain function through a process called synaptogenesis. Scientists at Yale University found that ketamine not only improved depression-like behavior in rats but also promoted the growth of new synaptic connections between neurons in the brain.

Patients often describe a kind of lucid dreaming or dissociative state in which they lose track of time and feel separated from their bodies. Many enjoy it; some don’t. But studies at NIMH and elsewhere suggest that the psychedelic experience may play a small but significant role in the drug’s efficacy.

As a drug once known almost exclusively to anesthesiologists, ketamine now falls into a gray zone. As the use of ketamine looks likely to grow, many psychiatrists say that use of ketamine for depression should be left to them. “The bottom line is you’re treating depression,” says psychiatrist David Feifel, director of the Center for Advanced Treatment of Mood and Anxiety Disorders at the University of California at San Diego. “And this isn’t garden-variety depression. The people coming in for ketamine are people who have the toughest, potentially most dangerous depressions. I think it’s a disaster if anesthesiologists feel competent to monitor these patients.”

Full article: The Washington Post

Onetime party drug hailed as miracle for treating severe depression


A Ketamine intravenous drip being prepared. (Amarett Jans/Courtesy of Enrique Abreu)

February 1, 2016

It was November 2012 when Dennis Hartman, a Seattle business executive, managed to pull himself out of bed, force himself to shower for the first time in days and board a plane that would carry him across the country to a clinical trial at the National Institute of Mental Health (NIMH) in Bethesda.

After a lifetime of profound depression, 25 years of therapy and cycling through 18 antidepressants and mood stabilizers, Hartman, then 46, had settled on a date and a plan to end it all. The clinical trial would be his last attempt at salvation.

For 40 minutes, he sat in a hospital room as an IV drip delivered ketamine through his system. Several more hours passed before it occurred to him that all his thoughts of suicide had evaporated.

“My life will always be divided into the time before that first infusion and the time after,” Hartman says today. “That sense of suffering and pain draining away. I was bewildered by the absence of pain.”

Ketamine could be speedy depression treatment

Ketamine is being used by researchers at The National Institutes of Health as a treatment for major depression. 

Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile.

Since 2006, dozens of studies have reported that it can also reverse the kind of severe depression that traditional antidepressants often don’t touch. The momentum behind the drug has now reached the American Psychiatric Association, which, according to members of a ketamine task force, seems headed toward a tacit endorsement of the drug for treatment-resistant depression.

Experts are calling it the most significant advance in mental health in more than half a century. They point to studies showing ketamine not only produces a rapid and robust antidepressant effect; it also puts a quick end to suicidal thinking.

Traditional antidepressants and mood stabilizers, by comparison, can take weeks or months to work. In 2010, a major study published in JAMA, the journal of the American Medical Association, reported that drugs in a leading class of antidepressants were no better than placebos for most depression.

A growing number of academic medical centers, including Yale University, the University of California at San Diego, the Mayo Clinic and the Cleveland Clinic, have begun offering ketamine treatments off-label for severe depression, as has Kaiser Permanente in Northern California.

The ‘next big thing’

“This is the next big thing in psychiatry,” says L. Alison McInnes, a San Francisco psychiatrist who over the past year has enrolled 58 severely depressed patients in Kaiser’s San Francisco clinic. She says her long-term success rate of 60 percent for people with treatment-resistant depression who try the drug has persuaded Kaiser to expand treatment to two other clinics in the Bay Area. The excitement stems from the fact that it’s working for patients who have spent years cycling through antidepressants, mood stabilizers and various therapies.

“Psychiatry has run out of gas” in trying to help depressed patients for whom nothing has worked, she says. “There is a significant number of people who don’t respond to antidepressants, and we’ve had nothing to offer them other than cognitive behavior therapy, electroshock therapy and transcranial stimulation.”

McInnes is a member of the APA’s ketamine task force, assigned to codify the protocol for how and when the drug will be given. She says she expects the APA to support the use of ketamine treatment early this year.

The guidelines, which follow the protocol used in the NIMH clinical trial involving Hartman, call for six IV drips over a two-week period. The dosage is very low, about a tenth of the amount used in anesthesia. And when it works, it does so within minutes or hours.

“It’s not subtle,” says Enrique Abreu, a Portland, Ore., anesthesiologist who began treating depressed patients with it in 2012. “It’s really obvious if it’s going to be effective.

“And the response rate is unbelievable. This drug is 75 percent effective, which means that three-quarters of my patients do well. Nothing in medicine has those kind of numbers.”

So far, there is no evidence of addiction at the low dose in which infusions are delivered. Ketamine does, however, have one major limitation: Its relief is temporary. Clinical trials at NIMH have found that relapse usually occurs about a week after a single infusion.

Ketamine works differently from traditional antidepressants, which target the brain’s serotonin and noradrenalin systems. It blocks N-methyl-D-aspartate (NMDA), a receptor in the brain that is activated by glutamate, a neurotransmitter.

In excessive quantities, glutamate becomes an excitotoxin, meaning that it overstimulates brain cells.

“Ketamine almost certainly modifies the function of synapses and circuits, turning certain circuits on and off,” explains Carlos Zarate Jr., NIMH’s chief of neurobiology and treatment of mood disorders, who has led the research on ketamine. “The result is a rapid antidepressant effect.”

Rapid effect

study published in the journal Science in 2010 suggested that ketamine restores brain function through a process called synaptogenesis. Scientists at Yale University found that ketamine not only improved depression-like behavior in rats but also promoted the growth of new synaptic connections between neurons in the brain.

mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists.

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

Psychedelics Promote Structural and Functional Neural Plasticity.

Even a low-dose infusion can cause intense hallucinations. Patients often describe a kind of lucid dreaming or dissociative state in which they lose track of time and feel separated from their bodies. Many enjoy it; some don’t. But studies at NIMH and elsewhere suggest that the psychedelic experience may play a small but significant role in the drug’s efficacy.

“It’s one of the things that’s really striking,” says Steven Levine, a Princeton, N.J., psychiatrist who estimates that he has treated 500 patients with ketamine since 2011. “With depression, people often feel very isolated and disconnected. Ketamine seems to leave something indelible behind. People use remarkably similar language to describe their experience: ‘a sense of connection to other people,’ ‘a greater sense of connection to the universe.’ ”

Although bladder problems and cognitive deficits have been reported among long-term ketamine abusers, none of these effects have been observed in low-dose clinical trials. In addition to depression, the drug is being studied for its effectiveness in treating obsessive-compulsive disorder, post-traumatic stress disorder, extreme anxiety and Rett syndrome, a rare developmental disorder on the autism spectrum.

Booster treatments

The drug’s fleeting remission effect has led many patients to seek booster infusions. Hartman, for one, began his search before he even left his hospital room in Bethesda.

Four years ago, he couldn’t find a doctor in the Pacific Northwest willing to administer ketamine. “At the time, psychiatrists hovered between willful ignorance and outright opposition to it,” says Hartman, whose depression began creeping back a few weeks after his return to Seattle.

It took nine months before he found an anesthesiologist in New York who was treating patients with ketamine. Soon, he was flying back and forth across the country for bimonthly infusions.

Upon his request, he received the same dosage and routine he’d received in Bethesda: six infusions over two weeks. And with each return to New York, his relief seemed to last a little longer. These days, he says that his periods of remission between infusions often stretch to six months. He says he no longer takes any medication for depression besides ketamine.

“I don’t consider myself permanently cured, but now it’s something I can manage,” Hartman says, “like diabetes or arthritis. Before, it was completely unmanageable. It dominated my life and prevented me from functioning.”

In 2012 he helped found the Ketamine Advocacy Network, a group that vets ketamine clinics, advocates for insurance coverage and spreads the word about the drug.

And word has indeed spread. Ketamine clinics, typically operated by psychiatrists or anesthesiologists, are popping up in major cities around the country.

Levine, for one, is about to expand from New Jersey to Denver and Baltimore. Portland’s Abreu recently opened a second clinic in Seattle.

Depression is big business. An estimated 15.7 million adults in the United States experienced at least one major depressive episode in 2014, according to the NIMH.

“There’s a great unmet need in depression,” says Gerard Sanacora, director of the Yale Depression Research Program. “We think this is an extremely important treatment. The concern comes if people start using ketamine before CBT [cognitive behavioral therapy] or Prozac. Maybe someday it will be a first-line treatment. But we’re not there yet.”

Many unknowns

Sanacora says a lot more research is required. “It’s a medication that can have big changes in heart rate and blood pressure. There are so many unknowns, I’m not sure it should be used more widely till we understand its long-term benefits and risks.”

While a single dose of ketamine is cheaper than a $2 bottle of water, the cost to the consumer varies wildly, running anywhere between $500 and $1,500 per treatment. The drug itself is easily available in any pharmacy, and doctors are free to prescribe it — as with any medication approved by the Food and Drug Administration — for off-label use. Practitioners attribute the expense to medical monitoring of patients and IV equipment required during an infusion.

There is no registry for tracking the number of patients being treated with ketamine for depression, the frequency of those treatments, dosage levels, follow-up care and adverse effects.

“We clearly need more standardization in its use,” Zarate says. “We still don’t know what the proper dose should be. We need to do more studies. It still, in my opinion, should be used predominantly in a research setting or highly specialized clinic.”

As a drug once known almost exclusively to anesthesiologists, ketamine now falls into a gray zone.

“Most anesthesiologists don’t do mental health, and there’s no way a psychiatrist feels comfortable putting an IV in someone’s arm,” Abreu says.

It’s a drug, in other words, that practically demands collaboration. Instead, it has set off a turf war. As the use of ketamine looks likely to grow, many psychiatrists say that use of ketamine for depression should be left to them.

“The bottom line is you’re treating depression,” says psychiatrist David Feifel, director of the Center for Advanced Treatment of Mood and Anxiety Disorders at the University of California at San Diego. “And this isn’t garden-variety depression. The people coming in for ketamine are people who have the toughest, potentially most dangerous depressions. I think it’s a disaster if anesthesiologists feel competent to monitor these patients. Many of them have bipolar disorder and are in danger of becoming manic. My question [to anesthesiologists] is: ‘Do you feel comfortable that you can pick up mania?’ ”

But ketamine has flourished from the ground up and with little or no advertising. The demand has come primarily from patients and their families; Zarate, for instance, says he receives “at least 100 emails a day” from patients.

Nearly every one of them wants to know where they can get it.

 

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Approximately one-third to one-half of patients with generalized Social Anxiety Disorder (SAD) do not experience adequate clinical benefit from current evidence-based treatment for SAD. This includes treatment with conventional approaches such as selective serotonin reuptake inhibitors (SSRIs) or venlafaxine and cognitive behavioral therapy (CBT). Failure of anxiety relief in patients with SAD is a source of substantial morbidity, distress, and decreases in quality of life.
Symptoms
Feelings of shyness or discomfort in certain situations aren’t necessarily signs of social anxiety disorder, particularly in children. Comfort levels in social situations vary, depending on the individual’s personality traits and life experiences. Some people are naturally reserved and others are more outgoing.
In contrast to everyday nervousness, social anxiety disorder includes fear, anxiety and avoidance that interferes with your daily routine, work, school or other activities.

Emotional and behavioral symptoms
Signs and symptoms of social anxiety disorder can include persistent:
• Fear of situations in which you may be judged
• Worrying about embarrassing or humiliating yourself
• Concern that you’ll offend someone
• Intense fear of interacting or talking with strangers
• Fear that others will notice that you look anxious
• Fear of physical symptoms that may cause you embarrassment, such as blushing, sweating, trembling or having a shaky voice
• Avoiding doing things or speaking to people out of fear of embarrassment
• Avoiding situations where you might be the center of attention
• Having anxiety in anticipation of a feared activity or event
• Spending time after a social situation analyzing your performance and identifying flaws in your interactions
• Expecting the worst possible consequences from a negative experience during a social situation
For children, anxiety about interacting with adults or peers may be shown by crying, having temper tantrums, clinging to parents or refusing to speak in social situations.
Performance type of social anxiety disorder is when you experience intense fear and anxiety only during speaking or performing in public, but not in other types of social situations.
Physical symptoms
Physical signs and symptoms can sometimes accompany social anxiety disorder and may include:
• Fast heartbeat
• Upset stomach or nausea
• Trouble catching your breath
• Dizziness or lightheadedness
• Confusion or feeling “out of body”
• Diarrhea
• Muscle tension
Avoiding normal social situations
Common, everyday experiences that may be hard to endure when you have social anxiety disorder include, for example:
• Using a public restroom
• Interacting with strangers
• Eating in front of others
• Making eye contact
• Initiating conversations
• Dating
• Attending parties or social gatherings
• Going to work or school
• Entering a room in which people are already seated
• Returning items to a store
Social anxiety disorder symptoms can change over time. They may flare up if you’re facing a lot of stress or demands. Although avoiding anxiety-producing situations may make you feel better in the short term, your anxiety is likely to persist over the long term if you don’t get treatment.
Ketamine
Converging lines of evidence from neuroimaging and pharmacological studies support the importance of glutamate abnormalities in the pathogenesis of SAD. In a previously conducted clinical study, an elevated glutamate to creatinine ratio was found in the anterior cingulate cortex of SAD patients when compared to healthy controls. Elevated brain glutamine levels have also been demonstrated in patients with SAD. Moreover, nonclinical rodent studies have established a strong link between glutamate regulation and anxiety.
Ketamine is a potent antagonist of the N-methyl-D-aspartate (NMDA) receptor, a major type of glutamate receptor in the brain. Ketamine is routinely used for anesthetic induction because of its dissociative properties. However in research studies and in some physician accounts of off-label clinical use, ketamine is an effective treatment for reducing symptoms of depressive and anxiety disorders. In multiple controlled clinical studies, ketamine has produced a rapid antidepressant effect in unipolar and bipolar depression. Ketamine’s anti-depressant effects peak 1-3 days following infusion and is observed long after ketamine has been metabolized and excreted by the body and after ketamine’s sedative and dissociative effects have dissipated.
The results of several clinical studies suggest that ketamine may also have significant anxiolytic effects. Patients with major depressive disorder given a single ketamine infusion have shown strong and significant reductions in comorbid anxiety symptoms. A trial including 11 depressed patients demonstrated a significant reduction in anxiety symptoms (Hamilton Anxiety Rating Scale (HAM-A)) following ketamine infusion. This improvement is supported by one of the earlier placebo-controlled trials of ketamine which demonstrated that the psychic anxiety item was one of 4 (out of 21) items on the Hamilton Depression Rating Scale (HAM-D) demonstrating significant improvement after ketamine infusion.

 

The National Institute of Mental Health Highlights Ketamine for Depression

 August 25, 2018

The National Institute of Mental Health (NIMH) issued a highlight on ketamine for treating depression.

The most commonly used antidepressants are largely variations on a theme; they increase the supply within synapses of a class of neurotransmitters believed to play a role in depression. While these drugs relieve depression for some, there is a weeks-long delay before they take effect, and some people with “treatment-resistant” depression do not respond at all.

The delay in effectiveness has suggested to scientists that the medication-induced changes in neurotransmitters are several steps away from processes more central to the root cause of depression. One possibility for a more proximal mechanism is glutamate, the primary excitatory, or activating, neurotransmitter in the brain. Preliminary studies suggested that inhibitors of glutamate could have antidepressant-like effects, and in a seminal clinical trial, the drug ketamine—which dampens glutamate signaling—lifted depression in as little as 2 hours in people with treatment-resistant depression.34

The discovery of rapidly acting antidepressants has transformed our expectations—we now look for treatments that will work in 6 hours rather than 6 weeks. But ketamine has some disadvantages; it has to be administered intravenously, the effects are transient, and it has side effects that require careful monitoring. However, results from clinical studies have confirmed the potential of the glutamate pathway as a target for the development of new antidepressants. Continuing research with ketamine has provided information on biomarkers that could be used to predict who will respond to treatment.35Clinical studies are also testing analogs of ketamine in an effort to develop glutamate inhibitors without ketamine’s side effects that can then be used in the clinic.36 Ketamine may also have potential for treating other mental illnesses; for example, a preliminary clinical trial reported that ketamine reduced the severity of symptoms in patients with PTSD. 37 Investigation of the role of glutamate signaling in other illnesses may provide the impetus to develop novel therapies based on this pathway.

Left: Change in the 21-item Hamilton Depression Rating Scale (HDRS) following ketamine or placebo treatment.
Right: Proportion of responders showing a 50 percent improvement on the HDRS following ketamine or placebo treatment.34

Source: Carlos Zarate, M.D., Experimental Therapeutics and Pathophysiology Branch, NIMH

One of the imperatives of clinical research going forward will be to demonstrate whether the ability of a compound to interact with a specific brain target is related to some measurable change in brain or behavioral activity that, in turn, can be associated with relief of symptoms. In a study of ketamine’s effects in patients in the depressive phase of bipolar disorder, ketamine restored pleasure-seeking behavior independent from and ahead of its other antidepressant effects. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom—loss of interest in pleasurable activities—which lasted up to 14 days.38 Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. This approach is consistent with the NIMH’s RDoC project, which calls for the study of functions—such as the ability to seek out and experience rewards—and their related brain systems that may identify subgroups of patients with common underlying dysfunctions that cut across traditional diagnostic categories.

The ketamine story shows that in some instances, a strong and repeatable clinical outcome stemming from a hypothesis about a specific molecular target (e.g., a glutamate receptor) can open up new arenas for basic research to explain the mechanisms of treatment response; basic studies can, in turn, provide data leading to improved treatments directed at that mechanism. A continuing focus on specific mechanisms will not only provide information on the potential of test compounds as depression medications, but will also help us understand which targets in the brain are worth aiming at in the quest for new therapies.

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22336 Alexandria Alexandria City
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22401 Fredericksburg Fredericksburg City
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22402 Fredericksburg Fredericksburg City
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22403 Fredericksburg Stafford
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22404 Fredericksburg Fredericksburg City
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22405 Fredericksburg Stafford
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22406 Fredericksburg Stafford
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22407 Fredericksburg Spotsylvania
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22408 Fredericksburg Spotsylvania
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22412 Fredericksburg Stafford
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22427 Bowling Green Caroline
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22428 Bowling Green Caroline
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22430 Brooke Stafford
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22432 Burgess Northumberland
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22433 Burr Hill Orange
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22435 Callao Northumberland
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22436 Caret Essex
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22437 Center Cross Essex
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22438 Champlain Essex
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22442 Coles Point Westmoreland
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22443 Colonial Beach Westmoreland
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22446 Corbin Caroline
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22448 Dahlgren King George
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22451 Dogue King George
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22454 Dunnsville Essex
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22456 Edwardsville Northumberland
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22460 Farnham Richmond
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22463 Garrisonville Stafford
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22469 Hague Westmoreland
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22471 Hartwood Stafford
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22472 Haynesville Richmond
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22473 Heathsville Northumberland
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22476 Hustle Essex
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22480 Irvington Lancaster
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22481 Jersey King George
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22482 Kilmarnock Lancaster
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22485 King George King George
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22488 Kinsale Westmoreland
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22501 Ladysmith Caroline
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22503 Lancaster Lancaster
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22504 Laneview Essex
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22507 Lively Lancaster
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22508 Locust Grove Orange
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22509 Loretto Essex
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22511 Lottsburg Northumberland
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22513 Merry Point Lancaster
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22514 Milford Caroline
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22517 Mollusk Lancaster
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22520 Montross Westmoreland
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22523 Morattico Lancaster
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22524 Mount Holly Westmoreland
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22526 Ninde King George
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22528 Nuttsville Lancaster
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22529 Oldhams Westmoreland
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22530 Ophelia Northumberland
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22534 Partlow Spotsylvania
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22535 Port Royal Caroline
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22538 Rappahannock Academy Caroline
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22539 Reedville Northumberland
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22542 Rhoadesville Orange
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22544 Rollins Fork King George
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22545 Ruby Stafford
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22546 Ruther Glen Caroline
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22547 Sealston King George
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22548 Sharps Richmond
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22552 Sparta Caroline
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22553 Spotsylvania Spotsylvania
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22554 Stafford Stafford
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22555 Stafford Stafford
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22556 Stafford Stafford
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22558 Stratford Westmoreland
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22560 Tappahannock Essex
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22565 Thornburg Spotsylvania
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22567 Unionville Orange
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22570 Village Richmond
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22572 Warsaw Richmond
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22576 Weems Lancaster
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22577 Sandy Point Westmoreland
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22578 White Stone Lancaster
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22579 Wicomico Church Northumberland
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22580 Woodford Caroline
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22581 Zacata Westmoreland
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22601 Winchester Winchester City
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22602 Winchester Frederick
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22603 Winchester Frederick
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22604 Winchester Winchester City
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22610 Bentonville Warren
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22611 Berryville Clarke
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22620 Boyce Clarke
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22622 Brucetown Frederick
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22623 Chester Gap Rappahannock
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22624 Clear Brook Frederick
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22625 Cross Junction Frederick
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22626 Fishers Hill Shenandoah
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22627 Flint Hill Rappahannock
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22630 Front Royal Warren
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22637 Gore Frederick
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22638 Winchester Frederick
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22639 Hume Fauquier
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22640 Huntly Rappahannock
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22641 Strasburg Shenandoah
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22642 Linden Warren
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22643 Markham Fauquier
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22644 Maurertown Shenandoah
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22645 Middletown Frederick
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22646 Millwood Clarke
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22649 Middletown Warren
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22650 Rileyville Page
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22652 Fort Valley Shenandoah
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22654 Star Tannery Frederick
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22655 Stephens City Frederick
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22656 Stephenson Frederick
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22657 Strasburg Shenandoah
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22660 Toms Brook Shenandoah
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22663 White Post Clarke
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22664 Woodstock Shenandoah
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22701 Culpeper Culpeper
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22709 Aroda Madison
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22711 Banco Madison
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22712 Bealeton Fauquier
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22713 Boston Culpeper
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22714 Brandy Station Culpeper
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22715 Brightwood Madison
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22716 Castleton Rappahannock
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22718 Elkwood Culpeper
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22719 Etlan Madison
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22720 Goldvein Fauquier
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22721 Graves Mill Madison
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22722 Haywood Madison
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22723 Hood Madison
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22724 Jeffersonton Culpeper
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22725 Leon Madison
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22726 Lignum Culpeper
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22727 Madison Madison
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22728 Midland Fauquier
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22729 Mitchells Culpeper
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22730 Oakpark Madison
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22731 Pratts Madison
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22732 Radiant Madison
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22733 Rapidan Culpeper
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22734 Remington Fauquier
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22735 Reva Madison
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22736 Richardsville Culpeper
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22737 Rixeyville Culpeper
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22738 Rochelle Madison
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22739 Somerville Fauquier
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22740 Sperryville Rappahannock
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22741 Stevensburg Culpeper
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22742 Sumerduck Fauquier
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22743 Syria Madison
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22746 Viewtown Culpeper
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22747 Washington Rappahannock
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22748 Wolftown Madison
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22749 Woodville Rappahannock
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22801 Harrisonburg Harrisonburg City
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22802 Harrisonburg Harrisonburg City
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22803 Harrisonburg Harrisonburg City
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22807 Harrisonburg Harrisonburg City
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22810 Basye Shenandoah
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22811 Bergton Rockingham
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22812 Bridgewater Rockingham
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22815 Broadway Rockingham
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22820 Criders Rockingham
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22821 Dayton Rockingham
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22824 Edinburg Shenandoah
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22827 Elkton Rockingham
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22830 Fulks Run Rockingham
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22831 Hinton Rockingham
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22832 Keezletown Rockingham
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22833 Lacey Spring Rockingham
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22834 Linville Rockingham
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22835 Luray Page
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22840 Mc Gaheysville Rockingham
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22841 Mount Crawford Rockingham
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22842 Mount Jackson Shenandoah
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22843 Mount Solon Augusta
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22844 New Market Shenandoah
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22845 Orkney Springs Shenandoah
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22846 Penn Laird Rockingham
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22847 Quicksburg Shenandoah
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22848 Pleasant Valley Rockingham
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22849 Shenandoah Page
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22850 Singers Glen Rockingham
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22851 Stanley Page
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22853 Timberville Rockingham
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22901 Charlottesville Albemarle
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22902 Charlottesville Charlottesville City
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22903 Charlottesville Charlottesville City
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22904 Charlottesville Charlottesville City
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22905 Charlottesville Charlottesville City
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22906 Charlottesville Charlottesville City
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22907 Charlottesville Charlottesville City
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22908 Charlottesville Charlottesville City
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22909 Charlottesville Albemarle
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22910 Charlottesville Charlottesville City
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22911 Charlottesville Albemarle
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22920 Afton Nelson
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22922 Arrington Nelson
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22923 Barboursville Orange
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22924 Batesville Albemarle
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22931 Covesville Albemarle
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22932 Crozet Albemarle
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22935 Dyke Greene
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22936 Earlysville Albemarle
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22937 Esmont Albemarle
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22938 Faber Nelson
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22939 Fishersville Augusta
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22940 Free Union Albemarle
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22942 Gordonsville Orange
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22943 Greenwood Albemarle
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22945 Ivy Albemarle
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22946 Keene Albemarle
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22947 Keswick Albemarle
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22948 Locust Dale Madison
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22949 Lovingston Nelson
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22952 Lyndhurst Augusta
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22957 Montpelier Station Orange
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22958 Nellysford Nelson
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22959 North Garden Albemarle
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22960 Orange Orange
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22963 Palmyra Fluvanna
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22964 Piney River Nelson
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22965 Quinque Greene
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22967 Roseland Nelson
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22968 Ruckersville Greene
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22969 Schuyler Nelson
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22971 Shipman Nelson
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22972 Somerset Orange
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22973 Stanardsville Greene
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22974 Troy Fluvanna
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22976 Tyro Nelson
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22980 Waynesboro Waynesboro City
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22987 White Hall Albemarle
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22989 Woodberry Forest Madison
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23001 Achilles Gloucester
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23002 Amelia Court House Amelia
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23003 Ark Gloucester
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23004 Arvonia Buckingham
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23005 Ashland Hanover
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23009 Aylett King William
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23011 Barhamsville New Kent
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23014 Beaumont Goochland
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23015 Beaverdam Hanover
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23018 Bena Gloucester
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23021 Bohannon Mathews
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23022 Bremo Bluff Fluvanna
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23023 Bruington King And Queen
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23024 Bumpass Louisa
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23025 Cardinal Mathews
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23027 Cartersville Cumberland
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23030 Charles City Charles City
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23031 Christchurch Middlesex
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23032 Church View Middlesex
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23035 Cobbs Creek Mathews
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23038 Columbia Goochland
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23039 Crozier Goochland
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23040 Cumberland Cumberland
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23043 Deltaville Middlesex
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23045 Diggs Mathews
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23047 Doswell Hanover
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23050 Dutton Gloucester
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23055 Fork Union Fluvanna
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23056 Foster Mathews
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23058 Glen Allen Henrico
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23059 Glen Allen Henrico
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23060 Glen Allen Henrico
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23061 Gloucester Gloucester
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23062 Gloucester Point Gloucester
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23063 Goochland Goochland
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23064 Grimstead Mathews
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23065 Gum Spring Goochland
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23066 Gwynn Mathews
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23067 Hadensville Goochland
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23068 Hallieford Mathews
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23069 Hanover Hanover
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23070 Hardyville Middlesex
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23071 Hartfield Middlesex
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23072 Hayes Gloucester
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23075 Highland Springs Henrico
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23076 Hudgins Mathews
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23079 Jamaica Middlesex
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23081 Jamestown James City
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23083 Jetersville Amelia
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23084 Kents Store Fluvanna
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23085 King And Queen Court House King And Queen
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23086 King William King William
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23089 Lanexa New Kent
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23090 Lightfoot York
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23091 Little Plymouth King And Queen
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23092 Locust Hill Middlesex
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23093 Louisa Louisa
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23101 Macon Powhatan
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23102 Maidens Goochland
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23103 Manakin Sabot Goochland
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23105 Mannboro Amelia
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23106 Manquin King William
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23107 Maryus Gloucester
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23108 Mascot King And Queen
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23109 Mathews Mathews
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23110 Mattaponi King And Queen
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23111 Mechanicsville Hanover
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23112 Midlothian Chesterfield
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23113 Midlothian Chesterfield
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23114 Midlothian Chesterfield
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23115 Millers Tavern Essex
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23116 Mechanicsville Hanover
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23117 Mineral Louisa
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23119 Moon Mathews
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23120 Moseley Chesterfield
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23123 New Canton Buckingham
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23124 New Kent New Kent
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23125 New Point Mathews
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23126 Newtown King And Queen
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23127 Norge James City
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23128 North Mathews
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23129 Oilville Goochland
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23130 Onemo Mathews
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23131 Ordinary Gloucester
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23138 Port Haywood Mathews
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23139 Powhatan Powhatan
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23140 Providence Forge New Kent
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23141 Quinton New Kent
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23146 Rockville Hanover
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23147 Ruthville Charles City
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23148 Saint Stephens Church King And Queen
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23149 Saluda Middlesex
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23150 Sandston Henrico
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23153 Sandy Hook Goochland
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23154 Schley Gloucester
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23155 Severn Gloucester
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23156 Shacklefords King And Queen
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23160 State Farm Goochland
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23161 Stevensville King And Queen
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23162 Studley Hanover
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23163 Susan Mathews
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23168 Toano James City
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23169 Topping Middlesex
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23170 Trevilians Louisa
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23173 University Of Richmond Richmond City
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23175 Urbanna Middlesex
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23176 Wake Middlesex
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23177 Walkerton King And Queen
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23178 Ware Neck Gloucester
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23180 Water View Middlesex
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23181 West Point King William
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23183 White Marsh Gloucester
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23184 Wicomico Gloucester
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23185 Williamsburg James City
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23186 Williamsburg Williamsburg City
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23187 Williamsburg Williamsburg City
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23188 Williamsburg James City
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23190 Woods Cross Roads Gloucester
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23192 Montpelier Hanover
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23218 Richmond Richmond City
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23219 Richmond Richmond City
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23220 Richmond Richmond City
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23221 Richmond Richmond City
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23222 Richmond Richmond City
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23223 Richmond Richmond City
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23224 Richmond Richmond City
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23225 Richmond Richmond City
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23226 Richmond Henrico
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23227 Richmond Henrico
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23228 Richmond Henrico
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23229 Richmond Henrico
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23230 Richmond Henrico
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23231 Richmond Henrico
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23232 Richmond Richmond City
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23233 Richmond Henrico
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23234 Richmond Chesterfield
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23235 Richmond Chesterfield
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23236 Richmond Chesterfield
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23237 Richmond Chesterfield
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23238 Richmond Henrico
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23240 Richmond Richmond City
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23241 Richmond Richmond City
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23242 Richmond Henrico
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23249 Richmond Richmond City
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23250 Richmond Henrico
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23255 Richmond Henrico
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23260 Richmond Richmond City
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23261 Richmond Richmond City
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23269 Richmond Richmond City
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23273 Richmond Richmond City
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23274 Richmond Richmond City
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23276 Richmond Richmond City
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23278 Richmond Richmond City
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23279 Richmond Richmond City
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23282 Richmond Richmond City
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23284 Richmond Richmond City
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23285 Richmond Richmond City
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23286 Richmond Richmond City
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23288 Richmond Henrico
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23289 Richmond Richmond City
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23290 Richmond Richmond City
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23291 Richmond Richmond City
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23292 Richmond Richmond City
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23293 Richmond Richmond City
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23294 Richmond Henrico
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23295 Richmond Richmond City
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23297 Richmond Chesterfield
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23298 Richmond Richmond City
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23301 Accomac Accomack
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23302 Assawoman Accomack
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23303 Atlantic Accomack
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23304 Battery Park Isle Of Wight
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23306 Belle Haven Accomack
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23307 Birdsnest Northampton
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23308 Bloxom Accomack
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23310 Cape Charles Northampton
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23313 Capeville Northampton
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23314 Carrollton Isle Of Wight
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23315 Carrsville Isle Of Wight
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23316 Cheriton Northampton
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23320 Chesapeake Chesapeake City
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23321 Chesapeake Chesapeake City
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23322 Chesapeake Chesapeake City
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23323 Chesapeake Chesapeake City
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23324 Chesapeake Chesapeake City
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23325 Chesapeake Chesapeake City
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23326 Chesapeake Chesapeake City
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23327 Chesapeake Chesapeake City
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23328 Chesapeake Chesapeake City
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23336 Chincoteague Island Accomack
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23337 Wallops Island Accomack
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23341 Craddockville Accomack
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23345 Davis Wharf Accomack
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23347 Eastville Northampton
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23350 Exmore Northampton
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23354 Franktown Northampton
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23356 Greenbackville Accomack
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23357 Greenbush Accomack
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23358 Hacksneck Accomack
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23359 Hallwood Accomack
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23389 Harborton Accomack
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23395 Horntown Accomack
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23396 Oak Hall Accomack
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23397 Isle Of Wight Isle Of Wight
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23398 Jamesville Northampton
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23399 Jenkins Bridge Accomack
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23401 Keller Accomack
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23404 Locustville Accomack
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23405 Machipongo Northampton
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23407 Mappsville Accomack
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23408 Marionville Northampton
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23409 Mears Accomack
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23410 Melfa Accomack
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23412 Modest Town Accomack
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23413 Nassawadox Northampton
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23414 Nelsonia Accomack
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23415 New Church Accomack
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23416 Oak Hall Accomack
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23417 Onancock Accomack
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23418 Onley Accomack
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23419 Oyster Northampton
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23420 Painter Accomack
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23421 Parksley Accomack
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23422 Pungoteague Accomack
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23423 Quinby Accomack
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23424 Rescue Isle Of Wight
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23426 Sanford Accomack
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23427 Saxis Accomack
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23429 Seaview Northampton
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23430 Smithfield Isle Of Wight
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23431 Smithfield Isle Of Wight
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23432 Suffolk Suffolk City
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23433 Suffolk Suffolk City
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23434 Suffolk Suffolk City
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23435 Suffolk Suffolk City
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23436 Suffolk Suffolk City
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23437 Suffolk Suffolk City
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23438 Suffolk Suffolk City
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23439 Suffolk Suffolk City
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23440 Tangier Accomack
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23441 Tasley Accomack
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23442 Temperanceville Accomack
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23443 Townsend Northampton
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23450 Virginia Beach Virginia Beach City
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23451 Virginia Beach Virginia Beach City
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23452 Virginia Beach Virginia Beach City
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23453 Virginia Beach Virginia Beach City
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23454 Virginia Beach Virginia Beach City
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23455 Virginia Beach Virginia Beach City
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23456 Virginia Beach Virginia Beach City
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23457 Virginia Beach Virginia Beach City
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23458 Virginia Beach Virginia Beach City
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23459 Virginia Beach Virginia Beach City
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23460 Virginia Beach Virginia Beach City
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23461 Virginia Beach Virginia Beach City
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23462 Virginia Beach Virginia Beach City
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23463 Virginia Beach Virginia Beach City
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23464 Virginia Beach Virginia Beach City
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23465 Virginia Beach Virginia Beach City
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23466 Virginia Beach Virginia Beach City
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23467 Virginia Beach Virginia Beach City
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23471 Virginia Beach Virginia Beach City
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23479 Virginia Beach Virginia Beach City
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23480 Wachapreague Accomack
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23482 Wardtown Northampton
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23483 Wattsville Accomack
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23486 Willis Wharf Northampton
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23487 Windsor Isle Of Wight
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23488 Withams Accomack
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23501 Norfolk Norfolk City
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23502 Norfolk Norfolk City
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23503 Norfolk Norfolk City
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23504 Norfolk Norfolk City
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23505 Norfolk Norfolk City
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23506 Norfolk Norfolk City
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23507 Norfolk Norfolk City
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23508 Norfolk Norfolk City
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23509 Norfolk Norfolk City
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23510 Norfolk Norfolk City
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23511 Norfolk Norfolk City
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23512 Norfolk Norfolk City
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23513 Norfolk Norfolk City
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23514 Norfolk Norfolk City
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23515 Norfolk Norfolk City
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23517 Norfolk Norfolk City
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23518 Norfolk Norfolk City
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23519 Norfolk Norfolk City
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23520 Norfolk Norfolk City
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23521 Norfolk Norfolk City
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23523 Norfolk Norfolk City
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23529 Norfolk Norfolk City
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23541 Norfolk Norfolk City
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23551 Norfolk Norfolk City
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23601 Newport News Newport News City
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23602 Newport News Newport News City
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23603 Newport News Newport News City
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23604 Fort Eustis Newport News City
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23605 Newport News Newport News City
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23606 Newport News Newport News City
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23607 Newport News Newport News City
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23608 Newport News Newport News City
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23609 Newport News Newport News City
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23612 Newport News Newport News City
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23628 Newport News Newport News City
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23630 Hampton Hampton City
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23651 Fort Monroe Hampton City
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23661 Hampton Hampton City
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23662 Poquoson Poquoson City
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23663 Hampton Hampton City
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23664 Hampton Hampton City
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23665 Hampton York
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23666 Hampton Hampton City
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23667 Hampton Hampton City
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23668 Hampton Hampton City
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23669 Hampton Hampton City
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23670 Hampton Hampton City
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23681 Hampton Hampton City
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23690 Yorktown York
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23691 Yorktown York
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23692 Yorktown York
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23693 Yorktown York
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23694 Lackey York
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23696 Seaford York
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23701 Portsmouth Portsmouth City
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23702 Portsmouth Portsmouth City
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23703 Portsmouth Portsmouth City
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23704 Portsmouth Portsmouth City
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23705 Portsmouth Portsmouth City
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23707 Portsmouth Portsmouth City
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23708 Portsmouth Portsmouth City
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23709 Portsmouth Portsmouth City
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23801 Fort Lee Prince George
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23803 Petersburg Petersburg City
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23804 Petersburg Petersburg City
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23805 Petersburg Petersburg City
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23806 Petersburg Petersburg City
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23821 Alberta Brunswick
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23822 Ammon Dinwiddie
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23824 Blackstone Nottoway
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23825 Blackstone Nottoway
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23827 Boykins Southampton
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23828 Branchville Southampton
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23829 Capron Southampton
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23830 Carson Dinwiddie
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23831 Chester Chesterfield
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23832 Chesterfield Chesterfield
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23833 Church Road Dinwiddie
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23834 Colonial Heights Colonial Heights City
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23836 Chester Chesterfield
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23837 Courtland Southampton
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23838 Chesterfield Chesterfield
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23839 Dendron Surry
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23840 Dewitt Dinwiddie
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23841 Dinwiddie Dinwiddie
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23842 Disputanta Prince George
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23843 Dolphin Brunswick
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23844 Drewryville Southampton
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23845 Ebony Brunswick
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23846 Elberon Surry
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23847 Emporia Greensville
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23850 Ford Dinwiddie
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23851 Franklin Franklin City
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23856 Freeman Brunswick
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23857 Gasburg Brunswick
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23860 Hopewell Hopewell City
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23866 Ivor Southampton
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23867 Jarratt Greensville
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23868 Lawrenceville Brunswick
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23870 Jarratt Greensville
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23872 Mc Kenney Dinwiddie
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23873 Meredithville Brunswick
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23874 Newsoms Southampton
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23875 Prince George Prince George
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23876 Rawlings Brunswick
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23878 Sedley Southampton
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23879 Skippers Greensville
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23881 Spring Grove Surry
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23882 Stony Creek Sussex
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23883 Surry Surry
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23884 Sussex Sussex
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23885 Sutherland Dinwiddie
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23887 Valentines Brunswick
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23888 Wakefield Sussex
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23889 Warfield Brunswick
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23890 Waverly Sussex
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23891 Waverly Sussex
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23893 White Plains Brunswick
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23894 Wilsons Dinwiddie
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23897 Yale Sussex
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23898 Zuni Isle Of Wight
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23899 Claremont Surry
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23901 Farmville Prince Edward
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23909 Farmville Prince Edward
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23915 Baskerville Mecklenburg
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23917 Boydton Mecklenburg
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23919 Bracey Mecklenburg
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23920 Brodnax Brunswick
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23921 Buckingham Buckingham
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23922 Burkeville Nottoway
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23923 Charlotte Court House Charlotte
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23924 Chase City Mecklenburg
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23927 Clarksville Mecklenburg
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23930 Crewe Nottoway
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23934 Cullen Charlotte
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23936 Dillwyn Buckingham
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23937 Drakes Branch Charlotte
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23938 Dundas Lunenburg
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23939 Evergreen Appomattox
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23941 Fort Mitchell Lunenburg
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23942 Green Bay Prince Edward
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23943 Hampden Sydney Prince Edward
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23944 Kenbridge Lunenburg
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23947 Keysville Charlotte
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23950 La Crosse Mecklenburg
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23952 Lunenburg Lunenburg
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23954 Meherrin Prince Edward
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23955 Nottoway Nottoway
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23958 Pamplin Appomattox
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23959 Phenix Charlotte
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23960 Prospect Prince Edward
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23962 Randolph Charlotte
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23963 Red House Charlotte
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23964 Red Oak Charlotte
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23966 Rice Prince Edward
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23967 Saxe Charlotte
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23968 Skipwith Mecklenburg
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23970 South Hill Mecklenburg
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23974 Victoria Lunenburg
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23976 Wylliesburg Charlotte
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24001 Roanoke Roanoke City
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24002 Roanoke Roanoke City
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24003 Roanoke Roanoke City
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24004 Roanoke Roanoke City
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24005 Roanoke Roanoke City
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24006 Roanoke Roanoke City
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24007 Roanoke Roanoke City
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24008 Roanoke Roanoke City
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24009 Roanoke Roanoke City
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24010 Roanoke Roanoke City
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24011 Roanoke Roanoke City
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24012 Roanoke Roanoke City
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24013 Roanoke Roanoke City
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24014 Roanoke Roanoke City
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24015 Roanoke Roanoke City
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24016 Roanoke Roanoke City
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24017 Roanoke Roanoke City
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24018 Roanoke Roanoke
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24019 Roanoke Roanoke
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24020 Roanoke Roanoke
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24022 Roanoke Roanoke City
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24023 Roanoke Roanoke City
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24024 Roanoke Roanoke City
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24025 Roanoke Roanoke City
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24026 Roanoke Roanoke City
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24027 Roanoke Roanoke City
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24028 Roanoke Roanoke City
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24029 Roanoke Roanoke City
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24030 Roanoke Roanoke City
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24031 Roanoke Roanoke City
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24032 Roanoke Roanoke City
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24033 Roanoke Roanoke City
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24034 Roanoke Roanoke City
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24035 Roanoke Roanoke City
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24036 Roanoke Roanoke City
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24037 Roanoke Roanoke City
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24038 Roanoke Roanoke City
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24040 Roanoke Roanoke City
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24042 Roanoke Roanoke City
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24043 Roanoke Roanoke City
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24044 Roanoke Roanoke City
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24045 Roanoke Roanoke City
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24048 Roanoke Roanoke City
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24050 Roanoke Botetourt
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24053 Ararat Patrick
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24054 Axton Henry
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24055 Bassett Henry
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24058 Belspring Pulaski
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24059 Bent Mountain Roanoke
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24060 Blacksburg Montgomery
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24061 Blacksburg Montgomery
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24062 Blacksburg Montgomery
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24063 Blacksburg Montgomery
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24064 Blue Ridge Botetourt
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24065 Boones Mill Franklin
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24066 Buchanan Botetourt
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24067 Callaway Franklin
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24068 Christiansburg Montgomery
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24069 Cascade Pittsylvania
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24070 Catawba Roanoke
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24072 Check Floyd
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24073 Christiansburg Montgomery
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24076 Claudville Patrick
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24077 Cloverdale Botetourt
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24078 Collinsville Henry
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24079 Copper Hill Floyd
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24082 Critz Patrick
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24083 Daleville Botetourt
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24084 Dublin Pulaski
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24085 Eagle Rock Botetourt
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24086 Eggleston Giles
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24087 Elliston Montgomery
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24088 Ferrum Franklin
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24089 Fieldale Henry
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24090 Fincastle Botetourt
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24091 Floyd Floyd
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24092 Glade Hill Franklin
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24093 Glen Lyn Giles
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24095 Goodview Bedford
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24101 Hardy Franklin
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24102 Henry Franklin
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24104 Huddleston Bedford
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24105 Indian Valley Floyd
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24111 Mc Coy Montgomery
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24112 Martinsville Martinsville City
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24113 Martinsville Martinsville City
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24114 Martinsville Martinsville City
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24115 Martinsville Martinsville City
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24120 Meadows Of Dan Patrick
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24121 Moneta Bedford
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24122 Montvale Bedford
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24124 Narrows Giles
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24126 Newbern Pulaski
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24127 New Castle Craig
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24128 Newport Giles
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24129 New River Pulaski
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24130 Oriskany Botetourt
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24131 Paint Bank Craig
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24132 Parrott Pulaski
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24133 Patrick Springs Patrick
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24134 Pearisburg Giles
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24136 Pembroke Giles
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24137 Penhook Franklin
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24138 Pilot Montgomery
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24139 Pittsville Pittsylvania
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24141 Radford Radford
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24142 Radford Radford
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24143 Radford Radford
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24146 Redwood Franklin
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24147 Rich Creek Giles
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24148 Ridgeway Henry
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24149 Riner Montgomery
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24150 Ripplemead Giles
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24151 Rocky Mount Franklin
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24153 Salem Salem
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24155 Roanoke Salem
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24157 Roanoke Salem
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24161 Sandy Level Pittsylvania
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24162 Shawsville Montgomery
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24165 Spencer Henry
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24167 Staffordsville Giles
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24168 Stanleytown Henry
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24171 Stuart Patrick
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24174 Thaxton Bedford
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24175 Troutville Botetourt
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24176 Union Hall Franklin
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24177 Vesta Patrick
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24178 Villamont Bedford
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24179 Vinton Roanoke
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24184 Wirtz Franklin
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24185 Woolwine Patrick
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24201 Bristol Bristol
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24202 Bristol Washington
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24203 Bristol Bristol
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24209 Bristol Bristol
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24210 Abingdon Washington
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24211 Abingdon Washington
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24212 Abingdon Washington
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24215 Andover Wise
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24216 Appalachia Wise
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24217 Bee Dickenson
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24218 Ben Hur Lee
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24219 Big Stone Gap Wise
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24220 Birchleaf Dickenson
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24221 Blackwater Lee
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24224 Castlewood Russell
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24225 Cleveland Russell
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24226 Clinchco Dickenson
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24228 Clintwood Dickenson
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24230 Coeburn Wise
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24236 Damascus Washington
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24237 Dante Russell
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24239 Davenport Buchanan
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24243 Dryden Lee
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24244 Duffield Scott
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24245 Dungannon Scott
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24246 East Stone Gap Wise
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24248 Ewing Lee
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24250 Fort Blackmore Scott
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24251 Gate City Scott
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24256 Haysi Dickenson
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24258 Hiltons Scott
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24260 Honaker Russell
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24263 Jonesville Lee
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24265 Keokee Lee
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24266 Lebanon Russell
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24269 Mc Clure Dickenson
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24270 Mendota Washington
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24271 Nickelsville Scott
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24272 Nora Dickenson
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24273 Norton Norton City
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24277 Pennington Gap Lee
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24279 Pound Wise
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24280 Rosedale Russell
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24281 Rose Hill Lee
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24282 Saint Charles Lee
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24283 Saint Paul Wise
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24290 Weber City Scott
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24292 Whitetop Grayson
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24293 Wise Wise
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24301 Pulaski Pulaski
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24311 Atkins Smyth
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24312 Austinville Wythe
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24313 Barren Springs Wythe
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24314 Bastian Bland
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24315 Bland Bland
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24316 Broadford Tazewell
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24317 Cana Carroll
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24318 Ceres Bland
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24319 Chilhowie Smyth
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24322 Cripple Creek Wythe
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24323 Crockett Wythe
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24324 Draper Pulaski
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24325 Dugspur Carroll
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24326 Elk Creek Grayson
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24327 Emory Washington
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24328 Fancy Gap Carroll
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24330 Fries Grayson
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24333 Galax Galax City
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24340 Glade Spring Washington
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24343 Hillsville Carroll
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24347 Hiwassee Pulaski
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24348 Independence Grayson
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24350 Ivanhoe Wythe
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24351 Lambsburg Carroll
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24352 Laurel Fork Carroll
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24354 Marion Smyth
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24360 Max Meadows Wythe
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24361 Meadowview Washington
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24363 Mouth Of Wilson Grayson
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24366 Rocky Gap Bland
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24368 Rural Retreat Wythe
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24370 Saltville Smyth
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24374 Speedwell Wythe
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24375 Sugar Grove Smyth
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24377 Tannersville Tazewell
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24378 Troutdale Grayson
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24380 Willis Floyd
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24381 Woodlawn Carroll
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24382 Wytheville Wythe
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24401 Staunton Staunton City
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24402 Staunton Staunton City
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24411 Augusta Springs Augusta
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24412 Bacova Bath
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24413 Blue Grass Highland
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24415 Brownsburg Rockbridge
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24416 Buena Vista Buena Vista City
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24421 Churchville Augusta
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24422 Clifton Forge Alleghany
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24426 Covington Covington City
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24430 Craigsville Augusta
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24431 Crimora Augusta
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24432 Deerfield Augusta
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24433 Doe Hill Highland
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24435 Fairfield Rockbridge
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24437 Fort Defiance Augusta
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24438 Glen Wilton Botetourt
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24439 Goshen Rockbridge
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24440 Greenville Augusta
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24441 Grottoes Rockingham
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24442 Head Waters Highland
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24445 Hot Springs Bath
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24448 Iron Gate Alleghany
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24450 Lexington Lexington City
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24457 Low Moor Alleghany
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24458 Mc Dowell Highland
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24459 Middlebrook Augusta
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24460 Millboro Bath
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24463 Mint Spring Augusta
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24464 Montebello Nelson
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24465 Monterey Highland
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24467 Mount Sidney Augusta
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24468 Mustoe Highland
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24469 New Hope Augusta
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24471 Port Republic Rockingham
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24472 Raphine Rockbridge
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24473 Rockbridge Baths Rockbridge
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24474 Selma Alleghany
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24476 Steeles Tavern Augusta
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24477 Stuarts Draft Augusta
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24479 Swoope Augusta
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24482 Verona Augusta
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24483 Vesuvius Rockbridge
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24484 Warm Springs Bath
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24485 West Augusta Augusta
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24486 Weyers Cave Augusta
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24487 Williamsville Bath
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24501 Lynchburg Lynchburg City
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24502 Lynchburg Lynchburg City
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24503 Lynchburg Lynchburg City
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24504 Lynchburg Lynchburg City
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24505 Lynchburg Lynchburg City
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24506 Lynchburg Lynchburg City
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24512 Lynchburg Lynchburg City
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24513 Lynchburg Lynchburg City
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24514 Lynchburg Lynchburg City
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24515 Lynchburg Lynchburg City
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24517 Altavista Campbell
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24520 Alton Halifax
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24521 Amherst Amherst
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24522 Appomattox Appomattox
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24523 Bedford Bedford
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24526 Big Island Bedford
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24527 Blairs Pittsylvania
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24528 Brookneal Campbell
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24529 Buffalo Junction Mecklenburg
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24530 Callands Pittsylvania
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24531 Chatham Pittsylvania
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24533 Clifford Amherst
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24534 Clover Halifax
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24535 Cluster Springs Halifax
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24536 Coleman Falls Bedford
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24538 Concord Campbell
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24539 Crystal Hill Halifax
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24540 Danville Danville City
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24541 Danville Danville City
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24543 Danville Danville City
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24544 Danville Danville City
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24549 Dry Fork Pittsylvania
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24550 Evington Campbell
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24551 Forest Bedford
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24553 Gladstone Nelson
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24554 Gladys Campbell
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24555 Glasgow Rockbridge
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24556 Goode Bedford
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24557 Gretna Pittsylvania
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24558 Halifax Halifax
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24562 Howardsville Buckingham
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24563 Hurt Pittsylvania
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24565 Java Pittsylvania
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24566 Keeling Pittsylvania
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24569 Long Island Pittsylvania
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24570 Lowry Bedford
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24571 Lynch Station Campbell
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24572 Madison Heights Amherst
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24574 Monroe Amherst
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24576 Naruna Campbell
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24577 Nathalie Halifax
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24578 Natural Bridge Rockbridge
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24579 Natural Bridge Station Rockbridge
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24580 Nelson Mecklenburg
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24581 Norwood Nelson
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24586 Ringgold Pittsylvania
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24588 Rustburg Campbell
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24589 Scottsburg Halifax
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24590 Scottsville Albemarle
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24592 South Boston Halifax
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24593 Spout Spring Appomattox
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24594 Sutherlin Pittsylvania
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24595 Sweet Briar Amherst
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24597 Vernon Hill Halifax
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24598 Virgilina Halifax
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24599 Wingina Buckingham
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24601 Amonate Tazewell
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24602 Bandy Tazewell
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24603 Big Rock Buchanan
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24604 Bishop Tazewell
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24605 Bluefield Tazewell
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24606 Boissevain Tazewell
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24607 Breaks Dickenson
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24608 Burkes Garden Tazewell
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24609 Cedar Bluff Tazewell
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24612 Doran Tazewell
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24613 Falls Mills Tazewell
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24614 Grundy Buchanan
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24619 Horsepen Tazewell
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24620 Hurley Buchanan
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24622 Jewell Ridge Tazewell
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24624 Keen Mountain Buchanan
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24627 Mavisdale Buchanan
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24628 Maxie Buchanan
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24630 North Tazewell Tazewell
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24631 Oakwood Buchanan
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24634 Pilgrims Knob Buchanan
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24635 Pocahontas Tazewell
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24637 Pounding Mill Tazewell
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24639 Raven Buchanan
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24640 Red Ash Tazewell
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24641 Richlands Tazewell
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24646 Rowe Buchanan
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24647 Shortt Gap Buchanan
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24649 Swords Creek Russell
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24651 Tazewell Tazewell
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24656 Vansant Buchanan
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24657 Whitewood Buchanan
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24658 Wolford Buchanan
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24701 Bluefield Mercer
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24712 Athens Mercer
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24714 Beeson Mercer
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24715 Bramwell Mercer
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24716 Bud Wyoming
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24719 Covel Wyoming
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24724 Freeman Mercer
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24726 Herndon Wyoming
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24729 Hiawatha Mercer
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24731 Kegley Mercer
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24732 Kellysville Mercer
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24733 Lashmeet Mercer
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24736 Matoaka Mercer
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24737 Montcalm Mercer
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24738 Nemours Mercer
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24739 Oakvale Mercer
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24740 Princeton Mercer
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24747 Rock Mercer
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24751 Wolfe Mercer
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24801 Welch Mcdowell
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24808 Anawalt Mcdowell
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24811 Avondale Mcdowell
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24813 Bartley Mcdowell
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24815 Berwind Mcdowell
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24816 Big Sandy Mcdowell
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24817 Bradshaw Mcdowell
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24818 Brenton Wyoming
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24822 Clear Fork Wyoming
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24823 Coal Mountain Wyoming
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24824 Coalwood Mcdowell
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24826 Cucumber Mcdowell
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24827 Cyclone Wyoming
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24828 Davy Mcdowell
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24829 Eckman Mcdowell
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24830 Elbert Mcdowell
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24831 Elkhorn Mcdowell
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24834 Fanrock Wyoming
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24836 Gary Mcdowell
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24839 Hanover Wyoming
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24842 Hemphill Mcdowell
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24843 Hensley Mcdowell
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24844 Iaeger Mcdowell
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24845 Ikes Fork Wyoming
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24846 Isaban Mcdowell
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24847 Itmann Wyoming
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24848 Jenkinjones Mcdowell
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24849 Jesse Wyoming
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24850 Jolo Mcdowell
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24851 Justice Mingo
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24853 Kimball Mcdowell
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24854 Kopperston Wyoming
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24855 Kyle Mcdowell
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24857 Lynco Wyoming
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24859 Marianna Wyoming
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24860 Matheny Wyoming
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24861 Maybeury Mcdowell
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24862 Mohawk Mcdowell
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24866 Newhall Mcdowell
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24867 New Richmond Wyoming
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24868 Northfork Mcdowell
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24869 North Spring Wyoming
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24870 Oceana Wyoming
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24871 Pageton Mcdowell
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24872 Panther Mcdowell
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24873 Paynesville Mcdowell
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24874 Pineville Wyoming
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24878 Premier Mcdowell
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24879 Raysal Mcdowell
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24880 Rock View Wyoming
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24881 Roderfield Mcdowell
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24882 Simon Wyoming
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24884 Squire Mcdowell
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24887 Switchback Mcdowell
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24888 Thorpe Mcdowell
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24892 War Mcdowell
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24894 Warriormine Mcdowell
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24895 Wilcoe Mcdowell
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24898 Wyoming Wyoming
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24901 Lewisburg Greenbrier
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24902 Fairlea Greenbrier
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24910 Alderson Greenbrier
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24915 Arbovale Pocahontas
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24916 Asbury Greenbrier
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24918 Ballard Monroe
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24920 Bartow Pocahontas
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24924 Buckeye Pocahontas
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24925 Caldwell Greenbrier
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24927 Cass Pocahontas
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24931 Crawley Greenbrier
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24934 Dunmore Pocahontas
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24935 Forest Hill Summers
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24938 Frankford Greenbrier
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24941 Gap Mills Monroe
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24943 Grassy Meadows Greenbrier
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24944 Green Bank Pocahontas
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24945 Greenville Monroe
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24946 Hillsboro Pocahontas
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24951 Lindside Monroe
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24954 Marlinton Pocahontas
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24957 Maxwelton Greenbrier
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24961 Neola Greenbrier
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24962 Pence Springs Summers
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24963 Peterstown Monroe
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24966 Renick Greenbrier
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24970 Ronceverte Greenbrier
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24974 Secondcreek Monroe
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24976 Sinks Grove Monroe
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24977 Smoot Greenbrier
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24981 Talcott Summers
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24983 Union Monroe
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24984 Waiteville Monroe
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24985 Wayside Monroe
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24986 White Sulphur Springs Greenbrier
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24991 Williamsburg Greenbrier
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24993 Wolfcreek Monroe
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25002 Alloy Fayette
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25003 Alum Creek Kanawha
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25005 Amma Roane
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25007 Arnett Raleigh
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25008 Artie Raleigh
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25009 Ashford Boone
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25011 Bancroft Putnam
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25015 Belle Kanawha
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25019 Bickmore Clay
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25021 Bim Boone
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25022 Blair Logan
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25024 Bloomingrose Boone
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25025 Blount Kanawha
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25026 Blue Creek Kanawha
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25028 Bob White Boone
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25030 Bomont Clay
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25031 Boomer Fayette
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25033 Buffalo Putnam
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25035 Cabin Creek Kanawha
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25036 Cannelton Fayette
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25039 Cedar Grove Kanawha
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25040 Charlton Heights Fayette
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25043 Clay Clay
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25044 Clear Creek Raleigh
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25045 Clendenin Kanawha
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25047 Clothier Logan
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25048 Colcord Raleigh
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25049 Comfort Boone
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25051 Costa Boone
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25053 Danville Boone
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25054 Dawes Kanawha
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25057 Deep Water Fayette
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25059 Dixie Nicholas
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25060 Dorothy Raleigh
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25061 Drybranch Kanawha
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25062 Dry Creek Raleigh
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25063 Duck Clay
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25064 Dunbar Kanawha
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25067 East Bank Kanawha
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25070 Eleanor Putnam
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25071 Elkview Kanawha
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25075 Eskdale Kanawha
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25076 Ethel Logan
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25079 Falling Rock Kanawha
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25081 Foster Boone
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25082 Fraziers Bottom Putnam
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25083 Gallagher Kanawha
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25085 Gauley Bridge Fayette
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25086 Glasgow Kanawha
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25088 Glen Clay
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25090 Glen Ferris Fayette
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25093 Gordon Boone
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25102 Handley Kanawha
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25103 Hansford Kanawha
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25106 Henderson Mason
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25107 Hernshaw Kanawha
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25108 Hewett Boone
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25109 Hometown Putnam
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25110 Hugheston Kanawha
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25111 Indore Clay
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25112 Institute Kanawha
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25113 Ivydale Clay
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25114 Jeffrey Boone
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25115 Kanawha Falls Fayette
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25118 Kimberly Fayette
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25119 Kincaid Fayette
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25121 Lake Logan
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25123 Leon Mason
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25124 Liberty Putnam
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25125 Lizemores Clay
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25126 London Kanawha
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25130 Madison Boone
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25132 Mammoth Kanawha
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25133 Maysel Clay
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25134 Miami Kanawha
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25136 Montgomery Fayette
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25139 Mount Carbon Fayette
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25140 Naoma Raleigh
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25141 Nebo Clay
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25142 Nellis Boone
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25143 Nitro Kanawha
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25148 Orgas Boone
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25149 Ottawa Boone
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25152 Page Fayette
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25154 Peytona Boone
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25156 Pinch Kanawha
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25159 Poca Putnam
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25160 Pond Gap Kanawha
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25161 Powellton Fayette
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25162 Pratt Kanawha
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25164 Procious Clay
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25165 Racine Boone
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25168 Red House Putnam
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25169 Ridgeview Boone
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25173 Robson Fayette
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25174 Rock Creek Raleigh
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25177 Saint Albans Kanawha
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25180 Saxon Boone
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25181 Seth Boone
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25183 Sharples Logan
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25185 Mount Olive Fayette
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25186 Smithers Fayette
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25187 Southside Mason
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25193 Sylvester Boone
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25201 Tad Kanawha
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25202 Tornado Kanawha
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25203 Turtle Creek Boone
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25204 Twilight Boone
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25205 Uneeda Boone
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25206 Van Boone
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25208 Wharton Boone
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25209 Whitesville Boone
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25211 Widen Clay
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25213 Winfield Putnam
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25214 Winifrede Kanawha
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25231 Advent Jackson
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25234 Arnoldsburg Calhoun
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25235 Chloe Calhoun
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25239 Cottageville Jackson
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25241 Evans Jackson
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25243 Gandeeville Roane
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25244 Gay Jackson
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25245 Given Jackson
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25247 Hartford Mason
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25248 Kenna Jackson
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25251 Left Hand Roane
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25252 Le Roy Jackson
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25253 Letart Mason
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25259 Looneyville Roane
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25260 Mason Mason
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25261 Millstone Calhoun
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25262 Millwood Jackson
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25264 Mount Alto Mason
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25265 New Haven Mason
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25266 Newton Roane
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25267 Normantown Gilmer
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25268 Orma Calhoun
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25270 Reedy Roane
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25271 Ripley Jackson
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25275 Sandyville Jackson
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25276 Spencer Roane
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25285 Wallback Clay
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25286 Walton Roane
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25287 West Columbia Mason
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25301 Charleston Kanawha
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25302 Charleston Kanawha
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25303 Charleston Kanawha
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25304 Charleston Kanawha
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25305 Charleston Kanawha
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25306 Charleston Kanawha
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25309 Charleston Kanawha
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25311 Charleston Kanawha
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25312 Charleston Kanawha
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25313 Charleston Kanawha
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25314 Charleston Kanawha
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25315 Charleston Kanawha
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25317 Charleston Kanawha
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25320 Charleston Kanawha
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25321 Charleston Kanawha
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25322 Charleston Kanawha
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Ketamine IV for Depression Webinar | Ketamine Doctors | Ketamine for Depression | 703-844-0184 | Fairfax, Virginia 22304 |

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Ask The Doctor: “Ketamine For Depression: Progress And Pitfalls” With Dr. Cristina Cusin, M.D.  < Webinar Link

Old Club Drug Is Repurposed Into Depression Treatment

A North Texas woman said a popular club drug and animal tranquilizer saved her from a life of depression and suicidal thoughts.

You may have heard of the drug before, as Special K on the street. it was designed as a horse tranquilizer, but Ketamine is gaining popularity as a treatment for depression.

Some doctors believe the controversial drug will become a game-changer in slowing the nation’s suicide epidemic.

Tiffany McCombie, a 40-year-old mother of one, knows what depression feels like in its darkest moments.

“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

Ketamine IV reduces depression in Adolescents |703-844-0184 | Ketamine therapy for Anxiety and Depression| IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |

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Below is a recent study regarding the treatment of adolescents with Ketamine for refractory depression. There seems to be good success and longer lasting results:

Intravenous Ketamine for Adolescents with Treatment-Resistant Depression: An Open-Label Study

The average response rate in published studies testing ketamine for adult TRD is 67% (Wan et al. 2015), which is considerably higher than TRD interventions (e.g., the average response rate for transcranial magnetic stimulation is 45%
(Conelea et al. 2017).

Background: Novel interventions for treatment-resistant depression (TRD) in adolescents are urgently needed. Ketamine has been studied in adults with TRD, but little information is available for adolescents. This study investigated efficacy and tolerability of intravenous ketamine in adolescents with TRD, and explored clinical response predictors.

Methods: Adolescents, 12–18 years of age, with TRD (failure to respond to two previous antidepressant trials) were administered six ketamine (0.5 mg/kg) infusions over 2 weeks. Clinical response was defined as a 50% decrease in Children’s Depression Rating Scale-Revised (CDRS-R); remission was CDRS-R score ≤28. Tolerability assessment included monitoring vital signs and dissociative symptoms using the Clinician-Administered Dissociative States Scale (CADSS).

Results: Thirteen participants (mean age 16.9 years, range 14.5–18.8 years, eight biologically male) completed the protocol. Average decrease in CDRS-R was 42.5% (p = 0.0004). Five (38%) adolescents met criteria for clinical response. Three responders showed sustained remission at 6-week follow-up; relapse occurred within 2 weeks for the other two responders. Ketamine infusions were generally well tolerated; dissociative symptoms and hemodynamic symptoms were transient. Higher dose was a significant predictor of treatment response.

Conclusions: These results demonstrate the potential role for ketamine in treating adolescents with TRD. Limitations include the open-label design and small sample; future research addressing these issues are needed to confirm these results. Additionally, evidence suggested a dose–response relationship; future studies are needed to optimize dose. Finally, questions remain regarding the long-term safety of ketamine as a depression treatment; more information is needed before broader clinical use.

Intravenous Ketamine for Adolescents – PDF

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Below is the latest on CBS for Ketmine treatment for Depression. Don’t Just walk through life..enjoy it.

Ketamine has been very successful in treating depression and suicidality in many patients over a long period of time:

Image result for suicidal person
703-844-0184 | Ketamine for Depression | Virginia |Fairfax | Loudon | Alexandria Ketamine infusions | PTSD | Anxiety

Ketamine gaining popularity as a treatment for the severely depressed

Anne Stallings says she has been battling severe depression for most of her life. She tried anti-depressants and even electroconvulsive therapy, but nothing worked until she went to a Ketamine  clinic  and tried ketamine, reports CBS News correspondent Paula Reid. 
 
“It was like the fifth treatment in and I had come home from the grocery store and I was putting away the groceries and I was like, ‘Wow, this is how you don’t feel depressed.’ It was like from turning on a black and white TV to a color TV,” Stallings said.   
 
Ketamine was approved by the FDA in the 1970s to sedate patients during medical procedures. It is more commonly known as an animal tranquilizer and in powder form as “Special K,” a club drug used to get high.
 
Today, ketamine is being provided legally off-label to treat depression at an estimated 250 clinics across the U.S.

ctm-saturday-clean-feed-20180203-cr470c-0700-0900-01-frame-72699.jpg

Anne Stallings

 CBS NEWS

Dr. Steve Levine offers intravenous ketamine infusions at several clinics around the country as an alternative to common anti-depressants. He says he treats about 70-80 patients across all the offices on any given day.

“Everything for the past 50 years has been based on the chemical imbalance theory of depression which has never held water,” Levine said. “So all these medicines, while they do help a lot of people, are based upon a flawed theory. And that is probably one of the reasons why they do take so long to work. They all take weeks to months to work so here is a medicine that people can take infrequently that is based upon a theory of the brain that makes a lot more sense and it works almost immediately.”
 
Stallings didn’t have time to wait. She had an especially hard time over the holidays and when her father got sick, she thought about taking her own life.
 
“I actually had suicidal ideations and the one thing about ketamine was that I was able to get in here emergently because I knew what was going on and when I left here my suicidal thoughts were gone,” Stallings said. 
 
That is in line with what Columbia University discovered in one of the largest studies yet on ketamine. Researchers found the drug was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients. The effects lasted up to six weeks.
 
Twenty-two-year-old Marc Nelson ditched his antidepressants for ketamine and talk therapy. He says he now feels more like himself, but it came at a cost. He has spent more than $10,000 on treatments.
 
“So many different drugs that I am now off of all of them, which you know, the side effects were just not tolerable to me. They make me a zombie. I was not happy,” Nelson said. 
 
But these infusions can have their own pitfalls. Ketamine can cause people to feel detached from their bodies.

ctm-saturday-clean-feed-20180203-cr470c-0700-0900-01-frame-74486.jpg

Marc Nelson receives a ketamine treatment 

 CBS NEWS

“The 45-minute period of very floatiness, I sometimes get nauseous,” Nelson said. “It’s a very interesting process. … I just lost my train of thought.”
 
Once the treatment was finished, Nelson said he felt “clear, cognizant” and “definitely able to pronounce” his words again.
 
Asked to address critics who say he’s making money by giving people the opportunity to get high, Levine said, “I would say that if you ask any of our patients none of them feel that they are getting high.”

“People tend to focus on the party use of ketamine, because it is more exciting, it’s sexier in some way. It does it a disservice because that’s a very small fraction of its use,” Levine added. “And as far as the money making aspect of this, if you were doing things in the right way you’re not gonna make a lot of money.”

Ketamine has piqued the interest of some major pharmaceutical companies. There are half a dozen drugs in development that mimic the way ketamine works, with some undergoing FDA clinical trials for approval as antidepressants.

For decades, Dr. Gerry Sanacora has been studying ketamine at Yale.

“What we’re trying to understand is what does it change in the brain that allows that sustained anti-depressant like response?” Sanacora said. 
 
He says the drug is not addictive in the way opioids are, but could still be harmful in the long run.
 
“There is at least evidence in animal models that these type of medications can actually cause some structural damage in the brain. That’s usually at higher doses, that’s usually at longer term exposure but we don’t know where that level is,” Sanacora said. 
 
Dr. Levine said he monitors patients closely. 

“In our population even people who have been having ketamine on a maintenance basis for up to six years now we haven’t seen any sign of that,” Levine said.

But for Anne Stallings, despite the unknowns, she’s content with a chance to feel normal.
 
“If I can live a quality, happy life, and be productive, be able to go to work, to be able to have my family, to enjoy life – not walk through life but enjoy life – then it’s worth it.”

Ketamine for rapid reduction of suicidal thoughts 2017  <article out of Colombia University

In major depression with clinically significant suicidal ideation,
a single subanesthetic ketamine infusion, adjunctive to ongoing
pharmacotherapy, was associated with a greater reduction
in suicidal thoughts at day 1, the primary outcome measure,
compared with midazolam control infusion. The adjusted
mean difference of 4.96 points on the clinician-rated SSI, a
Cohen’s d of 0.75, and a number needed to treat of 4 for
response represent a medium-sized effect. Adverse effects—
mainly blood pressure increase and dissociative symptoms—
were similar to those reported in other ketamine studies (37)
and were mostly mild to moderate, and transient, typically
resolving within minutes to hours after infusion. Improvement
in suicidal ideation largely persisted during the 6-week period of uncontrolled observation, during which
standard pharmacological treatments were also optimized.
To our knowledge, there is no established definition of a
clinically meaningful reduction in score on a standard suicidal
ideation scale. A prospective study (N=6,891) of patients
with depressive disorders (23) found that a baseline SSI
score .2 predicted suicide during up to 20 years of follow-up.
In a prospective study of 562 inpatients (64% with a mood
disorder) who endorsed suicidal thoughts (38), those who
experienced a 50% reduction within 24 hours from a severe
level (suicidal ideation “most of the time”) had one-third the
risk of subsequent self-harm events during a mean length of
stay of 24 days, compared with those whose suicidal thoughts
remained elevated. Given concerns about ketamine’s 1- to 2-week antidepressant
effect in previous studies (11), it is notable that the
improvement in suicidal ideation in this trial was largely
maintained through the 6-week follow-up ratings. This may
be partly explained by the fact that patients continued prior
psychotropic medication, which was optimized after completion
of day 1 postinfusion ratings. Our result is consistent
with the Hu et al. trial (41), in which patients with major depression
who were randomly assigned to receive a single
ketamineinfusion onday 1 of escitalopram therapy experienced
a faster response compared with patients who received a saline
control infusion, and the benefits were maintained for 4 weeks.

We found greater reductions in overall mood disturbance,
depression, and fatigue, assessed with the POMS, on day 1 after
ketamine compared with midazolam.A
secondary analysis of adjunctive ketamine (N=14) found
a reduction in suicidal ideation even when depression did
not remit (17)Ketamine is mechanistically distinct from
currently approved antidepressants, its therapeutic effects
possiblyinvolving rapid synapse formation (44)

Montgomery-Asberg Depression Rating Scale

In summary, in this randomized trial in suicidal depressed
patients, a single adjunctive subanesthetic ketamine infusion
was associated with a clinically significant reduction
in suicidal ideation at day 1 that was greater than with the
midazolam control infusion. In the context of standard, optimized
treatment after the ketamine infusion, this improvement
appeared to persist for at least 6 weeks. The
clinical applicability of our findings was improved with infusion
administration by a psychiatrist and without a medication
washout, as has been done in some studies

Profile of mood states

_Modified_Scale_for_Suicidal_Ideation

KETAMINE INFUSIONS |KETAMINE DEPRESSION | KETAMINE DOCTORS IN VIRGINIA | FAIRFAX KETAMINE | 703-844-0184 | KETAMINE AND DEPRESSION TREATMENT – Newsweek Article | 22308 |22305 | 22304 | 22191 |22192 |22193 | 20118 | 20104 | KETAMINE TREATMENT FOR DEPRESSION |CRPS |RSD |KETAMINE INFUSIONS FOR PAIN | SPRINGFIELD , VA KETAMINE |

NOVA Health Recovery  <<< Ketamine infusion center in Alexandria, Virginia 703-844-0184  – consider ketamine for addiction treatment

CAll 703-844-0184 for an immediate appointment!

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

email@novahealthrecovery.com

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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.

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KETAMINE | FAIRFAX | ALEXANDRIA | 703-844-0184| KETAMINE THERAPY | KETAMINE AS AN ANTI-DEPRESSANT – NIH -| Dr. Sendi | Ketamine Springfield, Va | Ketamine Loudon | Ketamine for depression| Lyme disease | email@novahealthrecovery.com| Ketamine Woodbridge||Ketamine for Lyme disease –

NOVA Health Recovery  <<< Ketamine infusion center in Alexandria, Virginia 703-844-0184  – consider ketamine for addiction treatment

CAll 703-844-0184 for an immediate appointment!

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

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

NovaKetamine : Ketamine treatments for depression, PTSD, anxiety, pain, and CRPS

NOVA KETAMINE – IV ketamine therapies in Virginia

Ketamine press article for Lyme Disease treatment

_______________________________________________________________________

Here is a knock off of the article from Ascend Ketamine in Houston:

There is an undeniable connection between depression and chronic pain. While depression is a clinical mental health disorder, it manifests with inexplicable psychical ailments: migraine headaches, back pain, etc. And while chronic pain is a clinically physical condition, it manifests with inexplicable mental ailments: elevated stress levels, poor quality of sleep, low self-esteem, etc. And the worst part: these mental and physical conditions perpetuate each other. Chronic pain exacerbates depressive symptoms. Depressive symptoms result in heightened levels of pain. And so on…

Breaking the Pain-Depression Cycle

Being proactive is the most important step an individual can take in an effort to break the pain-depression cycle. Acute pain can easily become chronic pain if left unaddressed. Advocate for yourself and speak to a physician if you notice any of these symptoms, even if you don’t think they are anything to be concerned about:

  • Depression, sadness or anxiety
  • Poor quality sleep or trouble falling asleep
  • Loss of hope
  • Loss of interest in enjoyable activities
  • Changes to your appetite
  • Inability to become motivated

Be mindful of—and avoid—stressful situations, as stress can result in heightened pain levels. And don’t assume that depressive symptoms will be resolved when your pain is minimized. It’s better to talk about what you’re experiencing now than it is to spend months or years suffering in the future.

Ketamine Infusions for Chronic Pain & Depression

Ketamine treatments are proven to reduce chronic pain and alleviate the symptoms of depression in up to 70% of patients. If chronic pain and depression are negatively impacting your life, ketamine infusions may be an option for you. Taking a multi-disciplinary approach to treating chronic pain, depression, and other psychiatric disorders, however, is a more high yield approach than any one therapy. Other treatment options to consider include:

  • Psychotherapy or counseling
  • Exercise, meditation, journaling, and other mind-body solutions
  • Medicinal or pharmacological solutions

Ketamine infusions coupled with any of the above treatments will likely yield the most promising results, minimizing chronic pain and effectively reducing depressive symptoms before they become untreatable. 

 

_________________________________________________

Ketamine press article for Lyme Disease treatment

CBS News Features Dr. Ashraf Hanna Discussing How IV Ketamine is Successfully Treating Lyme Disease

TAMPA, Fla.Feb. 22, 2016 /PRNewswire/ — CBS news just broadcast a featured story on Lyme disease and itsfar-reaching complications. There are over 400,000 new cases of the disease diagnosed each year, and the rate has been increasing dramatically.

Dr. Ashraf Hanna, a board certified physician and director of pain management at the Florida Spine Institute in ClearwaterFL discusses this tragic disease: “Lyme disease is a infectious disease caused by bacteria which is transmitted by ticks. The symptoms include rash, fatigue, arthritis of the joints, joint pain, muscle aches, and headaches, numbness, tingling and pain. 70-80% of patients get relief from antibiotics within a few weeks by their primary care or infectious disease physician, but 20-30% may continue with chronic pain symptoms.”

“For the remaining 20-30%, it is not a simple infection anymore; it is a complex, multi-system disease. We have to treat the different types of co-existing infections, autonomic dysfunction, hormonal deficiency, food allergies, etc. But the major contributing factor with persistence of those symptoms after antibiotic treatment is neuro-inflammation and immune-mediated reactions,” stated Dr. Hanna.

IV Ketamine appears to be the best treatment for late stage Lyme disease, after failed antibiotic treatments, and other therapies. Many Lyme patients are reporting remarkable success after treatments with IV Ketamine.

One of the Lyme Patients being treated by Dr. Hanna was Krysten Fernandez: “A few weeks after my tick bite, my symptoms began getting worse, I had extreme pain and was becoming lethargic and weak. I visited over 40 doctors, and after having being misdiagnosed and trying many failed remedies and treatments that were actually worse for my condition, I was finally diagnosed with Late Stage Lyme Disease. At this point I could not work or even walk. I used to be independent and active, was a yoga instructor and had a successful Internet business. Everyday was a struggle to do the simplest tasks.”

“After years of suffering and depression, I found Dr. Ashraf Hanna at the Florida Spine Institute and he recommended IV Ketamine for the treatment of my late stage Lyme disease. After only a few treatments, I had incredible results! My pain levels were reduced, and I felt better than I have felt in years! I am so thankful that Dr. Hanna was able to treat me with IV Ketamine. I can now walk again, have increased function in my limbs and I am getting back to a normal life and feeling great!” said Krysten.

“IV Ketamine Infusion simply blocks receptors in the brain that are responsible for releasing chemicals that cause inflammation of the nervous system that in turn can cause painful symptoms. What makes our program different is that we incorporate physical therapy so that we not only improve pain, but also improve function, and we have seen amazing results. We want patients to get their life back and live productive, fulfilling lives,” Said Dr. Hanna.

EFFECTS OF INTRAVENOUS KETAMINE IN A PATIENT WITH POST-TREATMENT LYME DISEASE SYNDROME:

Effects of intravenous ketamine in a patient with post-treatment Lyme disease syndrome

Discussion and conclusion
A recent double-blind, randomized, placebo-controlled
clinical trial was conducted to evaluate the efficacy of IV
ketamine in patients with treatment-resistant depression.15
These investigators reported that IV ketamine was effective at
reducing depressive symptoms in this patient population. The
results of our case report and evidence from similar studies
and preceding case reports substantiate the antidepressant
efficacy of ketamine.4,16–18 To our knowledge, there have
been no other reports in the literature that have assessed the
effects of IV ketamine in a patient with PTLDS until now.
In this patient with whole-body chronic pain associated
with PTLDS, IV ketamine drastically reduced pain levels
(Figure 1). The patient’s depression and suicidal ideations
were also eliminated post-ketamine infusion. Although we19,20
and others21,22 have reported the efficacy of IV ketamine for
the treatment of chronic pain, this patient’s results were not
typical. In this case, the drastic reductions in pain levels (VAS
reduced from 7 to 2) were followed by an eventual return to
baseline. However, when the patient’s pain did return, shorter
booster infusions were sufficient to maintain analgesia for
months at a time. This is in contrast to, for example, our
previous documentation of a patient with fibromyalgia who
achieved complete remission for more than a year postinfusion
without additional treatment.19
The current PTLDS patient’s pain levels were adequately
controlled using IV ketamine infusions for a duration of
~1–2 months from the last infusion session. Given that the
elimination half-life of IV ketamine is only 2.5 hours,23,24
this means that the duration of analgesia produced in this
case did not require the sustained pharmacological action
of ketamine, since it would have been eliminated within
the first day following the last infusion. This observation
supports theories that chronic pain associated with PTLDS
may be neuropathic in nature25 and that ketamine’s analgesic
efficacy is centrally mediated.
“Central sensitization” has been coined to describe
numerous neuropathic pain conditions resulting from a
nociceptive insult that triggers a prolonged but reversible
increase in the excitability and synaptic efficacy of neurons
in central nociceptive pathways.26 Ketamine is thought to
de-sensitize centrally mediated pain via repeated NMDA
receptor blockade.27 However, it is likely that ketamine acts
via multiple mechanisms to produce analgesia in neuropathic
pain conditions. Neuropathic pain has been associated with
increased glial activation and subsequent release of proinflammatory
cytokines. Interestingly, ketamine produces
pharmacological effects that reduce cell excitotoxicity via
NMDA antagonism and reduce inflammation by suppressing
the hyperactivation of microglia.28 Moreover, ketamine
produces immunomodulatory actions that may also be
uniquely beneficial to conditions that may have an autoimmune
component, such as PTLDS. Thus, ketamine appears
to produce a robust polypharmacological “entourage effect”
that is highly effective in treating neuropathic pain conditions
– which are notoriously difficult to treat with more
conventional analgesic drugs.
In conclusion, the pain relief (~71% decrease) described
in this case report was achieved without the use of increasing
doses of opioid analgesics and, in fact, afforded the
patient’s fentanyl dosage to be reduced from 125 µg to 75 µg
(40% decrease) every 48 hours. Opioid-sparing therapies,
such as ketamine, should be used more frequently for the
management of chronic pain. This is especially important
given the frequency of opioid dependence and abuse, which
has reached such severity to be widely regarded as an “epidemic”.29
Future studies should be conducted to optimize
ketamine for the management of chronic pain conditions
without the use of opioids, where appropriate.

 

Breakthrough Treatment IV Ketamine Infusions for CRPS, Fibromyalgia, Depression, PTSD, Chronic Lyme, Rheumatoid Arthritis and More Now Covered By Insurance!

CLEARWATER, Fla.Dec. 22, 2017 /PRNewswire/ — Chronic pain, inflammation and depression are major components of many conditions such as CRPS, RSD, Fibromyalgia, treatment-resistant depression, PTSD and Chronic Lyme Disease. IV Ketamine Infusions have successfully helped thousands of patients for which conventional treatments had failed. In the past, most insurance companies did not cover Ketamine treatments limiting many patient’s access to the drug. Now, many insurance companies have recognized the significant effectiveness of Ketamine and are beginning to cover many treatments.

Dr. Ashraf Hanna, a board certified physician and director of pain management at the Florida Spine Institute in Clearwater, FL discusses this breakthrough treatment: “IV Ketamine Infusions offer hope to my patients and give them relief from their pain and suffering. We are happy to announce that many insurance companies are now covering Ketamine treatments!”

“The insurance companies can no longer ignore the overwhelming research studies by top universities and hospitals regarding the use of Ketamine for numerous difficult-to-treat medical conditions. We use IV Ketamine Infusions for chronic pain as well as treatment-resistant depression, PTSD, OCD, anxiety and many more,” stated Dr. Hanna. “The fact that insurance is now accepted has really opened up the possibility of this treatment for many patients from around the world.”

IV Ketamine has been a safe and effective FDA-approved drug for nearly 50 years. At a molecular level, Ketamine blocks the NMDA receptor. The NMDA receptor is responsible for the body’s underlying neural network (similar to a computer network) and it’s ability to process pain signals to the central nervous system. Over-activation of this receptor can result in excitotoxicity, resulting in a myriad of pain disorders. Ketamine is thought to correct this over-activation by blocking the NMDA receptor. However, the therapeutic effects of ketamine far outlast the actual drug levels in the body leading many to hypothesize that ketamine induces secondary changes that produce long-lasting therapeutic effects in a myriad of disease states.

“While not all insurance companies cover every Ketamine treatment, we hope to continue to add new Ketamine-compliant insurance companies in 2018. Our goal is to help as many patients as possible with this amazing treatment. I have provided over 8,000 Ketamine infusions and have seen so many incredible successes over the past 5 years. Some of my patients were unable to move a limb or walk and now have complete mobility and can walk unaided,” stated Dr. Hanna.

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SOURCE ivketamine.com

Chronic Pain

Title: Ketamine for chronic pain: risks and benefits.Screenshot at Aug 25 06-54-08
Authors: Niesters, M., Martini, C. and Dahan, A.
Journal: Journal of Clinical Pharmacology
Abstract: The anaesthetic ketamine is used to treat various chronic pain syndromes, especially those that have a neuropathic component. Low dose ketamine produces strong analgesia in neuropathic pain states, presumably by inhibition of the N-methyl-D-aspartate receptor although other mechanisms are possibly involved, including enhancement of descending inhibition and anti-inflammatory effects at central sites. Current data on short term infusions indicate that ketamine produces potent analgesia during administration only, while three studies on the effect of prolonged infusion (4–14 days) show long-term analgesic effects up to 3 months following infusion. The side effects of ketamine noted in clinical studies include psychedelic symptoms (hallucinations, memory defects, panic attacks), nausea/vomiting, somnolence, cardiovascular stimulation and, in a minority of patients, hepatoxicity. The recreational use of ketamine is increasing and comes with a variety of additional risks ranging from bladder and renal complications to persistent psychotypical behaviour and memory defects. Blind extrapolation of these risks to clinical patients is difficult because of the variable, high and recurrent exposure to the drug in ketamine abusers and the high frequency of abuse of other illicit substances in this population. In clinical settings, ketamine is well tolerated, especially when benzodiazepines are used to tame the psychotropic side effects. Irrespective, close monitoring of patients receiving ketamine is mandatory, particularly aimed at CNS, haemodynamic, renal and hepatic symptoms as well as abuse. Further research is required to assess whether the benefits outweigh the risks and costs. Until definite proof is obtained ketamine administration should be restricted to patients with therapy-resistant severe neuropathic pain.
Link to Full Text

Title: Influence of ketamine and morphine on descending pain modulation in chronic pain patients: a randomized placebo-controlled cross-over proof-of-concept studyScreenshot at Aug 25 06-56-46
Authors: M. Niesters, L. Aarts, E. Sarton and A. Dahan
Journal: British Journal of Anesthesia
Abstract: Background Descending inhibition of pain, part of the endogenous pain modulation system, is important for normal pain processing. Dysfunction is associated with various chronic pain states. Here, the effect of ketamine and morphine on descending inhibition is examined using the conditioned pain modulation (CPM) paradigm in chronic neuropathic pain patients.
Methods CPM responses were obtained in 10 adult neuropathic pain subjects (two men/eight women). All subjects had peripheral neuropathy as defined by abnormal quantitative sensory testing. The effects of S(+)-ketamine (0.57 mg kg–1 h–1 for 1 h) and morphine (0.065 mg kg−1 h−1 for 1 h) were tested in a randomized, placebo-controlled double-blind study. CPM was measured at baseline and 100 min after the start of treatment and was induced by immersion of the leg into a cold-water bath. The test stimulus was a 30 s static thermal stimulus to the skin of the forearm.
Results Without treatment, no CPM was detectable. Treatment with ketamine, morphine, and placebo produced CPM responses of 40.2 (10.9)%, 28.5 (7.0)%, and 22.1 (12.0)%, respectively (for all treatments, CPM effect P<0.05), with no statistical difference in the magnitude of CPM among treatments. The magnitude of CPM correlated positively with the magnitude and duration of spontaneous pain relief.
Conclusions The observed treatment effects in chronic pain patients suggest a role for CPM engagement in analgesic efficacy of ketamine, morphine, and placebo treatment.
Link to Full Text

Title: The Dose-Dependent Effect of S(+)-Ketamine on Cardiac Output in Healthy Volunteers and Complex Regional Pain Syndrome Type 1 Chronic Pain PatientsScreenshot at Aug 25 06-58-20
Authors: Olofsen, Erik MSc; Sigtermans, Marnix MD, PhD; Noppers, Ingeborg MD, PhD; Niesters, Marieke MD, Msc; Mooren, Rene MSc; Bauer, Martin MD; Aarts, Leon MD, PhD; Sarton, Elise MD, PhD; Dahan, Albert MD, PhD
Journal: Anesthesia & Analgesia
Abstract: BACKGROUND: Ketamine is used as an analgesic for treatment of acute and chronic pain. While ketamine has a stimulatory effect on the cardiovascular system, little is known about the concentration–effect relationship. We examined the effect of S(+)-ketamine on cardiac output in healthy volunteers and chronic pain patients using a pharmacokinetic–pharmacodynamic modeling approach.
METHODS: In 10 chronic pain patients (diagnosed with complex regional pain syndrome type 1 [CRPS1] with a mean age 43.2 ± 13 years, disease duration 8.4 years, range 1.1 to 21.7 years) and 12 healthy volunteers (21.3 ± 1.6 years), 7 increasing IV doses of S(+)-ketamine were given over 5 minutes at 20-minute intervals starting with 1.5 mg with 1.5-mg increments. Cardiac output (CO) was calculated from the arterial pressure curve obtained from an arterial catheter in the radial artery. Ketamine and norketamine plasma concentrations were measured. A novel pharmacokinetic–pharmacodynamic model was constructed to quantify the direct stimulatory effect of ketamine on CO and the following adaptation/inhibition.
RESULTS: Significant differences in pharmacokinetic estimates were observed between study groups with 15% and 40% larger S(+)-ketamine S(+)-norketamine concentrations in healthy volunteers compared to CRPS1 patients. S(+)-ketamine had a dose-dependent stimulatory effect on CO in patients and volunteers. After infusion an inhibitory effect on CO was observed. Pharmacodynamic model parameters did not differ between CRPS1 patients and healthy volunteers. The concentration of S(+)-ketamine causing a 1 L/min increase in CO was 243 ± 54 ng/mL with an onset/offset half-life of 1.3 ± 0.21 minutes. The inhibitory component was slow (time constant of 67.2 ± 17.0 minutes).
CONCLUSIONS: S(+)-ketamine pharmacokinetics but not pharmacodynamics differed between study populations, related to differences in disease state (CRPS1 or not) or age. The dose-dependent effect of S(+)-ketamine on CO was well described by the biphasic dynamic model. The effect of S(+)-ketamine on CO was similar between study groups with respect to its stimulatory and inhibitory components, despite group differences in age and health.
Link to Full Text

Title: Intravenous Infusions in Chronic Pain ManagementScreenshot at Aug 25 06-59-16
Authors: Boleslav Kosharskyy, MD, Wilson Almonte, MD, Naum Shaparin, MD, Marco Pappagallo, MD, and Howard Smith, MD
Journal: Pain Physician
Abstract: In the United States, millions of Americans are affected by chronic pain, which adds heavily to national rates of morbidity, mortality, and disability, with an ever-increasing prevalence. According to a 2011 report titled Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research by the Institute of Medicine of the National Academies, pain not only exacts its toll on people’s lives but also on the economy with an estimated annual economic cost of at least $560 – 635 billion in health care costs and the cost of lost productivity attributed to chronic pain. Intravenous infusions of certain pharmacologic agents have been known to provide substantial pain relief in patients with various chronic painful conditions. Some of these infusions are better, and although not necessarily the first therapeutic choice, have been widely used and extensively studied. The others show promise, however are in need of further investigations. This article will focus on non-opiate intravenous infusions that have been utilized for chronic painful disorders such as fibromyalgia, neuropathic pain, phantom limb pain, post-herpetic neuralgia, complex regional pain syndromes (CRPS), diabetic neuropathy, and central pain related to stroke or spinal cord injuries. The management of patients with chronic pain conditions is challenging and continues to evolve as new treatment modalities are explored and tested. The following intravenous infusions used to treat the aforementioned chronic pain conditions will be reviewed: lidocaine, ketamine, phentolamine, dexmedetomidine, and bisphosphonates. This overview is intended to familiarize the practitioner with the variety of infusions for patients with chronic pain. It will not, however, be able to provide guidelines for their use due to the lack of sufficient evidence.
Link to Full Text

Title: The Use of Ketamine in Neuropathic PainScreenshot at Aug 25 07-05-58
Authors: Sarah Lee O’Brien • Sanjog Pangarkar • Joshua Prager
Journal: Curr Phys Med Rehabil Rep
Abstract: Hyperactivity of N-methyl-D-aspartate (NMDA) receptors may be one of the factors in the genesis of neuropathic pain (NP). Ketamine is a dissociative anesthetic and analgesic that is the most potent NMDA receptor antagonist currently available for human use. There is a growing body of literature for three decades suggesting efficacy of subanaesthetic doses of ketamine in the treatment of NP, particularly the pain in complex regional pain syndromes. The primary limitations of ketamine use are secondary to psychotomimetic and, to a lesser extent, sympathetic activation. The purpose of this article is to review the history, pharmacology, pharmacodynamics, clinical benefits, and limitations of ketamine for treatment of NP. Methods of administration and management of adverse effects are highlighted based on the clinical experience of the authors.
Link to Full Text

CRPS/RSD

Title: Ketamine: a growing global health-care needScreenshot at Aug 25 07-10-14
Authors: T. T. Dong, J. Mellin-Olsen and A. W. Gelb
Journal: British Journal of Anesthesia
Abstract: Ketamine was first synthesized in 1962, patented in Belgium in 1963, and approved for human use by the US Food and Drug Administration in 1970. Unlike inhalation anaesthetics, ketamine provides analgesia, preserves airway reflexes, offers haemodynamic stability, and maintains respiratory drive, which gives ketamine an excellent safety profile. It is therefore a favoured choice for trauma triage, use in man-made and natural disasters, and for many other patients with compromized haemodynamic stability. However, side-effects, such as agitation, hallucinations, and panic attacks, have limited its clinical use as an anaesthetic in affluent countries. Lately, ketamine has found new uses in clinical medicine in addition to renewed threats to its availability.
Link to Full Text

Title: Ketamine-induced affective switch in a patient with treatment-resistant depressionScreenshot at Aug 25 07-01-29
Authors: Girish Banwari, Prutha Desai, and Prahlad Patidar
Journal: Indian Journal of Pharmacology
Abstract: There is growing evidence to support the rapid, albeit short-lived antidepressant effect of subanesthetic dose of ketamine, a noncompetitive glutamate N-methyl-D-aspartate receptor antagonist in treatment-resistant unipolar and bipolar depression. Ketamine is known to cause transient mood elevation or euphoria, psychotomimetic effects, and dissociative symptoms, but its use in unipolar or bipolar depression has not been reported to induce an affective switch amounting to persistent or prolonged hypomania/mania or manic-like syndrome. We report the case of a 52-year-old male with first episode, continuous, nonpsychotic, treatment-resistant, unipolar major depression of 10 years duration, who manifested a switch from depression to mania while being treated with subanesthetic dose of ketamine, given intramuscularly. This case suggests that polarity switch should be considered as a potential side effect while using ketamine for treatment-resistant depression.
Link to Full Text

Title: Antidepressant Efficacy of Ketamine in Treatment-Resistant Major Depression: A Two-Site Randomized Controlled TrialScreenshot at Aug 25 07-02-37
Authors: James W. Murrough, , M.D., Dan V. Iosifescu, , M.D., Lee C. Chang, , M.D., Rayan K. Al Jurdi, , M.D., Charles E. Green, , Ph.D., Andrew M. Perez, , M.D., Syed Iqbal, , M.D., Sarah Pillemer, , B.A., Alexandra Foulkes, , M.S., Asim Shah, , M.D., Dennis S. Charney, , M.D., Sanjay J. Mathew, , M.D.
Journal: American Journal of Psychiatry
Abstract:Intravenous ketamine demonstrated rapid antidepressant effects in an optimized study design, improving depression severity in 64% of treatment-resistant patients 24 hours after a single dose. The double-blind trial provides evidence for the role of the N-methyl-d-aspartate glutamate receptor in depression, a receptor not currently activated by existing antidepressant drugs.
Objective
Ketamine, a glutamate N-methyl-d-aspartate (NMDA) receptor antagonist, has shown rapid antidepressant effects, but small study groups and inadequate control conditions in prior studies have precluded a definitive conclusion. The authors evaluated the rapid antidepressant efficacy of ketamine in a large group of patients with treatment-resistant major depression.
Method
This was a two-site, parallel-arm, randomized controlled trial of a single infusion of ketamine compared to an active placebo control condition, the anesthetic midazolam. Patients with treatment-resistant major depression experiencing a major depressive episode were randomly assigned under double-blind conditions to receive a single intravenous infusion of ketamine or midazolam in a 2:1 ratio (N=73). The primary outcome was change in depression severity 24 hours after drug administration, as assessed by the Montgomery-Åsberg Depression Rating Scale (MADRS).
Results
The ketamine group had greater improvement in the MADRS score than the midazolam group 24 hours after treatment. After adjustment for baseline scores and site, the MADRS score was lower in the ketamine group than in the midazolam group by 7.95 points (95% confidence interval [CI], 3.20 to 12.71). The likelihood of response at 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18; 95% CI, 1.21 to 4.14), with response rates of 64% and 28%, respectively.
Conclusions
Ketamine demonstrated rapid antidepressant effects in an optimized study design, further supporting NMDA receptor modulation as a novel mechanism for accelerated improvement in severe and chronic forms of depression. More information on response durability and safety is required before implementation in clinical practice.
Link to Full Text

Title: Intravenous Therapies in the Management of Neuropathic Pain: A Review on the Use of Ketamine and Lidocaine in Chronic Pain ManagementScreenshot at Aug 25 07-05-03
Authors: Harsha Shanthanna
Journal: Neuropathic Pain
Abstract: Neuropathic Pain is a term referred to “pain arising as a direct consequence of a lesion affecting the somatosensory system”. As a first line option, oral medications are mostly used, as they are easily available, relatively safe, and do not need much resources. They include antidepressants in the form of tricyclics, newer selective reuptake inhibitors of serotonin and norepinephrine, gabapentin, pregabalin etc. Although neuropathic pain conditions do share some common clinical features, they are quite diverse when considered individually according to their etiology and pathogenesis. Hence not all patients and not all types of neuropathic pain respond to such oral therapy. In practice patients are given a form of such neuropathic pain medication along with or without an opioid, depending upon the extent of pain that the patient suffers. Opioids are potent analgesics but are not a good choice for neuropathic pain conditions. With time the clinician is left with fewer alternatives and furthermore, with the the increasing knowledge that escalation of opioid therapy will perhaps lead to hyperalgesia and tolerance, it becomes necessary to explore other options. Among the other options one can always consider to explore treatment with intravenous medication such as Ketamine, Lidocaine, and Magnesium etc. This chapter would highlight the use of ketamine and lidocaine in the form of drug profile, the pharmacological basis behind its use, strategies to use, important side effects and limitations and available evidence base, including a review of randomised controlled studies. Both are considered separately in two different parts. References for both the parts are given at the end, in separate sections.
Link to Full Text

Post-Treatment Lyme Syndrome

Title: Post-Treatment Lyme Syndrome and Central SensitizationScreenshot at Aug 25 07-07-22
Authors: Shweta Batheja, , M.B, B.S., Jenifer A. Nields, , M.D., Alla Landa, , Ph.D., Brian A. Fallon, , M.D., M.P.H.
Journal: Journal of Neuropsychiatry
Abstract: The authors of this clinically important article describe the process whereby chronic Lyme disease and its CNS sequelae can result in various treatment-resistant pain and anxiety disorders that are characterized by hypersensitivity to noxious and non-noxious stimuli. These may include skin reactions, fatigue, muscle weakness, extreme sensitivity to sound or smell, and, also, mood and cognitive symptoms. The article reviews several treatment approaches beyond antibiotics, including antidepressants and anti-epileptic drugs.
Central sensitization is a process that links a variety of chronic pain disorders that are characterized by hypersensitivity to noxious stimuli and pain in response to non-noxious stimuli. Among these disorders, treatments that act centrally may have greater efficacy than treatments acting peripherally. Because many individuals with post-treatment Lyme syndrome (PTLS) have a similar symptom cluster, central sensitization may be a process mediating or exacerbating their sensory processing. This article reviews central sensitization, reports new data on sensory hyperarousal in PTLS, explores the potential role of central sensitization in symptom chronicity, and suggests new directions for neurophysiologic and treatment research.
Link to Full Text

Fibromyalgia

Title: Review of pharmacological therapies in fibromyalgia syndromeScreenshot at Aug 25 07-09-06
Authors: Winfried Häuser, Brian Walitt, Mary-Ann Fitzcharles and Claudia Sommer
Journal: Arthritis Research & Therapy
Abstract: This review addresses the current status of drug therapy for the management of fibromyalgia syndrome (FMS) and is based on interdisciplinary FMS management guidelines, meta-analyses of drug trial data, and observational studies. In the absence of a single gold-standard medication, patients are treated with a variety of drugs from different categories, often with limited evidence. Drug therapy is not mandatory for the management of FMS. Pregabalin, duloxetine, milnacipran, and amitriptyline are the current first-line prescribed agents but have had a mostly modest effect. With only a minority of patients expected to experience substantial benefit, most will discontinue therapy because of either a lack of efficacy or tolerability problems. Many drug treatments have undergone limited study and have had negative results. It is unlikely that these failed pilot trials will undergo future study. However, medications, though imperfect, will continue to be a component of treatment strategy for these patients. Both the potential for medication therapy to relieve symptoms and the potential to cause harm should be carefully considered in their administration.
Link to Full Text

Lichen Sclerosus

Title: Effects of Intravenous Ketamine Infusions in a Neuropathic Pain Patient with Lichen Sclerosus et Atrophicus
Authors: Ashraf F. Hanna, Josh S. Armstrong, Adam J. Smith
Journal: Karger Open Access
Abstract: A patient reported to the Florida Spine Institute (Clearwater, Fla., USA) with severe lichen sclerosus of the anogenital region and legs. The patient’s pain presentation was neuropathic with hypersensitivity, allodynia, swelling, and weakness. The patient had failed multiple pain management modalities including opioid therapy, anticonvulsants, and antidepressants. The patient completed a standard intravenous ketamine infusion regimen developed at the Florida Spine Institute and reported complete abolishment of her pain syndrome. For the first time, we report that ketamine infusions also dramatically improved a patient’s lichen sclerosus. That ketamine is known to have immunomodulatory properties, and given the clinical observations described in this case report,suggests that ketamine should be explored as a possible new therapeutic option for managing lichen sclerosus, especially in cases that are refractory to conventional therapies.

Title: Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviewsScreenshot at Aug 25 07-08-17
Authors: Neil E O’Connell, Benedict M Wand, James McAuley, Louise Marston, G Lorimer Moseley
Journal: Cochrane Database of Systematic Reviews
Abstract: Complex regional pain syndrome (CRPS) is characterised by persistent pain, usually in the hands or feet, that is not proportionate inseverity to any underlying injury. It often involves a variety of other symptoms such as swelling, discolouration, stiffness, weakness and changes to the skin. This over view sought to summarise and report all of the available evidence arising from systematic reviews for all treatments for this condition regarding how well they work and any potential harm that they might cause. We identified six Cochrane reviews and 13 non-Cochrane systematic reviews that included evidence relating to a broad range of treatments, from drugs to surgical procedures, rehabilitation and alternative therapies. For most treatments there were only a small number of published trials and the quality of these trials was mixed. As such, most of the evidence for most treatments is of low or very low quality and can not be regarded as reliable.We found low quality evidence that a daily course of the drug ketamine delivered intravenously may effectively reduce pain, although it is also associated with a variety of side effects. We found low quality evidence that the bisphosphonate class of drugs, calcitonin and programmes of graded motor imagery may be effective for CRPS, and that mirror therapy may be effective in people who develop CRPS after suffering a stroke. Low quality evidence suggested that physiotherapy and occupational therapy did not lead to clinically important benefits at one year follow up, and that blocking sympathetic nerves with local anaesthetic is not effective. There is moderate quality evidence that an intravenous regional blockade using the drug guanethidine is not effective and may be associated with complications.For a range of other interventions we found only very low quality evidence or no evidence at all. No conclusions should be drawn regarding the value of these interventions based on this level of evidence.Based on the existing evidence it is difficult to draw firm conclusions as to which therapies should be offered to patients with CRPS.Better quality research is vital to reduce uncertainty in this area and is necessary before confident recommendations can be made.
Link to Full Text

Depression

Title: Glutamate Receptor Antagonists as Fast-Acting Therapeutic Alternatives for the Treatment of Depression: Ketamine and Other CompoundsScreenshot at Aug 25 07-00-19
Authors: Mark J. Niciu, Ioline D. Henter, David A. Luckenbaugh, Carlos A. Zarate Jr., and Dennis S. Charney
Journal: Annu Rev Pharmacol Toxicol.
Abstract: The N-methyl-d-aspartate (NMDA) receptor antagonist ketamine has rapid and potent antidepressant effects in treatment-resistant major depressive disorder and bipolar depression. These effects are in direct contrast to the more modest effects seen after weeks of treatment with classic monoaminergic antidepressants. Numerous open-label and case studies similarly validate ketamine’s antidepressant properties. These clinical findings have been reverse-translated into preclinical models in an effort to elucidate ketamine’s antidepressant mechanism of action, and three important targets have been identified: mammalian target of rapamycin (mTOR), eukaryotic elongation factor 2 (eEF2), and glycogen synthase kinase-3 (GSK-3). Current clinical and preclinical research is focused on (a) prolonging/maintaining ketamine’s antidepressant effects, (b) developing more selective NMDA receptor antagonists free of ketamine’s adverse effects, and (c) identifying predictor, mediator/moderator, and treatment response biomarkers of ketamine’s antidepressant effects.
Link to Full Text

 

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Here is an interesting piece regarding the rapid effects of Ketamine on reversing depression, in specific, making events more pleasurable through modulating the action of Glutamate in the brain.

This article was written by Dr. Zarate:

Ketamine and depression – NIH

Highlight: Ketamine: A New (and Faster) Path to Treating Depression

Two charts show the effect of ketamine or placebo on the Hamilton Depression Rating Scale.

Left: Change in the 21-item Hamilton Depression Rating Scale (HDRS) following ketamine or placebo treatment.
Right: Proportion of responders showing a 50 percent improvement on the HDRS following ketamine or placebo treatment.34

Source: Carlos Zarate, M.D., Experimental Therapeutics and Pathophysiology Branch, NIMH

The most commonly used antidepressants are largely variations on a theme; they increase the supply within synapses of a class of neurotransmitters believed to play a role in depression. While these drugs relieve depression for some, there is a weeks-long delay before they take effect, and some people with “treatment-resistant” depression do not respond at all.

The delay in effectiveness has suggested to scientists that the medication-induced changes in neurotransmitters are several steps away from processes more central to the root cause of depression. One possibility for a more proximal mechanism is glutamate, the primary excitatory, or activating, neurotransmitter in the brain. Preliminary studies suggested that inhibitors of glutamate could have antidepressant-like effects, and in a seminal clinical trial, the drug ketamine—which dampens glutamate signaling—lifted depression in as little as 2 hours in people with treatment-resistant depression.34

The discovery of rapidly acting antidepressants has transformed our expectations—we now look for treatments that will work in 6 hours rather than 6 weeks. But ketamine has some disadvantages; it has to be administered intravenously, the effects are transient, and it has side effects that require careful monitoring. However, results from clinical studies have confirmed the potential of the glutamate pathway as a target for the development of new antidepressants. Continuing research with ketamine has provided information on biomarkers that could be used to predict who will respond to treatment.35Clinical studies are also testing analogs of ketamine in an effort to develop glutamate inhibitors without ketamine’s side effects that can then be used in the clinic.36 Ketamine may also have potential for treating other mental illnesses; for example, a preliminary clinical trial reported that ketamine reduced the severity of symptoms in patients with PTSD. 37 Investigation of the role of glutamate signaling in other illnesses may provide the impetus to develop novel therapies based on this pathway.

One of the imperatives of clinical research going forward will be to demonstrate whether the ability of a compound to interact with a specific brain target is related to some measurable change in brain or behavioral activity that, in turn, can be associated with relief of symptoms. In a study of ketamine’s effects in patients in the depressive phase of bipolar disorder, ketamine restored pleasure-seeking behavior independent from and ahead of its other antidepressant effects. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom—loss of interest in pleasurable activities—which lasted up to 14 days.38 Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. This approach is consistent with the NIMH’s RDoC project, which calls for the study of functions—such as the ability to seek out and experience rewards—and their related brain systems that may identify subgroups of patients with common underlying dysfunctions that cut across traditional diagnostic categories.

The ketamine story shows that in some instances, a strong and repeatable clinical outcome stemming from a hypothesis about a specific molecular target (e.g., a glutamate receptor) can open up new arenas for basic research to explain the mechanisms of treatment response; basic studies can, in turn, provide data leading to improved treatments directed at that mechanism. A continuing focus on specific mechanisms will not only provide information on the potential of test compounds as depression medications, but will also help us understand which targets in the brain are worth aiming at in the quest for new therapies.

PET scan data superimposed on anatomical MRI

PET scans revealed that ketamine rapidly restored bipolar depressed patients’ ability to anticipate pleasurable experiences by boosting activity in the dorsal anterior cingulate cortex (yellow) and related circuitry. Picture shows PET scan data superimposed on anatomical MRI.38

References

1 Analysis based on: US Burden of Disease Collaborators. (2013). The state of US health, 1990–2010: Burden of diseases, injuries, and risk factors.JAMA, 310(6), 591–608. (PubMed ID: 23842577)

2 Walker E. R., McGee R. E., & Druss B. G. (2015). Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis.JAMA Psychiatry72(4), 334-341. (PubMed ID: 25671328)

3 Centers for Disease Control and Prevention (CDC). (2013). Web-based Injury Statistics Query and Reporting System(WISQARSTM). Atlanta, GA: National Center for Injury Prevention and Control, CDC.

4 Insel, T. R. (2008). Assessing the economic cost of serious mental illness.American Journal of Psychiatry, 165(6), 663–665. (PubMed ID: 18519528)

5 Soni, A. (2009). The five most costly conditions, 1996 and 2006: Estimates for the US civilian noninstitutionalized population (Statistical Brief# 248). Rockville, MD: Agency for Healthcare Research and Quality.

6 Murray, F. E. (2012). Evaluating the role of science philanthropy in American research universities (Working Paper No. 18146). Cambridge, MA: National Bureau of Economic Research.

7 Terry, S. F. & Terry, P. F. (2011). Power to the people: Participant ownership of clinical trial dataScience Translational Medicine3(69), 69cm3. (PubMed ID: 21307299)

8 Calculated from: McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortalityEpidemiologic Reviews30(1), 67–76. (PubMed ID: 18480098)

9 Addington, J., Heinssen, R. K., Robinson, D. G., Schooler, N. R., Marcy, P., Brunette, M. F., … & Kane, J. M. (2015). Duration of untreated psychosis in community treatment settings in the United StatesPsychiatric Services: A Journal of the American Psychiatry Association. [Epub ahead of print] (PubMed ID: 25588418)

10 Marshall, M., Lewis, S., Lockwood, A., Drake, R., Jones, P., & Croudace, T. (2005). Association between duration of untreated psychosis and outcome in cohorts of first-episode patients: A systematic reviewArchives of General Psychiatry62(9), 975–983. (PubMed ID: 16143729)

11 Clementz, B., Sweeney, J., Hamm J., Ivleva, E., Ethridge, L., Pearlson, G., … & Tamminga C. (2016). Identification of distinct psychosis biotypes using brain-based biomarkers.American Journal of Psychiatry. (PubMed ID: 26651391)

12 Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox, N. A., Leibenluft, E., … & Pine, D. S. (2010). Attention bias modification treatment: A meta-analysis toward the establishment of novel treatment for anxiety.Biological Psychiatry68(11), 982–990. (PubMed ID: 20887977)

13 Britton, J. C., Bar‐Haim, Y., Carver, F. W., Holroyd, T., Norcross, M. A., Detloff, A., … & Pine, D. S. (2012). Isolating neural components of threat bias in pediatric anxiety.Journal of Child Psychology and Psychiatry53(6), 678–686. (PubMed ID: 22136196)

14 Lent, R., Azevedo, F. A., Andrade‐Moraes, C. H., & Pinto, A. V. (2012). How many neurons do you have? Some dogmas of quantitative neuroscience under revisionEuropean Journal of Neuroscience, 35(1), 1–9. (PubMed ID: 22151227)

15 Zhang, Y., Pak, C., Han, Y., Ahlenius, H., Zhang, Z., Chanda, S., … & Südhof, T. C. (2013). Rapid single-step induction of functional neurons from human pluripotent stem cellsNeuron78(5), 785–798. (PubMed ID: 23764284)

16 Krey, J. F., Paşca, S. P., Shcheglovitov, A., Yazawa, M., Schwemberger, R., Rasmusson, R., & Dolmetsch, R. E. (2013). Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neuronsNature Neuroscience16(2), 201–209. (PubMed ID: 23313911)

17 Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium. (2011). Genome-wide association study identifies five new schizophrenia lociNature Genetics43(10), 969–976. (PubMed ID: 21926974)

18 Schizophrenia Working Group of the Psychiatric Genomics Consortium. (2014). Biological insights from 108 schizophrenia-associated genetic lociNature511(7510), 421–427. (PubMed ID: 25056061)

19 Nishimasu, H., Ran, F.A., Hsu, P. D., Konermann, S., Shehata, S. I., Dohmae, N., … & Nureki, O. (2014). Crystal structure of Cas9 in complex with guide RNA and target DNACell156(5), 935–949. (PubMed ID: 24529477)

20 Chung, K., Wallace, J., Kim, S. Y., Kalyanasundaram, S., Andalman, A. S., Davidson, T. J., … & Deisseroth, K. (2013). Structural and molecular interrogation of intact biological systemsNature497(7449), 332–337. (PubMed ID: 23575631)

21 Colantuoni, C., Lipska, B. K., Ye, T., Hyde, T. M., Tao, R., Leek, J. T., … & Kleinman, J. E. (2011). Temporal dynamics and genetic control of transcription in the human prefrontal cortexNature, 478(7370), 519–523. (PubMed ID: 22031444)

22 Kang, H. J., Kawasawa, Y. I., Cheng, F., Zhu, Y., Xu, X., Li, M., … & Šestan, N. (2011). Spatio-temporal transcriptome of the human brainNature, 478(7370), 483–489. (PubMed ID: 22031440)

23 Li, G., Wang, L., Shi, F., Lyall, A. E., Lin, W., Gilmore, J. H., & Shen, D. (2014). Mapping longitudinal development of local cortical gyrification in infants from birth to 2 years of ageThe Journal of Neuroscience34(12), 4228–4238. (PubMed ID: 24647943)

24 Hill, J., Inder, T., Neil, J., Dierker, D., Harwell, J., & Van Essen, D. (2010). Similar patterns of cortical expansion during human development and evolutionProceedings of the National Academy of Sciences107(29), 13135–13140. (PubMed ID: 20624964)

25 Hawrylycz, M. J., Lein, E. S., Guillozet-Bongaarts, A. L., Shen, E. H., Ng, L., Miller, J. A., … & Jones, A.R. (2012). An anatomically comprehensive atlas of the adult human brain transcriptomeNature,489(7416), 391–399. (PubMed ID: 22996553)

26 Miller, J. A., Ding, S. L., Sunkin, S. M., Smith, K. A., Ng, L., Szafer, A., … & Lein, E.S. (2014). Transcriptional landscape of the prenatal human brainNature508(7495), 199–206. (PubMed ID: 24695229)

27 Willsey, A. J., Sanders, S. J., Li, M., Dong, S., Tebbenkamp, A. T., Muhle, R. A., … & State, M. W. (2013). Coexpression networks implicate human midfetal deep cortical projection neurons in the pathogenesis of autismCell155(5), 997–1007. (PubMed ID: 24267886)

28 Gulsuner, S., Walsh, T., Watts, A. C., Lee, M. K., Thornton, A. M., Casadei, S., … & McClellan, J. M. (2013). Spatial and temporal mapping of de novo mutations in schizophrenia to a fetal prefrontal cortical networkCell154(3), 518–529. (PubMed ID: 23911319)

29 Whiteford, H. A., Degenhardt, L., Rehm, J., Baxter, A. J., Ferrari, A. J., Erskine, H. E., … & Vos, T. (2013). Global burden of disease attributable to mental and substance use disorders: Findings from the Global Burden of Disease Study 2010Lancet382(9904), 1575–1586. (PubMed ID: 23993280)

30 Insel, T. R. (2012). Next-generation treatments for mental disordersScience Translational Medicine4(155), 155ps19. (PubMed ID: 23052292)

31 Hyman, S. E. (2012). Revolution stalledScience Translational Medicine4(155), 155cm11. (PubMed ID: 23052291)

32 Biomarkers Definitions Working Group (2001). Biomarkers and surrogate endpoints: Preferred definitions and conceptual frameworkClinical Pharmacology and Therapeutics, 69(3), 89–95. (PubMed ID: 11240971)

33 McGrath, C. L., Kelley, M. E., Holtzheimer, P. E., Dunlop, B. W., Craighead, W. E., Franco, A. R., … & Mayberg, H. S. (2013). Toward a neuroimaging treatment selection biomarker for major depressive disorderJAMA Psychiatry70(8), 821–829. (PubMed ID: 23760393)

34 Zarate Jr, C. A., Singh, J. B., Carlson, P. J., Brutsche, N. E., Ameli, R., Luckenbaugh, D. A., … & Manji, H. K. (2006). A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depressionArchives of General Psychiatry63(8), 856–864. (PubMed ID: 16894061)

35 Cornwell, B. R., Salvadore, G., Furey, M., Marquardt, C. A., Brutsche, N. E., Grillon, C., & Zarate Jr, C. A. (2012). Synaptic potentiation is critical for rapid antidepressant response to ketamine in treatment-resistant major depressionBiological Psychiatry72(7), 555–561. (PubMed ID: 22521148)

36 Zarate Jr, C. A., Mathews, D., Ibrahim, L., Chaves, J. F., Marquardt, C., Ukoh, I., … & Luckenbaugh, D. A. (2013). A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depressionBiological Psychiatry,74(4), 257–264. (PubMed ID: 23206319)

37 Feder, A., Parides, M. K., Murrough, J. W., Perez, A. M., Morgan, J. E., Saxena, S., … & Charney, D. S. (2014). Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder: A randomized clinical trialJAMA Psychiatry, 71(6), 681-688. (PubMed ID: 24740528)

38 Lally N., Nugent A. C., Luckenbaugh D. A., Ameli R., Roiser J. P., & Zarate C. A. (2014). Anti-anhedonic effect of ketamine and its neural correlates in treatment-resistant bipolar depression.Translational Psychiatry. [E-pub ahead of print] (PubMed ID: 25313512)

39 Smith, M., Saunders, R., Stuckhardt, L., & McGinnis, J. M. (Eds.). (2013). Best care at lower cost: The path to continuously learning health care in America. Washington, DC: National Academies Press. (PubMed ID: 24901184)

40 Chambers, D.A., Glasgow, R.E., & Stange, K.C. (2013). The dynamic sustainability framework: Addressing the paradox of sustainment amid ongoing change.Implementation Science, 8(1), 117. (PubMed ID: 24088228)

41 Ben-Zeev, D., Schueller, S. M., Begale, M., Duffecy, J., Kane, J. M., & Mohr, D. C. (2015). Strategies for mHealth research: Lessons from 3 mobile intervention studiesAdministration and Policy in Mental Health and Mental Health Services Research, 42(2), 157-167. (PubMed ID: 24824311)

42 Mohr, D. C., Burns, M. N., Schueller, S. M., Clarke, G., & Klinkman, M. (2013). Behavioral intervention technologies: Evidence review and recommendations for future research in mental healthGeneral Hospital Psychiatry,35(4), 332–338. (PubMed ID: 23664503)

43 Aitken, M., & Gauntlett, C. (2013). Patient apps for improved healthcare from novelty to mainstream.Parsippany, NJ: IMS Institute for Healthcare Informatics.

https://www.nimh.nih.gov/about/strategic-planning-reports/highlights/index.shtml


I also threw in a reprint of the article from NIH regarding strategic principle #2 to find biomarkers of mental health disorders:

Highlight: GPS for the Brain? BrainSpan Atlas Offers Clues to Mental Illnesses

Image from BrainSpan Atlas shows the location and expression level of the gene TGIF1 in a brain from 21 weeks postconception.

The recently created BrainSpan Atlas of the Developing Human Brain incorporates gene activity or expression (left) along with anatomical reference atlases (right) and neuroimaging data (not shown) of the mid-gestational human brain. In this figure, the location and expression level of the gene TGIF1 is shown in a brain from 21 weeks postconception.

Source: Allen Institute for Brain Science

Technologies have come a long way in mapping the trajectory of mental illnesses. Early efforts provided information on anatomical changes that occur over the course of development. In a step that has been hailed as providing a “GPS for the brain,” the BrainSpan Atlas of the Developing Brain, a partnership among the Allen Institute for Brain Science, Yale University, the University of Southern California, and NIMH—has created a comprehensive 3-D brain blueprint.25 The Atlas details not only the anatomy of the brain’s underlying structures, but also exactly where and when particular genes are turned on and off during mid-pregnancy—a time during fetal brain development when slight variations can have significant long-term consequences, including heightened risk for autism or schizophrenia.26 Knowledge of the location and time when a particular gene is turned on can help us understand how genes are disrupted in mental illnesses, providing important clues to future treatment targets and early interventions. The Atlas resources are freely available to the public on the Allen Brain Atlas data portal. Already, the BrainSpan Atlas has been used to identify genetic networks relevant to autism and schizophrenia.27,28 In both of these studies, the fetal pattern of gene expression revealed relationships that could not be detected by studying gene expression in the adult brain. As most mental illnesses are neurodevelopmental, mapping where and when genes are expressed in the brain provides a fundamental atlas for charting risk.

Brain Atlas NIH