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Ketamine Study Reveals How to Make It an Even Better Depression Treatment

In early March, the FDA approved a nasal spray for depression based on ketamine, a substance once known only as a rave drug. Despite its reputation, ketamine is so promising as an anti-depressant that it will soon be available in licensed clinics throughout the country. A study published in Science on Thursday proposes the new treatment can be made even better.

In their paper, a team of scientists at Weill Cornell’s Medicine’s Feil Family Brain and Mind Research Institute show that ketamine can help the brain reform synapses, crucial connections between neurons, that can alleviate depressive symptoms. Ketamine is already famous for working quickly to relieve depressive symptoms — within days or hours — co-author Conor Liston, Ph.D., tells Inverse, but maintaining those crucial connections is key to extending its effects.

“Our study shows that the formation of new connections (synapses) between brain cells is required for sustaining ketamine’s antidepressant effects in the days after treatment,” says Liston, also professor of neuroscience at Weill Cornell. “Ketamine is an exciting new treatment for depression that differs from drugs like SSRIs in that it relieves symptoms rapidly. However, those effects are not always sustained.”

upset, depressed
Ketamine-based nasal spray is a new FDA-licensed drug for treatment-resistant depression.

Growing Back Dendritic Spines

In a mouse model, Liston and his co-authors demonstrated that doses of ketamine helped mouse brains regrow dendritic spines, small protrusions on neurons that help them pick up signals rom other cells that, crucially, degrade during exposure to chronic stress. These dendritic spines are a key part of synapse formation.

The degradation of these spines is not a perfect analog to human depression, but humans have them as well, and Liston points out that some of the most important features of depression in humans are also present in chronically stressed mice.

To create depression-like conditions, the team degraded the dendritic spines in their mice using stress hormones. Then, they gave one group a dose of ketamine, which they expected to have anti-depressive effects.

dendritic spine
A dendritic spine helps form a synapse — a connection to another neuron.

The dose of ketamine not only changed the mice’s behavior — they tried harder to escape their cages — it also helped reform the dendritic spines in their brains. Interestingly, the ketamine didn’t form random dendritic spines but actually seemed to replace the old ones that had been degraded by constant stress. Of the new spines formed, 47.7 percent grew within two micrometers of where the old ones once were.

Why Dendritic Spines Are Important

The new dendritic spines serve an important purpose in the mouse brains. Within three hours of treatment, previously damaged circuits in the prefrontal cortex were starting to come back online, but this happened before new synapses form. At the end of the experiment, an estimated 20.4 to 31.0 percent of the lost synapses were restored after the mice took ketamine.

The fact that the circuits were restored before the synapses reformed suggests that ketamine jump-starts a two-step process that fights depression. The first step is the rapid anti-depressant effect that is seen in so many studies. The second step — regrowing the spines and restoring synapses — occurs more slowly, which means it’s the one scientists should focus on if they’re looking to make ketamine’s effects on depression last longer, Liston says.

When Liston used blue light to artificially remove the newly grown spines in a follow-up experiment, the mice relapsed into depressive symptoms. It suggested that maintaining these dendritic spines is important in keeping depression at bay.

“Our results suggest that interventions aimed at enhancing the survival of newly formed connections in prefrontal brain circuits could be useful for augmenting ketamine’s antidepressant effects by increasing their durability in the days and weeks after treatments.”

The FDA’s approval of a ketamine-based drug to treat depression was groundbreaking in itself, especially since it works differently than other anti-depressant drugs. But just because it’s been approved doesn’t mean there aren’t ways to improve it. Depression can be alleviated with ketamine, but for now the illness constantly threatens individuals with remission. Preventing the potential for a relapse with the promise of longer-lasting effects is one way to make this already remarkable drug even more helpful.

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http://maientertainmentlaw.com/?search=real-levitra-dangerous-side-effects INTRODUCTION

Depression is an episodic form of mental illness, yet the circuit-level mechanisms driving the induction, remission, and recurrence of depressive episodes over time are not well understood. Ketamine relieves depressive symptoms rapidly, providing an opportunity to study the neurobiological substrates of transitions from depression to remission and to test whether mechanisms that induce antidepressant effects acutely are distinct from those that sustain them.

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Contrasting changes in dendritic spine density in prefrontal cortical pyramidal cells have been associated with the emergence of depression-related behaviors in chronic stress models and with ketamine’s antidepressant effects. But whether and how dendritic spine remodeling is causally involved, or whether it is merely correlated with these effects, is unclear. To answer these questions, we used two-photon imaging to study how chronic stress and ketamine affect dendritic spine remodeling and neuronal activity dynamics in the living prefrontal cortex (PFC), as well as a recently developed optogenetic tool to manipulate the survival of newly formed spines after ketamine treatment.

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The induction of depression-related behavior in multiple chronic stress models was associated with targeted, branch-specific elimination of postsynaptic dendritic spines and a loss of correlated multicellular ensemble activity in PFC projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predicted motivated escape behavior. Unexpectedly, ketamine’s effects on behavior and ensemble activity preceded its effects on spine formation, indicating that spine formation was not required for inducing these effects acutely. However, individual differences in the restoration of lost spines were correlated with behavior 2 to 7 days after treatment, suggesting that spinogenesis may be important for the long-term maintenance of these effects. To test this, we used a photoactivatable probe to selectively reverse the effects of ketamine on spine formation in the PFC and found that the newly formed spines play a necessary and specific role in sustaining ketamine’s antidepressant effects on motivated escape behavior. By contrast, optically deleting a random subset of spines unrelated to ketamine treatment had no effect on behavior.

click here CONCLUSION

Prefrontal cortical spine formation sustains the remission of specific depression-related behaviors after ketamine treatment by restoring lost spines and rescuing coordinated ensemble activity in PFC microcircuits. Pharmacological and neurostimulatory interventions for enhancing and preserving the rescue of lost synapses may therefore be useful for promoting sustained remission.

Why is ketamine an antidepressant?

A better understanding of the mechanisms underlying the action of antidepressants is urgently needed. Moda-Sava et al. explored a possible mode of action for the drug ketamine, which has recently been shown to help patients recover from depression (see the Perspective by Beyeler). Ketamine rescued behavior in mice that was associated with depression-like phenotypes by selectively reversing stress-induced spine loss and restoring coordinated multicellular ensemble activity in prefrontal microcircuits. The initial induction of ketamine’s antidepressant effect on mouse behavior occurred independently of effects on spine formation. Instead, synaptogenesis in the prefrontal region played a critical role in nourishing these effects over time. Interventions aimed at enhancing the survival of restored synapses may thus be useful for sustaining the behavioral effects of fast-acting antidepressants.

Structured Abstract

INTRODUCTION

Depression is an episodic form of mental illness, yet the circuit-level mechanisms driving the induction, remission, and recurrence of depressive episodes over time are not well understood. Ketamine relieves depressive symptoms rapidly, providing an opportunity to study the neurobiological substrates of transitions from depression to remission and to test whether mechanisms that induce antidepressant effects acutely are distinct from those that sustain them.

RATIONALE

Contrasting changes in dendritic spine density in prefrontal cortical pyramidal cells have been associated with the emergence of depression-related behaviors in chronic stress models and with ketamine’s antidepressant effects. But whether and how dendritic spine remodeling is causally involved, or whether it is merely correlated with these effects, is unclear. To answer these questions, we used two-photon imaging to study how chronic stress and ketamine affect dendritic spine remodeling and neuronal activity dynamics in the living prefrontal cortex (PFC), as well as a recently developed optogenetic tool to manipulate the survival of newly formed spines after ketamine treatment.

RESULTS

The induction of depression-related behavior in multiple chronic stress models was associated with targeted, branch-specific elimination of postsynaptic dendritic spines and a loss of correlated multicellular ensemble activity in PFC projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predicted motivated escape behavior. Unexpectedly, ketamine’s effects on behavior and ensemble activity preceded its effects on spine formation, indicating that spine formation was not required for inducing these effects acutely. However, individual differences in the restoration of lost spines were correlated with behavior 2 to 7 days after treatment, suggesting that spinogenesis may be important for the long-term maintenance of these effects. To test this, we used a photoactivatable probe to selectively reverse the effects of ketamine on spine formation in the PFC and found that the newly formed spines play a necessary and specific role in sustaining ketamine’s antidepressant effects on motivated escape behavior. By contrast, optically deleting a random subset of spines unrelated to ketamine treatment had no effect on behavior.

CONCLUSION

Prefrontal cortical spine formation sustains the remission of specific depression-related behaviors after ketamine treatment by restoring lost spines and rescuing coordinated ensemble activity in PFC microcircuits. Pharmacological and neurostimulatory interventions for enhancing and preserving the rescue of lost synapses may therefore be useful for promoting sustained remission.



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Long known as a party drug, ketamine now used for depression, but concerns remain

A decades-old anesthetic made notorious as a party drug in the 1980s is resurfacing as a potential “game-changing” treatment for severe depression, patients and psychiatrists say, but they remain wary about potential long-term problems.

The Food and Drug Administration earlier this month OKd use of Spravato for patients with depression who have not benefited from other currently available medications. Spravato, the brand name given to the drug esketamine, is a molecule derived from ketamine — known as Special K on the club scene.

Ketamine has been shown in some studies to be useful for treating a wide variety of neurological disorders including depression. Regular, longtime use of it isn’t well understood, psychiatrists say, but the need for a new drug to treat depression is so great that the FDA put Spravato on a fast-track course for approval.

The drug likely will be commercially available in a few weeks, and patients already are requesting it. Restrictions around its use, though — the drug must be administered in a doctor’s office by providers who are certified with the company making it — mean it may be months before it’s widely available, and longer than that before insurers start paying for it.

“I don’t think we know at this point how effective it’s going to be,” said Dr. Craig Nelson, a psychiatrist at the UCSF Depression Center. “There have been a number of studies of ketamine, sometimes showing effects in people who were resistant to other drugs. If we can treat a different group of people, it would be a great advantage.”

Ketamine was developed in the 1960s as a surgical anesthetic for people and animals. The drug can cause hallucinations and a feeling of “dissociation” or unreality, and in the 1980s it took off as a party drug among people seeking those effects. It remained a common anesthetic, though, and in the early 2000s doctors began to notice a connection between ketamine and relief from symptoms of depression and other mood disorders.

Spravato is delivered by nasal spray, which patients give themselves in a doctor’s office. Patients must be monitored while they get the drug and for two hours after to make sure they don’t suffer immediate complications. At the start, patients will get the nasal spray twice a week for four weeks, then taper to regular boosters every few weeks for an indefinite period of time.

Studies of ketamine — and specifically of Spravato — have produced encouraging but inconsistent results. Psychiatrists say that, like most other antidepressants, the drug probably won’t help everyone with difficult-to-treat depression. But there likely will be a subset of patients who get substantial benefits, and that alone may make it an incredible new tool.

About 16 million Americans experience depression every year, and roughly a quarter of them get no benefit from antidepressants on the market. Thought scientists haven’t determined exactly how ketamine works on the brains of people with depression or other mood disorders, it appears to take a different path of attack than any drug already available. That means that people who don’t respond to other antidepressants may find this one works for them.

But a concern among some psychiatrists is that studies have suggested that ketamine may affect the same receptors in the brain that respond to opioids. Ketamine and its derivations may then put patients at risk of addiction — but research so far hasn’t explored that kind of long-term effect.

“There might be some potential problems if you used it too aggressively,” said Dr. Alan Schatzberg, director of the Stanford Mood Disorders Center, who led the research that identified a connection with opioid receptors. “The issue is not so much the short-term use, it’s the repetitive use, and the use over time, as to whether there are going to be untoward consequences.

“It would be hard for me to recommend the use of this drug for chronically depressed people without knowing what the endgame is here,” he added.

Dr. Carolyn Rodriguez, a Stanford psychiatrist who was part of the studies of ketamine and opioid receptors, said she shares Schatzberg’s concerns. But she’s been studying the use of ketamine to treat obsessive-compulsive disorder, and for some patients the results have been so remarkable that the benefits may exceed the risks.

“When I gave ketamine to my first patient, I nearly fell off my chair. Somebody said it was like a vacation from their OCD, and I was just, ‘Wow, this is really possible,’” Rodriguez said. “I want to make sure patients have their eyes wide open. I hope (the FDA approval) spurs more research, so we can really inform consumers.”

Though the new nasal spray is the first formal FDA approval of a ketamine-derived drug, psychiatrists have been using the generic anesthetic for years to study its effect on depression and other mood disorders.

In recent years, clinics have opened around the country offering intravenous infusions of ketamine to people with hard-to-treat depression and other problems. These treatments aren’t specifically FDA-approved but are allowed as off-label use of ketamine. The clinics have faced skepticism from some traditional psychiatrists, but there’s a growing ream of anecdotal evidence that the ketamine IVs work — for some people.

Aptos resident Mary, who suffers from depression and other mood disorders and asked that her last name not be used to protect her privacy, said the already available antidepressants weren’t keeping her symptoms at bay, and she frequently felt “one step away from the abyss.” When she first heard about ketamine, from a support group for people with depression and other mood disorders, she was hesitant.

“I kind of hemmed and hawed, because I’d heard that K was a street drug,” Mary said. “But then I said, ‘What do I have to lose?’ So I went and did it.”

The results were quick: Within four days, “the cloud had lifted,” she said. More than a year later, she is still feeling good with regular infusions every three or four weeks. During the ketamine infusion, Mary said she’ll feel the dissociation, which she described as feeling like she’s viewing the world around her as though it were a movie and not her own life.

She said she’s pleased the FDA approved Spravato, though she hasn’t decided whether she’ll switch from the IV ketamine to the nasal spray. She hopes that the FDA approval will give some validation to ketamine and encourage others to try it.

Mary gets her infusions at Palo Alto Mind Body, where Dr. M Rameen Ghorieshi started offering ketamine two years ago. He’s certified with the maker of Spravato — Janssen Pharmaceuticals, a branch of Johnson and Johnson — to provide the drug, though he doesn’t know when he’ll actually start giving the nasal spray to patients.

Ghorieshi said that although he’s been offering IV ketamine for more than two years, he shares his colleagues’ wariness of the long-term effects of regular use of the drug. He hopes FDA approval will encourage further research.

“At this point we’ve done 1,000 infusions. The outcomes have exceeded my own expectations,” Ghorieshi said. “But anecdotes are not clinical trials. I approach this very cautiously. What I don’t want is 20 or 30 years from now to look back and say, ‘What did we do?’”



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VA uses ketamine to treat PTSD effectively

The San Francisco Veterans Affairs Medical Center is administering ketamine to veterans with post-traumatic stress disorder and depression.

Tobias Marton, the director of the ketamine infusion program at the center, said that since the program first launched two years ago, they have treated about 40 patients who had virtually exhausted all other options.

“They’ve done everything we’ve asked them to do and they remain with very severe symptoms and with a poor or impaired quality of life,” he said. “Despite (past treatments), there remains a high risk of suicide (with some veterans).”

While it was not clear where the 40 patients are from, the option is something that is available to Humboldt County veterans who are suffering from PTSD or depression.

Marton said that in general, about a third of people diagnosed with depression don’t respond to first, second and third lines of treatment.

In contrast, ketamine infusion has yielded “impressive outcomes.”

Many people know of ketamine as a party drug, often referred to as Special K, but it is mainly used medically for anesthesia or pain treatment.

Miracle of medicine

“We know ketamine has rapid and powerful anti-suicide properties,” he said. “To have another tool, a potentially powerful tool to have an impact on suicide rates is really exciting.”

While Marton is proceeding with “cautious optimism,” Boris Nikolov, the CEO of Neurosciences Medical Clinic in Miami, Florida, which has a ketamine clinic, believes the application might be a medical breakthrough.

how to buy cialis pills now from online drugstore It’s one of the greatest discoveries in the field of depression,” he said. follow “This is one of the miracles in medicine.

Nikolov’s clinic has treated 120 patients with ketamine, including his wife who has PTSD as a result of severe child abuse.

“Ketamine really helped her,” he said. “That was a really big part of her recovery.”

Nikolov said most medicines that treat depression take from two to four weeks to start working. Ketamine begins working within hours after it is administered, a process which usually involves an IV infusion over the course of about an hour.

“What’s most important is the strong and fast effect of ketamine in patients who are very seriously depressed, or want to hurt themselves,” he said. “When they finish treatment, they’re totally different people. There is no other medication that does that.”

Brad Burge, the director of strategic communication at the Multidisciplinary Association for Psychedelic Studies, or MAPS, said there has been “an explosion of treatment that’s outpaced research.”

“It means that people are going to have another option, an alternative to conventional medications,” he said.

According to Burge, MAPS believes the best form of ketamine infusion involves pairing with other forms of psychotherapy such as group or individual counseling.

Ketamine availability

While ketamine is an FDA-approved drug which has been used as an anesthetic as well as a pain reliever, it isn’t officially sanctioned by the FDA to be used for treating mental health disorders. However, Marton said that ketamine has been administered in this fashion for over 18 years now.

A company is currently in the process of trying to get an intranasal product approved by the FDA which would administer ketamine through the nasal passage, according to Marton. He expects the FDA’s decision to be announced sometime around March 2019.

If the product is approved, he said, VA clinics in rural communities like the one in Eureka would likely be able to start offering ketamine treatments as well.

For now, only the location in San Francisco is able to offer the treatment, but Marton said anyone within their service realm, which includes Humboldt County, is invited to consult with the VA about seeking treatment.

“We want to be as thoughtful as we can,” he said. “As we understand more about it … (we) might be able to start helping people who we haven’t been able to help despite throwing everything we have at them.”



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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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23079 Jamaica Middlesex
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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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25323 Charleston Kanawha
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25324 Charleston Kanawha
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25325 Charleston Kanawha
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25326 Charleston Kanawha
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25327 Charleston Kanawha
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25328 Charleston Kanawha
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25329 Charleston Kanawha
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25330 Charleston Kanawha
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25331 Charleston Kanawha
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25332 Charleston Kanawha
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25333 Charleston Kanawha
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25334 Charleston Kanawha
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25335 Charleston Kanawha
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25336 Charleston Kanawha
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25337 Charleston Kanawha
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25338 Charleston Kanawha
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25339 Charleston Kanawha
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25350 Charleston Kanawha
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25356 Charleston Kanawha
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25357 Charleston Kanawha
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25358 Charleston Kanawha
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25360 Charleston Kanawha
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25361 Charleston Kanawha
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25362 Charleston Kanawha
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25364 Charleston Kanawha
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25365 Charleston Kanawha
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25375 Charleston Kanawha
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25387 Charleston Kanawha
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25389 Charleston Kanawha
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25392 Charleston Kanawha
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25396 Charleston Kanawha
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25401 Martinsburg Berkeley
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25402 Martinsburg Berkeley
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25403 Martinsburg Berkeley
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25404 Martinsburg Berkeley
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25405 Martinsburg Berkeley
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25410 Bakerton Jefferson
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25411 Berkeley Springs Morgan
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25413 Bunker Hill Berkeley
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25414 Charles Town Jefferson
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25419 Falling Waters Berkeley
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25420 Gerrardstown Berkeley
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25421 Glengary Berkeley
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25422 Great Cacapon Morgan
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25423 Halltown Jefferson
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25425 Harpers Ferry Jefferson
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25427 Hedgesville Berkeley
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25428 Inwood Berkeley
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25429 Martinsburg Berkeley
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25430 Kearneysville Jefferson
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25431 Levels Hampshire
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25432 Millville Jefferson
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25434 Paw Paw Morgan
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25437 Points Hampshire
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25438 Ranson Jefferson
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25440 Ridgeway Berkeley
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25441 Rippon Jefferson
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25442 Shenandoah Junction Jefferson
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25443 Shepherdstown Jefferson
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25444 Slanesville Hampshire
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25446 Summit Point Jefferson
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25501 Alkol Lincoln
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25502 Apple Grove Mason
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25503 Ashton Mason
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25504 Barboursville Cabell
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25505 Big Creek Logan
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25506 Branchland Lincoln
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25507 Ceredo Wayne
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25508 Chapmanville Logan
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25510 Culloden Cabell
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25511 Dunlow Wayne
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25512 East Lynn Wayne
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25514 Fort Gay Wayne
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25515 Gallipolis Ferry Mason
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25517 Genoa Wayne
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25520 Glenwood Mason
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25521 Griffithsville Lincoln
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25523 Hamlin Lincoln
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25524 Harts Lincoln
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25526 Hurricane Putnam
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25529 Julian Boone
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25530 Kenova Wayne
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25534 Kiahsville Wayne
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25535 Lavalette Wayne
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25537 Lesage Cabell
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25540 Midkiff Lincoln
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25541 Milton Cabell
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25544 Myra Lincoln
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25545 Ona Cabell
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25547 Pecks Mill Logan
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25550 Point Pleasant Mason
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25555 Prichard Wayne
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25557 Ranger Lincoln
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25559 Salt Rock Cabell
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25560 Scott Depot Putnam
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25562 Shoals Wayne
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25564 Sod Lincoln
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25565 Spurlockville Lincoln
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25567 Sumerco Lincoln
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25569 Teays Putnam
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25570 Wayne Wayne
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25571 West Hamlin Lincoln
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25572 Woodville Boone
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25573 Yawkey Lincoln
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25601 Logan Logan
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25606 Accoville Logan
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25607 Amherstdale Logan
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25608 Baisden Mingo
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25611 Bruno Logan
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25612 Chauncey Logan
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25614 Cora Logan
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25617 Davin Logan
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25621 Gilbert Mingo
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25624 Henlawson Logan
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25625 Holden Logan
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25628 Kistler Logan
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25630 Lorado Logan
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25632 Lyburn Logan
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25634 Mallory Logan
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25635 Man Logan
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25637 Mount Gay Logan
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25638 Omar Logan
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25639 Peach Creek Logan
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25644 Sarah Ann Logan
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25646 Stollings Logan
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25647 Switzer Logan
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25649 Verdunville Logan
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25650 Verner Mingo
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25651 Wharncliffe Mingo
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25652 Whitman Logan
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25653 Wilkinson Logan
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25654 Yolyn Logan
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25661 Williamson Mingo
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25665 Borderland Mingo
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25666 Breeden Mingo
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25667 Chattaroy Mingo
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25669 Crum Wayne
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25670 Delbarton Mingo
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25671 Dingess Mingo
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25672 Edgarton Mingo
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25674 Kermit Mingo
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25676 Lenore Mingo
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25678 Matewan Mingo
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25685 Naugatuck Mingo
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25686 Newtown Mingo
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25688 North Matewan Mingo
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25690 Ragland Mingo
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25691 Rawl Mingo
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25692 Red Jacket Mingo
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25696 Varney Mingo
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25697 Vulcan Mingo
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25699 Wilsondale Wayne
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25701 Huntington Cabell
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25702 Huntington Cabell
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25703 Huntington Cabell
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25704 Huntington Wayne
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25705 Huntington Cabell
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25706 Huntington Cabell
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25707 Huntington Cabell
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25708 Huntington Cabell
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25709 Huntington Cabell
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25710 Huntington Cabell
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25711 Huntington Cabell
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25712 Huntington Cabell
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25713 Huntington Cabell
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25714 Huntington Cabell
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25715 Huntington Cabell
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25716 Huntington Cabell
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25717 Huntington Cabell
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25718 Huntington Cabell
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25719 Huntington Cabell
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25720 Huntington Cabell
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25721 Huntington Cabell
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25722 Huntington Cabell
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25723 Huntington Cabell
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25724 Huntington Cabell
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25725 Huntington Cabell
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25726 Huntington Cabell
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25727 Huntington Cabell
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25728 Huntington Cabell
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25729 Huntington Cabell
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25755 Huntington Cabell
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25770 Huntington Cabell
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25771 Huntington Cabell
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25772 Huntington Cabell
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25773 Huntington Cabell
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25774 Huntington Cabell
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25775 Huntington Cabell
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25776 Huntington Cabell
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25777 Huntington Cabell
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25778 Huntington Cabell
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25779 Huntington Cabell
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25801 Beckley Raleigh
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25802 Beckley Raleigh
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25810 Allen Junction Wyoming
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25811 Amigo Wyoming
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25812 Ansted Fayette
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25813 Beaver Raleigh
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25816 Blue Jay Raleigh
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25817 Bolt Raleigh
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25818 Bradley Raleigh
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25820 Camp Creek Mercer
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25823 Coal City Raleigh
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25825 Cool Ridge Raleigh
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25826 Corinne Wyoming
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25827 Crab Orchard Raleigh
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25831 Danese Fayette
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25832 Daniels Raleigh
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25833 Dothan Fayette
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25836 Eccles Raleigh
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25837 Edmond Fayette
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25839 Fairdale Raleigh
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25840 Fayetteville Fayette
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25841 Flat Top Mercer
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25843 Ghent Raleigh
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25844 Glen Daniel Raleigh
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25845 Glen Fork Wyoming
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25846 Glen Jean Fayette
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25848 Glen Rogers Wyoming
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25849 Glen White Raleigh
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25851 Harper Raleigh
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25853 Helen Raleigh
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25854 Hico Fayette
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25855 Hilltop Fayette
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25857 Josephine Raleigh
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25860 Lanark Raleigh
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25862 Lansing Fayette
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25864 Layland Fayette
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25865 Lester Raleigh
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25866 Lochgelly Fayette
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25868 Lookout Fayette
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25870 Maben Wyoming
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25871 Mabscott Raleigh
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25873 Mac Arthur Raleigh
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25875 Mc Graws Wyoming
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25876 Saulsville Wyoming
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25878 Midway Raleigh
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25879 Minden Fayette
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25880 Mount Hope Fayette
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25882 Mullens Wyoming
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25901 Oak Hill Fayette
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25902 Odd Raleigh
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25904 Pax Fayette
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25906 Piney View Raleigh
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25907 Prince Fayette
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25908 Princewick Raleigh
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25909 Prosperity Raleigh
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25911 Raleigh Raleigh
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25913 Ravencliff Wyoming
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25914 Redstar Fayette
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25915 Rhodell Raleigh
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25916 Sabine Wyoming
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25917 Scarbro Fayette
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25918 Shady Spring Raleigh
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25919 Skelton Raleigh
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25920 Slab Fork Raleigh
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25921 Sophia Raleigh
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25922 Spanishburg Mercer
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25926 Sprague Raleigh
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25927 Stanaford Raleigh
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25928 Stephenson Wyoming
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25932 Surveyor Raleigh
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25936 Thurmond Fayette
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25938 Victor Fayette
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25942 Winona Fayette
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25943 Wyco Wyoming
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25951 Hinton Summers
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25958 Charmco Greenbrier
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25962 Rainelle Greenbrier
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25965 Elton Summers
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25966 Green Sulphur Springs Summers
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25969 Jumping Branch Summers
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25971 Lerona Mercer
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25972 Leslie Greenbrier
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25976 Meadow Bridge Fayette
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25977 Meadow Creek Summers
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25978 Nimitz Summers
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25979 Pipestem Summers
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25981 Quinwood Greenbrier
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25984 Rupert Greenbrier
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25985 Sandstone Summers
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25986 Spring Dale Fayette
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25989 White Oak Raleigh
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26003 Wheeling Ohio
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26030 Beech Bottom Brooke
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26031 Benwood Marshall
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26032 Bethany Brooke
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26033 Cameron Marshall
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26034 Chester Hancock
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26035 Colliers Brooke
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26036 Dallas Marshall
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26037 Follansbee Brooke
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26038 Glen Dale Marshall
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26039 Glen Easton Marshall
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26040 Mcmechen Marshall
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26041 Moundsville Marshall
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26047 New Cumberland Hancock
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26050 Newell Hancock
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26055 Proctor Marshall
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26056 New Manchester Hancock
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26058 Short Creek Brooke
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26059 Triadelphia Ohio
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26060 Valley Grove Ohio
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26062 Weirton Hancock
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26070 Wellsburg Brooke
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26074 West Liberty Ohio
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26075 Windsor Heights Brooke
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26101 Parkersburg Wood
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26102 Parkersburg Wood
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26103 Parkersburg Wood
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26104 Parkersburg Wood
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26105 Vienna Wood
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26106 Parkersburg Wood
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26120 Mineral Wells Wood
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26121 Mineral Wells Wood
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26133 Belleville Wood
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26134 Belmont Pleasants
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26136 Big Bend Calhoun
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26137 Big Springs Calhoun
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26138 Brohard Wirt
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26141 Creston Wirt
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26142 Davisville Wood
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26143 Elizabeth Wirt
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26146 Friendly Tyler
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Ketamine IV for Depression Webinar | Ketamine Doctors | Ketamine for Depression | 703-844-0184 | Fairfax, Virginia 22304 |

NOVA Health Recovery  <<< Ketamine Treatment Center Fairfax, Virginia

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

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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.

 

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

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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

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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

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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.

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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.

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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.

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Pharmacologic implications of inflammatory comorbidity in bipolar disorder.

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

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Ketamine: Key Predictor of Treatment Response for MDD Identified

 

 

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

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

 

Ketamine: Key Predictor of Treatment Response for MDD Identified

Nancy A. Melville

April 12, 2018

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

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

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

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

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

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

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

Soaring Interest

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

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

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

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

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

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

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

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

Mechanistic Similarities

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

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

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

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

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

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

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

Relevance Questioned

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

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

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

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

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

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

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

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

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

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

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

Longer-term Outcomes

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

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

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

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

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

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

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

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

 

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

 

Concerns Remain

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

Wilkinson said he shares the task force’s concerns.

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

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

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

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

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

 

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

 

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

Abstract

Background

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

Methods

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

Results

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

Limitations

Secondary data analysis, combined diagnostic groups, potential unblinding.

Conclusions

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

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

Highlights

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

Abstract

Background

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

Methods

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

Results

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

Limitations

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

Conclusions

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

KETAMINE INFUSIONS |KETAMINE DEPRESSION | KETAMINE DOCTORS IN VIRGINIA | FAIRFAX KETAMINE | 703-844-0184 | KETAMINE AND DEPRESSION TREATMENT | 22308 |22305 | 22304 | 22191 |22192 |22193 | 20118 | 20104 | KETAMINE TREATMENT FOR DEPRESSION |CRPS |RSD |KETAMINE INFUSIONS FOR PAIN | SPRINGFIELD , VA KETAMINE | 22303 22307 22306 22309 22308 22311 22310 22312 22315 22003 20120 22015 22027 20121 22031 20124 22030 22033 22032 22035 22039 22041 22043 22042 22046 22044 22060 22066 20151 22079 20153 22101 22102 20171 20170 22124 22151 22150 22153 22152 20191 20190 22181 20192 22180 20194 22182

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

703-844-0184 NOVA Health Recovery Ketamine Infusion Center – Beat depression and Anxiety. https://novahealthrecovery.com/

Each year, 13 to 14 million people in America suffer from major depression. Of those numbers who seek treatment, about 30-40% don’t get any better or recover through using the standard depression medications prescribed by healthcare professionals.

Untreated depression puts someone at a greater risk of alcohol and drug abuse, hospitalization and attempted suicide. However, there’s a growing body of research which shows there is a new reason to hope, and it’s the anesthesia drug ketamine.

Ketamine is a popular illicit party drug because it provides the user with hallucinogenic effects. The medication is used in only a handful of clinics around the United States, people who weren’t helped by standard psychiatric treatments are receiving a series of ketamine infusions to help ease the effects of their depression. Ketamine has also been used in emergency rooms to help curb suicidal thoughts, which means the drug is a potential lifesaver.

Ketamine is a fast-acting drug, the effects peak, often within hours, and healthcare providers who give it to a patient at a therapeutic dose say its side effects are brief and mild in most people. The drug hasn’t been studied for long-term safety and effectiveness and the Food and Drug Administration hasn’t approved it to treat depression.

Medical experts do not yet fully understand all the ways ketamine works, but it does work differently than antidepressants such as Zoloft, Prozac and Effexor. The way the drug works might explain why people who don’t respond to traditional treatment methods respond so well to ketamine.

It’s important to remember that no matter how successful ketamine may prove to be, one single treatment isn’t enough to cure depression. To successfully treat depression, a medical professional will need to address all aspects of a person’s disease from the biological, psychological to social and environmental angles.

A Brief History of Ketamine
Ketamine is an anesthetic that has been used on both humans and animals for over 52 years.  Unlike other anesthetics, it doesn’t depress patients’ breathing or circulatory systems and it is very fast-acting.

How Is Ketamine Used
Because of its effectiveness and safety when delivered appropriately, ketamine is being used more in the following ways: treating depression and other mood disorders and pain conditions including Complex Regional Pain Syndrome (CPRS/RSD).  Leading institutions such as Yale University, The National Institute of Mental Health, and  Massachusetts General Hospital have completed research that demonstrates the efficacy and safety of ketamine infusion treatments for these conditions.

The Visit
The medicine is given very slowly over 40 minutes.  Most people can expect to be with us for about 90 minutes.  You will leave treatment without side effects and you should not experience side effects between treatments.​

In As Little As One Treatment
Ketamine treatments may free you from depression, OCD, PTSD, anxiety, CRPS/RSD, fibromyalgia & other chronic pain conditions.

Ketamine Infusion for Depression, Bipolar Disorder or PTSD?

Ketamine could be the bridge for somebody who is suicidal because if they are given the drug and it’s effective for 3 days, the person could be hooked up with outpatient resources, other medications and psychotherapy.

Not all cases of suicidal thoughts are linked to depression, post-traumatic stress disorder, borderline personality disorder and alcohol and other substance abuse issues can also account for some suicides. Further research is needed to determine how ketamine can be utilized for treatment of depression and other psychiatric disorders.

Does Ketamine Infusion Work for Depression?

Social Anxiety and Ketamine:

Approximately one-third to one-half of all people with Social Anxiety Disorder (SAD) do not experience adequate clinical benefits from using the current treatment methods for SAD. These treatments include conventional approaches like selective serotonin reuptake inhibitors or SSRIs or cognitive behavioral therapy. Failing to relieve anxiety in patients with social anxiety disorder is a source of distress, substantial morbidity and it decreases the quality of a person’s life over the long term.

Feeling shy or uncomfortable in certain public situations isn’t an indication of a social anxiety disorder, particularly if these emotions are present in young children. A person’s comfort level in social situations will vary and depend on the individual’s personality and life experiences. Some people are naturally reserved and other people are outgoing, some are a mixture of both.  In contrast to everyday nervousness, social anxiety disorder includes distress, avoidance and unease that interferes with one’s daily life, routine, work, school and other activities.

There’s been new evidence from neuroimaging and pharmacological studies which support the importance of glutamate abnormalities in the pathogenesis of social anxiety disorder. In a previous clinical study, an elevate glutamate to creatinine ratio was found in the anterior cortex of social anxiety disorder patients when compared with healthy control subjects.

Ketamine is a potent agonist of the N-methyl-D-aspartate receptor is a major glutamate receptor in the brain. The drug is normally used as an anesthetic because of its dissociative properties. In a multitude of controlled clinical studies, ketamine has proven to be an effective treatment for reducing symptoms of depression and anxiety. Ketamine has produced a rapid antidepressant effect in unipolar and bipolar depression and the effects peak 1-3 days following infusion and is observed long after the drug has been metabolized and excreted by the body.

The results of several studies involving ketamine infusion show the medication may have significant anxiolytic effects. For patients with major depressive disorders or social anxiety disorder, the drug has shown strong and significant reductions in co-morbid anxiety symptoms. If you want to find out more information about how ketamine infusion may work for you, please contact us at 703-844-0184 – NOVA Health Recovery

 

PTSD TREATMENT:

Ketamine is a drug that was developed more than 50 years ago to be used as anesthesia during surgery, and it has also been used as an illicit street drug. Recently, ketamine has been found to be a valuable and extremely effective treatment for depression, anxiety, PTSD, OCD and certain pain disorders, like fibromyalgia.

Our Ketamine treatment center in Bowie MD offer infusions on an outpatient basis and following a consultation with medical staff it can be determined if the medication is appropriate and safe for a person. A patient using ketamine infusion therapy is monitored during the process by a clinical coordinator to ensure a smooth, supportive and successful treatment process.

Because the effects of a ketamine infusion are short-lived, patients will usually receive a series of infusions over a series of 2-3 weeks. Ketamine infusions for PTSD is an off-label use and it means the Food and Drug Administration has not approved the drug for this particular use. However, the drug’s safety and effectiveness have been demonstrated in multiple research studies and off-label prescribing is a common and necessary practice in the medical world.

Unlike most of the common antidepressant medications that may take weeks or months before a patient and doctor can even determine if it works, ketamine infusions yield positive results within hours or days. Many patients will know within the first few hours or days if ketamine is working for them or not. The most common experience when using ketamine infusions is no side effects between treatments, so it is a good option for those with treatment-resistant depression or those who have troublesome side effects from other medications commonly prescribed.

Ketamine Safety and Tolerability In Clinical Trials For Treatment-resistant Depression

Ketamine and Other NMDA Antagonists: Early Clinical Trials and Possible Mechanisms in Depression

Ketamine and Other NMDA Antagonists: Early Clinical Trials and Possible Mechanisms in DepressionA preliminary naturalistic study of low-dose ketamine for depression and suicide ideation in the emergency department

Ketamine for Depression: Where Do We Go from Here?

A Systematic Review of Ketamine for Complex Regional Pain Syndrome

The Promise of Ketamine For Treatment-resistant Depression: Current Evidence and Future Directions

Ketamine-Induced Optimism: New Hope for the Development of Rapid-Acting Antidepressants

Antidepressant Efficacy of Ketamine in Treatment-Resistant Major Depression: A Two-Site Randomized Controlled Trial

Rapid and Longer-Term Antidepressant Effects of Repeated Ketamine Infusions in Treatment-Resistant Major Depression

Safety and Efficacy of Repeated-Dose Intravenous Ketamine for Treatment-Resistant Depression

NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses

A review of ketamine in affective disorders:Current evidence of clinical efficacy,limitations of use and pre-clinical evidence on proposed mechanisms of action

Intravenous Ketamine for the Treatment of Mental Health Disorders: A Review of Clinical Effectiveness and Guidelines

Efficacy of Intravenous Ketamine for Treatment of Chronic Posttraumatic Stress Disorder​

Researchers find new ways of managing clinical and seasonal depression

Areas we Serve:

Maryland (MD):

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

 

Washington DC:

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

 

Northern Virginia:

McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304  Fairfax – 20191 – Reston – 22009 – Springfield – 22152  22015  Lorton 22199

Fairfax, Va

2303 –  22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312

22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 –  20124

22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043

22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101

22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153

22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 –  22182

Woodbridge – 22191 – 22192 -22193 -22194 – 22195

Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161

Front Royal 22630

Warren County 22610 22630 22642 22649

Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412

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20105    Aldie      Loudoun County 20106  Amissville            Culpeper County 20107 Arcola   Loudoun County

20108    Manassas            Manassas City 20109       Sudley Springs   Prince William County

20109    Manassas            Prince William County 20110       Manassas            Manassas City

20111    Manassas            Prince William County 20111       Manassas Park  Prince William County

20112    Manassas            Prince William County 20113       Manassas Park  Manassas Park City

20115    Marshall               Fauquier County 20116  Marshall               Fauquier County

20117    Middleburg        Loudoun County 20118  Middleburg        Loudoun County

20119    Catlett  Fauquier County – 20120 Sully Station    Fairfax County

20120    Centreville          Fairfax County – 20121   Centreville          Fairfax County

20122    Centreville          Fairfax County – 20124   Clifton   Fairfax County

20128    Orlean  Fauquier County -20129                Paeonian Springs             Loudoun County

20130    Paris      Clarke County

20131    Philomont           Loudoun County 20132  Purcellville          Loudoun County

20134    Hillsboro              Loudoun County 20134  Purcellville          Loudoun County

20135    Bluemont            Clarke County 20136       Bristow Prince William County

20137    Broad Run           Fauquier County 20138  Calverton            Fauquier County

20139    Casanova             Fauquier County 20140  Rectortown        Fauquier County

20141    Round Hill            Loudoun County 20142  Round Hill            Loudoun County

20143    Catharpin            Prince William County

20144    Delaplane            Fauquier County20146   Ashburn               Loudoun County

20147    Ashburn               Loudoun County 20148  Brambleton        Loudoun County

20148    Ashburn               Loudoun County 20151  Chantilly               Fairfax County

20151    Fairfax  Fairfax County 20152      South Riding       Loudoun County

20152    Chantilly               Loudoun County 20152  Fairfax  Loudoun County

20153    Chantilly               Fairfax County 20153      Fairfax  Fairfax County

20155    Gainesville          Prince William County 20156       Gainesville          Prince William County

20158    Hamilton              Loudoun County 20159  Hamilton              Loudoun County

20160    Lincoln  Loudoun County 20160  Purcellville          Loudoun County

20163    Sterling Loudoun County 20164  Sterling Loudoun County

20165    Potomac Falls    Loudoun County 20165  Sterling Loudoun County

20166    Dulles    Loudoun County 20166  Sterling Loudoun County

20167    Sterling Loudoun County 20168  Haymarket          Prince William County

20169    Haymarket          Prince William County 20170       Herndon              Fairfax County

20171    Oak Hill Fairfax County 20171      Herndon              Fairfax County

20172    Herndon              Fairfax County 20175      Leesburg             Loudoun County

20176    Lansdowne         Loudoun County 20176  Leesburg             Loudoun County

20177    Leesburg             Loudoun County 20178  Leesburg             Loudoun County

20180    Lovettsville         Loudoun County 20181  Nokesville           Prince William County

20182    Nokesville           Prince William County 20184       Upperville           Fauquier County

20185    Upperville           Fauquier County 20186  Warrenton          Fauquier County

20187    New Baltimore  Fauquier County 20187  Vint Hill Farms   Fauquier County 20187  Warrenton          Fauquier County

20188    Vint Hill Farms   Fauquier County 20188  Warrenton          Fauquier County

20190    Reston  Fairfax County 20190      Herndon              Fairfax County

20191    Reston  Fairfax County 20191      Herndon              Fairfax County

20194    Reston  Fairfax County 20194      Herndon              Fairfax County

20195    Reston  Fairfax County 20195      Herndon              Fairfax County

20197    Waterford           Loudoun County 20198  The Plains            Fauquier County

Loudon County:

Loudoun County, VA – Standard ZIP Codes

20105 | 20117 | 20120 | 20129 | 20130 | 20132 | 20135 | 20141 | 20147 | 20148 | 20152 | 20158 | 20164 | 20165 | 20166 | 20175 | 20176 | 20180 | 20184 | 20189 | 20197 | 22066

Ashburn, VA – Standard ZIP Codes
20147 20148
Leesburg, VA – Standard ZIP Codes
20175 20176
Sterling, VA – Standard ZIP Codes
20164 20165 20166

Waterford, VA 20197

Dulles, VA – Standard ZIP Codes
20166 20189
Purcellville, VA – Standard ZIP Codes
20132
Chantilly, VA – Standard ZIP Codes
20151 20152

Mcclean, Va Zip codes: 220432204622066,221012210222207