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Is Ketamine Safe and Effective for Depression?

The anesthetic ketamine, used in both humans and animals, is perhaps best known as an illegal party drug due to its hallucinogenic effects. However, a growing body of research indicates that the drug may have a powerful new medical use: as a fast-acting antidepressant without the side effects seen in most prescription antidepressants.

As Nature reports, in many clinical trials to date people who have not responded to standard antidepressant treatment — such as SSRIs including Prozac — seem to respond to ketamine. And while it can take weeks to feel better after starting a prescription antidepressant, the therapeutic effects of ketamine are seen in a matter of hours.

Despite the seemingly “miracle drug” nature of ketamine, there are serious concerns about its use in depression. First, it is unclear how the drug works to alleviate depression. Second, there are no long-term studies on its long-term use. Studies that have already been done indicate the antidepressant effects of ketamine can last from between a few days to a few weeks.

And due to the addictive nature of ketamine itself, there are worries that sustained use of it may lead to dependence.

On May 4, Nature published the results of the latest trial involving ketamine, bolstering its potential as an antidepressant treatment. Researchers, examining the drug in mice, found that that the mood boosting effects may not be caused by ketamine itself, but instead by one of the metabolites ((2R,6R)-hydroxynorketamine) formed when the drug is broken down into smaller pieces.

Even more promising, the ketamine given to the rats did not increase side effects, even though the dose was much stronger than what would be given to humans for depression. The researchers say they want to take the metabolite into testing in humans, though that is likely years away.

The largest trial ever of ketamine in depression was done in 2013 with 73 participants. The drug lead to a decline in depression symptoms 24 hours after treatment in 64% of patients, all of whom had tried at least 3 other drugs without any results.  Antidepressant Efficacy of Ketamine in Treatment resistant depression

Despite the lack of clear-cut evidence of its benefits and unknowns about its long-term risk, many doctors are already offering ketamine as a depression treatments to patients, though this is an off-label use.

Side effects of ketamine can include confusion, lucid daydreaming, fuzzy vision, and a “high” feeling, though they tend to go away quickly, according to these doctors. Patients, who are usually given ketamine via infusion, are carefully monitored and must have pre-arranged transport home. They can’t drive or use heavy machinery for 24 hours.

Drug companies are even trying to cash in on the ketamine craze. Janssen Pharmaceutical is testing a form of ketamine it developed, called esketamine, in 5 clinical trials. It would be given via a nasal spray. Another is rapastinel, under development by Allergan. Both drugs had “breakthrough therapy designation” from the FDA, meaning they will go through the regulatory process at a much quicker rate.

NMDAR inhibition-independent antidepressant actions of ketamine metabolites

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Reasons to treat depression rapidly – Depression causes rapid aging> Consider using a rapid – acting antidepressant!

Depression ‘makes us biologically older’  BBC Article

Major depressive disorder and accelerated cellular aging

Patients with major depressive disorder (MDD) have an increased onset risk of aging-related somatic diseases such as heart disease,
diabetes, obesity and cancer. This suggests mechanisms of accelerated biological aging among the depressed, which can be
indicated by a shorter length of telomeres. We examine whether MDD is associated with accelerated biological aging, and whether
depression characteristics such as severity, duration, and psychoactive medication do further impact on biological aging. Data are
from the Netherlands Study of Depression and Anxiety, including 1095 current MDD patients, 802 remitted MDD patients and 510
control subjects. Telomere length (TL) was assessed as the telomere sequence copy number (T) compared to a single-copy gene
copy number (S) using quantitative polymerase chain reaction. This resulted in a T/S ratio and was converted to base pairs (bp).
MDD diagnosis and MDD characteristics were determined by self-report questionnaires and structured psychiatric interviews.
Compared with control subjects (mean bp = 5541), sociodemographic-adjusted TL was shorter among remitted MDD patients
(mean bp = 5459; P = 0.014) and current MDD patients (mean bp = 5461; P = 0.012). Adjustment for health and lifestyle variables did
not reduce the associations. Within the current MDD patients, separate analyses showed that both higher depression severity
(P<0.01) and longer symptom duration in the past 4 years (P = 0.01) were associated with shorter TL. Our results demonstrate that
depressed patients show accelerated cellular aging according to a ‘dose–response’ gradient: those with the most severe and
chronic MDD showed the shortest TL. We also confirmed the imprint of past exposure to depression, as those with remitted MDD
had shorter TL than controls

In this large cohort study we demonstrated that currently
depressed persons had shorter TL than never-depressed controls.
Based on an estimated mean telomere shortening rate of 14–20
bp per year as found in this and other studies,20,23,26 the
differences observed indicate 4–6 years of accelerated aging for
the current MDD sample as compared to controls. We also showed
evidence for the imprint of past exposure to depression since
those with remitted MDD also had shorter TL than control
subjects. These observed associations remained significant after
controlling for lifestyle and somatic health variables, suggesting that the shortened telomeres were not simply due to unhealthylifestyle or poorer somatic health among depressed persons.
Finally, the association between MDD and TL showed a ‘dose–
response’ gradient, since the most severely and chronically
depressed patients had the shortest telomeres.

MDD is thus associated with shortened TL, which resembles
accelerated biological aging. The disorder has previously also been
associated with dysregulations of the hypothalamus–pituitary–
adrenal (HPA) axis,43,45 the immune system,46,47 the autonomic
nervous system (ANS)48,49 and increased oxidative stress.50
Shortened telomeres, in turn, are suggested to be a consequence
or a concomitant of these dysregulated biological stress systems.
In line with this, several in vitro and in vivo studies found increased
cortisol,51 oxidative stress52 and pro-inflammatory cytokines53
to be associated with shorter TL. Dysregulations of these stress systems could contribute to telomere shortening in MDD patients.9,12
However, the exact biological mechanisms that mediate the relation
between depression and telomere shortening, as well as the
direction of the link, remain to be further explored.

Oxidative stress shortens telomeres

Elevated DNA Oxidation and DNA Repair Enzyme Expression in Brain White Matter in Major Depressive Disorder.

The Role of Oxidative Stress in Depressive Disorders

Abstract:

Studies of the World Health Organization suggest that in the year 2020, depressive disorder will be the illness with the highest
burden of disease. Especially unipolar depression is the psychiatric disorder with the highest prevalence and incidence, it is cost-intensive and has a relatively high morbidity. Lately, the biological process involved in the aetiology of depression has been the focus of research.
Since its emergence, the monoamine hypothesis has been adjusted and extended considerably. An increasing body of evidence points to
alterations not only in brain function, but also in neuronal plasticity. The clinical presentations demonstrate these dysfunctions by accompanying cognitive symptoms such as problems with memory and concentration. Modern imaging techniques show volume reduction of the hippocampus and the frontal cortex. These findings are in line with post-mortem studies of patients with depressive disorder and they point to a significant decrease of neuronal and glial cells in cortico-limbic regions which can be seen as a consequence of alterations in
neuronal plasticity in this disorder. This could be triggered by an increase of free radicals which in turn eventually leads to cell death and consequently atrophy of vulnerable neuronal and glial cell population in these regions. Therefore, research on increased oxidative stress in unipolar depressive disorder, mediated by elevated concentrations of free radicals, has been undertaken. This review gives a comprehensive overview over the current literature discussing the involvement of oxidative stress and free radicals in depression.

Membrane damage in blood of patients with depression has
been shown by elevated of omega 3- fatty-acids [45] and by increased
lipid peroxidation products in patients with DD [42, 45,
[46, 47]. Furthermore, DNA-strand brakes have been reported in
the blood of these patients [48]. DD has been linked to increased
serum levels of malondialdehyde (MDA), a breakdown product of
oxidized apolipoprotein B-containing lipoproteins, and thus a
marker of the rate of peroxide breakdown [49, 50].

In patients with DD (Depressive Disorders), elevated levels of MDA adversely affect
the efficiency of visual-spatial and auditory-verbal working memory,
short-term declarative memory and delayed recall declarative
memory [51]. Higher concentration of plasma MDA in patients
with recurrent depression is associated with the severity of depressive
symptoms, both at the beginning of antidepressant pharmacotherapy,
and after 8 weeks of treatment. Statistically significant
differences were found in the intensity of depressive symptoms,
measured on therapy onset versus the examination results after
8 weeks of treatment [51]. Although this is used as a marker of lipid peroxidation, it is considered to be less stable than 8-iso-PGF2a, and more susceptible to confounding factors such as antioxidants from diet [52]. Therefore, the best way to investigate oxidative disruptions to lipids in humans is via assessing levels of F2-
isoprostanes [52-54]. These are stable compounds produced in the
process of lipid peroxidation [52, 54]. 8-iso-PGF2a are specific F2-
isoprostane molecules produced during the peroxidation of arachnidonic acid. However, the mean serum level of 8-iso-PGF2a was shown to be significantly higher in a group of patients with DD,
controlling for lifestyle variables such as body mass index, alcohol
consumption, and physical activity [55, 56]. Cerebral membrane
abnormalities and altered membrane phospholipids have been suggested by an increased choline-containing compound seen in the
putamen of patients with DD [57] which has been interpreted as a
result of increased oxidative stress in patients with DD.

A Meta-Analysis of Oxidative Stress Markers in Depression

Results
115 articles met the inclusion criteria. Lower TAC was noted in acute episodes (AEs) of depressed patients (p<0.05). Antioxidants, including serum paraoxonase, uric acid, albumin,
high-density lipoprotein cholesterol and zinc levels were lower than controls (p<0.05); the serum uric acid, albumin and vitamin C levels were increased after antidepressant therapy
(p<0.05). Oxidative damage products, including red blood cell (RBC) malondialdehyde (MDA), serum MDA and 8-F2-isoprostanes levels were higher than controls (p<0.05). After
antidepressant medication, RBC and serum MDA levels were decreased (p<0.05). Moreover, serum peroxide in free radicals levels were higher than controls (p<0.05). There were
no difference

Conclusion
This meta-analysis supports the facts that the serum TAC, paraoxonase and antioxidant levels are lower, and the serum free radical and oxidative damage product levels are higher
than controls in depressed patients. Meanwhile, the antioxidant levels are increased and the oxidative damage product levels are decreased after antidepressant medication. The
pathophysiological relationships between oxidative stress and depression, and the potential benefits of antioxidant supplementation deserve further research.

Some studies have demonstrated that depressed patients’ oxidative product levels in their peripheral blood [3, 4], red blood cells (RBC) [4], mononuclear cells [5], urine [6], cerebrospinal
fluid [7] and postmortem brains [8] were abnormal. Antioxidant system disturbance in peripheral blood has also been reported [9]. Autoimmune responses against neoepitopes
induced by oxidative damage of fatty acid and protein membranes have been reported [10, 11].
Lower glutathione (GSH) levels [12] and a negative relationship between anhedonia severity
and occipital GSH levels [13] were found through magnetic resonance spectroscopy (MRS).

Oxidative stress is defined as a persistent imbalance between oxidation and anti-oxidation, which leads to the damage of cellular macromolecules [14, 15]. The free radicals consist of reactive
oxygen species (ROS) and reactive nitrogen species (RNS). The main ROS includes superoxide anion, hydroxy radical and hydrogen peroxide, and the RNS consists of nitric oxide
(NO), nitrogen dioxide and peroxynitrite. Nitrite is often used as a marker of NO activity. Interestingly, the brain appears to be more susceptible to the ROS/RNS because of the high
content of unsaturated fatty acids, high oxygen consumption per unit weight, high content of key ingredients of lipid peroxidation (LP) and scarcity of antioxidant defence systems [16].
The oxidative products include products of oxidative damage of LP, protein and DNA in depression. As a product of LP, abnormal malondialdehyde (MDA) levels in depression have
been reported [17]. 8-F2-isoprostane (8-iso-PGF2α) is another product of LP [18] that is considered
to be a marker of LP because of its chemical stability [19]. The protein carbonyl (PC), 8-hydroxy-2-deoxyguanosine (8-OHdG) and 8-oxo-7, 8-dihydroguanosine (8-oxoGuo) are
the markers of protein, DNA and RNA oxidative damage, respectively [3, 20, 21]. The oxidative damage to cellular macromolecules changes the structure of original epitopes, which leads to the generation of new epitopes modified (neoepitopes). The antibodies against oxidative neoepitopes
in depression have been found [10, 11, 22–24]. On the other hand, the antioxidant defence systems can be divided into enzymatic and non-enzymatic antioxidants. The nonenzymatic
antioxidants include vitamins C and E, albumin, uric acid, high-density lipoprotein cholesterol (HDL-C), GSH, coenzyme Q10 (CoQ10), ceruloplasmin, zinc, selenium, and so on.
The enzymatic antioxidants include superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), glutathione reductase (GR), paraoxonase 1 (PON1), and so on.

Discussion
The present findings support oxidative stress may be disordered in depressed patients, which is demonstrated by abnormal oxidative stress marker levels. In this meta-analysis, at first we
found in depressed patients: 1) the serum TAC, PON, uric acid, albumin, HDL-C and zinc levels were lower than controls; 2) the serum peroxide, MDA, 8-iso-PGF2α and RBC MDA levels
were higher than controls. To explore the effect of the antidepressant therapy to oxidative stress
markers, we reviewed the studies which had changes. And it came to the conclusions: 1) the serum uric acid, albumin, and vitamin C levels were increased; 2) the serum nitrite, RBC and
serum MDA levels were decreased.

The serum antioxidant levels are significantly lower in depression in our study and previous
reports, including PON, albumin, zinc, uric acid HDL-C, CoQ10 [146] and GSH [4, 38].
Meanwhile, the oxidative damage product levels are significantly higher. The body couldn’t
scavenge the excess free radicals (peroxide), leading to damages of main parts of cellular macromolecules
such as fatty acids, protein, DNA, RNA and mitochondria. The longitudinal antidepressant
therapy can reverse these abnormal oxidative stress parameters. It has proved
these phenomena occur in depression, such as increased levels of MDA, 8-iso-PGF2α, 8-oxoGuo
and 8-OHdG [3, 21]. Oxidative stress plays a crucial role in the pathophysiology of
depression. Some genes may be a potential factor. Lawlor et al (2007) reported the R allele of
PON1Q192R was associated with depression [147]. In addition, poor appetite, psychological
stressors, obesity, metabolic syndrome, sleep disorders, cigarette smoking and unhealthy lifestyle
may also contribute to it [148]. Furthermore, oxidative stress activates the immuneinflammatory
pathways [148]. But some studies supported decrease in albumin, zinc and
HDL-C levels was probably related to increased levels of pro-inflammatory cytokines (such as
interleukin-1 (IL-1) and IL-6) [59, 70–72, 117] during an acute phase response, which illustrated the activated immune-inflammatory pathways also activates the oxidative stress. These two mechanisms influence each other. On the other hand, the oxidative damage to cellular macromolecules changes the structure of original epitopes, which leads to generation of newepitopes modified (neoepitopes). Oxidative neoepitopes reported up to now include the conjugated oleic and azelaic acid, MDA, phosphatidyl inositol (Pi), NO-modified adducts and oxidized low density lipoprotein (oxLDL) [11, 22–24]. Maes et al reported the levels of serum IgG antibody against the oxLDL and IgM antibodies against the conjugated oleic and azelaic acid, MDA, Pi and NO-modified adducts were increased in depression [11, 22–24]. Depleted antioxidant defence in depression suggests that antioxidant supplements may be useful in clinical management. Preliminary evidence has indicated that patients treated with CoQ10 showed improvement in depressive symptoms and decrease in hippocampal oxidative DNA damage [149]. In our analyses, vitamin C and E levels did not differ between depressed patients and controls, but many studies have reported that vitamin C and E supplements could improve depressive moods [150, 151].

Malondialdehyde plasma concentration correlates with declarative and working memory in patients with recurrent depressive disorder

Abstract

Oxidative stress has been implicated in the cognitive decline, especially in memory impairment. The purpose of this study was to determine the concentration of malondialdehyde (MDA) in patients with recurrent depressive disorders (rDD) and to define relationship between plasma levels of MDA and the cognitive performance. The study comprised 46 patients meeting criteria for rDD. Cognitive function assessment was based on: The Trail Making Test , The Stroop Test, Verbal Fluency Test and Auditory-Verbal Learning Test. The severity of depression symptoms was assessed using the Hamilton Depression Rating Scale (HDRS). Statistically significant differences were found in the intensity of depression symptoms, measured by the HDRS on therapy onset versus the examination results after 8 weeks of treatment (P < 0.001). Considering the 8-week pharmacotherapy period, rDD patients presented better outcomes in cognitive function tests. There was no statistically significant correlation between plasma MDA levels, and the age, disease duration, number of previous depressive episodes and the results in HDRS applied on admission and on discharge. Elevated levels of MDA adversely affected the efficiency of visual-spatial and auditory-verbal working memory, short-term declarative memory and the delayed recall declarative memory. 1. Higher concentration of plasma MDA in rDD patients is associated with the severity of depressive symptoms, both at the beginning of antidepressants pharmacotherapy, and after 8 weeks of its duration. 2. Elevated levels of plasma MDA are related to the impairment of visual-spatial and auditory-verbal working memory and short-term and delayed declarative memory.

Antioxidant /Antidepressant-like Effect of Ascorbic acid (Vitamine
C) and Fluoxetine
Another study investigated the influence of ascorbic acid
(which is an antioxidant with antidepressant-like effects in animals)
on both depressive-like behaviour induced by a chronic unpredictable
stress (CUS) paradigm and on serum markers of oxidative
stress and in cerebral cortex and hippocampus of mice [120]. The
CUS-model is an animal model for induced depression-like behaviour
in animals. Depressive-like behaviour induced by CUS was
accompanied by significantly increased lipid peroxidation (cerebral
cortex and hippocampus), decreased catalase (CAT) (cerebral cortex
and hippocampus) and glutathione reductase (GR) (hippocampus)
activities and reduced levels of glutathione (cerebral cortex).
Repeated ascorbic acid as well as fluoxetine administration significantly
reversed CUS-induced depressive-like behaviour as well as
oxidative damage. No alterations were observed in locomotor activity
and glutathione peroxidase (GPx) activity in the same sample.
These findings pointed to a rapid and robust effect of ascorbic acid
in reversing behavioural and biochemical alterations induced in an
animal model [120].  Ascorbic acid treatment, similarly to fluoxetine, reverses depressive-like behavior and brain oxidative damage induced by chronic unpredictable stress.

 

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

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

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

______________________________________

Characterizing the course of suicidal ideation response to ketamine

Characterizing the course of suicidal ideation response to ketamine PDF

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

 

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

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

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Ketamine Consultants Blog

What is Ketamine?

Ketamine, also known as Ketalar, Ketaset, and Ketanest, is a medication that’s currently FDA approved only as an anesthetic but it’s showing great potential as a treatment for severe depression. In fact, numerous Ketamine Clinics have begun to appear throughout the United States to solve this problem. Depressed patients with stubborn symptoms get relief within hours rather than weeks with conventional anti-depressants. Doctors can only prescribe ketamine for depression off-label because studies are relatively new, but experts are saying that ketamine is one of the biggest breakthroughs in severe depression treatment to come along in decades [1].

Ketamine is a powerful pain reliever and a relaxant, but at higher doses it can also induce unconsciousness and disturbances in how a person experiences sight and sound. In high doses, it can produce hallucinations and delusions and its ability to create strong dissociative experiences have made it popular in the club scene where it’s known as “Special K”. An overdose of ketamine can be fatal and it can be addictive if patients don’t follow their doctor’s prescription guidelines. Currently, ketamine is scheduled as a class III drug and it’s created a lot of controversy among experts who disagree about whether it’s safe for doctors to prescribe it as a treatment for chronic depression. Despite the intrigue and the need for additional research to establish its safety and efficacy, ketamine clinics are now offering infusion treatments to patients all over the United States [1][2][8][9].

Effects of Ketamine

As a street drug, ketamine creates a sense of dissociation and can change a person’s sense of hearing and sight, but for patients with severe depression, ketamine relieves mood problems within hours or sometimes moments for about 85% of those treated. While conventional anti-depressants can take several weeks to take effect, studies have shown that ketamine often improves depression symptoms almost immediately. Patients typically feel better within hours [1][2].

Doctors, dentists, and psychiatrists prescribe ketamine to help their patients achieve a variety of different health goals. Doctors often use ketamine in FDA approved situations such as procedures involving cardiac catheterization, orthopedics, skin grafting, or diagnostics involving the eye, ear, nose, and throat. Surgical dentists may also use ketamine as an anesthesia during tooth extractions. After other treatment options have been attempted and failed, doctors may use ketamine to treat certain types of seizures in patients with status epilepticus [2].

Researchers demonstrated in 2014 that ketamine reduced symptoms of post-traumatic stress disorder in 41 patients and there are other exciting possibilities on the horizon in terms of PTSD treatment. Treatment-resistant depression and substance use disorders could both be treated with this drug, though many medical professionals view ketamine treatment for these mental health issues as controversial [2].

Ketamine for Pain Management (CRPS)

Central Sensitization is a process the central nervous system goes through which causes Complex Regional Pain Syndrome (CRPS/RSD) and other types of chronic pain. In central sensitization the number of NMDA receptors increases which amplifies a patients’ experience of pain. Ketamine interferes with NMDA receptors which puts a damper on pain signaling, providing pain relief and a desensitization to pain for patients affected by CRPS [8].

At low doses, ketamine can relieve chronic pain and potentiate the effects of sedatives. Researchers believe that ketamine could provide an alternative to more addictive painkillers like morphine if the FDA approves it for this use [1][8].

Ketamine for Anesthesia

In the 1960’s doctors used ketamine as an anesthetic on the battlefields in Vietnam because administration lends itself well to use in disaster zones; doctors don’t need electricity, an oxygen supply, or even highly trained staff to give patients ketamine. Since that time, the FDA has only approved ketamine for use as an anesthetic in hospitals and medical settings. As an anesthetic, ketamine doesn’t lower the patient’s breathing rate or blood pressure, which makes it safer than other anesthesia options. It’s for this reason that veterinarians use ketamine more than any other type of anesthetic for surgery on animals [1][2].

Ketamine for Depression

Depression is a major issue in the United States and though there are many anti-depressants on the market, about one-third of patients don’t experience any relief from their symptoms using the drugs that are currently available. Ketamine acts on depression by rebalancing a different set of neurotransmitters and receptors (the NMDA/glutamate receptors and GABA receptors) than the old-school Selective Serotonin Reuptake Inhibitors (which function by blocking reabsorption of serotonin). By blocking glutamate receptors in the brain, the majority of patients with ‘Treatment Resistant Depression’ are able to experience relief from their symptoms using ketamine [1].

Even though ketamine has yet to be approved by the FDA for use in treating depression, patients are flocking to ketamine clinics to receive the treatment off-label. It provides fast relief, which is vitally important in cases where patients feel suicidal and for depressed patients who have tried all of the other anti-depressants available with no luck, ketamine offers new hope. Infusion treatments take about 1 hour at a clinic, but the results are long-lasting with most patients returning only once every one to two weeks over a specified period of time. The treatment is expensive, but the results are promising enough that patients are willing to pay out-of-pocket for it [5][8][9].

The FDA hasn’t yet approved ketamine for use as an anti-depressant, but both Esketamine and Rapastinel (developed by Johnson & Johnson and Allergan respectively) have been fast-tracked as breakthrough drugs. The demand for these two medications is projected to grow rapidly in the coming years.  Still, doctors can only prescribe ketamine for depression off-label since ketamine has been FDA approved for use as an anesthetic, not as an anti-depressant. Researchers have cautioned doctors to avoid over-prescribing this drug because the long-term health and well-being of patients could be at risk. Ketamine has a high potential for abuse, after all and experts claim that the evidence does not exist to prove that this drug is safe [1][2][6].

Ketamine as Drugs of Abuse

Ketamine is abused as a recreational drug and it has effects that are similar to Phenylcyclidine (PCP), LSD, dextromethorphan (DXM) and nitrous oxide (laughing gas). Ketamine is a dissociative anesthetic that can alter one’s sense of sight and sound and also produce profound relaxation, hallucinations, and delusions for about an hour. The effects of the drug come on almost immediately. It has been used as a rape drug that can render women unable to speak or to move [1][2].

People who abuse ketamine have developed serious bladder and kidney problems such as ulcerative cystitis, stomach issues, and memory loss. In fact, street users even risk developing depression as a result of addiction and dependence on the drug [2].

How is Ketamine used for depression?

Doctors may prescribe ketamine by itself or in tandem with other anti-depressants [3]. Many experts on depression recommend that ketamine only be used as a short-term depression treatment option while other anti-depressants are taking effect. Though there are convenient ketamine nasal sprays in research and development by Johnson & Johnson, the high-potential for abuse of this drug has made many doctors and psychiatrists wary of using this drug to treat depression long-term. Further, some medical organizations are concerned that the long-term effects of chronic ketamine use is not well-understood. According to these organizations, more research is needed to establish the safety of this drug [1][2][6].

Promising Remedy for ‘Treatment Resistant Depressions’

Thomas Insel, the director of the National Institute of Mental Health says, “Recent data suggest that ketamine, given intravenously might be the most important breakthrough anti-depressant in decades.” Conventional anti-depressants aren’t able to help about one-third of patients with major depression, but new ketamine drugs such as esketamine (in development by Johnson and Johnson) may offer new hope. Infusion therapies available through ketamine clinics across the United States report a high success rate of 60% to 70% treating Treatment Resistant Depression as well as Major Depression with risk of suicide [1][3][5][6].

Fast-Tracked by FDA

Two drugs, Johnson & Johnson’s Esketamine and Allergan’s Rapastinel, were both upgraded to ‘fast-track’ status by the FDA in 2016 due to their importance and promise in treating treatment resistant depression.

Depression is the leading cause of disability in the world and currently, 12% of Americans (about 29 million people) are taking anti-depressant medications. The suicide rate is higher now than it has been in over 30 years. And about one-third of depressed Americans don’t experience relief taking conventional anti-depressants. In the interest of capitalizing on the market value of depression, which is projected to almost double by the year 2024, the FDA will review the use of these new ketamine-based depression drugs in 2018 and 2019, allowing Johnson & Johnson and Allergan to go through an abbreviated version of the normally lengthy FDA approval process for new drug therapies [5][6].

Experimental Trials

Drug trials have shown that 60% to 70% of patients with Treatment-Resistant Depression have been responsive to ketamine. Esketamine, a nasal spray developed by Johnson & Johnson, is in Phase III clinical trials right now. They are expected to receive FDA approval later in 2018, and once that happens, it will open doors for administering ketamine outside a clinic setting.

Rapastinel, which was developed by Allergan, is out of Phase III and awaiting FDA approval. The drug can be administered within 30 seconds intravenously and Allergan is working to develop an oral version of the drug as well [2][3][5].

How Ketamine Therapy Works

Ketamine therapy is usually performed at a ketamine clinic. Patients receive an intravenous infusion of the drug with relief from depression symptoms that can last for several weeks.

Ketamine Infusion or Intravenous Therapy (Infusion Process)

Ketamine can be injected directly into muscle tissue or it can be given intravenously. Researchers for Johnson & Johnson have also recently developed new treatment protocol called Esketamine that’s awaiting FDA approval. Using Esketamine, patients will be able to self-administer the drug as a nasal mist [2][3].

Patients must receive a referral from a doctor to go to a ketamine clinic. There, patients can receive an intravenous infusion of ketamine. On the first visit, a doctor will assess the patient before hooking the patient up to a ketamine IV. Patients then experience a variety of sensations during the infusion and for up to 2 hours following the infusion. Many patients report feeling a sense of deep relaxation and the ability to reflect on past traumas and anxieties calmly [7][9].

How does it work?

Researchers have demonstrated that a deficiency in certain vital connections between certain neurons in the brain may cause depression. Ketamine works as an NMDA receptor antagonist (NMDA is a glutamate receptor also known as N-methyl-d-aspartate) and an AMPA receptor stimulator. As such, ketamine stimulates the development of new receptors and synapses in the brain which helps patients regulate their mood, sleep better, and experience better focus [2][8].

Ketamine works by interfering with and rebalancing the glutamatergic system (glutamate and GABA) to stimulate new synaptic connections, better memory, and brain plasticity [8]. During ketamine infusions, patients may feel capable of exploring traumatic memories more calmly to reframe the past or they may feel a pleasant sensation of relaxation or floating [7]. Effects from an infusion can last for up to a week or two.

Intranasal ketamine formulas work by binding to a receptor called N-methyl-d-aspartate. In the brain, ketamine blocks the neurotransmitter glutamate which causes communication between the conscious mind and other parts of the mind (such as mood centers) to be blocked. In low doses, it relieves depression, but in higher doses, it can cause patients to feel an uncomfortable sense of dissociation from the body similar to a near death experience [2][3][4].

While most anti-depressant medications must build up in the body over the course of several weeks in order to have an effect, ketamine’s mood-altering benefits happen as the drug leaves the body. Researchers don’t know why this is the case, or even exactly how the drug achieves its strong anti-depressant effects but the fact is, ketamine works quickly to relieve depression symptoms in 85% of patients who are resistant to other forms of therapy [1]. Standard anti-depressants target the neurotransmitters serotonin, norepinephrine, and dopamine, but ketamine is different. Ketamine blocks glutamate and stimulates synaptic plasticity or the ability of the brain to change and grow [5].

Doctors don’t fully understand how ketamine works or the potential effects that patients may experience from taking tiny doses of this drug over and over again. What is known is that recreational users can suffer ulcerative cystitis or cognitive issues as a result of prolonged use [5].

Ketamine Infusion Dose/Dosage

Researchers are working to find the perfect ketamine dose for depression patients. The risk of overdosing on this drug is high for the recreational user because there is only a slight difference between a dosage that leads to desirable effects and one that can cause a lethal overdose. The goal for researchers is to find an exact dosage that’s high enough to get rid of symptoms of depression but low enough to prevent patients from experiencing hearing and sight disturbances as well as the other negative effects from the drug [1][2][9]. Ketamine produces only temporary effects on severe depression. Patients must continue to return to the clinic for infusions every few weeks to keep their depression symptoms in check [5].

Ketamine therapy cost? Is ketamine therapy covered by insurance?

Ketamine therapy is rarely covered by insurance and it’s pricey. Patients typically pay between $400 and $800 per infusion. On a bi-weekly schedule for ketamine treatments, patients can expect to pay about $15,000 out-of-pocket annually [5].

Ketamine Infusion Side-Effects

Ketamine use can cause a variety of side effects including:

  • Extreme fatigue or exhaustion
  • Nervousness or restlessness
  • Sweating
  • Amnesia
  • Puffy or swollen eyelids, lips, or tongue
  • Hives, itching, or rash
  • Delusions
  • Difficulty thinking or learning
  • Loss of appetite
  • Nausea
  • Fast heartbeat, slow heartbeat, irregular heartbeat
  • Dizziness, fainting
  • Difficulty swallowing
  • Confusion
  • Convulsions
  • Difficulty breathing
  • Chest pain or discomfort
  • Blurry vision
  • Inability to control eye movement
  • Slurred speech
  • Difficulty urinating, frequent urination, cloudy or bloody urine
  • Paleness, bluish lips, skin, or fingernails
  • Increased pressure in the brain and the eyes [1][2]
  • What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |
    What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |

    Ketamine for Depression: Does it work?

    What is Ketamine?

    Ketamine, also known as Ketalar, Ketaset, and Ketanest, is a medication that’s currently FDA approved only as an anesthetic but it’s showing great potential as a treatment for severe depression. In fact, numerous Ketamine Clinics have begun to appear throughout the United States to solve this problem. Depressed patients with stubborn symptoms get relief within hours rather than weeks with conventional anti-depressants. Doctors can only prescribe ketamine for depression off-label because studies are relatively new, but experts are saying that ketamine is one of the biggest breakthroughs in severe depression treatment to come along in decades [1].

    Ketamine is a powerful pain reliever and a relaxant, but at higher doses it can also induce unconsciousness and disturbances in how a person experiences sight and sound. In high doses, it can produce hallucinations and delusions and its ability to create strong dissociative experiences have made it popular in the club scene where it’s known as “Special K”. An overdose of ketamine can be fatal and it can be addictive if patients don’t follow their doctor’s prescription guidelines. Currently, ketamine is scheduled as a class III drug and it’s created a lot of controversy among experts who disagree about whether it’s safe for doctors to prescribe it as a treatment for chronic depression. Despite the intrigue and the need for additional research to establish its safety and efficacy, ketamine clinics are now offering infusion treatments to patients all over the United States [1][2][8][9].

    Effects of Ketamine

    As a street drug, ketamine creates a sense of dissociation and can change a person’s sense of hearing and sight, but for patients with severe depression, ketamine relieves mood problems within hours or sometimes moments for about 85% of those treated. While conventional anti-depressants can take several weeks to take effect, studies have shown that ketamine often improves depression symptoms almost immediately. Patients typically feel better within hours [1][2].

    Doctors, dentists, and psychiatrists prescribe ketamine to help their patients achieve a variety of different health goals. Doctors often use ketamine in FDA approved situations such as procedures involving cardiac catheterization, orthopedics, skin grafting, or diagnostics involving the eye, ear, nose, and throat. Surgical dentists may also use ketamine as an anesthesia during tooth extractions. After other treatment options have been attempted and failed, doctors may use ketamine to treat certain types of seizures in patients with status epilepticus [2].

    Researchers demonstrated in 2014 that ketamine reduced symptoms of post-traumatic stress disorder in 41 patients and there are other exciting possibilities on the horizon in terms of PTSD treatment. Treatment-resistant depression and substance use disorders could both be treated with this drug, though many medical professionals view ketamine treatment for these mental health issues as controversial [2].

    Ketamine for Pain Management (CRPS)

    Central Sensitization is a process the central nervous system goes through which causes Complex Regional Pain Syndrome (CRPS/RSD) and other types of chronic pain. In central sensitization the number of NMDA receptors increases which amplifies a patients’ experience of pain. Ketamine interferes with NMDA receptors which puts a damper on pain signaling, providing pain relief and a desensitization to pain for patients affected by CRPS [8].

    At low doses, ketamine can relieve chronic pain and potentiate the effects of sedatives. Researchers believe that ketamine could provide an alternative to more addictive painkillers like morphine if the FDA approves it for this use [1][8].

    Ketamine for Anesthesia

    In the 1960’s doctors used ketamine as an anesthetic on the battlefields in Vietnam because administration lends itself well to use in disaster zones; doctors don’t need electricity, an oxygen supply, or even highly trained staff to give patients ketamine. Since that time, the FDA has only approved ketamine for use as an anesthetic in hospitals and medical settings. As an anesthetic, ketamine doesn’t lower the patient’s breathing rate or blood pressure, which makes it safer than other anesthesia options. It’s for this reason that veterinarians use ketamine more than any other type of anesthetic for surgery on animals [1][2].

    Ketamine for Depression

    Depression is a major issue in the United States and though there are many anti-depressants on the market, about one-third of patients don’t experience any relief from their symptoms using the drugs that are currently available. Ketamine acts on depression by rebalancing a different set of neurotransmitters and receptors (the NMDA/glutamate receptors and GABA receptors) than the old-school Selective Serotonin Reuptake Inhibitors (which function by blocking reabsorption of serotonin). By blocking glutamate receptors in the brain, the majority of patients with ‘Treatment Resistant Depression’ are able to experience relief from their symptoms using ketamine [1].

    Even though ketamine has yet to be approved by the FDA for use in treating depression, patients are flocking to ketamine clinics to receive the treatment off-label. It provides fast relief, which is vitally important in cases where patients feel suicidal and for depressed patients who have tried all of the other anti-depressants available with no luck, ketamine offers new hope. Infusion treatments take about 1 hour at a clinic, but the results are long-lasting with most patients returning only once every one to two weeks over a specified period of time. The treatment is expensive, but the results are promising enough that patients are willing to pay out-of-pocket for it [5][8][9].

    The FDA hasn’t yet approved ketamine for use as an anti-depressant, but both Esketamine and Rapastinel (developed by Johnson & Johnson and Allergan respectively) have been fast-tracked as breakthrough drugs. The demand for these two medications is projected to grow rapidly in the coming years.  Still, doctors can only prescribe ketamine for depression off-label since ketamine has been FDA approved for use as an anesthetic, not as an anti-depressant. Researchers have cautioned doctors to avoid over-prescribing this drug because the long-term health and well-being of patients could be at risk. Ketamine has a high potential for abuse, after all and experts claim that the evidence does not exist to prove that this drug is safe [1][2][6].

    Ketamine as Drugs of Abuse

    Ketamine is abused as a recreational drug and it has effects that are similar to Phenylcyclidine (PCP), LSD, dextromethorphan (DXM) and nitrous oxide (laughing gas). Ketamine is a dissociative anesthetic that can alter one’s sense of sight and sound and also produce profound relaxation, hallucinations, and delusions for about an hour. The effects of the drug come on almost immediately. It has been used as a rape drug that can render women unable to speak or to move [1][2].

    People who abuse ketamine have developed serious bladder and kidney problems such as ulcerative cystitis, stomach issues, and memory loss. In fact, street users even risk developing depression as a result of addiction and dependence on the drug [2].

    How is Ketamine used for depression?

    Doctors may prescribe ketamine by itself or in tandem with other anti-depressants [3]. Many experts on depression recommend that ketamine only be used as a short-term depression treatment option while other anti-depressants are taking effect. Though there are convenient ketamine nasal sprays in research and development by Johnson & Johnson, the high-potential for abuse of this drug has made many doctors and psychiatrists wary of using this drug to treat depression long-term. Further, some medical organizations are concerned that the long-term effects of chronic ketamine use is not well-understood. According to these organizations, more research is needed to establish the safety of this drug [1][2][6].

    Promising Remedy for ‘Treatment Resistant Depressions’

    Thomas Insel, the director of the National Institute of Mental Health says, “Recent data suggest that ketamine, given intravenously might be the most important breakthrough anti-depressant in decades.” Conventional anti-depressants aren’t able to help about one-third of patients with major depression, but new ketamine drugs such as esketamine (in development by Johnson and Johnson) may offer new hope. Infusion therapies available through ketamine clinics across the United States report a high success rate of 60% to 70% treating Treatment Resistant Depression as well as Major Depression with risk of suicide [1][3][5][6].

    Fast-Tracked by FDA

    Two drugs, Johnson & Johnson’s Esketamine and Allergan’s Rapastinel, were both upgraded to ‘fast-track’ status by the FDA in 2016 due to their importance and promise in treating treatment resistant depression.

    Depression is the leading cause of disability in the world and currently, 12% of Americans (about 29 million people) are taking anti-depressant medications. The suicide rate is higher now than it has been in over 30 years. And about one-third of depressed Americans don’t experience relief taking conventional anti-depressants. In the interest of capitalizing on the market value of depression, which is projected to almost double by the year 2024, the FDA will review the use of these new ketamine-based depression drugs in 2018 and 2019, allowing Johnson & Johnson and Allergan to go through an abbreviated version of the normally lengthy FDA approval process for new drug therapies [5][6].

    Experimental Trials

    Drug trials have shown that 60% to 70% of patients with Treatment-Resistant Depression have been responsive to ketamine. Esketamine, a nasal spray developed by Johnson & Johnson, is in Phase III clinical trials right now. They are expected to receive FDA approval later in 2018, and once that happens, it will open doors for administering ketamine outside a clinic setting.

    Rapastinel, which was developed by Allergan, is out of Phase III and awaiting FDA approval. The drug can be administered within 30 seconds intravenously and Allergan is working to develop an oral version of the drug as well [2][3][5].

    How Ketamine Therapy Works

    Ketamine therapy is usually performed at a ketamine clinic. Patients receive an intravenous infusion of the drug with relief from depression symptoms that can last for several weeks.

    Ketamine Infusion or Intravenous Therapy (Infusion Process)

    Ketamine can be injected directly into muscle tissue or it can be given intravenously. Researchers for Johnson & Johnson have also recently developed new treatment protocol called Esketamine that’s awaiting FDA approval. Using Esketamine, patients will be able to self-administer the drug as a nasal mist [2][3].

    Patients must receive a referral from a doctor to go to a ketamine clinic. There, patients can receive an intravenous infusion of ketamine. On the first visit, a doctor will assess the patient before hooking the patient up to a ketamine IV. Patients then experience a variety of sensations during the infusion and for up to 2 hours following the infusion. Many patients report feeling a sense of deep relaxation and the ability to reflect on past traumas and anxieties calmly [7][9].

    How does it work?

    Researchers have demonstrated that a deficiency in certain vital connections between certain neurons in the brain may cause depression. Ketamine works as an NMDA receptor antagonist (NMDA is a glutamate receptor also known as N-methyl-d-aspartate) and an AMPA receptor stimulator. As such, ketamine stimulates the development of new receptors and synapses in the brain which helps patients regulate their mood, sleep better, and experience better focus [2][8].

    Ketamine works by interfering with and rebalancing the glutamatergic system (glutamate and GABA) to stimulate new synaptic connections, better memory, and brain plasticity [8]. During ketamine infusions, patients may feel capable of exploring traumatic memories more calmly to reframe the past or they may feel a pleasant sensation of relaxation or floating [7]. Effects from an infusion can last for up to a week or two.

    Intranasal ketamine formulas work by binding to a receptor called N-methyl-d-aspartate. In the brain, ketamine blocks the neurotransmitter glutamate which causes communication between the conscious mind and other parts of the mind (such as mood centers) to be blocked. In low doses, it relieves depression, but in higher doses, it can cause patients to feel an uncomfortable sense of dissociation from the body similar to a near death experience [2][3][4].

    While most anti-depressant medications must build up in the body over the course of several weeks in order to have an effect, ketamine’s mood-altering benefits happen as the drug leaves the body. Researchers don’t know why this is the case, or even exactly how the drug achieves its strong anti-depressant effects but the fact is, ketamine works quickly to relieve depression symptoms in 85% of patients who are resistant to other forms of therapy [1]. Standard anti-depressants target the neurotransmitters serotonin, norepinephrine, and dopamine, but ketamine is different. Ketamine blocks glutamate and stimulates synaptic plasticity or the ability of the brain to change and grow [5].

    Doctors don’t fully understand how ketamine works or the potential effects that patients may experience from taking tiny doses of this drug over and over again. What is known is that recreational users can suffer ulcerative cystitis or cognitive issues as a result of prolonged use [5].

    Ketamine Infusion Dose/Dosage

    Researchers are working to find the perfect ketamine dose for depression patients. The risk of overdosing on this drug is high for the recreational user because there is only a slight difference between a dosage that leads to desirable effects and one that can cause a lethal overdose. The goal for researchers is to find an exact dosage that’s high enough to get rid of symptoms of depression but low enough to prevent patients from experiencing hearing and sight disturbances as well as the other negative effects from the drug [1][2][9]. Ketamine produces only temporary effects on severe depression. Patients must continue to return to the clinic for infusions every few weeks to keep their depression symptoms in check [5].

    Ketamine therapy cost? Is ketamine therapy covered by insurance?

    Ketamine therapy is rarely covered by insurance and it’s pricey. Patients typically pay between $400 and $800 per infusion. On a bi-weekly schedule for ketamine treatments, patients can expect to pay about $15,000 out-of-pocket annually [5].

    Ketamine Infusion Side-Effects

    Ketamine use can cause a variety of side effects including:

    • Extreme fatigue or exhaustion
    • Nervousness or restlessness
    • Sweating
    • Amnesia
    • Puffy or swollen eyelids, lips, or tongue
    • Hives, itching, or rash
    • Delusions
    • Difficulty thinking or learning
    • Loss of appetite
    • Nausea
    • Fast heartbeat, slow heartbeat, irregular heartbeat
    • Dizziness, fainting
    • Difficulty swallowing
    • Confusion
    • Convulsions
    • Difficulty breathing
    • Chest pain or discomfort
    • Blurry vision
    • Inability to control eye movement
    • Slurred speech
    • Difficulty urinating, frequent urination, cloudy or bloody urine
    • Paleness, bluish lips, skin, or fingernails
    • Increased pressure in the brain and the eyes [1][2]

    Where can you get ketamine therapy?

    Off-label ketamine infusion therapy is an unregulated business that has gotten the attention of both clinicians and medical organizations. There are currently ketamine clinics in a number of cities throughout the United States [10].

    Actify Neurotherapies

    1-888-566-8774

    With locations in 9 different states including:

    • Maryland
    • Pennsylvania
    • Colorado
    • New York
    • New Jersey
    • Florida
    • North Carolina
    • California

    Portland Ketamine Clinic

    503-207-4992

    Ketamine Clinic of West Texas

    432-704-2133

    Northwest Ketamine Clinics

    425-214-1495

    Ketamine Clinics of Alabama

    334-699-8231

    Sierra Ketamine Clinics

    775-276-5454

    Ketamine Clinics of Los Angeles

    424-343-8889

    Is ketamine therapy addictive?

    Patients who use ketamine long-term may develop a tolerance and addiction to the drug over time. In medical settings, ketamine is safe to use because the dosage is carefully calibrated and monitored, but there is a high potential for abuse when patients use ketamine recreationally as  a street drug. If patients don’t follow their doctor’s prescription for ketamine it can have extremely negative mental and physical effects particularly on the brain and bladder [2].

    Ketamine-Based Drugs in Late Stage Trials

    Both Rapastinel and Esketamine are ketamine-based drugs that have been ‘fast-tracked’ by the FDA because the FDA has identified them as “breakthrough drugs” [5].

    Rapastinel

    Allergan developed Rapastinel, a ketamine drug that can be administered in 30 seconds intravenously. It works on the same receptors as ketamine, but it doesn’t produce hallucinations. An oral version of Rapastinel is also in development. The FDA considers Rapastinel to be a “breakthrough drug” which means that Allergan can speed through the lengthy drug approval process and get the drug to market by 2019 [5].

    Esketamine

    The FDA has designated Esketamine a “breakthrough therapy”, which means that the drug developers, a subsidiary of Johnson & Johnson, can speed through the lengthy drug approval process to get the drug on the market more quickly. Esketamine can be administered like a nasal decongestant, which would make it more convenient than intravenous therapy for depression patients. Experts feel that Esketemine would be most appropriately used as an adjunct therapy in combination with other anti-depressant medications, not as a standalone treatment for depression [5][6].

    According to one recent study, when administered in combination with other oral antidepressants, Esketamine reduced patients’ depression symptoms more than oral anti-depressants alone. The anti-depressant effects of using a conventional anti-depressant in conjunction with Esketamine occurred within only about 1 week. When used alone, Esketamine effects seem to last 1 to 7 days in most patients. Esketamine is in Phase 3 testing with the FDA for use as a drug for ‘Treatment Resistant Depression’ and Major Depression with risk of suicide. Johnson & Johnson will file for FDA approval for this drug as a depression treatment in 2018 [3][6].

    Risks of Ketamine Abuse

    Ketamine abuse is a serious problem. It is possible to become addicted to ketamine. Patients may begin to need higher doses of the drug in order to experience the positive effects. An overdose of ketamine can be deadly. The effects of using ketamine chronically over a long period of time have not been established, but recreational drug users who have used ketamine long-term have developed ulcerative cystitis as well as cognitive issues [1][2].

    The Ketamine Controversy

    While ketamine can literally save lives by relieving the symptoms of major, Treatment Resistant Depression, including the risk of suicide, research still has not established the safety of ketamine for long-term use. The lethal dose of ketamine is only slightly higher than the therapeutic dose and its addictive properties mean that it could cause depressed patients more problems than it solves. Ketamine clinics have popped up all over the country to cash in on the high demand for a depression treatment that really works, but the research hasn’t demonstrated that this drug is safe for chronic use. So this is an instance where the buyer needs to beware. The FDA has fast-tracked these drugs because it’s constituents see market potential, but important research still needs to be done on this drug to demonstrate it’s safety and long-term efficacy.

    Resources:

    [1] Collins, S. (2005-2018). What you need to know about ketamine’s effects. Retrieved April 3, 2018 from https://www.webmd.com/depression/features/what-does-ketamine-do-your-brain#1

    [2] Davis, K. (2017). What are the uses of ketamine? Retrieved April 3, 2018 from https://www.medicalnewstoday.com/articles/302663.php
    [3] Pagliarulo, N. (2018). J& J builds case for ketamine-based depression drug. Retrieved April 3, 2018 from https://www.biopharmadive.com/news/jj-builds-case-for-ketamine-based-depression-drug/513866/
    [4] No Author (2007-2018). Special K and X. Retrieved April 3, 2018 from http://goaskalice.columbia.edu/answered-questions/special-k-and-x
    [5] Oaklander, M. (2017). New Hope for Depression. Retrieved April 3, 2018 from http://time.com/4876098/new-hope-for-depression/
    [6] Oberhaus, D. (2017). Ketamine Nasal Spray Will Totally Change the Market for Antidepressant Drugs. Retrieved April 3, 2018 from https://tonic.vice.com/en_us/article/wjxd9b/ketamine-nasal-spray-will-totally-change-the-market-for-antidepressant-drugs
    Source: https://www.depressionalliance.org/ketamine-for-depression/
    _________________________________________

    What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |
    What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |

    Learn How Ketamine Can Treat Post Traumatic Stress Disorder ICD 10

    For decades, ketamine has been used as a medicinal intervention for treating depression, anxiety, mood disorders, and post-traumatic stress disorder (PTSD). While most ketamine advocates recognize its therapeutic potential for treating depression, the many benefits available to those suffering from PTSD are less understood.

    Do you or a loved one suffer from post-traumatic stress disorder? If so, ketamine infusion therapy may be able to help alleviate your symptoms and provide the relief you need. However, public knowledge about medicinal ketamine is lacking. In this article, we go over everything there is to know about ketamine for treating PTSD.

    PTSD 101: What You Need to Know

    Post-traumatic stress disorder has a medical diagnostic code of ICD-10, which is the code used for reimbursing treatment through your insurance provider. PTSD, unlike other mental illnesses, is characterized by its triggering from a single or series of traumatic events. This explains why PTSD is common among military veterans and first responders.

    According to a summary article from Mayo Clinic, PTSD is a mental health condition triggered by a terrifying experience. The sufferer subsequently experiences flashbacks, night terrors, and anxiety attacks that they cannot control as a result of the event. It takes a significant amount of time, therapy, and self-care to overcome the trauma of PTSD.

    There is no known cure for PTSD. However, many experimental medicinal interventions are breaking ground when it comes to finding a cure. For example, the psychoactive drugs MDMA and ketamine have both been studied for their potential to alleviate the negative effects of PTSD.

    Ketamine Infusion Therapy

    Since the early 2000s, ketamine has gained popularity among medical providers for its application in infusion therapies. In recent years, clinics all around the world have embraced the healing power of ketamine by offering ketamine infusion therapy. This unique therapy involves one or more intravenous injections of ketamine under the supervision of an anesthesiologist.

    What Is Ketamine?

    Although ketamine has garnered a reputation as a party drug, its primary value is in its ability to provide fast-acting and potent relief for those with chronic pain issues. Ketamine was first synthesized in the 1960s and was later adopted as an anesthetic in veterinary medicine by the end of the decade. However, use in humans was initially sparse.

    Ketamine is both an analgesic and anesthetic drug, which means its primary quality is to reduce or prevent pain. This makes ketamine highly effective for treating major depressive disorder, chronic back pain, and PTSD.

    Ketamine and PTSD

    What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |
    What is Ketamine | 703-844-0184 | Ketamine therapy for PTSD | IV Ketamine for depression, PTSD, bipolar disorder, and others | Ketamine therapy for depression | 703-844-0184 | Fairfax, Va 22304 |

    Ketamine infusion clinics across the United States are now offering specialty treatments for those suffering from PTSD. For example, the renowned Ketamine Clinics of Los Angeles has treated hundreds of PTSD patients over the years. Led by Dr. Steven Mandel, M.D., the team at Ketamine Clinics of LA has a proven track record of helping relieve the pain of PTSD.

    An increasing amount of scientific research has proven that ketamine is effective in treating PTSD. Most notably, a breakthrough 2014 study in JAMA Psychiatry discovered that a single intravenous subanesthetic dose of ketamine resulted in “significant and rapid reduction in PTSD symptom severity.”

    Over the past few years, many articles and news reports have heralded ketamine as a potential wonder drug for treating PTSD. A recent article published by Medscape discussed how a team of researchers at the Icahn School of Medicine at Mount Sinai in New York City used ketamine to fight depressive symptoms in patients with PTSD and severe depression.

    Is Ketamine Safe for PTSD?

    There is no doubt that ketamine is a novel treatment for many PTSD sufferers. Since it is a relatively new medicinal intervention, there is some skepticism within the medical community regarding whether it is safe for human use. However, many of these doubts have been quelled over the years thanks to numerous studies and experiences that have proven its safety.

    The most compelling evidence suggesting that ketamine infusion is safe in humans comes from a 2014 clinical study. This study managed to safely administer low doses of ketamine to treat neuropathic pain states in adults. Over the two-week monitoring period, the patients exhibited numerous benefits while experiencing only marginal or negligible side effects.

    It should be noted that ketamine is not safe if taken recreationally. Since its inception, ketamine has gained a reputation as a party drug for its ability to induce dissociative states and euphoria. However, ketamine is not safe to use unless administered by a licensed physician. It is possible to overdose on ketamine, and the side effects of using high doses of ketamine can be fatal.

    Ketamine: A PTSD Prevention Tool?

    Interestingly, ketamine has found success as a tool for preventing the onset of PTSD. In one case, a research team gave a family of mice a low dose of ketamine before exposing them to electric shocks. Usually, mice exhibit symptoms of PTSD after being exposed to such a severe stressor. However, the mice that were given ketamine did not exhibit these symptoms at all.

    Typically, traumatized mice freeze up when they are placed back in the cage in which they were shocked. In this case, the mice who were sedated with ketamine did not freeze when placed in the cage or froze for a significantly reduced duration. This led the research team to believe that ketamine may have value in both preventing and treating PTSD in humans.

    Is Ketamine Right for You?

    Ketamine may be an appropriate treatment option for you if you have treatment-resistant PTSD. In other words, you must first be diagnosed with PTSD and have sought the traditional frontline treatments for the condition before considering ketamine infusion therapy.

    We recommend speaking with your doctor about your PTSD symptoms and the appropriate therapies available to you. Usually, SSRIs or benzodiazepine pharmaceutical drugs, in conjunction with cognitive behavioral therapy (CBT) is the first method of treatment. However, if you do not respond well to this treatment option you should consider seeking ketamine therapy.

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

CAll 703-844-0184 for an immediate appointment!

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

email@novahealthrecovery.com

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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

 

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Ketamine in Fairfax | Alexandria |Lyme disease treatment| 703-844-0184 | Dr. Sendi | Alexandria | Virginia Ketamine | www.novahealthrecovery.com|22308

 

Ketamine has been found to be useful in a range of painful conditions and metal health disorders. There is a report, listed below, of Ketamine used for Lyme disease treatment. Seeing the neuropathic nature of Lyme disease infection, Ketamine treatment presents an opportunity to lessen suffering and better one’s pain management:

 ketamine-help-manage-pain-patients-post-treatment-lyme-disease-syndrome

 Can Ketamine Help Lyme disease treatment?

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

Could ketamine help manage pain in patients with post-treatment
Lyme disease syndrome?
Sunday, September 17, 2017
http://danielcameronmd.com/ketamine-help-manage-pain-patients-post-treatment-lyme-diseasesyndrome/
by Daniel J. Cameron, MD, MPH
In the International Medical Case Reports Journal, researchers describe a 31-year-old woman with
PTLDS “whose pain was refractory to treatment options such as radiofrequency ablation, vitamin
infusion therapy, opioid analgesics, and other pharmacotherapies.” [2] Her pain began gradually, 3 years
prior and a short time after being diagnosed and treated for Lyme disease, explains Hanna from the
Florida Spine Institute in Clearwater, Florida. “The patient complained of diffuse body pain (6–7/10),
fatigue, headache, and brain fog (7–8/10).” [2]
The woman’s pain worsened despite treatment, increasing during everyday activity. “Her current
treatment regimen,” according to Hanna and colleagues, “included fentanyl transdermal patches,
clonazepam, oxycodone hydrochloride, and citalopram hydrobromide.” Physical therapy, IV vitamin
infusions, trigger point injections and a radiofrequency ablation procedure did not alleviate her pain.
The authors’ surmised that the woman’s pain may be related to an immune dysfunction brought on by
the infection. Ketamine exhibits anti-inflammatory and immunomodulatory actions, explains Hanna,
which may be useful in the treatment of PTLDS. [2] It is also an anesthetic and has been proven
successful “in placebo-controlled clinical trials for the treatment of depression, suicidal ideations, and
pain.”
The patient was prescribed ketamine off label for pain. “Ketamine has been utilized off-label as an
effective option for treating certain neuropathic pain conditions that currently do not have gold standard
treatment options such as complex regional pain syndrome (CRPS) and fibromyalgia,” states Hanna. [2]
Ketamine was found to effectively lessen the woman’s pain, decreasing it by approximately 71%.
Furthermore, her pain relief was achieved without using increased doses of opioid analgesics. And, in
fact, the patient was able to reduce her fentanyl dosage by 40%, from 125 ?g to 75 ?g, every 48 hours,
explains Hanna. “The patient’s depression and suicidal ideations were also eliminated post-ketamine
infusion.”
Given these findings, Hanna suggests, “Opioid-sparing therapies, such as ketamine, should be used more
frequently for the management of chronic pain.”
The authors did not address the concerns raised by physicians as to whether a persistent Lyme disease
infection or tick-borne co-infection might underlie the illness.

“Central sensitization” has been coined to describe
numerous neuropathic pain conditions resulting from a
nociceptive insult that triggers a prolonged but reversible
increase in the excitability and synaptic efficacy of neurons
in central nociceptive pathways.26 Ketamine is thought to
de-sensitize centrally mediated pain via repeated NMDA
receptor blockade.27 However, it is likely that ketamine acts
via multiple mechanisms to produce analgesia in neuropathic
pain conditions. Neuropathic pain has been associated with
increased glial activation and subsequent release of proinflammatory
cytokines. Interestingly, ketamine produces
pharmacological effects that reduce cell excitotoxicity via
NMDA antagonism and reduce inflammation by suppressing
the hyperactivation of microglia.28 Moreover, ketamine
produces immunomodulatory actions that may also be
uniquely beneficial to conditions that may have an autoimmune
component, such as PTLDS. Thus, ketamine appears
to produce a robust polypharmacological “entourage effect”
that is highly effective in treating neuropathic pain conditions
– which are notoriously difficult to treat with more
conventional analgesic drugs.

Ketamine in Fairfax |Lyme disease treatment| 703-844-0184 | Dr. Sendi | Alexandria | Virginia Ketamine | www.novahealthrecovery.com

Ketamine in Fairfax |Lyme disease treatment| 703-844-0184 | Dr. Sendi | Alexandria | Virginia Ketamine | www.novahealthrecovery.com

Lyme Disease Causes, Diagnosis and Treatment

Lyme disease is a bacterial infection transmitted by ticks. Lyme disease was first recognized in 1975, after researchers investigated why unusually large numbers of children were being diagnosed with juvenile rheumatoid arthritis in Lyme, Conn., and two neighboring towns.

The investigators discovered that most of the affected children lived near wooded areas likely to harbor ticks. They also found that the children’s first symptoms typically started in the summer months coinciding with the height of the tick season.

Several of the patients reported having a peculiar skin rash just before developing arthritis symptoms, and many also recalled being bitten by a tick at the rash site.

Further investigations resulted in the discovery that tiny deer ticks infected with a spiral-shaped bacterium or spirochete (which was later named Borrelia burgdorferi) were responsible for the outbreak of arthritis in Lyme. Ordinary “wood ticks” and “dog ticks” do not carry the infection.

The ticks most commonly infected with B. burgdorferi usually feed and mate on deer during part of their life cycle. The recent growth of the deer population in the northeast and the building of suburban developments in rural areas where deer ticks are commonly found have probably contributed to the increasing number of people with the disease.

The number of reported cases of Lyme disease, as well as the number of geographic areas in which it is found, has been increasing. Lyme disease has been reported in nearly all states in this country, although most cases are concentrated in the coastal northeast, Mid-Atlantic States, Wisconsin, and Minnesota, and northern California. Lyme disease is also found in large areas of Asia and Europe. Recent reports suggest that it is present in South America, too.

In addition to causing arthritis, Lyme disease can also cause heart, brain, and nerve problems.

lyme

How Is Lyme Disease Transmitted?

Lyme disease is transmitted through a bite from a specific type of tick. The animals that most often carry these insects are white-footed field mice, deer, racoons, opossums, skunks, weasels, foxes, shrews, moles, chipmunks, squirrels, and horses. The majority of these ticks have been found in New York, Connecticut, Massachusetts, Maryland, New Jersey, Minnesota, and Wisconsin.

 

What Are the Symptoms of Lyme Disease?

In the early stages of Lyme disease, you may experience flu-like symptoms that can include a stiff neck, chills, fever, swollen lymph nodes, headaches, fatigue, muscle aches, and joint pain. You also may experience a large, expanding skin rash around the area of the tick bite. In more advanced disease, nerve problems and arthritis, especially in the knees, may occur.

Here are some more details:

  • Erythma migrans. Erythema migrans is the telltale rash which occurs in about 70% to 80% of cases and starts as a small red spot that expands over a period of days or weeks, forming a circular, triangular, or oval-shaped rash. Sometimes the rash resembles a bull’s-eye because it appears as a red ring surrounding a central clear area. The rash, which can range in size from that of a dime to the entire width of a person’s back, appears between three days and a few weeks of a tick bite, usually occurring at the site of a bite. As infection spreads, several rashes can appear at different sites on the body.

    Erythema migrans is often accompanied by symptoms such as fever, headache, stiff neck, body aches, and fatigue. These flu-like symptoms may resemble those of common viral infections and usually resolve within days or a few weeks.

  • Arthritis. After several weeks of being infected with Lyme disease, approximately 60% of those people not treated with antibiotics develop recurrent attacks of painful and swollen joints that last a few days to a few months. The arthritis can shift from one joint to another; the knee is most commonly affected and usually one or a few joints are affected at any given time. About 10% to 20% of untreated patients will go on to develop lasting arthritis. The knuckle joints of the hands are only very rarely affected.
  • Neurological symptoms. Lyme disease can also affect the nervous system, causing symptoms such as stiff neck and severe headache (meningitis), temporary paralysis of facial muscles (Bell’s palsy), numbness, pain or weakness in the limbs, or poor coordination. More subtle changes such as memory loss, difficulty with concentration, and a change in mood or sleeping habits have also been associated with Lyme disease. People with these latter symptoms alone usually don’t have Lyme disease as their cause.

    Nervous system abnormalities usually develop several weeks, months, or even years following an untreated infection. These symptoms often last for weeks or months and may recur. These features of Lyme disease usually start to resolve even before antibiotics are started. Patients with neurologic disease usually have a total return to normal function.

  • Heart problems. Fewer than one out of 10 Lyme disease patients develops heart problems, such as an irregular, slow heartbeat, which can be signaled by dizziness or shortness of breath. These symptoms rarely last more than a few days or weeks. Such heart abnormalities generally appear several weeks after infection, and usually begin to resolve even before treatment.
  • Other symptoms. Less commonly, Lyme disease can result in eye inflammation and severe fatigue, although none of these problems is likely to appear without other Lyme disease symptoms being present.

Lyme disease imitates a variety of illnesses and its severity can vary from person to person. If you have been bitten by a tick and live in an area known to have Lyme disease, see your doctor right away so that a proper diagnose can be made and treatment started

How Is Lyme Disease Diagnosed?

Lyme disease may be difficult to diagnose because many of its symptoms mimic those of other disorders. Although a tick bite is an important clue for diagnosis, many patients cannot recall having been bitten by a tick. This is not surprising because the tick is tiny, and a tick bite is usually painless.

The easiest way for a doctor to diagnose Lyme disease is to see the unique bull’s-eye rash. If there is no visible rash (as is the case in about one-fourth of those infected), the doctor might order a blood test three to four weeks after the onset of the suspected infection to look for antibodies against the bacteria. Unfortunately, the Lyme disease bacterium itself is difficult to isolate or culture from body tissues or fluids. These blood tests are:

  • ELISA. This blood test measures the levels of antibodies against the Lyme disease bacteria that are present in the body. Antibodies are molecules or small substances tailor-made by the immune system to lock onto and destroy specific microbial invaders.
  • Western blot. This blood test identifies antibodies directed against a panel of proteins found on the Lyme bacteria. The test is ordered when the ELISA result is either positive or uncertain.

The presence of antibodies, however, does not prove that the bacterium is the cause of a patient’s symptoms. The presence of specific antibodies suggests a prior infection, which may or may not still be active.

Note: In the first few weeks following infection (when the rash first appears), antibody tests are not reliable because a patient’s immune system has not produced enough antibodies to be detected. Antibiotics given to a patient early during infection may also prevent antibodies from reaching detectable levels, even though the Lyme disease bacterium is the cause of the patient’s symptoms.

Other tests. Some patients experiencing nervous system symptoms may also undergo a spinal tap. A spinal tap is a procedure in which spinal fluid is removed from the spinal canal for the purpose of diagnosis in a laboratory. Through this procedure, doctors can detect brain and spinal cord inflammation and can look for antibodies against the Lyme disease bacterium in the spinal fluid.

How Is Lyme Disease Treated?

In its early stages, Lyme disease can be effectively treated with antibiotics. In general, the sooner such therapy is begun following infection, the quicker and more complete the recovery. Antibiotics, such as doxycycline or amoxicillin taken orally for two to four weeks, can speed the healing of the rash and can usually prevent subsequent symptoms such as arthritis or neurological problems. There is no compelling evidence that prolonged antibiotic therapy is more effective than two weeks of therapy. Prolonged antibiotic use may have serious side effects.

Intravenous (IV) antibiotics may be used for more serious cases and for someone whose nervous system has been affected. Lyme disease with arthritis also can be treated with antibiotics. Most patients experience full recovery.

Patients younger than 9 years or pregnant or lactating women with Lyme disease are treated with amoxicillin or penicillin because doxycycline can stain the permanent teeth developing in young children or unborn babies. Patients allergic to penicillin are given erythromycin or related antibiotics.

Doctors prefer to treat Lyme disease patients experiencing heart symptoms with antibiotics such as Rocephin, Claforan, or penicillin given intravenously for about two weeks. If these symptoms persist or are severe enough, patients may also be treated with corticosteroids or given a temporary internal cardiac pacemaker. People with Lyme disease rarely experience long-term heart damage.

Following treatment for Lyme disease, some people still have persistent fatigue and achiness. This general malaise can take months to slowly disappear, although it generally does so spontaneously without the use of additional antibiotic therapy. There is no evidence that the Borrelia infection causes systemic exertion intolerance disease (formerly called chronic fatigue syndrome) or fibromyalgia. Although some patients with Lyme disease may develop these problems, as with other patients who get SEID or fibromyalgia, long-term antibiotics will not hasten recovery.

womawithdoctors

A new, innovative treatment for pain associated with Chronic Lyme Disease is IV Ketamine Infusions. At the Florida Spine Institute, Dr. Ashraf Hanna’s treatment protocols are individually planned depending on the nature of the patient’s pain and responsiveness to initial sessions. Dr. Hanna’s chronic Lyme patients have experienced very successful results with IV Ketamine treatments.

 

How Can I Prevent Getting Lyme Disease?

Fortunately, the cause of Lyme disease is known and the disease can be prevented. Essential to prevention is the avoidance of deer ticks. Although generally only about one percent of all deer ticks are infected with the Lyme disease bacterium, in some areas more than half of them harbor the microbe.

Most people with Lyme disease become infected during the late spring, summer, and early fall when immature ticks are out looking for their meal. Except in warm climates, few people are bitten by deer ticks during winter months.

Deer ticks are most often found in wooded areas and nearby grasslands, and are especially common where the two areas merge, including neighborhood yards where deer occasionally roam. Ticks do not survive long on sunny lawns, they dry out quickly and die.

Try these tips to prevent tick bites:

  • Wear long sleeves and tightly woven clothing that is light in color when walking in wooded areas so the ticks can be seen more easily.
  • Wear your shirt tucked into your pants, and your pants tucked into your socks or boots.
  • Walk in the center of trails through the woods to avoid picking up ticks from overhanging grass and brush.
  • Keep grass trimmed as short as possible.
  • Apply tick repellents with DEET to your clothing, shoes and socks before going out. Another tick repellent called permethrin, designed to be placed on the clothing can be used alone or in combination with DEET. (Although highly effective, these repellents can cause some serious side effects, particularly when high concentrations are used repeatedly on the skin. Infants and children may be especially at risk for adverse reactions.)
  • Check yourself, your family, and your pets routinely for ticks, especially after a trip outdoors.
  • Shower and shampoo your hair if you think you may have been exposed to ticks.
  • Check your clothes for ticks and wash them immediately in order to remove any ticks.

If an infected tick bites, it will not transmit the infection until it has had the opportunity to have its blood meal. This takes time, thus there is value in inspecting your body after outdoor activities in areas where Lyme disease is known to occur. Newly attached ticks can be easily removed before they transmit the infection.

Pregnant women should be especially careful to avoid ticks in Lyme disease areas because the infection can be transferred to the unborn child. Such a prenatal infection can make the woman more likely to miscarry.

Preventative antibiotics are not generally used following all tick bites, but may be used in some special circumstances; a recent study showed that such preventive use of antibiotics is very effective.

If you are bitten by a tick, the best way to remove it is by taking the following steps:

  • Tug gently but firmly with blunt tweezers near the “head” of the tick until it releases its hold on the skin
  • To lessen the chance of contact with the bacterium, try not to crush the tick’s body or handle the tick with bare fingers
  • Swab the bite area thoroughly with an antiseptic to prevent infection
  • DO NOT use kerosene, Vaseline, fingernail polish, or a cigarette butt
  • DO NOT squeeze the tick’s body with your fingers or tweezers.

 

Is There a Vaccine for Lyme Disease?

In 1998, the FDA approved a vaccine for Lyme disease called LYMErix. Although some people reported getting sick from the vaccine, the FDA found no evidence that it was dangerous. However, in February 2002, the makers of the vaccine pulled it off the market due to poor sales. Currently, there is no available vaccine on the market for Lyme disease.

What Is the Outlook for People With Lyme Disease?

Most people with Lyme disease respond well to antibiotic therapy and recover fully. Some people may have persistent symptoms or symptoms that recur, making further antibiotic treatment necessary. If left untreated, Lyme disease can cause permanent damage to the heart, nervous system, and joints.

A bout with Lyme disease and successful treatment are no guarantee that the illness will be prevented in the future. The disease can strike more than once in the same individual if he or she is bitten by another tick and re-infected with the Lyme disease bacterium. The antibody test usually remains positive for months to many years after an infection. The presence of antibodies in the blood is not sufficient reason for continued or re-treatment with antibiotics.

Reference

SOURCES:
Centers for Disease Control and Prevention (CDC).
American College of Rheumatology.
National Institute of Allergy and Infectious Diseases.