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Recent research has shown that ketamine has considerable promise for treating a wide range of treatment-refractory neuropsychiatric disorders, including obsessive compulsive disorder (OCD), post-traumatic stress disorder (PTSD), bipolar disorder, suicide ideation, addiction and, most notably, treatment-resistant major depressive disorder (MDD). Although this research has taken place almost exclusively within the past two decades, evidence of ketamine’s neuropsychiatric effects appeared long before this. For example, ketamine was used throughout the 1970s in Mexico as part of psychedelic therapy sessions that combined traditional healing practices with psychoanalytic techniques.

In 2000, researchers found that ketamine had strong, fast-acting, and long-term effects in depression. In a randomized, placebo-controlled, crossover design study, patients with depression received 0.5 mg/kg of ketamine or saline on the first day of testing. Treatments were switched 1 week later. Researchers found that the antidepressant effects of ketamine began within 4 hours, peaked at 72 hours, and lasted for 1 to 2 weeks thereafter.1 In a 2006 study, this finding was replicated in an independent group of 18 patients with major depressive disorder who were resistant to other treatments. Compared with participants who received placebo, those who received ketamine showed significant improvement in symptoms within 110 minutes, with 35% maintaining significant response for at least 1 week.

Many of today’s depression treatments are monoaminergic-based, including monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin-norepinephrine reuptake inhibitors. These treatments have been proven effective for a large number of patients. However, a significant subset of patients with major depressive disorder do not respond to these agents. Despite its undisputed value to the field, the monoamine hypothesis of depression cannot fully explain the heterogeneity of MDD. In the 1990s, animal models began to implicate glutamate – one of the major excitatory neurotransmitters in the mammalian central nervous system (CNS) – as well as its ionotropic NMDA receptor in the etiology and treatment of mood disorders .

Existing antidepressant treatments [MAOIs, TCAs, SSRIs, and serotonin-norepinephrine reuptake inhibitors (SNRIs)] are monoaminergic-based treatments. Although they have been in use for decades and have helped many patients, a significant subset of MDD patients showed little to no therapeutic benefit in response to these agents. For instance, the NIMH-funded, communitybased Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study of >4000 MDD patients found that, even after four unique medication trials, augmentation, or switch, 33% of the patients did not respond to standard monoaminergic-based treatments .

In 2000, Berman and colleagues discovered that ketamine exerted rapid, robust, and relatively sustained antidepressant effects in depressed patients . Using a randomized, placebo-controlled, crossover design, each patient received an i.v. infusion of 0.5 mg/kg of either ketamine or saline on the first test day. On the following test day, which took place at least 1 week later, treatments were switched. The authors found that ketamine exerted antidepressant effects that began within 4 h of the infusion, peaked at 72 h, and persisted for 1–2 weeks post-infusion. .Ketamine has also been shown to have distinct and independent antisuicidal and anti-anhedonic effects in patients with mood disorders .

Another limitation of currently available antidepressants is that their clinical effects take more time to reach their full therapeutic potential (for instance, the mean onset for paroxetine is 13 days). This is a substantial disadvantage during an acute depressive crisis. Furthermore, even when these agents do alleviate depressive symptoms, evidence regarding their ability to successfully reduce suicide ideation and behavior remains inconclusive . In contrast, a single dose (0.5 mg/kg) of i.v. ketamine exerts rapid and profound antidepressant effects within hours to days of administration . Ketamine also rapidly reduces suicidel ideation, an effect that appears to occur independently of its antidepressant properties . Ketamine has dose-dependent neuropsychological effects even at subanesthetic doses, with antidepressant properties peaking at 0.5–1.0 mg/kg.

Ketamine’s pan-therapeutic effects also include alleviating fatigue and anhedonia as well as improving sleep measures such as circadian rhythm and slow-wave activity in MDD patients .

The positive effects of Ketamine has led to research into other rapidly acting antisdepressants, including nasal ketamine. Lapidus and colleagues demonstrated that intranasal ketamine had antidepressant effects and led to sufficiently high ketamine plasma concentrations. We use a compounded intranasal ketamine miuxture in our office at NOVA Health Recovery. There is also an FDA approved version more recently, which has only the S-Ketamine in it . There are heavy restrictions and high costs to the FDA approved version, yet efficacy may not be any better.

Noitrois Oxide also has antidepressant effects. Like ketamine, it exhibits NMDA receptor antagonism, has partial agonism for mu, kappa, and delta opioid receptors, inhibits AMPA, kainite, and gamma-aminobutyric acid receptors A and C (GABAA, GABAC), affects serotonin-3 receptors (5-HT3), and releases dopamine . In a double-blind, placebo-controlled, crossover trial, depressive symptoms improved for participants receiving nitrous oxide within 2 h compared with those receiving placebo, an effect that remained significant at 1 day post-treatment. Phase I and II trials are ongoing to determine optimal dose, safety, and efficacy.

Sarcosine also has antidepressant effects. t, sarcosine (also known as N-methylglycine), is an amino acid that functions as a glycine transporter-1 inhibitor and a 6- week, double-blind, randomized, citalopram-controlled trial in 20 MDD patients found that sarcosine possessed superior antidepressant properties compared with citalopram after 2 weeks . Notably, and in contrast to ketamine, sarcosine did not result in rapid-acting effects on the timescale of several days. Sarcosine has co-agonistic properties at the NMDA receptor and is an agonist at the inhibitory glycine receptor. It also exhibits NMDA-enhancing properties, suggesting that AMPA-receptor-mediated or other downstream mechanisms might elicit antidepressant effects. NMDA receptor downregulation might also play a part .

Suboxone (Buprenorphine) also has antidepressant effects as well. Intrigued by the potential of nonaminergic antidepressant mechanisms, researchers have begun to re-evaluate the role of endogenous opioids in depression. For instance, buprenorphine (BUP), a drug currently used to treat opioid addiction and pain disorders, is being explored as a treatment for MDD. The compound has a wide variety of actions throughout the brain, including partial agonism at the mu opioid receptor and antagonism at the kappa and delta opioid receptors ; these are connected to intracellular signaling cascades that potentially mediate antidepressant effects Several open-label studies of BUP in MDD have shown promising preliminary results, and a double-blind, randomized, placebo-controlled trial examining the effect of low-dose BUP on suicidal ideation similarly yielded positive results .

NOVA Health Recovery has used buprenorphine succesfully in the treatment of depression.

Ketamine and Future Depression Treatments

1. Kraus C, Wasserman D, Henter ID, Acevedo-Diaz E, Kadriu B, Zarate CA Jr. The influence of ketamine on drug discovery in depression [published online August 2, 2019]. Drug Discov Today. doi: 10.1016/j.drudis.2019.07.007

2. Zarate CA Jr, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depressionArch Gen Psychiatry. 2006;63(8):856-64.

3. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trialBiol Psychiatry. 2015;78(1):10-18.

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KETAMINE For Obsessive-Compulsive Disorder | Depression | 703-844-0184 | FAIRFAX, VA | LOUDON, VA| LORTON, VA | |Ketamine For Obsessive Compulsive Disorder| 22308 |22304

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

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Randomized Controlled Crossover Trial of Ketamine in
Obsessive-Compulsive Disorder: Proof-of-Concept

Ketamine for Obsessive-compulsive disorder  <ARTICLE

Ketamine has effectiveness on the short run when it comes to treating Obsessive-compulsive disorders:

Serotonin reuptake inhibitors (SRIs), the first-line pharmacological treatment for obsessive-compulsive disorder (OCD), have two
limitations: incomplete symptom relief and 2–3 months lag time before clinically meaningful improvement. New medications with faster
onset are needed. As converging evidence suggests a role for the glutamate system in the pathophysiology of OCD, we tested whether a
single dose of ketamine, a non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, could achieve rapid antiobsessional
effects. In a randomized, double-blind, placebo-controlled, crossover design, drug-free OCD adults (n ¼ 15) with near-constant
obsessions received two 40-min intravenous infusions, one of saline and one of ketamine (0.5 mg/kg), spaced at least 1-week
apart. The OCD visual analog scale (OCD-VAS) and the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) were used to assess OCD
symptoms. Unexpectedly, ketamine’s effects within the crossover design showed significant (po0.005) carryover effects (ie, lasting
longer than 1 week). As a result, only the first-phase data were used in additional analyses. Specifically, those receiving ketamine (n ¼ 8)
reported significant improvement in obsessions (measured by OCD-VAS) during the infusion compared with subjects receiving placebo
(n ¼ 7). One-week post-infusion, 50% of those receiving ketamine (n ¼ 8) met criteria for treatment response (X35% Y-BOCS
reduction) vs 0% of those receiving placebo (n ¼ 7). Rapid anti-OCD effects from a single intravenous dose of ketamine can persist for at
least 1 week in some OCD patients with constant intrusive thoughts. This is the first randomized, controlled trial to demonstrate that a
drug affecting glutamate neurotransmission can reduce OCD symptoms without the presence of an SRI and is consistent with a
glutamatergic hypothesis of OCD.

 

Ketamine is a noncompetitive antagonist of the NMDA
receptor (a type of glutamate receptor). Studies in patients
with unipolar and bipolar depression have found that a
single intravenous infusion of ketamine can have antidepressant
effects within 40 min of starting the infusion.
These effects persist for 3–18 days, long after the drug has
cleared the patient’s system (Berman et al, 2000;
Diazgranados et al, 2010a, b; Murrough et al, 2012; Valentine
et al, 2011; Zarate et al, 2006, 2012a). We treated an
unmedicated individual with OCD with ketamine (0.5 mg/kg
IV over 40 min) and found rapid anti-obsessional effects that
returned to baseline by 1-week post-infusion (Rodriguez
et al, 2011). Bloch et al (2012) conducted an open ketamine
trial in 10 subjects with OCD and found modest but
statistically significant improvement in OCD symptoms
over days 1–3 following ketamine infusion compared with
baseline; however, most subjects in this study were taking
multiple other medications at the time of infusion.

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

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

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

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

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

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

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

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

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

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

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

Intravenous Ketamine for Adolescents – PDF

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Traditional antidepressants may take weeks to work on individuals. There have been associations with increased suicidality in some studies. The need for a more rapidly acting antidepressant is important. The study below investigated the antidepressant effect of Ketamine by looking through an FDA database and observing associations of pain and depression reduction with the use of Ketamine. They were clearly present. Of note, minocycline and Diclofenac also seemed to be associated with improved depression parameters.

Ketamine provides both pain relief and anti-depression effects in refractory patients, who by definition, have failed multiple therapies.   ::

 

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Ketamine for Pain Management, Treatment of Depression << Article Link

Article below:

Ketamine may alleviate depression, pain, and adverse effects associated with opioid treatment, and may thus represent an attractive adjunct therapy for pain management, according to a novel population analysis recently published in Scientific Reports.1

Nearly half of all patients with depression taking conventional antidepressants discontinue their treatment prematurely.2 Researchers have sought alternatives to standard antidepressants, for which therapeutic effects are delayed by 2 to 10 weeks.3

Ketamine, an N-methyl-D-aspartate antagonist, was shown to provide acute benefits for treatment-resistant depression, bipolar depression, and major depressive disorder with suicidal ideation, when administered intravenously, however, those studies were conducted on limited samples (20 to 57 participants).4-7

The history of ketamine as an illicit drug favored for its hallucinogenic effects presents ethical obstacles to its use in large clinical trials. Researchers from the University of California San Diego in La Jolla, therefore employed an Inverse-Frequency Analysis approach to investigate whether ketamine, when administered in addition to other therapeutics, has antidepressant properties.

The team applied the inverse frequency analysis method, which looks for negative statistical patterns in the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) post-marketing database of more than 8 million patient records. They observed reductions in depression and pain in patients receiving ketamine, as indicated by negative log odds ratio (logOR) values (logOR, -0.67 ± 0.034 and logOR, -0.41 ± 0.019, respectively). “The data we analyzed are indirect and skewed by cases of bad or lethal adverse effects. Nevertheless the statistics were sufficient to notice the trends,” explained study co-author, Ruben Abagyan, PhD, in an interview with Clinical Pain Advisor.

According to Dr Abagyan, a study recently published by a British team indicates that ketamine might be effective in nearly 40% of patients with severe, treatment-resistant depression, results that are concordant with those from the current study.8

The IFA method was also used to evaluate ketamine efficacy and associated side effects reported in the FAERS database. The investigators found significant reductions in a number of side effects associated with opioid therapies, including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) compared with other drug combinations used for pain management.

The authors concluded that their findings are in line with those from smaller studies, indicating beneficial effects for ketamine as a monotherapy or adjunctive therapy for depression, particularly treatment-resistant depression, with particular indication for patients with suicide ideation, because of its rapid onset of action. “The results should serve as a motivation to conduct a proper clinical trial for the rapid onset treatment of severe depression,” Dr Abagyan noted.

The novel analysis employed in this study may help investigate off-label indications for other drugs. “Ideally the method we proposed should be applied to the actual clinical data rather than the somewhat biased set of un-normalized FAERS reports,” Dr Abagyan added. “The method [can be used] to observe unexpected effects of a treatment by looking at the reduction of the baseline of this effect upon treatment. It can be applied to any effect that is being recorded including cancer, viral diseases mortality, longevity.” he concluded.

 

References

  1. Cohen IV, Makunts T, Atayee R, Abagyan R. Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indicationsSci Rep 2017;7:1450.
  2. Sansone RA, Sansone LA. Antidepressant adherence: are patients taking their medications?. Innov Clin Neurosci. 2012;9(5-6):41-46.
  3. Frazer A, Benmansour S. Mol Psychiatry. Delayed pharmacological effects of antidepressantsMol Psychiatry 2002;7:S23-8.
  4. Price RB, Iosifescu DV, Murrough JW,  et al. Effects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant depressionDepress Anxiety 2014;31:335-343.
  5. DiazGranados N, Ibrahim LA, Brutsche NE, et al. Rapid resolution of suicidal ideation after a single infusion of an N-methyl-D-aspartate antagonist in patients with treatment-resistant major depressive disorderJ Clin Psychiatry 2010;71:1605-1611.
  6. Alberich S, Martínez-Cengotitabengoa M, López P,et al. Efficacy and safety of ketamine in bipolar depression: A systematic reviewRev Psiquiatr Salud Ment 2017;10:104-112.
  7. Larkin, G. L. & Beautrais, A. L. A preliminary naturalistic study of low-dose ketamine for depression and suicide ideation in the emergency departmentInt J Neuropsychopharmacol 2011;8:1127-31.
  8. Singh I, Morgan C, Curran V, et al. Ketamine treatment for depression: opportunities for clinical innovation and ethical foresightLancet Psychiatry 2017;4:419-42

 

Population scale data reveals the antidepressant effects of Ketamine  ::  << Article below

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

Isaac V. Cohen, Tigran Makunts, Rabia Atayee & Ruben Abagyan

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

We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics
had signifcantly lower frequency of reports of depression than patients who took any other combination of drugs
for pain (LogOR−0.67±0.034)

Te analysis of the whole FAERS database revealed several other unintentional depression reducing drugs
among antibiotics, cosmeceuticals and NSAIDS.Our data supported previous studies that observed the
psychiatric polypharmacology of minocycline, a tetracycline antibiotic.The NSAID, diclofenac, was also
observed to have some antidepressant properties.It is theorized that both of these drugs may accomplish
antidepressant effects through an anti-inflammatory mechanism.Because of the antidepressant activity of several
NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to
patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression
event rates remained low (LogOR−0.56±0.035).As an important side note, we also evaluated efcacy and side efects with the use of ketamine for pain management.
We found that patients who were on ketamine had reduced opioid induced side effects including constipation, vomiting, and nausea. Our data supports ketamine’s
opioid-sparing properties and alludes to the fact that patients may receive benefts of improved pain, reduced
requirement of opioids, and ultimately less opioid reduced side effects.

References
1. Murray, C. J. & Lopez, A. D. Evidence-based health policy–lessons from the Global Burden of Disease Study. Science 274, 740–743,
doi:10.1126/science.274.5288.740 (1996).
2. Kessler, R. C. et al. Te epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication
(NCS-R). JAMA 289, 3095–3105, doi:10.1001/jama.289.23.3095 (2003).
3. Bromet, E. et al. Cross-national epidemiology of DSM-IV major depressive episode. BMC Med 9, 90, doi:10.1186/1741-7015-9-90
(2011).
4. Andrade, L. et al. The epidemiology of major depressive episodes: results from the International Consortium of Psychiatric
Epidemiology (ICPE) Surveys. Int J Methods Psychiatr Res 12, 3–21, doi:10.1002/(ISSN)1557-0657 (2003).
5. Sansone, R. A. & Sansone, L. A. Antidepressant adherence: are patients taking their medications? Innov Clin Neurosci 9, 41–46
(2012).
6. Frazer, A. & Benmansour, S. Delayed pharmacological effects of antidepressants. Mol Psychiatry 7, S23–28, doi:10.1038/
sj.mp.4001015 (2002). Suppl 1.
7. Braun, C., Bschor, T., Franklin, J. & Baethge, C. Suicides and Suicide Attempts during Long-Term Treatment with Antidepressants:
A Meta-Analysis of 29 Placebo-Controlled Studies Including 6,934 Patients with Major Depressive Disorder. Psychother Psychosom
85, 171–179, doi:10.1159/000442293 (2016).
8. Seemüller, F. et al. Te controversial link between antidepressants and suicidality risks in adults: data from a naturalistic study on a
large sample of in-patients with a major depressive episode. Int J Neuropsychopharmacol 12, 181–189, doi:10.1017/
S1461145708009139 (2009).
9. Rush, A. J. et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D
report. Am J Psychiatry 163, 1905–1917, doi:10.1176/ajp.2006.163.11.1905 (2006).
10. Price, R. B. et al. Efects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant
depression. Depress Anxiety 31, 335–343, doi:10.1002/da.22253 (2014).

11. DiazGranados, N. et al. Rapid resolution of suicidal ideation afer a single infusion of an N-methyl-D-aspartate antagonist in
patients with treatment-resistant major depressive disorder. J Clin Psychiatry 71, 1605–1611, doi:10.4088/JCP.09m05327blu (2010).
12. Alberich, S. et al. Efcacy and safety of ketamine in bipolar depression: A systematic review. Rev Psiquiatr Salud Ment (2016).
13. Larkin, G. L. & Beautrais, A. L. A preliminary naturalistic study of low-dose ketamine for depression and suicide ideation in the
emergency department. Int J Neuropsychopharmacol 14, 1127–1131, doi:10.1017/S1461145711000629 (2011).
14. Miyaoka, T. et al. Minocycline as adjunctive therapy for patients with unipolar psychotic depression: an open-label study. Prog
Neuropsychopharmacol Biol Psychiatry 37, 222–226, doi:10.1016/j.pnpbp.2012.02.002 (2012).
15. Rosenblat, J. D. et al. Anti-infammatory agents in the treatment of bipolar depression: a systematic review and meta-analysis.
Bipolar Disord 18, 89–101, doi:10.1111/bdi.2016.18.issue-2 (2016).
16. FDA Adverse Event Reporting System (FAERS): Latest Quarterly Data Files. http://www.fda.gov/Drugs/
GuidanceComplianceRegulatoryInformation/Surveillance/AdverseDrugEfects/ucm082193.htm (Accessed 2016).
17. The Adverse Event Reporting System (AERS): Older Quarterly Data Files. http://www.fda.gov/Drugs/
GuidanceComplianceRegulatoryInformation/Surveillance/AdverseDrugEfects/ucm083765.htm (Accessed 2016).
18. Questions and Answers on FDA’s Adverse Event Reporting System (FAERS) http://www.fda.gov/Drugs/
GuidanceComplianceRegulatoryInformation/Surveillance/AdverseDrugEfects/default.htm (Acessed 2016).

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

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

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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

 

Ketamine therapy Fairfax| Alexandria |703-844-0184 | Lyme disease treatment with Ketamine | Virginia Ketamine | Maryland Ketamine | Ketamine depression treatment | www.novahealthrecovery.com | Ketamine infusions | Suboxone| CRPS | Sublocade

 Virginia Ketamine Treatment Center<<< Link

  NOVA Health Recovery Ketamine Specialists<<< Link

Ketamine center in Fairfax, Virginia    << Ketamine infusions

NOVA Health Recovery – KETAMINE SYSTEMS<< Link

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

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.