A single very low intravenous dose of a medication historically employed for anesthesia – and experimentally for FM pain – can provide significant relief or remission of treatment-resistant major depression in less than two hours, according to a new study by the National Institute of Mental Health. Further, for 35 percent of the patients, the response to the single dose was sustained for at least one week. The patients who took part in this randomized, placebo-controlled, double-blind crossover trial had previously tried an average of six antidepressants without symptom relief.
These findings have potentially “enormous public health implications,” according to the NIMH. By comparison, most currently-used antidepressants require eight weeks to demonstrate benefits – if they work at all – for patients diagnosed with treatment-resistant major depression. And usually four to six weeks are required even for “more responsive” patients, the researchers explain.
The drug involved - Ketamine - corrects a chemical imbalance in the brain that interferes with the regulation of normal electrical flow between brain cells. It is able to act so much more swiftly than other antidepressants because it intervenes in the same mood-regulating chemical chain of events as they do, only several stages “downstream.”
However, because Ketamine has become known in club-drug circles for its “psychedelic” side effects since the 1960s, the NIMH researchers caution that an altered version of the drug will be necessary for use as an antidepressant, to avoid addiction or disorientation. And in the process, they believe, they’ll come closer to understanding why depression occurs in the first place – while possibly identifying biological markers that may aid in diagnosis.
The report on the NIMH trial, “A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression,” by Carlos A. Zarate, Jr., MD, et al., was published in the August 2006 issue of the Archives of General Psychiatry. See also the NIMH press release at www.nimh.nih.gov/press/ketamine.cfm
Implications regarding the mechanism of Fibromyalgia pain. In technical terms, Ketamine’s antidepressant quality is thought to result from its ability to block the brain protein N-methyl-D-aspartate (NMDA) receptor. Researchers believe that this same “NMDA antagonist” action may account for Ketamine’s ability to reduce some Fibromyalgia patients’ pain and tender point sensitivity, as demonstrated in various trials.1,2 The inference is that Fibromyalgia pain may result from “NMDA receptor activation in the spinal cord” – causing an increase in the neurons’ response to pain stimuli (“central sensitization”).3
1. Go to the ImmuneSupport.com archive http://www.immunesupport.com/library/showarticle.cfm/id/2554/searchtext/ketamine to find an abstract of the article “Pain analysis in patients with Fibromyalgia (FM). Effects of intravenous morphine, lidocaine, & ketamine,” by J. Sorenson, et al., published in the November-December 1995 issue of the Scandinavian Journal of Rheumatology.
2. Go to the Immune Support.com archive http://www.immunesupport.com/library/showarticle.cfm/id/5209/searchtext/ketamine to find an abstract of the article “Ketamine in chronic pain management: An evidence-based review,” by G. Hocking & M.J. Cousins, published in the December 2003 issue of the journal Anesthesia and Analgesia.
3. Go to http://opioids.com/nmda/receptor.html to review an abstract of the article “Update on the neurophysiology of pain transmission and modulation: Focus on the NMDA-Receptor,” by G.J. Bennett, published in the January 2000 issue of the Journal of Pain Symptom Management.