Friday, 5 October 2012

Ketamine, good news bad news

The mind is a unique an  crazy computer which tends to spring up every now and again with useful bits of news. I was half surprised by the fact that magic mushrooms can actually turn off or dampen the areas of the brain to depression and anxiety. But along the way you must experience the hallucinations of a psilocybin, the active ingredient that creates the cure. In most cases, going on a indian vision quest every time you get the blues seems a little impractical, despite the claim that one mushroom session could have a positive lasting effect for a good few years. Fast forward to today and Scientists say they have figured out how an experimental drug called ketamine is able to relieve major depression in hours instead of weeks.
Researchers from Yale and the National Institute of Mental Health say ketamine seems to cause a burst of new connections to form between nerve cells in parts of the brain involved in emotion and mood. The discovery, described in Science, should speed development of the first truly new depression drugs since the 1970s, the researchers say. "It's exciting," says Ron Duman, a a psychiatarist and neurobiologist at Yale University. "The hope is that this new information about ketamine is really going to provide a whole array of new targets that can be developed that ultimately provide a much better way of treating depression." Ketamine is an FDA-approved anesthetic. It's also a popular club drug that can produce out-of-body experiences. Not exactly the resume you'd expect for a depression drug. But a few years ago, researchers discovered that ketamine could help people with major depression who hadn't responded to other treatments. What's more, the relief came almost instantly.
Depression is associated with a loss of so-called synaptic connections between nerve cells, Duman says. So he and other scientists began to study mice exposed to stresses that produce symptoms a lot like those of human depression. The stressed mice lost connections in certain parts of the brain. But a dose of ketamine was able to "rapidly increase these connections and also to rapidly reverse the deficits that are caused by stress," Duman says. A team at the National Institute of Mental Health also has found evidence that ketamine works by encouraging synaptic connections.
It's possible to see the change just by studying rodent brain cells with a microscope, says Carlos Zarate from the Mood and Anxiety Disorders Program at NIMH. A healthy neuron looks like a tree in spring, he says, with lots of branches and leaves extending toward synaptic connections with other neurons. "What happens in depression is there's a shriveling of these branches and these leaves and It looks like a tree in winter. And a drug like ketamine does make the tree look like one back in spring." And there's also indirect evidence that ketamine is restoring synaptic connections in people, Zarate says. His team studied 30 depressed patients who got ketamine.
And they found changes in brainwave activity that indicated the drug had strengthened connections between neurons in areas of the brain involved in depression. All of this research is intended to produce drugs that will work like ketamine, but without the hallucinations. And several of these alternative drugs are already being tried in people.

In a another example of a benefits Ketamine, in the most severe cases of reflex sympathetic dystrophy (RSD), inducing a five-day coma may be the only effective treatment. The method is akin to rebooting the central nervous systems of patients whose nerve cells have gone haywire. The FDA has yet to approve coma therapy, which is induced by administering large bolus injections of ketamine and midazolam at up to 50 times the normal dose. But that has not stopped U.S. doctors from pioneering the use of a “ketamine coma” in American patients treated at hospitals in Germany and Mexico.
For the better part of four years, Robert Schwartzman, MD, chairman of the Department of Neurology at Drexel University College of Medicine in Philadelphia, and colleagues have been studying the effects of ketamine treatment, including induced comas, in patients with RSD. Their results suggest that the coma therapy may provide long-term and perhaps permanent relief in as many as half of the most severe cases.
Ketamine is the most potent clinically available inhibitor of N-methyl-D-aspartate (NMDA) receptors. These receptors permit the transfer of electrical signals between neurons in the brain and the spinal column. Studies support the idea that RSD results from a dynamic change in the physiology and structure of central pain neurons mediated by NMDA receptors. When these receptors malfunction, enzymatic and metabolic cascades occur in pain cells, and the degree of pain is magnified out of proportion to the physical injury causing it. In a study of infusions of low-dose ketamine (Pain Physician 2005;8:175-179), Dr. Schwartzman and colleagues found that a critical factor in central sensitization seems to be the release of magnesium on the NMDA receptor, with an influx of calcium and the initiation of intracellular cascades. As an NMDA antagonist, ketamine blocks central sensitization. Drugs such as dextromethorphan, amantadine and memantine (Namenda, Forest Pharmaceuticals) also could be used, but they appear to have a low potential for blocking the sensitization process.
As well as medical benefits, long time users take ketamine for recreational purposes, as it can cause euphoria, vivid dreams and hallucinations. Chronic use of ketamine may lead to cognitive impairments including memory problems. In 1989, psychiatry professor John Olney reported that ketamine caused irreversible changes in two small areas of the rat brain, which however has significant differences in metabolism from the human brain and therefore may not occur in humans.
According to a recent systematic review, 110 documented reports of irritative urinary tract symptoms from ketamine dependence exist. Urinary tract symptoms have been collectively referred as ketamine-induced ulcerative cystitis or ketamine-induced vesicopathy, and they include urge incontinence, decreased bladder compliance, decreased bladder volume, detrusor overactivity, and painful haematuria (blood in urine). Despite the long term negative effects for ketamine, the medical use of this drug could out weigh the bad stuff. Ketamine's bad reputation of a party drug, whereby club users wound take 20 times the doses of a clinical measure at a poor grade of Ketamine.
And finally, a Russian doctor Evgeny Krupitsky (Clinical Director of Research for the Saint Petersburg Regional Center for Research in Addiction and Psychopharmacology) has claimed to have encouraging results by using ketamine as part of a treatment for alcohol addiction which combines psychedelic and aversive techniques. Controlled ketamine use and group therapy, and resulted in 60 of the 86 alcoholic males selected for the study remaining fully abstinent through one year of treatment. For heroin addiction, the same researcher reached the conclusion that one ketamine-assisted psychotherapy session was significantly more effective than active placebo in promoting abstinence from heroin during one year without any adverse reactions. The Use of recreational drugs such as mushrooms and now ketamine might open doors for a relaxed attitude to at least study them for any benefits. Hopefully In the future there may not be a underground black-market for certain Class A drugs, for which has a criminal element to it.

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