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Rebooting pain sensors with ketamine coma

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For some chronic pain sufferers, `Special K' may be the answer


Knight Ridder Newspapers

PHILADELPHIA - (KRT) - At his worst, Brett Lovell, 32, of Lebanon, Pa., experienced such searing pain that he couldn't straighten his arm, and the fingers of his left hand curled up like a claw. The pain had him downing 25 pills a day.

Then he undertook an experimental treatment - a seven-day coma in which he was pumped full of a drug called ketamine, which doctors use as an anesthetic and street dealers refer to as the recreational drug "Special K."

The experimental procedure gave him fleeting hallucinations, but it helped. "I can enjoy life better today," said Lovell, who is down to just one pill a day and can maneuver a computer mouse.

Ketamine is now being touted as a revolutionary treatment for a severe pain disorder.

In the treatment, ketamine is infused intravenously and continuously while patients are supported by a ventilator - and are virtually dead - for days.

Robert Schwartzman, chairman of neurology at Drexel University College of Medicine, is the U.S. pioneer of the experimental treatment, which resets the link between the pain sensory neurons and the brain.

He equates the brain to a computer. "For five days we turn your computer off so you're not having any pain," he said. When the brain is turned back on, the pain system is "rebooted."

Considered a safe anesthetic, ketamine - known in street parlance as K or Special K - is chemically similar to PCP and causes inebriation, hallucinations and dissociation, a sensation that patients are not in their bodies. These side effects have led to its popularity at raves and reports of its use as a date-rape drug.

That history was not lost on Sandra Lovell, who watched her son Brett in his coma. "All I can describe it as is seeing your child laying there dead," she said. "The worst part was when he was coming out of it. It's like coming off one of the worst trips from LSD."

One of his hallucinations was of his brother, a police officer, trying to shoot him, a vision that greatly distressed his parents.

Yet for Lovell, the trip - which cost about $30,000 - was worth it.

The extreme nature of treatment speaks to the desperation of those with chronic regional pain syndrome or reflex sympathetic dystrophy, a condition that affects 1.5 million Americans, according to the Reflex Sympathetic Dystrophy Syndrome Association.

The syndrome produces intense, burning pain, and causes normally non-painful sensations - touch, movement and temperature - to be agonizing.

"It makes you feel like you've been doused in gasoline and set on fire," said Cynthia Toussaint, 44, a sufferer in Valley Village, Calif., who runs a nonprofit organization to help women in pain.

The condition can result from any type of injury, such as a turned ankle or carpal tunnel syndrome. It develops in 1 to 2 percent of fractures and 2 to 5 percent of peripheral nerve injuries.

The body's pain system, which is necessary to telling us something is wrong, goes awry in these cases.

When pain fibers from the injury site activate, they trigger a chain reaction that changes the structure of the pain neurons. These changes provoke the neurons to fire even more - like a car engine revving out of control - which creates more pain, said Daniel Carr, chief executive officer of IDDS, a New York City-based company that is testing a ketamine nasal spray.

The syndrome often goes misdiagnosed and mistreated, said Schwartzman. Most of his patients have already seen 10 other doctors by the time they find him.

And, many, especially children, face skepticism from their doctors, who think the patients are just trying to get attention.

"I got such horrible looks from doctors, like I had two heads," said Megan Vanatta, 21, of Washingtonville, N.Y., who has had the disorder since she was 7. "Doctors would ask, 'Are your parents fighting? Do your parents abuse you?'"

The earlier the condition is treated, the more effective it seems to be - but there is no cure and no one treatment works universally, experts say. The ketamine coma is only for the most serious cases.

A number of U.S. doctors use ketamine in small doses to treat pain while patients are awake, but Schwartzman and two German colleagues, Ralph-Thomas Kiefer and Peter Rohr, are the first to infuse it in comatose patients for up to seven days.

So far, the trio has treated 26 American patients in Germany. All patients received significant temporary pain relief, and nine remain completely pain-free from nine months to three years after the infusion.

Ketamine is FDA-approved in the United States for two-day use when the patient is awake, but Schwartzman holds out little hope that the coma procedure will ever be allowed here.

At Hahnemann University Hospital in Philadelphia, Schwartzman studies ketamine use for less severe patients and as boosters for those who have returned from Germany.

He just finished a study of 50 patients who were awake during five days of ketamine use - also not enough, he said - and plans to go back to the FDA in a couple of months for approval to try 10-day outpatient infusions.

It may seem strange for a mind-altering substance to be used medically, but the history of ketamine is like many other drugs - if it works for one thing, scientists say, let's see if it works for another.

"The problem unfortunately is that we have so many horrible diseases related to the brain and so few drugs," said Bita Moghaddam, neuroscience professor at the University of Pittsburgh who uses ketamine in rats to mimic schizophrenic symptoms. "If you have a drug you think is relatively safe, you have to use what you have."

Ketamine has also been used to study alcoholism and dementia, and explored as a treatment for sleep apnea and addictions and an aid in psychotherapy.

While many severe pain sufferers are enthusiastic about the ketamine coma, researchers are more cautious.

"Initial observations are exciting," said Srinivasa Raja, director of pain medicine at Johns Hopkins University School of Medicine. "But it has to be tempered with the fact that they are not blinded observations. They have to be followed through over time."

Timothy Lubenow, a pain specialist at Rush University Medical Center in Chicago, had a patient who went to Germany and "had great pain relief up until the plane ride back," he said. "She bumped her knee, which was the affected part, and the pain came back."

Schwartzman hopes that continuing research on treatments for severe pain will yield alternatives to the ketamine coma and that in the future "we won't need the ketamine sleep."

But, "right now, for dreadful patients, the only thing I've seen work is to have them go to sleep," he said.


© 2005, The Philadelphia Inquirer.

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IV k for 5 days straight... i wonder what the chances are of developing olney's lesions? have always wondered what it'd be like to be hooked up to a drip!

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twix: I heard that there is new research indicating that Ketamine doesn't actually cause Olney's Lesions. I would love it if someone could prove, or disprove, this?

But, 5 days of I.V. K sounds wonderful! I reckon I could reprogram my brain quite well in that amount of time aswell. And not just the pain part of it.

I could come out of that a totally different person, by choice!

How surprising is it that a metaprogramming drug could have such profound effects on the human brain? Not surprising to this psychonaut!

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benz there's a good section of karl jansen's book ketamine dreams and realities devoted to the question of olney's lesions. unfortunately i don't have it on hand, but i remember in part that jansen argued that the doses needed to cause toxicity were far beyond recreational dose and frequency. i just figure that these people on IVs are going to get as close to olney's as anyone else will.

although an IV sounds divine i don't think you'd remember anything except having vaguely gone somewhere! recall that k is an NMDA antagonist and disrupts long-term potentiation.

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"twix: I heard that there is new research indicating that Ketamine doesn't actually cause Olney's Lesions. I would love it if someone could prove, or disprove, this?"

Like Benz said it would be good to get a hold of some good scientific info proving/disproving the Theory (is it a theory or fact?) of Olneys legions.

"How surprising is it that a metaprogramming drug could have such profound effects on the human brain? Not surprising to this psychonaut!"

I don't really know much on Ketamine and Metaprogramming could anyone recomend some good reading on the subject? Also what are some other Metaprogramming drugs? besides K and Cid :P

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From The DXM Zine:

I've seen no evidence for this except with very frequent high-dose use (e.g., third or fourth plateau several times a week for several months); furthermore, people who do report DXM becoming less pleasant with time haven't said it's that much faster with high dose trips (whereas any brain damage problem would be). Technically speaking, the damage that Olney et al found with dissociatives is way beyond the fourth plateau dosage level, and I'm not convinced that normal users would ever experience it.


From The DXM Zine:

On the other hand, Onley's lesions have never been found at human

recreational levels, and DXM has received little attention. Ketamine

users, some of whom have used ketamine for many years, don't typically

show mental impairment. Even the few DXM users who do show impairment

typically return to normal after staying off DXM for several months, and

at least one paper suggests the mental impairment from dissociatives may

be caused by depression, not brain damage


From The DXM Zine:

Consider Coenzyme Q10 supplementation. One paper suggested that Q10

 might be useful in some types of neural lesions. It has been

 suggested that, as a mitochondrial energy substrate, it may prevent

 brain cells from "running out of fuel".


i also remember reading that olney's lesions are not an issue with recreational dxm/ketamine usage although a quick flick through my docos and i cant find it, this was the most relavent.

the info that i cant find pretty much disproved william whites theory.

of course there could very well be some individuals who are more susceptable than others, but i feel with sensible (as can be) recreational usage the chances of developing something like this are almost non-existant.

hell, if anyone was gonna have em apart from mr. 5 days of coma and k it'd probably be me. a couple of years back me and a mate went on a bit of a binge, well i guess the 'bit' part is a fairly big lie. we binged for about a year only dropping below 3rd plateau for about a month absolute max. and below second 3-4 times max. in a whole year.

if anything i would dare say i came out of it a better person with a *much* more positive outlook on life, not to mention everything else. with no lasting effects (that i dont find beneficial anyway) the person that accompanied me through a fair portion of this didnt experiance any long lasting negative effects either

BTW i do realise that what we did was rather if not extremely dangerous and do not suggest that anyone attempt anything like this under any circumstances

obviously we didnt sit down and draw up a plan to be completely off guts for 12 months straight, it just happened

i must also add that i do NOT regret the above experience in any way and actually feel it has benefited me in more ways that one

[ 02. September 2005, 09:27: Message edited by: dracos6 ]

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oh yeah, thats what i was originally gonna say

5 days of straight K ***HOLY F#CKIN SHIT***

ah well we can dream, hey benz? :D

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the info that i cant find pretty much disproved william whites theory.

probably this article http://www.erowid.org/chemicals/dxm/dxm_health2.shtml

here's an excerpt from karl jansen:

In 1989, psychiatry professor John Olney reported that ketamine caused reversible changes in two small areas of the rat brain. 40mg/kg resulted in fluid-filled bags ("vacuoles") appearing inside cells. The bags disappeared after several days, unless high doses of the far more toxic PCP or close relative MK801 were repeatedly given, in which case some cell death was seen. Roland Auer injected monkeys with MK801 and was unable to produce any vacuoles. I asked Auer in 1998 whether persons undergoing anesthesia with Ketalar were at risk of these changes. His reply was that he doubted that it was even a remote possibility because of fundamental differences in metabolism between the rat and human brain. As discussed in chapter 4, ketamine can block excito-toxicity (brain damage due to low oxygen, low sugar, epilepsy, trauma etc.) but it can also excite the brain at low doses by switching off the inhibitory system. Why isn't this damaging in monkeys and humans? The answer probably lies in the fact that ketamine binds to an increasingly wide range of different receptors as the dose level rises, and some of these receptors act to shut down the excitement. In humans, by the time a potentially toxic dose is reached, the "excitement window" has been passed and the drug is starting to activate other systems that switch cells off again, a result of ketamine's promiscuity that improves its safety relative to MK801. MK801 binds very specifically to N-P receptors. The other part of the explanation is that rats have rates of brain metabolism that are almost twice as high as those in humans to start with. It is because of this higher base rate of metabolism that ketamine causes over-excitement in rats at doses below those at which it activates shutdown systems.

Frank Sharp also works in this area. I discussed with Sharp how this issue stood in 1998. His view was that reversible toxic changes in the rat started to appear at 40mg/kg and reached a level at which no further changes occurred (a plateau) at 100mg/kg, when a little cell death could be seen - but matters would not progress beyond this point. Extensive attempts to produce toxic changes in monkeys had been a total failure at doses up to 10mg/kg i.m. These monkey studies are unpublished.

I sought the view of Olney's colleague, Nuri Farber. The work of his team indicated that N-P receptors must be blocked for at least 2 hours to cause reversible changes, and at least 24 hours to produce some cell death, in rats. Ketamine has a short half- life (the time required for the blood level to fall to half its original level): only 20 minutes in the rat. His team thus had no ethical qualms about using Ketalar in humans. However, he thought that the methods used in monkey studies so far were unsatisfactory, because the animals were probably too young. Only adult rats show the toxic changes. He was not prepared to accept a clean bill of health for the drug in primates until this work with older monkeys had been done, and until the drug companies published their monkey studies to support their claims of harmlessness.

There is thus no published evidence at this time (January 2000) that ketamine can produce toxic cell changes in monkeys. The unpublished monkey data that we know about, that of Frank Sharp, actually shows that there is no damage at doses up to 10mg/kg. The failure to produce toxic changes in monkeys is probably one reason why the FDA did not remove Ketalar from the market. Some people see 40 mg/kg as so far above the human dose level as to be irrelevant in any case. This is not the most useful way to look at this issue. When given by intramuscular injection, humans are at least 10 times more sensitive to the anesthetic effects than rats. When rats are given 30 mg/kg, the experimenters describe this as a 'subanesthetic dose,' versus a 'high anesthetic dose' of about 150 mg/kg. In humans, an equivalent subanesthetic dose is about 1 mg/kg and the topc anesthetic dose would be about 13 mg/kg. However, humans are much less sensitive to the neurotoxic effects.

These two matters are directly related: humans are protected from the toxic changes by the rising anesthesia, which cuts in above a certain dose and calms cells down. This also happens in rats, hence the 100 mg/kg plateau, but it happens too late to completely avoid some toxic changes as rats are already running hot because of their twice-as-fast metabolic rate."

These brain cell changes do not appear if rats are pretreated with certain drugs. The list of drugs which can block the toxic changes is long and diverse. Most of these drugs block toxic changes in rats by switching on a range of different "calming" systems, depending on the drug used. Ketamine is highly promiscuous and eventually binds to the same receptors as some of the protective agents listed above, which shutdown the over-excitement. So the toxic effects happen via one neurochemical system (glutamate) and this is switched off by other systems activated at higher ketamine levels (e.g. the opioid system). In humans, the opioid system (amongst others) cuts in before activation of the glutamate systems reaches the point where cell damage occurs, but in rats this is not the case.

young tripper, maybe try read "the human biocomputer" by john lilly?

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