Posted by Ame Sans Vie on January 27, 2003, at 3:29:40
In reply to Questions about Benzo's/GABA, and AED's!!!, posted by titleistguy on January 26, 2003, at 23:37:14
I'm kind of unclear on this myself... I know they bind to BZD receptors, but do they bind to GABA-A receptors? I had read in a few different sources that the benzodiazepine receptor, as well as the barbiturate/convulsion-promoting drug receptor, was just a way to 'fire up' the BZD receptors so that they would in turn activate GABA channels, causing g-aminobutyrate's 'gates' to open more frequently... I don't know, it's all just a bit confusing when you've only read all that technical jargon in about 15 minutes...
The extent of my knowledge on the photosensitivity that often accompanies withdrawal is only that it's caused by melatonin suppression. Can anyone else expand on this? I find it rather interesting.
Quitting a benzo cold is quite often uncomfortable at the least, and sometimes life-threating (i.e., in the event of a seizure). However, quitting cold usually will reduce the length of withdrawal. By the way, and this plays a big role in this, which benzos were you taking?
As implied above, discontuing a benzo by tapering the dose gradually is usually less troublesome. Often they'll switch you from the benzo you're on to an equivalent dose of Valium (diazepam), which has the longest half-life of all the benzodiazepines (yet it's also the shortest-acting). The slower rate of elimination from the body as you're tapering down can be a great help. Finally, one more rather unorthodox suggestion is to use dextromethorphan to ease withdrawal. It's the active ingredient in Robitussin Maximum Strength Cough and Vicks 44 Cough (definitely don't buy a cough syrup that contains other active ingredients, with the possible exception of guaifenesin-- acetaminophen, pseudoephredine, and especially phenylpropanolamine [sp?... you know, PPA-- that stuff they're saying is causing people to have strokes] can wreak some serious havoc on your body if you take them regularly. Not to mention the horrible addiction potential for DXM itself; it is a stereo-isomer of levomethorphan, a narcotic many times more potent than morphine. Though it doesn't bind to any opiate receptors, the drug has a tendency to make you feel 'happy' as it builds up in your body. And I've been through dextromethorphan abuse- not a place you wanna be. I guzzled two 8oz bottles of Robitussin every night for several months straight; DXM is classified as a dissociative anesthetic, just like PCP and ketamine. Just take the doses as directed on the bottle-- DXM has been shown time and time again to be quite helpful in withdrawal of everything from tobacco to alcohol to cocaine. But once you feel the withdrawal symptoms are subsiding, lower the dose.
I'll respond to each of the drugs you listed individually:
Neurontin: Probably the best of the anticonvulsants for anxiety, statistically speaking. I still don't think anyone's quite sure how it works, though it is structurally related to GABA.
Gabitril: Essentially worthless-- it acts solely on the GABA-B receptors. A very few people have claimed to have been helped by this med (though from what I've heard, always for depression; not anxiety). FWIW, not long after starting this medication, I ended up going into a catatonic state followed by three hours in status epilepticus... they told me I definitely beat the odds by far when I came out of it. They'd already told my parents that the chance of my survival was, "at this juncture... minimal"!
Depakote: I'd give this a pretty close second, after Neurontin, for anxiolysis. I mean, it works very well, but the weight gain... the cognitive dulling... the possible hair loss... those are things you've got to consider. It works (but only at pretty high doses) to increase the action of GABA within the brain. It achieves this by inhibiting GABA amino-transferase, the enzyme that breaks down GABA in the brain.
Topamax: I don't know what to say about this one... it worked all right for me. I can't say for sure whether the GABA receptors are at work here, but topiramate is a carbamate derivative: so are Equanil (meprobamate, a powerful anxiolytic) and Soma (carisoprodol, a muscle-relaxant. My experience with Equanil and Soma has been very positive-- Equanil I'd describe as mixing a couple bars of Xanax along with 300mg phenobarbital. Soma feels practically the same (its active metabolite is meprobamate) except you also get those great tension-relieving, euphoric muscle relaxant properties.
Tegretol: One of very few psychiatric drugs I've yet to try, though I *have* tried Trileptal (same thing as Tegretol, just altered a bit to alleviate many of the bothersome side effects). It had no effect on me whatsoever, good or bad. It seems that it works (at least partially) like lithium-- limiting the influx of sodium ions across cell membrane in the motor cortex. This inhibits nerve impulses. I believe Tegretol/Trileptal is involved in the GABA 'cycle', as (if I remember correctly) sodium ions are a key component in the g-aminobutyrate system, and many drugs useful in treatment of anxiety (I believe Depakote may be one of them...?) also act on this sodium ion transport system.
A couple others worth mentioning: Lamictal (lamotrigine; which acts by inhibiting glutamate release) and Dilantin (phenytoin). All I know about Dilantin is that it alters ion transport.
The only other drug I can recommend that's available in the States is Rilutek (riluzole), typically prescribed for amyotrophic lateral sclerosis (ALS). It potentiates GABA at sites A and B (possibly also C), inhibits glutamate (an excitatory neurotransmitter-- MSG, monosodium glutamate, is nothing but a salt form of glutamate), interferes with binding of amino acid receptors, and inactivates voltage-dependent sodium channels. This is one drug I'm going to try next (also Parnate and a few TCAs... the only things I haven't tried yet).
Drugs that solely act on the BZD receptors... hmm... well, there's flumazenil, but I doubt you want a BZD-antagonist, lol. Other than that, all I can think of is muscimol, a psychoactive chemical found in the Fly Agaris mushroom (you've probably seen these; they're red with white scales... just like on Super Mario Bros., lol). These mushrooms are often taken in large amounts, both by spiritualists and recreational drug users, to induce a type of 'vision quest'. Nothing like LSD-- while on LSD, very rarely does one believe the hallucinations they are having are real (which, technically, forces you to refer to these as 'visuals', since these are not *true* hallucinations). The same goes for your run-of-the-mill psilocybe mushrooms. But the Fly Agaris (or amanita, as it's often called) induces true states of psychosis. *Muscimol*, however, can be extracted and can easily be ordered through the net. The mushroom and all chemicals contained within are 100% legal by federal law. If you decide to try this route, make sure to read up on muscimol and what doses are therapeutic and which ones are fatal.
Lastly, I'm just curious-- why did you go off the benzos in the first place? Any drug that acts on the BZD receptors/GABA system and has an immediate effect (such as Ambien, muscimol, g-hydroxybutyrate [GHB] and its derivatives/precursors like 1,4-butanediol and g-butyrolactone [GBL]) is most likely going to be every bit as addictive as the benzos. So, just wondering what your motivation(s) for getting off the benzos was. Anyway, hope this helped!
--Michael
poster:Ame Sans Vie
thread:137721
URL: http://www.dr-bob.org/babble/20030125/msgs/137739.html