^ you're absolutely right and I didn't mean to imply there is NO clinical utility, in fact there is a lot. I just thought saying it's 'more than enough' across the board was overstating it.
As far as it's anticonvulsant efficacy, as mentioned in the other thread, it's so poor of an anticonvulsant that it requires concomitant administration with another anticonvulsant to treat seizures.
For mild-moderate benzo and alcohol withdrawal, I would agree that it's preferable to using benzos in many cases. I was strictly speaking about severe cases where grand-mal seizures and even death (primarily in the case of alcohol) are real possibilities. One of my professors in the addictions counseling program had a gentlemen come in for an assessment who was intoxicated and their normal protocol was to have them wait to sober up enough to drive home but he was so severely dependent that he would experience severe DT's if his BAC dropped below the legal limit so they had to call his wife in and instruct her on how much alcohol to give him in order to prevent him from seizing while transporting him to detox. I was more so speaking about cases in severity closer to this.
behindblueeyes said:
I don't binge every night anymore (just my nights off work), but the cravings are still there. And I know this is contributing to my depression/anxiety.
The OP has clearly indicated that their habit is not severe. So what you're "strictly speaking about" is impertinent to the OP. As for gabapentin and its anti-convulsant properties, it is an anti-convulsant, but as you've stated and I have in dozens of tramadol threads, it's not sufficient at treating grand mal seizures, and is usually used an adjunct therapy to other anti-convulsants. There are however, over 40 different kinds of seizures, with each working differently. Nonetheless, their efficacy is more than proven in alcohol and benzodiazepine withdrawal, and I'm glad the studies provided were sufficient for you to change your perspective on outdated methodologies in treatment of gabaergic withdrawal (eg. stand-alone diazepam).
Cane2Left said:
As discussed in the other thread linked above, gabapentin's effects are primarily due to non-GABAergic mechanisms of action and is absolutely, undeniably NOT a GABAA agonist and therefore is NOT sufficient to treat alcohol or benzo withdrawal alone if someone was strongly physically dependent.
There's a difference between "more than effective" and "more than enough". More than effective means that the suggested medication itself is effective, at doing what it's intended to do. "More than enough" suggests that the medication is sufficient on its own. I don't think I negated that benzodiazepines should be tapered or used in alcohol withdrawal.
Alcohol (and gabaergic withdrawal in general) cause down-regulation of gaba-a and possibly an implication at gaba-b receptors, plus an up-regulation of glutamate. An abundance of glutamate induces excitotoxicity, or hyperexcitability of neurons due to NMDA activation through increased activity at calcium-channels. This is turn leads to cell suicide, and upsets the stimulatory/inhibitory balance in the brain. Here is where seizures, neuropathy, and damage to the nervous system come into the picture. These "non-gabaergic mechanisms" you speak of are completely irrelevant (or completely relevant as the case may be) when an understanding is achieved on how gabaergic withdrawal works. Allow me to elaborate:
Of course it's always ideal to taper, lowering the benzodiazepine doses in fragments allows glutamate to adjust slowly, instead of suddenly denying your brain of gaba-agonism, and leaving it exposed to a glutaminergic storm. There is an aspect however, that benzodiazepines alone don't address, which is the most important aspect, docking high glutaminergic transmission through calcium-channel-blockade. Gabapentin/pregabalin, tend to be very potent calcium-channel-blockers. While the benzodiazepine, would only be effective at maintaining gaba enhancement at starved receptors. Hence why most of the time, if not almost always during extremely heavy alcohol and GHB habits, users can be completely resistant to the effect of benzodiazepines (as seen in various case reports). On top of that, there's a gaba-b aspect in alcohol withdrawal which benzodiazepines alone don't cover.
Hyperexcitability following chronic alcohol exposure appears to result in enhanced activation of glutamatergic synapses in the brain. This enhanced glutamatergic transmission probably results from a combination of increased NMDA receptor activation, decreased GABAA receptor activation and increased function of voltage-activated calcium channels.
Source:
http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.1993.tb00720.x/abstract
the studies reviewed here provide suggestive evidence that PGB might constitute a novel efficacious and safe pharmacological treatment in both chronic and heavy alcohol and BDZ abuse and dependence. Moreover, PGB could also help in the treatment of symptoms of protracted withdrawal from alcohol, which extend up to 1 year beyond its cessation, such as anxiety and sleep disturbances [35]. This could enrich the available pharmacological armamentarium, which asfar, includes virtually only carbamazepine [36]
Pregabalin in the Treatment of Alcohol and Benzodiazepines Dependence
Related reading:
Chronic ethanol exposure enhacing NMDA activity and increasing sensitivity to excitotoxicity
Glutamate excitotoxicity in ethanol withdrawal
Ethanol inhibits excitotoxicity
Protective effect of gabapentin on N-methyl-D-aspartate-induced excitotoxicity in rat hippocampal CA1 neurons.
Baclofen In Ethanol Withdrawal
Role of GABA-B in Ethanol Withdrawal
Baclofen, an anti-convulsant, and a benzodiazepine (taper) are
always things I suggest during gabaergic withdrawal. With the baclofen exclusively in gaba-b withdrawal. It honestly baffles me that people still think that benzodiazepines are alone sufficient at treating GHB, alcohol, and benzodiazepine withdrawal. Sometimes doctors opt to inject people with double, and even sometime triple digit milligrams of benzodiazepines to patients who are irresponsive, when the solution is right under their nose -- adding an anti-convulsant. In time though, the perspective will change, and they will become less underrated, something which is currently happening gradually.
As an aside, there is a huge amount of concomitant pregabalin/benzodiazepine users that can easily rotate both substances, myself included. Even though you did well to elaborate on the pharmacology of gabapentin/pregbalin in the thread provided, it still remains unknown, and a cross-tolerance is still suspect to many users. My guess would be due to their previously suggested action on GAD.
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