Vastness
Bluelight Crew
- Joined
- Mar 10, 2006
- Messages
- 2,306
I am having some trouble nailing down any specifics about the relation between benzodiazepine consumption and the known risk of seizures upon discontinuation or withdrawal.
I'm asking primarily for personal reasons because I know for a fact I've been taking benzos too often recently. But I would like to understand more about the mechanism from a neuropharmacological perspective regardless.
I have found this one study which may include a sufficiently data-oriented answer to my question - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635822/ - but am having trouble parsing the data, not being a neuroscientist myself and not understanding fully the statistical measures given.
Can anyone help me out here? Obviously what I would really like to see is a nice neat graph with "net benzodiazepine consumption" over a given period on one axis, and "percentage likelihood of seizure incidence" on the other - but perhaps that is something I am not going to find.
I am aware that the majority of seizures of this type are grand-mal and result in coma or death a significant percentage of the time. I'm also aware that there appears to be a lot of variation between individuals as far as exactly how much benzodiazepine consumption and over what period leads to an increased likelihood of these serious outcomes - and, I suppose, increased likelihood for development of persistent epilepsy of some form, with some individuals having serious negative outcomes after just relatively short treatment periods, while others have no serious outcomes even after comparatively long and heavy dose periods of use. What is the cause of these differences? Is there any way to predict before such a serious incident, the likelihood of said incident occurring in any given individual?
Are certain benzodiazepines or classes of benzodiazepines more or less likely to prime the brain for these epileptic symptoms?
As an aside - I am curious why the same risks do not seem to exist with other GABAergics, as far as I am aware - for example, I am aware of a few case studies of very, very high dose zolpidem abuse involving very very rapid cessation which would be categorically unsafe with almost any benzodiazepine - which did not result in any serious outcome (when I speak of "serious outcomes" in this post, I am always referring to induction of epilepsy in previously non-epileptic individuals, manifesting as at least one seizure of some form - whether grand-mal or not - of course there are other negative outcomes to be considered - but please consider these outside the scope of this topic). Moving a little further away from the benzodiazepine receptors specifically, do gabapentinoids carry similar risks, if of a lower magnitude? To my knowledge, there are no recorded incidences at all of serious outcomes from rapid phenibut cessation for example - psychosis and delirium, yes - epileptic symptoms, no. I haven't looked into the other 2 personally but my sense is that while the risk may be non-zero - it is not high.
Alcohol of course is another notorious epileptinoid, if you'll excuse my invented term, but does alcohol interact with benzodiazepine receptors? Perhaps it is the "dirty" receptor profile that is at play here?
Obviously I would like to believe that my own neurochemistry is somewhat epilepsy resistant based on 1) wishful thinking, 2) I have never had a seizure before and have no family history of epilepsy of any kind - but is this just delusional thinking? Again, is there any way to tell?
Are there any preventative measures to be taken? (Besides, obviously, keeping benzodiazepine use to an absolute minimum.)
As this turned into a somewhat lengthy post I went back and bolded the key questions - and italicised some other relevant stuff - that ended up being more of a large chunk of this post than I planned, there is a lot I want to understand, heh, but I hope it makes it more readable, at least.
I was going to post in "Other Drugs" but feel that (hopefully) I'll get some answers more to my liking here, maybe I will just post a request for some personal experiences in that forum.
Thanks in advance for any responses.
I'm asking primarily for personal reasons because I know for a fact I've been taking benzos too often recently. But I would like to understand more about the mechanism from a neuropharmacological perspective regardless.
I have found this one study which may include a sufficiently data-oriented answer to my question - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635822/ - but am having trouble parsing the data, not being a neuroscientist myself and not understanding fully the statistical measures given.
Can anyone help me out here? Obviously what I would really like to see is a nice neat graph with "net benzodiazepine consumption" over a given period on one axis, and "percentage likelihood of seizure incidence" on the other - but perhaps that is something I am not going to find.
I am aware that the majority of seizures of this type are grand-mal and result in coma or death a significant percentage of the time. I'm also aware that there appears to be a lot of variation between individuals as far as exactly how much benzodiazepine consumption and over what period leads to an increased likelihood of these serious outcomes - and, I suppose, increased likelihood for development of persistent epilepsy of some form, with some individuals having serious negative outcomes after just relatively short treatment periods, while others have no serious outcomes even after comparatively long and heavy dose periods of use. What is the cause of these differences? Is there any way to predict before such a serious incident, the likelihood of said incident occurring in any given individual?
Are certain benzodiazepines or classes of benzodiazepines more or less likely to prime the brain for these epileptic symptoms?
As an aside - I am curious why the same risks do not seem to exist with other GABAergics, as far as I am aware - for example, I am aware of a few case studies of very, very high dose zolpidem abuse involving very very rapid cessation which would be categorically unsafe with almost any benzodiazepine - which did not result in any serious outcome (when I speak of "serious outcomes" in this post, I am always referring to induction of epilepsy in previously non-epileptic individuals, manifesting as at least one seizure of some form - whether grand-mal or not - of course there are other negative outcomes to be considered - but please consider these outside the scope of this topic). Moving a little further away from the benzodiazepine receptors specifically, do gabapentinoids carry similar risks, if of a lower magnitude? To my knowledge, there are no recorded incidences at all of serious outcomes from rapid phenibut cessation for example - psychosis and delirium, yes - epileptic symptoms, no. I haven't looked into the other 2 personally but my sense is that while the risk may be non-zero - it is not high.
Alcohol of course is another notorious epileptinoid, if you'll excuse my invented term, but does alcohol interact with benzodiazepine receptors? Perhaps it is the "dirty" receptor profile that is at play here?
Obviously I would like to believe that my own neurochemistry is somewhat epilepsy resistant based on 1) wishful thinking, 2) I have never had a seizure before and have no family history of epilepsy of any kind - but is this just delusional thinking? Again, is there any way to tell?
Are there any preventative measures to be taken? (Besides, obviously, keeping benzodiazepine use to an absolute minimum.)
As this turned into a somewhat lengthy post I went back and bolded the key questions - and italicised some other relevant stuff - that ended up being more of a large chunk of this post than I planned, there is a lot I want to understand, heh, but I hope it makes it more readable, at least.
I was going to post in "Other Drugs" but feel that (hopefully) I'll get some answers more to my liking here, maybe I will just post a request for some personal experiences in that forum.
Thanks in advance for any responses.
