I've read and heard from doctors that klonopin can permanently alter one's brain chemistry if one uses it for a month or longer. I'm wondering if this is the case with all benzos, or if there are some that don't come with that problem. If there are ones that don't have that problem, which would you suggest as the strongest, most euphoric, least addictive?
I've read and heard from doctors that klonopin can permanently alter one's brain chemistry if one uses it for a month or longer. I'm wondering if this is the case with all benzos, or if there are some that don't come with that problem. If there are ones that don't have that problem, which would you suggest as the strongest, most euphoric, least addictive?
Permanently?? A Doc told you that? Your brain changes after long treatment with all Benzos, which results in withdrawal if the subject stops abruptly the medication, but this process is reversible and your brain will recover to baseline after benzos are out of the system
but if you've taken it for more htan a month before, and you've gottne over withdrawls, and you feel the same, then no need to wrry. it can (apparently) permanently affect your brain (i think the article i read said in 10-15% of people, but dont quote me on that), so if you feel fine, chances are it didnt permanently affect you.
It is true that benzos cause long-lasting changes in brain chemistry, although they are not permanent. The changes are quite major, since sudden discontinuation (after becoming physically addicted) can very well result in death and some symptoms can persist for months. This is a class effect of benzos, so there are none that don't alter brain chemistry.
It is true that benzos cause long-lasting changes in brain chemistry, although they are not permanent. The changes are quite major, since sudden discontinuation (after becoming physically addicted) can very well result in death and some symptoms can persist for months. This is a class effect of benzos, so there are none that don't alter brain chemistry.
What about soma? is this the same, or will it not effect the brain as much when one stops taking it?
Below are some studies suggesting neurotoxicity of benzos & a definition of neurotoxicity. So going by the strict definition they COULD theoretically alter specific brain functions irreversibly. That said with the scientific uncertainty of predicting IN VIVO neurotoxicity of drugs & compounds (Ricaurte comes to mind) SWIM would suggest the main serious concern with benzo's (as always) is still going to be addiction, tolerance, withdrawal syndrome etc (which in some cases can be severe). Many active drugs can probably be linked to some form of neurotoxicity (e.g alcohol) but determining the severity & relevance is another thing. (Also probably hard to prove one way or the other)
Definition:
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The term neurotoxic is used to describe a substance, condition or state that damages the nervous system and/or brain, usually by killing neurons. The term is generally used to describe a condition or substance that has been shown to result in observable physical damage. The presence of neurocognitive deficits alone is not usually considered sufficient evidence of neurotoxicity, as many substances exist which may impair neurocognitive performance without resulting in the death of neurons. This may be due to the direct action of the substance, with the impairment and neurocognitive deficits being temporary, and resolving when the substance is metabolised from the body. In some cases the level or exposure-time may be critical, with some substances only becoming neurotoxic in certain doses or time periods.
Effect of GABA agonists on the neurotoxicity and anticonvulsant activity of benzodiazepines.
Chweh AY, Swinyard EA, Wolf HH, Kupferberg HJ.
Progabide (50 mg/kg, i.p.), a GABA receptor agonist, significantly decreases the median minimal neurotoxic dose (TD50) of clobazam, chlordiazepoxide, and diazepam; the receptor binding of these substances is highly enhanced by muscimol. Progabide has no significant effect on the TD50 of clonazepam and triazolam; the receptor bindings of these substances is either only slightly enhanced or not altered by muscimol. Progabide also significantly decreases the median antimaximal electroshock dose (MES ED50) of all the benzodiazepines tested. However, progabide has no effect on the median antipentylenetetrazol dose (PTZ ED50) of the benzodiazepines. Likewise, THIP (2.5 mg/kg, i.p.) significantly decreases the TD50 of chlordiazepoxide but not that of triazolam. THIP significantly decreases the MES ED50 of chlordiazepoxide and triazolam but has no effect on the PTZ ED50 of these two substances. The above data suggest that benzodiazepine receptors linked to GABA receptors contribute to the minimal neurotoxicity and anti-MES activity but not to the anti-PTZ activity of benzodiazepines.
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Open study of clobazam in refractory epilepsy.
Munn R, Farrell K.
Department of Pediatrics; University of British Columbia, Vancouver, Canada.
Clobazam is a 1,5-benzodiazepine reported to have a wide spectrum of antiepileptic activity and is associated with less neurotoxicity than the 1,4-benzodiazepines, nitrazepam and clonazepam. The effect of clobazam on seizure control and neurologic behavior was examined prospectively in 115 children (average age: 8.4 years) with intractable seizures. Eighteen children (16%) became seizure free and a further 35 (31%) demonstrated a greater than 90% decrease in seizure frequency. Tolerance to the antiepileptic effect of clobazam was observed in 30 of 79 children (38%) who demonstrated an initial improvement in seizure control. Complete tolerance was observed in 9 patients, partial tolerance in 9, and partial tolerance that responded to an increased dose of clobazam in 12. Seventy-two percent of patients reported improvement and 26% worsening in at least one parameter of neurologic function after beginning clobazam. The improvement in neurologic function correlated poorly with change in seizure control. Patients who discontinued 1,4-benzodiazepine (n = 37) had a greater improvement in attention span, alertness, balance, drooling, and mood compared to the remainder of the group. These data suggest that clobazam is effective in the treatment of children with a wide range of epilepsies and seizure types and support the clinical impression that clobazam is associated with less neurotoxicity than the 1,4-benzodiazepines.
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I've read and heard from doctors that klonopin can permanently alter one's brain chemistry if one uses it for a month or longer
SWIM would suggest those discussing clonazepam in such a way are probably referring (possibly by using incorrect terminology) to tolerance, side effects and problems associated with using clonazepam for longer than a month (ignoring the exact mechanism I.e is it reversible or irreversible). As Clonazepam can cause tolerance, addiction & withdrawal within that time frame and they as professionals may only have 5minutes in a busy surgery to convey a message to a patient - you can see where they might be coming from.
I haven't done a lot of research on benzos specifically. However, judging from how they work by sensitizing gaba-a receptors. The result should be a reduced production of gaba in your brain, which would be easily reversible. AFAIK nmda receptors are the only that permanently change, but the cause is not similar to benzos. Permanent could mean that there is nothing that can reverse it other than time, which is true. However, if changes were permanent everyone who has every ceased using benzos would be really really messed up. My guess would be that they would sleep almost all the time due to an excess of gaba/gaba receptors.
07-01-2008, 10:28
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