hi everybody.
What can anybody tell me about how anticonvulsants work, like clonazepam e.g.?
I’m guessing that they work as some kind of neurotransmitter blocker- through either forcing higher rates of reuptake, or by desensitizing neurotransmitter receptors. And that this blocking action acts like tinder removal- when available neurotransmitter levels drop below a certain point (turning down the ‘volume’), there isn’t a way for seizurettes to spread (no ‘shrieking feedback’).
Am I at all near the base? Way off-base? Are the mechanisms by which anticonvulsants work even understood?
thanks y’all.
jb
Clonazepam is Chlonopin(sp?), right? Same class (benzodiazepenes) as Valium, Xanax, etc? Here is some info on them.
They’re Central Nervous System depressants - taking one is basically like taking a big shot of booze - has about the same effect on the body in any case. They’re not terribly good for you, but they tend to be fairly effective in the short term as far as I can tell - but I’ve only taken them for their anxiolitic properties.
Clonazepam is an anxiolytic. Its use as an anti-seiure drug has been diminishing with time, as better, non-addicting agents have been found.
Tegretal, Neurontin, Topamax, trileptal, keppra, and others are all coming to the forefront of seizure treatment, joining that good old standbys, depakote, dilantin, and phenobarb.
How they work depends on the individual drug. And a lot of how they work is still a mystery.
Some anticonvulsants/tranquilizers work by binding to chloride channels on the membranes of nerve cells and causing the channels (which are normally opened by the inhibitory neurotransmitter GABA) to open more easily or stay open longer. This lets more chloride ions stream into the cell, which increases the negative charge inside the cell and makes the cell less likely to fire. Barbiturates and drugs like clonazepam and Valium work this way, but other anti-seizure drugs work in different ways. Some of the drugs that don’t affect the chloride channels affect sodium channels in such a way that the cell is less likely to fire over and over again quickly.
I looked up mechanisms of action for the three antiseizure medications I’ve been on.
Here’s what I found:
From http://www.topamax.com/news/topamax-tonic.htm
Mechanism of Action—Although the exact mechanism of action is unknown, studies on cultured neurons suggest that TOPAMAX works in three ways to reduce seizure frequency:
It blocks non-NMDA subtype of the glutamate receptor, a neurotransmitter that increases nerve cell excitation in the brain.
It enhances the activity of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits nerve-cell excitation in the brain.
It blocks sodium channels.
The Mechanism of action for Keppra appears to be unknown but unrelated to other antiseizure drugs.
see http://www.emea.eu.int/humandocs/PDFs/EPAR/Keppra/198600en1.pdf
Tegretol- Mechanism of Action: Like phenytoin, it is known to block sustained repetitive firing in a frequency dependent manner. As with phenytoin, this is due to blockade of sodium channels and is believed to be largely responsible for its action.
See http://www.neuroskills.com/index.html?main=tbi/ac.shtml (also lists mechanisms for other antiseizure medications)
-Lil