Nowadays, most of oral drugs available for the treatment of epileptic seizures are anticonvulsants. However, most of temporal lobe epilepsy (TLE) seizures do not manifest in convulsions. I heard something about a new therapy with antiepilergic drugs that aims to modulate the neurotransmitter function (i.e., GABA) but I do not know the effectivity of this last.
I would like to ask the expert community about the new approximations to this complex disorder (benefits/side-effects) and more specifically if you recommend to try another pharmacological treatment different from antiepilergic drugs in the case of TLE.
Thanks in advance,
The naming anticonvulsants may be misleading, so mostly the term antiepileptic drugs is used, which is a synonym. Temporal lobe epilepsy is the type of epilepsy where most of the AED are studied before being allowed to be commercialized. Newer approaches include immunotherapy, but it may be difficult to prove immune pathogenesis in an individual patient. It may take some time to figure out which AED is effective and well-supported in an individual patient, and a significant proportion may be pharmacoresistant, so the question of surgery arises.
Hope this brief summary helps.
I fully agree with Dirks answer. The term "anticonvulsant" actually is kind of a misnomer, exactly because not all seizures result in "convulsions". Also the term "antiepileptic" may be misleading - if it is interpreted as "antiepileptogenic", which would imply that these drugs are able to reverse the process of epileptogenesis. If this were true, then it would imply that a patient could take these drugs and be "cured" after a while. If some of the newer drugs actually have "anti-epileptogenic" potential remains to be seen, up to now I am not aware of any study demonstrating such an effect in humans. The most accurate term for the current medical treatment probably is "seizure suppressive drugs".
In regard to modulation of GABA: some of the seizure suppressive drugs have already been implicated to have such effects, some of them were even rationally designed to "look like" GABA, for example Gabapentin (...and of course all the benzodiazepines act on GABA receptors).
Like Dirk mentioned, most of the models where drugs or other experiments are performed are generally TLE models. Unless we have specific genetic variations in genes relevant to pathways of epileptogenesis or hyperexcitability, the current drug schemes work well. Apart from TLE due to lesions or sclerosis, they are treatable but major major part is now seen to be drug-resistant and its quite a challenge to overcome in the field of epilepsy. Refractory seizures and being handled by combination of drugs. I was working with TLE sclerosis patient in collaboration and we find certain imp gene expression has gone haywire in kinase signalling (unpublished). So atleast now, there is nothing as dietary supplement for TLE like a ketogenic diet for treatment.
TLE is not a monolithic, homogenous entity. Seizures originating from the temporal lobe could be due to a calcified temporal lobe lesion, a focal cortical dysplasia, a gliotic scar, post encephalitic etiology (HSE), MTS etc. Not all seizures arising from the temporal lobe are difficult to control with anti seizure medication. In my experience, few patients do well on CBZ monotherapy or in combination with Clobazam.
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