Mesial temporal lobe epilepsy · Grey Matter

Mesial temporal lobe epilepsy is epilepsy whose seizures start in the inner face of the temporal lobe (the hippocampus, the amygdala and the cortex around them), and it is the most common focal epilepsy in adults and the one most often treated with surgery.

Mesial temporal lobe epilepsy. Mesial temporal lobe epilepsy is epilepsy whose seizures start in the inner face of the temporal lobe (the hippocampus, the amygdala and the cortex around them), and it is the most common focal epilepsy in adults and the one most often treated with surgery.

Its typical seizure begins with an aura the person remembers: a rising feeling from the stomach, a sudden intense déjà vu, fear, or a strange smell or taste. Awareness then fades into a fixed stare, often with automatisms (lip smacking, chewing, fumbling with the hands), lasting a minute or two, followed by confusion. The structure involved explains the signs: the hippocampus and amygdala are memory and emotion machinery, so their seizures are felt as memory and emotion.

Hippocampal sclerosis is the usual lesion. The hippocampus is shrunken and scarred on MRI, with heavy loss of pyramidal cells (CA1 worst) and of some interneurons, and an international classification grades the pattern of loss.

The circuit rewires. In sclerosis, the mossy fibres of dentate granule cells, which normally project forward, sprout back onto the granule cells themselves, forming recurrent excitatory loops; this sprouting is a candidate mechanism of the epilepsy, and how much it causes rather than accompanies is still argued.

It resists drugs. A large share of people with it keep having seizures despite medication, which is the reason it dominates epilepsy surgery: in a randomised trial, 58 % were free of seizures impairing awareness a year after temporal lobe surgery against 8 % with drugs alone.

Memory can suffer from both the seizures and the surgery, especially on the language-dominant side, which is why memory and language are mapped before an operation.

In mesial temporal epilepsy the scar and the seizures are thought to feed each other.

In the leading model, prolonged seizures kill vulnerable cells and rewire what remains, and the rewired hippocampus produces more seizures; how often this loop runs in people, rather than in animal models, is still studied.

Questions: How well does removing part of the temporal lobe stop seizures? In the randomised trial that settled the question, 80 people with drug-resistant temporal lobe epilepsy were assigned to surgery or to continued medication, and after one year 58 % of the surgical group were free of seizures that impair awareness against 8 % of the medical group. Surgery is considered once two appropriate, tolerated medicines have failed to give lasting freedom from seizures, the international definition of drug resistance. The risks, chiefly to memory and to part of the upper visual field on the side opposite the operation, are weighed with mapping of language and memory before the operation. Why is the hippocampus the most common starting point of focal epilepsy that resists drugs? The hippocampus is built for strong recurrent excitation and plasticity, which serve memory and also let activity spread and synchronise easily. Its pyramidal cells, CA1 above all, are among the most vulnerable in the brain to injury such as a prolonged febrile seizure, and their loss leaves a shrunken, scarred hippocampus, called hippocampal sclerosis. In the surviving circuit, the mossy fibres of dentate granule cells sprout back onto granule cells and form recurrent excitatory loops, and some inhibitory interneurons are lost, so the tissue becomes easier to synchronise and harder to calm with drugs.