Abstract

Background: The piriform cortex, known as area tempestas, has a high propensity to trigger limbic epileptic seizures. Recent studies on human patients indicate that a resection containing the piriform cortex produces a marked improvement in patients suffering from intractable limbic seizures. This calls for looking back at the pharmacological and anatomical data on area tempestas. Within the piriform cortex, status epilepticus can be induced by impairing the desensitization of AMPA receptors. The mechanistic target of rapamycin complex1 (mTORC1) is a promising candidate.

Objective: The present perspective aims to link the novel role of the piriform cortex with recent evidence on the modulation of AMPA receptors under the influence of mTORC1. This is based on recent evidence and preliminary data, leading to the formulation of interaction between mTORC1 and AMPA receptors to mitigate the onset of long-lasting, self-sustaining, neurotoxic status epilepticus.

Methods: The perspective grounds its method on recent literature along with the actual experimental procedure to elicit status epilepticus from the piriform cortex and the method to administer the mTORC1 inhibitor rapamycin to mitigate seizure expression and brain damage.

Results: The available and present perspectives converge to show that rapamycin may disrupt the seizure circuitry initiated in the piriform cortex to mitigate seizure duration, severity, and brain damage.

Conclusion: The perspective provides a novel scenario to understand refractory epilepsy and selfsustaining status epilepticus. It is expected to provide a beneficial outcome in patients suffering from temporal lobe epilepsy.

Keywords: Status epilepticus, area tempestas, piriform cortex, rapamycin, mTOR, autophagy.