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Endogenous anticonvulsant substances.

Neuroscience and Biobehavioral Reviews

|January 1, 1986

Summary

Epileptic seizures stop spontaneously due to endogenous anticonvulsant substances, not neuronal fatigue. These substances, including adenosine, prostaglandins, and opioids, also prevent further seizures, impacting epilepsy drug development.

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Area of Science:

Neuroscience
Pharmacology
Epileptology

Background:

Epileptic seizures typically cease abruptly and spontaneously.
Following a seizure, the brain exhibits a period of refractoriness to subsequent seizures.

Purpose of the Study:

To review potential mechanisms of seizure arrest.
To investigate the processes underlying post-ictal brain refractoriness.

Main Methods:

Literature review of existing data on seizure arrest and refractoriness.
Analysis of proposed endogenous anticonvulsant mechanisms.

Main Results:

Neuronal fatigue does not appear to be involved in seizure arrest or refractoriness.
Seizure arrest may involve the purine adenosine and other unknown factors.
Seizure refractoriness involves prostaglandins, opioid peptides, benzodiazepine systems, neuropeptides, and purines.

Conclusions:

Endogenous anticonvulsant substances, released during seizures, are key to both arrest and refractoriness.
Adenosine, prostaglandins, and opioid peptides are significant contributors.
Findings have implications for developing new anti-epileptic drugs and managing status epilepticus.

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