1981Annals of NeurologyRequires access

Postictal pleocytosis

James W. Schmidley, Roger P. Simon

Open publisher page 45 citations

Abstract

Six patients showed a transient and otherwise unexplained cerebrospinal fluid (CSF) pleocytosis following a flurry of generalized convulsions. Each had an obvious cause for repeated seizures. No evidence was found for an infectious, inflammatory, neoplastic, or other cause for the pleocytosis. All CSF specimens were clear and colorless, under normal pressure, and bacteriologically sterile. The maximal leukocyte count ranged from 9 to 80 per cubic millimeter and reached a maximum on the day after cessation of convulsions. No specimen contained more than 650 erythrocytes. Two patients initially had a mildly increased CSF protein; glucose values were unremarkable. We propose that the pleocytosis in these patients was a result of frequently repeated generalized convulsions. The mechanism of postictal pleocytosis is uncertain. It may result from transient breakdown of the blood-brain barrier, which has been demonstrated after seizures in experimental animals. Although infectious causes must first be considered and rigorously searched for, it appears that seizures alone may cause a transient CSF pleocytosis.

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Six patients showed a transient and otherwise unexplained cerebrospinal fluid (CSF) pleocytosis following a flurry of generalized convulsions. Each had an obvious cause for repeated seizures. No evidence was found for an infectious, inflammatory, neoplastic, or other cause for the pleocytosis. All CSF specimens were clear and colorless, under normal pressure, and bacteriologically sterile. The maximal leukocyte count ranged from 9 to 80 per cubic millimeter and reached a maximum on the day after cessation of convulsions. No specimen contained more than 650 erythrocytes. Two patients initially had a mildly increased CSF protein; glucose values were unremarkable. We propose that the pleocytosis in these patients was a result of frequently repeated generalized convulsions. The mechanism of postictal pleocytosis is uncertain. It may result from transient breakdown of the blood-brain barrier, which has been demonstrated after seizures in experimental animals. Although infectious causes must first be considered and rigorously searched for, it appears that seizures alone may cause a transient CSF pleocytosis.

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Available abstract

Six patients showed a transient and otherwise unexplained cerebrospinal fluid (CSF) pleocytosis following a flurry of generalized convulsions. Each had an obvious cause for repeated seizures. No evidence was found for an infectious, inflammatory, neoplastic, or other cause for the pleocytosis. All CSF specimens were clear and colorless, under normal pressure, and bacteriologically sterile. The maximal leukocyte count ranged from 9 to 80 per cubic millimeter and reached a maximum on the day after cessation of convulsions. No specimen contained more than 650 erythrocytes. Two patients initially had a mildly increased CSF protein; glucose values were unremarkable. We propose that the pleocytosis in these patients was a result of frequently repeated generalized convulsions. The mechanism of postictal pleocytosis is uncertain. It may result from transient breakdown of the blood-brain barrier, which has been demonstrated after seizures in experimental animals. Although infectious causes must first be considered and rigorously searched for, it appears that seizures alone may cause a transient CSF pleocytosis.

Key concepts: Pleocytosis, CSF pleocytosis, Cerebrospinal fluid, Medicine, Immunology, Pathology

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