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G. Bryan Young, MD; Kenneth G. Jordan, MD
From the University of Western Ontario, London, Ontario (Dr Young), and Jordan Neuroscience, San Bernardino, Calif (Dr Jordan).

Arch Neurol. 1998;55:117-119.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

NONCONVULSIVE seizures (NCSs) are heterogeneous and include absence, complex partial, and simple partial seizures without convulsive activity.¹ Although typical absence seizures do not damage the brain, other nonconvulsive seizures, usually complex partial status epilepticus (CPSE), can cause enduring cerebral dysfunction, affecting memory and other functions. Epileptic brain damage has been documented in humans and animals and includes cognitive impairment, recurring seizures, and neuronal death.^2-3

ANIMAL MODELS

In animal studies, prolonged NCSs can cause behavioral deficits.^4-7 Repeated NCSs and induced nonconvulsive status epilepticus (NCSE) have produced epilepsy in some animals.^8-11 The classic studies of Meldrum and Brierley¹² and Nevander et al¹³ demonstrated that, even without attendant hypoxemia, acidosis, hyperthermia, and hypoglycemia, ongoing seizures in primates and rats can cause neuronal death. Epileptic brain damage is likely caused by excitotoxic effects produced by glutamate or aspartate-activating N-methyl-D-asparate and other receptors with contributions by increased free-radical . . . [Full Text of this Article]

CLINICAL EVIDENCE

CONCLUSIONS


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