The term stroke refers to a neurologic deficit with sudden or rapid onset due to hemorrhagic or ischemic cerebrovascular disease, which lasts 24 hours or more. A deficit due to ischemia that lasts less than 24 hours is a transient ischemic attack (TIA).

Historical references for stroke as a cause of seizures or epilepsy date back to Hippocrates, but it was not until Hughlings Jackson in 1864 that brain damage from stroke was clearly defined as a cause of epilepsy.2

Subsequent studies have confirmed that cerebrovascular disease is the most common documented cause of seizures in the elderly, accounting for 22–69% of seizures in this age group.3–5 As the population ages, cerebrovascular disease will account for an increasingly high percentage of total cases of seizures and epilepsy.

An additional relationship between seizures and vascular disease concerns differential diagnosis: In some cases, it is difficult to determine whether the cause of transient neurologic dysfunction is ischemia (TIA) or seizure and, if from a seizure, whether the seizure itself results from a new vascular insult. These distinctions have major implications for treatment.

Cerebrovascular disease can result in seizures or epilepsy in several ways:

  • With stroke, as with other structural lesions of the brain, neuronal damage can alter the balance between excitation and inhibition. The resultant hyperexcitability can lead to acute symptomatic seizures, generally defined as occurring within 1 to 2 weeks of the stroke, and epilepsy, a chronic tendency toward recurrent unprovoked seizures. The occurrence of acute symptomatic seizures is neither necessary nor sufficient to predict the later development of epilepsy, but in most settings, acute seizures increase the risk of subsequent epilepsy.6 If the ischemia is of insufficient duration to produce neuronal damage, an acute symptomatic seizure is still possible, but permanent alterations leading to epilepsy should not occur. However, modern neuroimaging has established that the 24-hour definition of a TIA is insufficiently restrictive, as many TIAs lasting longer than a few minutes produce evidence of permanent neuronal damage that could potentially be epileptogenic.7
  • Cortical iron resulting from hemorrhagic strokes can make neuronal membranes more excitable, producing a chronic epileptic focus.8,9
  • Stroke treatment can result in seizures, most commonly by causing hemorrhage into an infarcted brain region (i.e., hemorrhagic conversion).
  • Measures for treating or preventing stroke can occasionally lead to seizures by causing new infarcts or acute elevation of blood pressure that disrupts autoregulation of cerebral blood flow and leads to localized cerebral edema.10,11

Adapted from: Bromfield, EB, and Henderson GV. Seizures and cerebrovascular disease. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;269–289.
With permission from Elsevier (www.elsevier.com). 

Authored by: EB Bromfield | GV Henderson | Steven C. Schachter, MD on 4/2004
Reviewed by: Steven C. Schachter, MD on 4/2004
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