Early Poststroke Seizures

Abstract

We define as early seizure (ES) those occurring within 7 days after stroke and late seizures those developing beyond 1 week after stroke. Seizures are well known to occur at the onset of intracerebral hemorrhage and serve as a clinical marker. Onset seizures may be focal or generalized, are usually brief and are associated with loss of consciousness in the setting of hemorrhage. A similar concept of immediate seizure occurs in traumatic brain injury. Predictive factors of ES can be classified of general and neurologic origin. An important question is whether ES per se worsen prognosis and outcome. The viability of the penumbral region in animal models of focal ischemia is influenced by the peri-infarct depolarization waves. If this also is true in humans, seizures in the immediate poststroke period might worsen outcome. Recently, hypercholesterolemia has been associated with better functional outcome at 1 month after a first-ever stroke, and multivariate analysis studies have shown that mean cholesterol values were lower in patients with ES compared with controls.

Seizures and epilepsy in patients with lacunar strokes

“…In contrast to previous studies [20,21], we do not observe that hypercholesterolemia is protective against stroke-related seizures.…”

Seizures in Acute Stroke: Incidence, Risk Factors and Prognosis

“…Early seizures (ES) are frequently defined as those occurring within the first 7–14 days after stroke, but some authors extend this definition up to the first 4 weeks [4,5,6,7,8,9]. Seizures appearing after this time are considered as late seizures.…”

Early post-acute stroke seizures: Clinical profile and outcome in a Nigerian stroke unit

“…[16,17] The Aiwansoba and Chukwuyem: Clinical profile and outcome of early post-acute stroke seizures dominant majority of western literature however associates EPASS more with hemorrhage than infarct. [1,2,4,6] This epidemiologic difference in the presentation of EPASS and the subtype of stroke may not be unrelated with the very high proportion of putaminothalamic (deep) bleeds of ruptured lenticulostriate arteries from chronic severe hypertension in Africans, which may provoke less seizures in contrast to cortical (superficial) bleeds as shown in the recent Kinshasa intracerebral hemorrhage score study in rural Congolese Africans. [18] Similar studies have divested EPASS to an extent from pathologic subtypes of stroke and have instead associated EPASS more with cerebral cortical location of a stroke than with the subtype of stroke.…”

“…[2][3][4] There are no strict guidelines currently in the definition of EPASS in reference to the number of days after a stroke; however, between 7 and 14 days have been used operationally. [5,6] EPASS usually begins within the first 24 h of a stroke, it could be solitary or multiple, focal or generalized, it may occasionally present as status epilepticus, and it is found more frequently in males than in females. [7,8] The pathophysiological changes that occur in the brain's cortical function shortly after a stroke is believed to be the neural substrate for EPASS and more often than not, as the acute alterations resolve, EPASS also resolves and usually does not progress to epilepsy (a tendency to recurrent seizures).…”