A few other causes of cerebrovascular insult do not correspond so well with the ischemic or hemorrhagic classifications:
Cerebral venous occlusions may occur spontaneously in patients with a hypercoagulable state (including pregnancy or recent parturition) or in those with intracranial infections, especially in parameningeal locations, such as the mastoid. These occlusions diminish local blood flow and typically produce hemorrhagic infarctions that do not conform to the usual arterial territories. Cortical vein thrombosis commonly produces acute symptomatic seizures, but epilepsy is a much less common sequela.28–30
The term hypertensive encephalopathy refers to an acute cerebrovascular syndrome precipitated by sudden, severe hypertension.11 When systemic blood pressure is raised suddenly, there is a loss of cerebral autoregulation from forced dilatation of cerebral resistance vessels. Pathologically, these vessels show abnormal permeability to protein, and the surrounding brain shows swelling of astrocytes, primarily of cortical layers 2 and 3.10 This process results in localized cerebral edema, often affecting the parieto-occipital regions and causing focal deficits and often acute symptomatic seizures.23,24 Patients usually make a good recovery. Although petechial hemorrhage is common, epilepsy rarely follows these insults. It is important to realize that the degree of hypertension need not be extreme, as long as it is unusually high for a given patient.
A clinically and radiographically similar process occurs among patients on immunosuppressant therapy, even in those with only minor elevations of blood pressure. Apparently, the immunosuppressant itself can directly affect vessel wall permeability.
Eclampsia may result from a similar pathophysiologic process.25 Again, acute symptomatic seizures are common, but epilepsy is rare. Treatment with magnesium is recommended (see Special situations). Magnesium can block the NMDA subtype of excitatory glutamate receptors, but it is not clear that systemic administration has such an effect across the blood-brain barrier, so its use in this syndrome may succeed because of its effects on the underlying vascular pathophysiology.25,26
A special situation that is closely related to the processes previously discussed is that of postendarterectomy hyperperfusion syndrome. This occurs usually a day or two after successful carotid endarterectomy. It is characterized by acute headache, hemispheric edema ipsilateral to the surgery, and acute symptomatic seizures.27 Pathophysiology is thought to be rapid restoration of perfusion pressure in a distal circulation that has been accustomed to much lower perfusion, resulting in a loss of autoregulation and associated dysfunction. Lowering blood pressure is the mainstay of treatment. Therapy with antiepileptic drugs is also important, to prevent focal seizures and the further localized blood flow increases associated with them.
Within each stroke category, cortical involvement increases the likelihood of seizures. This is not surprising in view of the well-established conception of seizures as cortical events. In addition, larger lesions and more severe deficits are associated with a higher risk of seizures and epilepsy in most, but not all, circumstances.
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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