The classification of cerebrovascular insults generally follows a mechanistic scheme, although lesion location is also important. The principal division is between those that result from interruption of blood flow, or ischemia, and those resulting primarily from blood vessel rupture, causing hemorrhage. Within each category, cortical involvement increases the likelihood of seizures. Larger lesions and more severe deficits are associated with a higher risk of seizures and epilepsy in most, but not all, circumstances.

Ischemic strokes are divided into several types:

  • Thrombotic
  • Embolic
    • Cardiac
    • Artery-to-artery
  • Small vessel (“lacunar”)
  • Hypoperfusion (“watershed”)
  • Coagulation-related
  • Vasospastic
    • Migrainous
    • Vasculitic

Ischemic infarcts result in neuronal death from localized loss of blood flow. Cell death occurs when energy-dependent processes, such as maintaining ionic gradients across cellular and intracellular membranes, fail. Excitotoxicity mediated by glutamate receptors also contributes.12 In addition, as the damage heals, inflammatory processes are activated and can cause further neuronal damage.

A frequent cause of ischemic infarcts is progressive atherosclerosis leading to critical stenosis or occlusion of major arteries, such as the internal carotid, vertebral, or basilar arteries. An unclear percentage of such vascular lesions may actually produce infarcts by the phenomenon of artery-to-artery embolisms arising from unstable plaques or thromboses.7,13

Cardiogenic emboli most often arise from a friable clot occurring on a diseased valvular or myocardial surface. They frequently lodge in large arteries at branching points, such as the origin of the middle cerebral artery (MCA) and its major subdivisions or the basilar bifurcation at the origin of the posterior cerebral arteries (PCAs). Less common are clots that result from nonbacterial thrombotic endocarditis or septic emboli from infectious endocarditis.

Embolic strokes usually affect the cortex of gray-white junction, where blood flow is highest and end arteries predominate; cortical involvement would be more likely to precipitate seizures and epilepsy than subcortical lesions.

Arterial dissection, occurring because of trauma to the vessel (sometimes trivial or forgotten), connective tissue disorders, or both, can cause embolic or thrombotic stroke in the involved vascular territory.

A common cause of ischemic stroke is progressive stenosis of small vessels, classically from damage to the vascular media caused by chronic hypertension, a process termed lipohyalinosis (probably a form of atherosclerosis). This usually affects the penetrating arteries that branch off the MCA or basilar artery, causing “lacunar” infarcts of the basal ganglia, deep white matter, or brain stem. Damage to these areas is less likely to cause acute symptomatic seizures or epilepsy than are strokes that affect cortex directly.

Global cerebral hypoperfusion that occurs in the setting of stenotic vessels can result in focal infarcts, usually occurring at cortical and subcortical border zone or “watershed” areas between territories of the major blood vessels, especially the anterior cerebral artery and MCA, or the MCA and PCA. Severe hypoperfusion or cardiac arrest can also cause selective damage to these areas, particularly if large vessels are narrowed from atherosclerosis, but more commonly results in widespread damage, sometimes diffusely affecting the middle layers of cortex, termed laminar necrosis. Less complete insults may cause selective damage of the hippocampus and cerebellum. Acute symptomatic seizures or status epilepticus(SE), especially myoclonic status, is common after hypoxic-ischemic insults.14

Hypercoagulable states, such as may be associated with malignancy, collagen vascular diseases, or genetic abnormalities of the thrombolytic system, cause in situ thrombosis of small or large vessels, often multiple. They are also associated with cardiogenic emboli from nonbacterial thrombotic endocarditis.13 Certain types of coagulation defects may promote venous rather than arterial thrombosis, leading to venous infarcts or, among patients with cardiac septal defects, arterial emboli.

Vasospasm is thought to be the main mechanism by which migraine causes occasional stroke. Platelet aggregation may also be a triggering event. Migrainous infarction is a rare complication of a common condition and is more likely to occur in those with focal neurologic symptoms as a component of their usual migraine.15 Vasospasm can also occur as a complication of angiography. (Patients with migraine may have a higher risk.) Branches of the PCA are most often affected.

Systemic or cerebral vasculitis is another potential cause of vasospasm and is due to autoimmune disease or drug abuse, particularly of cocaine.15 Inflammation of the arterial walls can also cause hemorrhage, although this is more common with inflammation caused by infections.

Nearly any kind of ischemic process, if rapidly reversible, can result in temporary dysfunction without permanent damage, manifested as a transient ischemic attack (TIA). Magnetic resonance imaging (MRI) has demonstrated that permanent structural changes (i.e., infarcts) can occur with TIAs lasting well under 24 hours, however, even though the clinical deficits appear to resolve completely.7 Therefore, not just acute symptomatic seizures but also epilepsy can result from a clinical TIA.

Hemorrhagic conversion of ischemic infarcts occurs when the vessel wall itself is sufficiently damaged to disturb its integrity. Clinically, this is more likely to occur with embolic infarcts than with other types. Furthermore, because current means of treating or preventing ischemic infarcts interfere with clot formation or maintenance, these therapeutic measures also pose a risk of hemorrhage. This risk is low for antiplatelet agents and moderate for anticoagulants and thrombolytic agents.

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 ( 

Reviewed By: 
Steven C. Schachter, MD
Thursday, April 1, 2004