The principal division in the classification of cerebrovascular insults is between those that result from ischemia and those resulting primarily from blood vessel rupture, causing hemorrhage. Hemorrhagic strokes are divided into various types:

  • Related to vascular malformations
    • Arteriovenous malformation
    • Cavernous angioma
    • Venous angioma
  • Subarachnoid (aneurysmal)
  • Spontaneous intracerebral
    • Hypertensive (deep, lobar)
    • Amyloid angiopathy
  • Coagulopathy-related

Mechanisms of damage

Hemorrhagic strokes share with ischemic processes a more or less sudden onset but cause cerebral damage in different ways:

  • An arterial leak results in a concussive insult to nearby neurons and axons, leading to neuronal dysfunction and, if sufficiently severe, neuronal death.
  • If the leak is not quickly sealed, then intracranial pressure rises, ultimately to the level of arterial pressure, and cerebral perfusion is precluded until communication between the arterial and extra-arterial cerebral space is ended. This elimination of perfusion pressure can result in global, multifocal, or localized ischemia.
  • Locally, a blood clot constitutes a mass lesion that exerts pressure on nearby neural and vascular structures and sometimes sufficiently interferes with arterial or venous blood flow to cause an infarct.
  • After intracerebral hemorrhage, as with ischemic infarcts, the inflammatory system is activated to dispose of cellular and hematologic debris, and this can cause vasospasm.
  • Blood products result in chronic exposure of neurons to iron-containing compounds, which may lead to peroxidation of lipid membranes and promote excitatory ionic currents.8

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

Congenital vascular malformations

Congenital vascular malformations are a common cause of intracerebral hemorrhage, especially in younger people. These are usually divided into three types:

  • Arteriovenous malformations (AVMs) have a direct arterial-to-venous connection without an intervening capillary bed. Most eventually become symptomatic, with the most common presentation being hemorrhage (40–50%) and the next most common being seizures (17–40%), especially in younger people and perhaps in those with larger malformations.4,16 AVMs may also produce progressive, and at times transient, ischemic deficits via a steal phenomenon from surrounding normal tissue.
  • Cavernous angiomas consist of vascular channels lined by endothelium without intervening neural tissue. Seizures are the most common presentation, occurring in at least 40–70% of patients.16 A sizable proportion, however, are incidental findings on MRI and are estimated to occur in 0.5% of the general population.17 Diagnosis usually depends on a characteristic heterogeneous pattern with evidence of surrounding blood products, implying at least minor hemorrhage.
  • Venous angiomas are aberrant venous channels that communicate with the normal venous system. Symptoms are uncommon, but of those venous angiomas that become symptomatic, most present with seizures, except those located in the cerebellum, which are the most likely ones to hemorrhage.

A fourth type of vascular malformation, capillary telangiectasias, consists of dilated capillary structures with intervening neural tissue. These are most often located in the pons and are rarely symptomatic.

Subarachnoid hemorrhage

Subarachnoid hemorrhage may result from AVMs or from coagulation or platelet defects, but the most common cause by far is rupture of a saccular aneurysm, thought to result from an area of congenital weakness in the arterial wall, usually located at branch points near the circle of Willis. The most common locations of these aneurysms are the junction of the posterior communicating artery and internal carotid artery and the anterior communicating artery. Next most common are the proximal middle cerebral artery and then the posterior circulation.7 Thought to be congenital, they are present in perhaps 5% of the population. The likelihood of rupture increases markedly with advancing age, as well as with hypertension and smoking.

Approximately one-third of ruptures are immediately fatal, another one-third result in significant disability, and another one-third of patients recover without major disability.

The major risks after the initial bleed are

  • rebleeding (may be prevented by surgery to occlude the aneurysmal neck)
  • vasospasm, causing focal or multifocal cerebral ischemia (This ischemia may in some cases be prevented by increasing perfusion pressure, but it is unsafe to do so unless the aneurysm has been secured.)
  • hydrocephalus (early or late)

Acute symptomatic seizures may occur at the time of the initial bleed, when they may be confused with syncope resulting from transient cessation of cerebral perfusion, caused by the acute rise in intracranial pressure to equal the systemic pressure. Epilepsy and acute symptomatic seizures may be related to hemorrhages that occur parenchymally, as well as in the subarachnoid space. Intracerebral extension of the hemorrhage is often associated with rupture of aneurysms that involve the anterior communicating artery and damage the orbitofrontal cortex.

Subarachnoid and subdural bleeding can result from another type of anomaly, dural arteriovenous fistulas, which may be acquired as a result of trauma or other insult. These can also cause seizures and epilepsy, but the usual presentation is chronic headache.18

Intracerebral hemorrhage

Intracerebral hemorrhages are most commonly due to acute and chronic hypertension. In these patients, most of the hemorrhages are located in the basal ganglia, especially the putamen. Although lobar hemorrhages are more likely to produce seizures and epilepsy, some deep hemorrhages, especially those involving the caudate,19 may also lead to seizures.

A substantial proportion of lobar hemorrhages may in fact be due to a different source of vascular damage than that produced by hypertension. The terms cerebral amyloid angiopathy (CAA), cerebral congophilic angiopathy, and cerebrovascular amyloidosis refer to a clinicopathologic entity characterized by hyaline eosinophilic staining properties.20 CAA is implicated as the cause of primary nontraumatic intracerebral hemorrhage in as many as 10–15% of patients over the age of 60 years and in nearly 20% of patients over the age of 70 years.21 This pathology may also produce seizures in the absence of gross hemorrhage; petechial hemorrhage is suspected.22

Other causes of intracerebral hemorrhage include coagulopathies. These may be congenital, such as the hemophilias, or acquired, often as a result of treatment with anticoagulants or 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
Wednesday, March 31, 2004