Working from the outside in, intracranial hemorrhage may be epidural, subdural, subarachnoid, intraparechymal, or intraventricular in origin (though many do not remain localized to a single compartment). The term “hemorrhagic stroke” only applies to subarachnoid and intraparenchymal hemorrhages. Epidural and subdural hematomas most often result from traumatic head injury. Intraventricular hemorrhage is an important affliction of premature infants. Intraparenchymal hemorrhages are most often associated with hypertension, but may also be due to vascular malformations (usually presenting in young patients) or amyloid angiopathy (nearly confined to elderly patients). The proximate pathogenesis of hypertensive brain hemorrhage is controversial.  In the setting of chronic hypertension, an abrubt increase in blood pressure associated with an increase in cerebral blood flow is hypothesized to produce bleeding from normal or injured vessels.  Active bleeding usually lasts less than an hour.  Progressive clinical deterioration after bleeding has stopped is usually due to cerebral edema or systemic metabolic derangements, although prolonged bleeding may occasionally be responsible, especially with continued uncontrolled hypertension. While hypertensive hemorrhages may occur anywhere within the brain, they are most commonly seen in the same locations as lacunar infarcts, and for the same reason (small vessels arising directly from large caliber arteries).

The most common cause of non-hypertensive intracerebral hemorrhage is cerebral amyloid angiopathy.  In this disorder, the walls of leptomeningeal and intracortical arteries are infiltrated by a protein which is nearly identical to that found in senile plaques of Alzheimer’s disease.  Necrosis of vascular smooth muscle ensues and the cerebrocortical arterioles become prone to rupture.  This leads to the typical clinical picture of lobar hemorrhages (which are often multiple and recurrent) in an elderly patient.

Arteriovenous malformations (AVMs) are the most clinically significant of the congenital vascular malformations (the others are less likely to become symptomatic and are more frequently incidental findings on examination of the brain for other reasons).  AVMs are congenital arterio-venous shunts or connections without intervening capillary beds.  Two thirds are diagnosed before the age of forty.  Ninety percent are in the cerebral hemispheres and most of these are in the middle cerebral artery distribution. AVMs tend to present either with intracerebral hemorrhages or seizures.

Subarachnoid hemorrhage may result from extension of an intracerebral hemorrhage. In the absence of intracerebral hemorrhage, subarachnoid hemorrhage occurs secondary to rupture of vessels within the subarachnoid space.  Trauma is the most common cause of subarachnoid hemorrhage, however in trauma, subarachnoid hemorrhage is not a major contributor to overall morbidity and mortality.

The most important etiology of subarachnoid hemorrhage is rupture of a saccular aneurysm. Ruptured saccular aneurysms account for about half of all non-traumatic subarachnoid hemorrhages and produce death or permanent disability immediately in up to 50% of patients. In the absence of surgical intervention, many patients die from rebleeding if they survive the initial hemorrhage. 

Saccular aneurysms are the most common form of intracranial aneurysm, and are found with a prevalence of 2-5% at autopsy.  Predisposing factors include a family history of saccular aneurysm, polycystic kidney disease, coarctation of the aorta, and diseases that affect the integrity of vascular walls, such as Marfan’s syndrome, Ehlers-Danlos syndrome and pseudoxanthoma elasticum. Subarachnoid hemorrhage produces increased intracranial pressure, which can exceed the cerebral areterial perfusion pressure.  This results from a variety of contributing factors including the volume of subarachnoid blood, vasogenic edema, blockage of CSF drainage, and impairment of cerebral venous drainage.

The exact cause of early mortality in SAH is often unclear but may be related to cardiorespiratory problems mediated by intense catecholeminergic output resulting from hypothalamic irritation. Cerebral vasospasm is the most important cause of morbidity and mortality in patients who survive the initial hemorrhage.  This occurs in about 25% of patients, usually between 4 and 12 days after the initial hemorrhage.  The clinical syndrome evolves over a period of hours or days, which differentiates it from rebleeding which is usually sudden.  Although the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage is far from completely understood, it seems to be related to the amount of blood surrounding the arteries at the base of the brain.  It has been hypothesized that the release of oxyhemoglobin from lysing subarachnoid red blood cells initiates arterial smooth muscle contraction.

Further reading

Cordonnier C, Leys D. Stroke: the bare essentials. Pract Neurol. 2008 Aug;8(4):263-72.