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From: Neuropsychiatry, Neuropsychology, Clinical Neuroscience (Lippincott, Williams & Wilkins)
by Rhawn Joseph, Ph.D.


Hemorrhage can occur anywhere throughout the brain and may be due to a number of causes, e.g., head injury, hypertension, rupture of an aneurysm or arterial venous malformation (AVM), the weakening of a segment of the vasculature secondary to emboli or thrombus, or vessel wall necrosis due to occlusion and ischemia (Adams & Victor 1993; Roos et al. 1995).

Hemorrhages are frequently classified in terms of gross anatomical location. These include, extradural, subdural, subarachnoid, intercerebral/cerebral, and cerebellar. Extradural and subdural hemorrhages are frequently secondary to head injury, whereas subarachnoid, cerebral and cerebellar hemorrhages are often related to arterial abnormalities. Bleeding from a hemorrhage may be minute and inconsequential, or profuse and extensive such that a large pool of blood rapidly develops. In some cases bleeding may occur at a very slow, albeit continuous pace such that the adverse effects are not detected for days.


Subarachnoid hemorrhage results from any condition which causes blood to leak into the subarachnoid space. Massive subarachnoid hemorrhage is usually due to rupture of an intracranial aneurysm, or bleeding from a cerebral angioma--in either case there is no warning and the onset is quite sudden and abrupt (Adams & Victor, 1994; Roos et al. 1995; Schievink et al. 1995). If the hemorrhage is severe it may lead to immediate coma and death, particularly if there is a buildup of over 20 ml of intraventricular blood (Roos et al. 1995). If moderate, the patient may pass into a semi-stuporous state, and/or become confused and irritable. If minor patients may complain only of severe headache and possibly develop focal deficits after hours or over the course of the first few days or weeks following hemorrhage. Vasospams and rebleeding are very common during the first two weeks.

Subarachnoid hemorrhage has a mortality of over 50% , a third of whom will die immediately or within the first 24 hours (Schievink et al. 1995). Only approximately 25% who survive will make a good recovery (Hijdra et al. 1987).

Subarachnoid hemorrhage occurs most often among individuals above age 50. When it occurs among among younger individuals it is often secondary to congenital vascular abnormaltiies, including angioma, ruptured aneurysms or via the rupture of an AVM on the brain surface (Adams & Victor, 1993; Brown et al. 1991; Schievink et al. 1995; Toole, 1990). Rupture or seepage into the ventricular system is not uncommon (Roos et al. 1995), and CSF is bloody in 90% of cases. Anemic and hemorrhagic infarction may coexist in the same lesion.

Headache and vomiting are immediate common sequela of hemorrhage (as well as cerebrovascular disease) and most patients will complain of severe backache and neck stiffness in the absence of demonstrable focal signs which develop later (Gorelick et al. 1986; Portenoy et al. 1984). Onset is sudden and the intensity is described as severe or violent. These headaches are diffusely distributed over the cranium and/or are localized to the frontal-parietal region (Gorelick et al., 1986). Headaches are usually due the pressure effects of escaping blood which distend, distort, or stretch pain-sensitive intracranial structures. Pain in or behind the eye is often associated with hemorrhage of posterior communicating-carotid aneurysms (Gorelick et al., 1986).


Cerebral hemorrhage is commonly caused by hypertension and associated rupture aneurysm and degenerative changes in the vessel wall of penetrating arteries which make them suceptible to rupture (Kase, 1986; Schievink et al. 1995). Onset is always sudden.

The rupture may be brought on by mental excitement of physical effort, or may ocur during rest or sleep. Usually the the patient complains of sudden headache and may vomit and become confused and dazed with progressive impairment of consciousness over several minutes or hours time (except in the most mildest of cases). However, it may evolve gradually taking hours or days to become fully developed, and there may be no warning signs (Mayer et al. 1994).

After a large hemorrhage the affected hemisphere becomes larger than the other due to swelling. As the pool of blood increases and begins to clot, surrounding tissues become compressed, the convolutions become flattened and pressure may be exerted against the opposite half of the brain causing damage in this region also. With large hemorrhages, coma and death may ensue due to compression of midline and vital brainstem nuclei (Adams & Victor, 1994; Mayer et al. 1994). If the patient survives and the clot is not surgically removed it is eventually absorbed and replaced by a glial scar. In these instances, however, patients are commonly incapacitated to varying degrees. Cerebral hemorrhages occur most often in the vicinity of the internal capsule, corona radiata, frontal lobe, pons, thalamus and putamen (Adams & Victor, 1994; Kase, 1986).

The neurological deficit is never transitory (good functional recovery being attained by less than 40% of the survivors) and 30 to 75% die within 30 days (Adams & Victor, 1994; Fieschi et al. 1988; Portenoy et al., 1987). Most patients suffer persistent, permanent, and severe neurological abnormalities. Good clinical outcome is related to lower age, the size of hemorrhage, the time period the patient was unconscious, high scores on the Gasgow Coma Scale, and post-operative neurological events (Meier 1991; Portenoy et al. 1987; Tidswell et al. 1995; Toole, 1990).

In over 60% of the cases, intracerebral hemorrhage is related to hypertensive cerebrovascular disease (Mohvr et al. 1978) which makes vessels susceptible to rupture. That is, hypertension can induce degenerative changes and may in fact induce the formation of microaneurysms particularly in the subcortical and perforating arteries (Kase, 1986). However, not all cerebral hemorrhages are due to hypertension.


When emboli and other debris build up or occlude the artery, the arterial wall will begin to die and then rupture, and the vessel with hemorrhage out its contents. Approximately 65% of those with a cerebral embolic stroke develop hemorrhagic infarction. Conversely, less than 20% of those with thrombosis will develop hemorrhage (Ott et al. 1986). Similarly, approximately 50% of all hemorrhagic infarcts are associated with embolic strokes (Fisher & Adams, 1951; Hart & Easton, 1986). Hence embolic strokes have a special propensity for hemorrhagic transformation and hemorrhagic infarction nearly always indicates embolism.

Blood vessels effected by embolism characteristically hemorrhage within 12-48 hours (Cerebral Embolism Study Group, 1984; Hart & Easton, 1986). However, the hemorrhage may take several days to fully develop (Laureno et al. 1987). Hemorrhagic transformation occurs when the emboli disintegrates and/or migrates distally thus allowing reperfusion of the damaged vessel (Fisher & Adams, 1951: Jorgensen & Torvic, 1969). That is, when a vesssel is occluded, it is damaged and weakened, and both the brain and the involved portion of the vessel may become necrotic. When the weakened portion of a previously occluded vessel is subsequently reexposed to the full force of arterial pressure it ruptures and hemorrhages. Fortunately, blood vessels have he capacity to regenerate.

Frequently embolic hemorrhages are asymptomatic (Hakim et al. 1983; Ott, et al., 1986) and supposedly benign since the tissue involved has already been damaged. However, if the hemmorhage is secondary to anticoagulant therapy the bleeding may be more profuse and cause significant neurological deterioration and even death.


Hemorrhage may occur secondary to drug use, anti-coagulant therapy, medication, AVMs, aneurysms, vessel wall necrosis, brain tumors, and various types of arterial pathology, including small vascular malformations, and cerebral amyloid angiopathy (Adams & Victor, 1993; Brown et al. 1991; Kase, 1986; Roos et al. 1995; Schievink et al. 1995; Toole, 1990).

ISCHEMIA & HEMORRHAGIC INFARCTS Ischemia not only results in the death of brain cells but necrosis of the local vasculature which is also deprived of metabolic support (Welch & Levine 1991). These vessel wall ischemic structural alterations make them very suceptible to rupture. Indeed, over 40% of those with cerebral ischemic infarction will become hemorrhagic within one to two weeks (Hornig et al. 1986).

These ischemic related hemorrhagic infarcts (HI) are not limited to a single vessel, however. Bleeding may be mutlifocal, particularly if the patient had suffered a large stroke.

In part, this is also due to the more extensive edema associated with large strokes. When swelling occurs not only is brain tissue compressed but the endothelium of various small vessels is also crushed and damaged. When these vessels are compressed blood flow is prevented which in turn makes these same vessels and their distal extensions more suceptible to rupture when blood flow is reestablished (Garcia et al., 1983). That is, with blockage of a vessel, the distal part of the vessel may become necrotic. Even with mild degrees of edema there is compressions and subsequent damage to various small vessels surrounding the lesion (Welch & Levine 1991).

Hemorrhagic infarcts are not usually associated with chronic hypertension (Hart & Easton, 1986). Frequently, however, they are secondary to the reestablishment of blood flow following occlusion. Because of this when anticoagulants are employed so as to remove the clot, the necrotic vessels rupture and hemorrhage. Hence anticoagulants can increase the risk of secondary hemorrhagic infarction particularly when used following large strokes and/or those accompanied by gross neurological disturbances (Cerebral Embolism Study Group, 1983; Hornig et al., 1986).


Aneurysm (also called saccular or berry aneurysms) take the form of small, thin walled blisters protruding from the various cerebral arteries (Brown et al. 1991). Aneurysms may be single or multiple, and are presumed to be due to developmental defects; e.g., a congenital weakness at the junction of two arteries. Often they are located at the bifurcations and branches of various arteries, particularly the internal carotid, the middle cerebral, or the junction of the anterior communicating and anterior cerebral arteries (Adams & Victor 1994; Brown et al. 1991).

Symptoms secondary to aneurysm (due to rupture or compression) may occur at any age. Prior to rupture they are usually asymptomatic. However, as there is a tendency for them to enlarge over time, which in turn makes them more suceptible to rupture, with increasing age there is increasing risk. The peak incidence of rupture is between 40 and 55 (Adams & Victor, 1994).

Aneurysms may rupture due to sudden increases in blood pressure, while engaged in strenuous activity, during sexual intercourse, or while straining during a bowel movement (Adams & Victor, 1994). One patient I examined suffered a ruptured aneurysm when hyperventilating in his swimming pool so that he could remain submerged for a long time period.

Occasionaly, if large and located near the base of the brain they may compress the optic nerves, hypothalamus or pituitary; and if within the cavernous sinus, compress the 3rd, 4th, 6th, or opthalamic division of the 5th nerve. Hence, a variety of visual, endocrine, and emotional alterations may hearld the presence of an aneurysm prior to rupture (Brown et al. 1991).

With large aneurysms, when rupture occurs, blood under high pressure may be forced into the subarachnoid space, and the patient may be striken with an excrutiating generalized headache and/or almost immediately fall unconscious to the ground, or they may suffer a severe headache but remain relatively lucid (Adams & Victor, 1994; Brown et al. 1991; Jorensen et al. 1994; Schievink et al. 1995). If the hemorrhage is confined to the subarachnoid space there are few or no lateralizing signs and no warning symptoms. In some cases, however, patient may complain of headache, transitory unilateral weakness, numbness or tingling, or speech disturbance in the days/weeks preceeding rupture --due to minor leakage of the aneurysm.

Often those who become unconscious following rupture develop decerebrate ridgity. This is usually due to compression effects (such as herniation) on the brainstem. Persistent deep coma is accompanied by irregular respiration, attacks of extensor rigidity, and finally respiratory arrest and circulatory collapse. In mild cases, consciousness, if lost, may be regained within minutes or hours. However, patients remain drowsiness, confused, and complain of headache and neck stiffness for several days (Jorgenson et al. 1994). Unfortunately, in mild or severe cases there is a tendency for the hemorrhage to reccur (Adams & Victor, 1993).

Cerebral amyloid angiopathy

Amyloid angiopathies are associated with the development of microaneurysms and the occlusion of arteries in the superfical layers of the cerebral cortex (Kase, 1986). Following amyloid occlusion, the arteries are often weakened thus making them susceptible to rupture.

Amyloid angiopathies are often associated with recurrent hemorrhages over a period of months which in turn may lead to the develpment of intracerebral hematomas. Sometimes a head trauma can trigger these later form of hemmorhages.


Arteriovenous malformations consist of a tangle of dilated blood vessels and are sometimes referred to as angiomas. It is a developmental abnormality, and may become symptomatic at any age, but most commonly between the ages of 20-30.

Frequently AVMs form abnormal collateral channels between arteries and veins thus bypassing the capillary system (Brown et al. 1991). When this occurs there may be an abnormal shunting of blood from the arteries to the veins. In consequence underlying brain tissue is not adequately irrigated and may become ischemic depending on the size of the AVM.

AVMs vary in size and tend to be located in the posterior portion of the cerebral hemispheres, near the surface, as well as deep within the brainstem, thalamus, and basal gnaglia. Frequently they are multiple and may be found in a variety of separate locations (Brown et al. 1991; Toole, 1990). They tend to be more common among males.

Like aneurysms, AVMs are present from birth and can grow larger and more complicated over time. It has been estimated that AVMs can increase in size by 2.8% per year and can become 56% larger over the span of a 20 year time period (Mendelow et al. 1987). As they increase in size the risk of them becoming symptomatic increases as there is a greater likelyhood of collateral shunting.

AVMs are often a cause of intracerebal and subarannoid hemmorhage (Brown et al. 1991; Drake, 1978). When hemorrhage occurs blood may enter the subarachnoid space thus mimicking an aneurysm. However, although the first symptom is usually a hemorrhage, 30% of patients with this disorder may suffer a seizure and 20% headaches or focal neurological symptoms.

Small vascular malformations often become symptomatic during the 30s and 40s and occurs more often among females (Kase, 1986). These often involve the subcortical whtie matter of the convexity.

Brain tumors can give rise to hemorrhage in a variety of ways, particularly if the tumor is malignant and is richly vascularized. That is, certain tumors have a tendency to become spontaneously necrotic. When this occurs, there supporting vasculature ruptures. However, frequently tumors are transmitted to the brain via the arterial system, whereas others, such as carcinomas, tend to invade the walls of blood vessels. In either instance, by adhering to or penetrating the walls of the blood vessels, tumors can make them more suceptible to rupture (see chapter 34).


Individuals with possible cerebrovascular abnormalities (such as aneurysm, AVM, or even tumor), and who abuse cocaine or amphetamines are at risk for suffering an intracranial hemorrhagic infarct (Golbe & Merkin, 1986; Lichtenfeld et al. 1984; Schwartz, & Cohen, 1984; Wojak & FLamm, 1987). Presumably these drug induced hemorrhages are due to transient increases in blood pressure and/or vasospasm which in turn act to rupture abnormal vessels.


Mortality rates for cerebrovascular diesase have declined in the U.S. over the course of the last 40 years (Gillum, 1986; Meier & Strauman 1991). Nevertheless, the initial death rate for individuals in the acute phase and up to 30 days after stroke is about 38%. However, 50% of those who survive this phase die over the course of the next 7 years (Dombovy et al. 1986). Moreover, mortality rates increase for those who suffer strokes during the winter months (Lanska & Hoffman, 1999).

The major determinants for short-term mortality are intraventicular hemorrhage, pulmonary edeman, impaired consciousness, leg weakneness, respiratory diease and increasing age (Chambers et al. 1987; Lanska & Hoffman, 1999; Roos et al. 1995; Schievink et al. 1995)-with level of consciousnes following stroke being the single most important predictor of short-term survival (Chambers et al. 1987). The major determinants for long term mortality are low activity level, advanced age, male sex, heart disease and hypertension. However, those who suffer intraventricular hemorrhagic infarcts have a higher mortality rate than those with infarcts due to other causes (Chambers, et al. 1987; Roos et al. 1995; Schievink et al. 1995). As noted in chapter 10, those with right hemisphere damage tend to have poorer outcomes as well as higher mortality rates. In particular right parietal lobule infarcts are associated with very poor outcomes (Valdimarsson et al. 1982).

Hyperglycemia and diabetes are also associated with poor neurological recovery, and higher short-term mortality as well as increasing the risk for stroke in general. This is because diabetes and hyperglycemia both accentuate ischemic damage (Bruno et al., 1999; Pulsinelli et al. 1983; Woo et al. 1988). Hyperglycemia also appears to have a negative effect on energy metabolism due to the generation of severe lactic acidosis (Rehncrona et al. 1980) --factors which act to retard neuronal recovery.

Some authors have argued that luxury perfusion and increased cerebral blood flow (CBF) within an infarcted cite is often indicative of a good prognosis, wheras low CBF is a bad prognosis (Olsen et al. 1981). Presumably increased flow acts to nourish damaged tissue. Other studies however, indiate that initial CBF levels are not predictive of clinical outcome (Burke et al. 1986). Apparently this is because once damage occurs during the initial period of ischemia, these cells cannot be salvaged (Heiss & Rosner, 1983).

Hence, blood flow increases only when undamaged neurons return to a functionally active state (Burke et al., 1986) rather than acting to rejuvinate injured tissue. In fact, hyperperfusion may endanger neuronal recovery (Mies et al. 1983). On the otherhand oxygen metabolism seems to correlates better with clinical status and functional recovery than does blood flow (Wise et al., 1983).

Recovery is often greatest during the first 30 days after stroke (Dombovy, et al., 1986; Lind, 1982), but continues up to 6 months in some patients (Wade & Hewer, 1987). It has been estimated that although about 60% of stroke patients are able to achieve total independence in activities of daily living (Meier & Strauman 1991; Wade & Hewer, 1987) only approximately 10 to 30% of initial survivors return to their jobs without gross or obvious disability (Bekson & Cummings 1991). Depending on the nature of the stroke, about 40% demonstate mild disability, 40% are severely disabled, and 10% require institutionalization (Stallones et al, 1972; Absher & Tool, 1996).

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