Trauma is a potential cause of intracranial bleeding— typical SDH or epidural hematomas or parenchymal contusions. A history of injury may be lacking when a patient is found unconscious and other clues must be sought, such as lacerations or soft-tissue swelling. Conversely, a patient with a primary hemorrhage may suffer secondary trauma.

Either acute or chronic arterial hypertension may be a cause of ICH. Chronic hypertension leads to degenerative changes in small penetrating arteries in the deep structures of the brain. Sudden, severe hypertension may overwhelm the autoregulatory responses of the cerebral vasculature and an arteriole may rupture. Acute and severe arterial hypertension may be secondary to acute glomerulonephritis, eclamp sia, severe emotional stress, or the use of a sympathomimetic agent. The most common sites for hypertensive ICH are the basal ganglia (putamen), thalamus, brainstem, cer ebellum, or lobar white matter. Hypertension should be considered as the likely cause
of a hematoma located in deep gray matter structures of the cerebral hemisphere if a patient has a history of hypertension. Other features of chronic hypertension, such as retinopathy, renal dysfunction, or left ventricular hypertrophy, support the diagnosis. Even though hemorrhagic stroke often is attributed to hypertension because of the presence of an elevated blood pressure measured upon arrival to an emergency department, arterial hypertension is common among acutely ill patients with intracranial hemorrhage, and the finding should not automatically lead to the diagnosis of hypertensive hemorrhage.

Rupture of a saccular aneurysm is the most common cause of nontraumatic SAH and it is an important cause of ICH. Approximately 1% to 5% of adults harbor intracranial aneurysms, but a minority of these lesions actually rupture. In general, the risk of rupture is correlated with the size of the aneurysm, with the highest risk found with aneurysms larger than 6 to 8 mm in diameter. Patients with autosomal dominant polycystic kidney disease have a high prevalence of intracranial
aneurysms. Approximately 10% of patients have a family history of cerebral aneurysms. Approximately 85% of saccular aneurysms are in the carotid circulation with the most common sites being the junction of the internal carotid artery—posterior communicating artery, the bifurcation of the middle cerebral artery, and the anterior communicating artery. The most common locations in the posterior circulation are the bifurcation of the basilar artery and the origin of the posterior inferior cerebellar artery.

Infective, neoplastic, and traumatic aneurysms are rare causes of intracranial hemorrhage. These lesions usually are located in peripheral branch pial arteries on the cortical surface of the cerebral hemispheres. They usually are smaller than saccular aneurysms, but they have a relatively high risk of hemorrhage. Dolichoectatic (fusiform) aneurysms are tortuous, elongated arterial enlargements most commonly found in the basilar arteries of patients with extensive atherosclerosis or young men with Fabry’s disease. Hemorrhage is an uncommon complication. Spontaneous or traumatic dissecting aneurysms of intracranial arteries, particularly of the basilar or distal vertebral arteries, are potential causes of atypical SAH.

Vascular malformations are classified as arteriovenous malformation (AVM), developmental venous anomaly, cavernous malformation, and telangiectasias. They may be located in any part of the brain. Although familial cases, as with hereditary hemorrhagic telangiectasia or familial cavernous malformations, may occur, most are sporadic. The prevalence of vascular malformations is less than that of saccular aneurysms, and most affected persons never have hemorrhage. ICH is the pre senting symptoms in approximately 50% of cases. Non-hemorrhagic symptoms include seizures, recurrent and stereotypic headache, or progressive neurologic impairments. Patients with large AVM leading to turbulent blood flow may have pulsatile tinnitus and a cranial bruit may be auscultated.

It (congophilic angiopathy) is a leading cause of lobar ICH in the elderly. With aging, amyloid is deposited in the walls of cortical and leptomeningeal arterioles. Presumably, the protein accumulation leads to vascular fragility and bleeding. The hemorrhages, which are most commonly located in the frontal and parietal lobes, usually arise at the junction of the white matter and cerebral cortex. Multiple or recurrent hemorrhages are common. Cerebellar hemorrhages may also develop. Amyloid angiopathy should be considered as the likely cause of lobar ICH among persons older than 75. Because approximately 70% of affected patients also have a history of Alzheimer’s disease, a past history of dementia or cognitive decline increases the likelihood that an ICH in an elderly patient is due to amyloid angiopathy.

Multisystem or isolated CNS vasculitis is a rare cause of intracranial hemorrhage. Bleeding is most often associated with a necrotizing vasculitis, such as polyarteritis nodosa. Vasculitis may be the cause of bleeding among some young patients who have hemorrhagic stroke after the use of a sympathomimetic drug.

Intracranial hemorrhage may complicate several inherited or acquired bleeding diatheses, including hemophilia, sickle cell disease, thrombocytopenia, or leukemia. It may also complicate the use of thrombolytic or antithrombotic agents. In general, the severity of bleeding is worse, and the prognosis is poorer among patients with bleeding secondary to a coagulation disorder than among persons with spontaneous hemorrhages. Intracranial bleeding is a side effect of treatment for oral anticoagulants or thrombin inhibitors, and this complication should be considered whenever a patient has acute neurologic symptoms while taking oral anticoagulants even if there is no other evidence of bleeding. The risk of ICH is especially high among the elderly and persons who have leukoaraiosis present on brain imaging studies. Persons with a past history of stroke or poorly controlled hypertension also have a high risk of bleeding secondary to oral anticoagulants. The risk of intracranial bleeding increases when the international normalized ratio (INR) exceeds 3 to 4. The frequency of hemorrhagic stroke is lower with antiplatelet agents than with oral anticoagulants. The combination of aspirin and clopidogrel is more likely to be associated with bleeding than the use of either medication alone especially among persons with a history of stroke. The combination of warfarin and aspirin has a higher risk of bleeding than the administration of either agent alone.

Intracranial hemorrhage has been attributed to the abuse of medications such as cocaine or methamphetamine. These agents may lead to bleeding because of sudden increases in blood pressure or because of the development of a vasculitis. Intracranial hemorrhage has also been associated with heavy alcohol use.

is an uncommon cause of hemorrhagic stroke among young adults and children. The arteriographic hallmark of moyamoya is occlusions of the major arteries of the anterior circulation and the appearance of a mesh of fine blood vessels at the base of the brain. Moyamoya disease is inherited on an autosomal dominant basis and is most common among persons of northeastern Asia. It is also diagnosed when the arteriographic findings occur among patients with a number of acquired disorders. Hemorrhages may be secondary to rupture of an aneurysm (most commonly in the posterior circulation) or rupture of small collateral channels.

Occlusion of a cortical vein (cortical venous thrombosis) or sinus (sinus thrombosis) is an uncommon etiology of hemorrhagic stroke. Bleeding is most common among patients with thrombosis of the superior sagittal sinus; in this situation, the areas of hemorrhage are parasagittal in location bilaterally and in a thumbprint pattern. The clinical course of venous thrombosis differs from that of most other hemorrhagic strokes. Most patients have worsening headaches, seizures, altered consciousness, and focal neurologic signs that evolve over a few days. Venous thrombosis often develops in the peripartum period, but it also occurs among persons who are dehydrated, have malignant disease, have undergone a recent cranial operation, or have an otolaryngologic infection.

Hemorrhage may be the initial symptom of a highly vascular primary or metastatic brain tumor, including choriocarcinoma, melanoma, or carcinoma of the kidney, thyroid, liver, lung, or breast. The most common primary tumors are glioblastoma or pilocytic astrocytoma. Patients may have a history of evolving neurologic symptoms such as headache or personality changes before the bleeding event. The presence of extensive brain edema in the first hours after hemorrhages or multiple hemorrhagic lesions should prompt consideration of an underlying brain tumor.

Modern brain imaging allows discovery of asymptomatic hemorrhagic changes in the ischemic lesion in a sizable proportion of patients with a recent stroke. A smaller percentage of patients have neurologic worsening secondary to hemorrhagic transformation of the infarction. The risk of this complication is increased with the use of a thrombolytic within the first hours after stroke.

1. Hemorrhagic stroke usually is a sudden, dramatic event. The patient or observers often relate the circumstances surrounding the onset of symptoms. A headache, of any quality and location, usually is described as intense and often is described as the “worst headache of my life.” A headache accompanied by a transient loss of consciousness or one that is of cataclysmic onset is a premier symptom of SAH. Approximately 40% of patients with ICH will complain of severe headache. Other symptoms include nausea, vomiting, prostration, photophobia, phonophobia, and nuchal rigidity. The presence of nausea and vomiting and focal signs suggestive of a stroke in a cerebral hemisphere is predictive of a hemorrhagic event.

2. Disturbances in consciousness are common. Prolonged unresponsiveness (coma) occurs among patients with major hemorrhages. Transient alteration in alertness at the time of bleeding (syncope) may also happen. Disorientation, confusion, or delirium may also
occur. Although focal or generalized seizures may develop, recurrent seizures or status epilepticus are uncommon.

3. Focal neurologic signs reflect the location of the hematoma. The most common pattern is a contralateral hemiparesis and hemisensory loss secondary to a hematoma in the basal ganglia. Patients with cerebellar hemorrhage often have a subacute course. They report headache, dizziness (vertigo), disturbed balance, nausea, and vomiting. Signs of increased intracranial pressure (ICP) or brainstem compression subsequently appear, including cranial nerve palsy, motor impairment, and disturbed consciousness. Although most patients with SAH or primary IVH do not have focal neurologic signs, some patients with aneurysms will have focal findings. The most common is a third nerve palsy secondary to a ruptured posterior communicating artery aneurysm.