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  1. What are the types of intracranial hemorrhage, and how are they identified?

  2. Which patients require emergent or nonemergent neurosurgical intervention?

  3. How are aneurysmal and traumatic subarachnoid hemorrhage differentiated?

  4. What medical treatments bear on the management of intracranial hemorrhage?

  5. How is raised intracranial pressure managed?

  6. Is anticoagulation safe after an intracranial hemorrhage?

  7. How is brain death determined?

  8. What tests should be obtained in patients with ventriculoperitoneal shunts and fever?

Intracranial hemorrhages can be divided into three main categories. The first two, spontaneous intracerebral hemorrhage (bleeding within the brain parenchyma) and subarachnoid hemorrhage from aneurysm rupture, are considered strokes. The third category is intracranial hemorrhage from trauma, which may result in parenchymal, subarachnoid, subdural, or epidural bleeding. For ease of exposition, we use the term intracranial hemorrhage for all forms of bleeding within the skull and the term intracerebral hemorrhage for the more restricted category of bleeding within the substance of the brain.

When bleeding secondary to head trauma is excluded, intracerebral hemorrhage accounts for 10% of strokes. In the United States, rates range between 7 and 11 cases per 100,000 yearly, with a higher incidence in African Americans and Hispanics. The highest incidence globally is found in Japan, where rates are as high as 61 per 100,000 population.


The most common underlying condition in patients with spontaneous intracerebral hemorrhage is hypertension. Other associated conditions are coagulopathy, tumor, cerebral venous thrombosis, vascular malformation, amyloid angiopathy, and hemorrhagic transformation of ischemic stroke. The frequency of hypertension in patients with cerebral hemorrhage has been ˜75% in many population studies. Certain subgroups of hypertensive patients are at high risk for intracranial hemorrhage, including those younger than 55 years, smokers, and especially patients who have stopped taking chronically administered antihypertensive medications. Several prospective trials have demonstrated that the risk of cerebral hemorrhage decreases with administration of antihypertensive medications. Coagulopathy has become an increasingly frequent cause of primary intracerebral hemorrhage, with both medical anticoagulation and disorders such as uremia and liver failure contributing to this increase.


Several clinical features may help distinguish cerebral hemorrhage from other forms of stroke, such as headache, nausea, vomiting, confusion, systemic hypertension, and in advanced cases, decreased level of consciousness and enlargement of the pupils. The most common location for spontaneous intracerebral hemorrhage is the basal ganglia, accounting for ˜65% of cases. The presenting features, in addition to the above-described signs common to all hemorrhages, are hemiplegia and confusion. Thalamic hemorrhage presents similarly, usually with hemiplegia and often with hemianesthesia. Pontine hemorrhage causes rapid coma, quadriplegia, pinpoint pupils, and loss of extraocular movements. Cerebellar hemorrhage represents a special case that causes vomiting, vertigo, dizziness, gait ataxia, and progressive coma from hydrocephalus. Lobar hemorrhages are becoming more common with the prevalence of anticoagulant and antiplatelet therapy and cause signs referable to the region of bleeding. The differential diagnosis in all these cases includes ischemic stroke, and ...

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