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INTRODUCTION

Spontaneous intracranial hemorrhage accounts for about 20% of all strokes, but they are often devastating, accounting for a disproportionately large proportion of morbidity and mortality among stroke patients. There are two types of hemorrhagic stroke. Intraparenchymal hemorrhage (IPH) is characterized by bleeding within the brain itself, whereas subarachnoid hemorrhage (SAH) is characterized by vessel rupture in the cerebrospinal fluid (CSF)–filled subarachnoid space surrounding the brain. IPH and SAH have distinct clinical presentations, radiologic findings, etiologies, and treatment modalities.

INTRAPARENCHYMAL HEMORRHAGE

ESSENTIALS OF DIAGNOSIS

  • Sudden-onset focal deficit, with worsening over seconds to minutes; headache, nausea, vomiting, and coma are common

  • Etiologies include hypertension, vascular malformations, vasculopathies, coagulopathies, and others

  • Computed tomography (CT) and magnetic resonance imaging (MRI) are exquisitely sensitive to acute IPH

  • Treatment and prevention of recurrence are based on etiology; there are no treatments for IPH that are known to improve outcome

General Considerations

A. Incidence

IPH accounts for 10–15% of all strokes. Incidence worldwide is 10–20 cases per 100,000 persons and increases with age. It is more common in men, blacks, and people of Asian descent. The high incidence in blacks may reflect the prevalence of hypertension in that population, as well as inadequate access to primary prevention services. In the United States, approximately 45,000 people per year have an IPH, of whom 38–50% die. Most survivors are left with major neurologic deficits. The incidence is expected to increase over the next 50 years due to aging of the population and changing racial demographics.

B. Risk Factors

The most prevalent modifiable risk factor for IPH is hypertension. IPH is a particular risk in hypertensive patients younger than 55 years, smokers, and patients who are noncompliant with antihypertensive regimens. Patients with IPH are usually hypertensive on presentation, in some cases probably due to the IPH itself. The presence of left ventricular hypertrophy or renal insufficiency may provide evidence of long-standing hypertension. Antihypertensive treatment lowers the risk of IPH by about 50%.

Other modifiable risk factors for IPH include smoking and heavy alcohol use. Chronic alcoholism may increase the risk of IPH by causing cirrhosis, thrombocytopenia, or both. Low serum cholesterol is associated with an increased risk of IPH, especially in patients with severe hypertension. High-intensity statin therapy may increase the risk of IPH in patients with a history of stroke.

There are genetic risk factors for IPH, as shown by a familial tendency in about 10% of patients. Important genes include the apolipoprotein E ε2 and ε4 alleles, which predispose to lobar hemorrhage by increasing the vasculopathic effects of amyloid deposition in cortical blood vessels. In patients with lobar hemorrhage, the presence of these alleles triples the risk of recurrent hemorrhage. As yet, screening of patients with IPH for genetic risk factors is not indicated in routine clinical practice.

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