eMedicine Specialties > Neurology > Neurological Emergencies

Intracranial Hemorrhage

Author: David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
Contributor Information and Disclosures

Updated: Apr 27, 2009

Introduction

Background

Intracranial hemorrhage (ie, the pathological accumulation of blood within the cranial vault) may occur within brain parenchyma or the surrounding meningeal spaces. Hemorrhage within the meninges or the associated potential spaces, including epidural hematoma, subdural hematoma, and subarachnoid hemorrhage, is covered in detail in other articles. Intracerebral hemorrhage (ICH) and extension of parenchymal bleeding into the ventricles (ie, intraventricular hemorrhage [IVH]) are detailed here.

Intracerebral hemorrhage accounts for 8-13% of all strokes and results from a wide spectrum of disorders. Intracerebral hemorrhage is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage. Intracerebral hemorrhage and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.

Pathophysiology

Nontraumatic intracerebral hemorrhage most commonly results from hypertensive damage to blood vessel walls (eg, hypertension, eclampsia, drug abuse), but it also may be due to autoregulatory dysfunction with excessive cerebral blood flow (eg, reperfusion injury, hemorrhagic transformation, cold exposure), rupture of an aneurysm or arteriovenous malformation (AVM), arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered hemostasis (eg, thrombolysis, anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg, tumor, infection), or venous outflow obstruction (eg, cerebral venous thrombosis). Nonpenetrating and penetrating cranial trauma are also common causes of intracerebral hemorrhage.

Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries.

Predilection sites for intracerebral hemorrhage include the basal ganglia (40-50%), lobar regions (20-50%), thalamus (10-15%), pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%).

Intraventricular hemorrhage occurs in one third of intracerebral hemorrhage cases from extension of thalamic ganglionic bleeding into the ventricular space. Isolated intraventricular hemorrhage frequently arise from subependymal structures including the germinal matrix, AVMs, and cavernous angiomas.

Frequency

United States

Each year, intracerebral hemorrhage affects approximately 12-15 per 100,000 individuals, including 350 hypertensive hemorrhages per 100,000 elderly individuals. The overall incidence of intracerebral hemorrhage has declined since the 1950s.

International

Asian countries have a higher incidence of intracerebral hemorrhage than other regions of the world.

Mortality/Morbidity

  • Annually, more than 20,000 individuals in the United States die of intracerebral hemorrhage.
  • Intracerebral hemorrhage has a 30-day mortality rate of 44%.
  • Pontine or other brainstem intracerebral hemorrhage has a mortality rate of 75% at 24 hours.
  • Hallevi et al reviewed the charts and CT scans of patients with intraventricular hemorrhage (IVH) to determine if the extension of the hemorrhage could be measured. Clinical outcome was determined by the modified Rankin Scale (mRS). IVH was also classified with an IVH score. The IVH score allowed rapid estimate of IVH volume by the practitioner and increased predictability for outcome.1

Race

Intracerebral hemorrhage has a higher incidence among populations with a higher frequency of hypertension, including African Americans. A higher incidence of intracerebral hemorrhage has been noted in Chinese, Japanese, and other Asian populations, possibly due to environmental factors (eg, a diet rich in fish oils) and/or genetic factors.

Sex

  • Intracerebral hemorrhage has a slight male predominance, though study results have been conflicting.
  • Cerebral amyloid angiopathy may be more common among women.
  • Phenylpropanolamine use has been associated with intracerebral hemorrhage in young women.2

Age

  • Incidence of intracerebral hemorrhage increases in individuals older than 55 years and doubles with each decade until age 80 years.
  • The relative risk of intracerebral hemorrhage is greater than 7 in individuals older than 70 years.
  • In individuals younger than 45 years, lobar hemorrhage is the most common site of and frequently is associated with AVMs.
  • Subependymal hemorrhage or germinal matrix hemorrhage is primarily seen in premature infants.

Clinical

History

  • Onset of symptoms of intracerebral hemorrhage is usually during daytime activity, with progressive (ie, minutes to hours) development of the following:
    • Alteration in level of consciousness (approximately 50%)
    • Nausea and vomiting (approximately 40-50%)
    • Headache (approximately 40%)
    • Seizures3 (approximately 6-7%)
    • Focal neurological deficits
  • Lobar hemorrhage due to cerebral amyloid angiopathy may be preceded by prodromal symptoms of focal numbness, tingling, or weakness.
  • A history of hypertension, trauma, illicit drug abuse, or a bleeding diathesis may be elicited.

Physical

Clinical manifestations of intracerebral hemorrhage are determined by the size and location of hemorrhage, but may include the following:

  • Hypertension, fever, or cardiac arrhythmias
  • Nuchal rigidity
  • Subhyaloid retinal hemorrhages
  • Altered level of consciousness
  • Anisocoria
  • Focal neurological deficits
    • Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia
    • Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
    • Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
    • Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
    • Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
    • Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Causes

More on Intracranial Hemorrhage

Overview: Intracranial Hemorrhage
Differential Diagnoses & Workup: Intracranial Hemorrhage
Treatment & Medication: Intracranial Hemorrhage
Follow-up: Intracranial Hemorrhage
Multimedia: Intracranial Hemorrhage
References
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References

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Further Reading

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Keywords

intracranial hemorrhage, intracerebral hemorrhage, intraparenchymal hemorrhage, intracranial hematoma, intracerebral hematoma, intraparenchymal hematoma, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, intracranial pressure

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Contributor Information and Disclosures

Author

David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey L Saver, MD, Director, Stroke Center, Professor, Department of Neurology, University of California at Los Angeles Medical Center
Jeffrey L Saver, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, and National Stroke Association
Disclosure: Boehringer-Ingelheim - Secondary Prevention Consulting fee Consulting; Talacris Consulting fee Consulting; ImaRx Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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