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Intracranial Hemorrhage Clinical Presentation

  • Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD  more...
Updated: May 10, 2016


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%)
  • Seizures[4] (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.



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


Possible causes are as follows:

Contributor Information and Disclosures

David S Liebeskind, MD Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California, Los Angeles, David Geffen School of Medicine; 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, Stroke Council of the American Heart Association, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Jeffrey L Saver, MD, FAHA, FAAN Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine

Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, National Stroke Association

Disclosure: Received the university of california regents receive funds for consulting services on clinical trial design provided to covidien, stryker, and lundbeck. from University of California for consulting.

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Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.
This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.
This MRI reveals hemorrhagic transformation of an ischemic infarct.
Table 1. MRI Appearance of Intracerebral Hemorrhage
Hyperacute< 24 hoursOxyhemoglobin (intracellular)Iso or hypoHyper
Acute1-3 daysDeoxyhemoglobin (intracellular)Iso or hypoHypo
Early subacute>3 daysMethemoglobinHyperHypo
Late subacute>7 daysMethemoglobin (extracellular)HyperHyper
Chronic>14 daysHemosiderin (extracellular)Iso or hypoHypo
Table 2. Grading of Subependymal Hemorrhage
GradeHemorrhage Location
ISubependymal hemorrhage
IIIntraventricular hemorrhage without ventriculomegaly
IIIIntraventricular hemorrhage with ventriculomegaly
IVIntraventricular hemorrhage with parenchymal hemorrhage
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