Cerebral Aneurysms Clinical Presentation

  • Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Feb 27, 2012
 

History

  • The clinical presentation of cerebral aneurysms includes symptoms associated with major aneurysmal rupture (eg, SAH), minor aneurysmal hemorrhage (eg, warning leak or sentinel bleed), nonhemorrhagic manifestations (eg, mass effects or cerebral ischemia), and asymptomatic scenarios (eg, incidental aneurysm detection or identification through screening[1] ).
  • Although aneurysmal SAH has characteristic historical features, the constellation of symptoms may vary with location, size, shape, and direction of the aneurysm.
  • Aneurysmal rupture also may present with intraparenchymal hemorrhage (more common with distal aneurysms), intraventricular hemorrhage (13-28%), or subdural hematoma (2-5%).
  • Minor aneurysmal hemorrhage may precede rupture with a wide variation in latency, although these warning leaks also may be clinically silent.
  • Giant aneurysms may compress brain parenchyma, resulting in focal neurological complaints.
  • Aneurysmal expansion may produce pain or herald new neurological manifestations.
  • Traumatic aneurysms may have a delayed presentation, with intracranial hemorrhage or recurrent epistaxis.
  • Symptoms associated with cerebral aneurysms and SAH are as follows:
    • Headache: This is characterized by the acute onset of severe pain, which patients often describe as "the worst headache of my life." Aneurysmal expansion, thrombosis, or intramural hemorrhage may cause a subacute, unilateral, periorbital headache. Headache does not always accompany aneurysmal SAH.
    • Facial pain: Cavernous-carotid aneurysms may produce facial pain.
    • Alterations in consciousness: The sudden elevation of intracranial pressure associated with aneurysmal rupture may lead to a precipitous decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in alertness also may be noted.
    • Seizures: Focal or generalized seizures are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset.
    • Manifestations of meningeal irritation: Neck pain or stiffness, photophobia, sonophobia, or other hyperesthesia may be noted with SAH.
    • Autonomic disturbances: Subarachnoid accumulation of products of blood degradation may elicit fever. Nausea or vomiting, sweating, chills, and cardiac arrhythmias also may be present.
    • Focal neurological complaints: Hemorrhage or ischemia may manifest with focal deficits including weakness, hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances. Focal symptoms are more common with giant aneurysms.
    • Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
    • Respiratory dysfunction or cardiovascular instability: These are ominous signs of brainstem compression.
    • Hormonal dysfunction: Intrasellar aneurysms may interfere with pituitary function.
    • Epistaxis: This is noted occasionally with traumatic aneurysms.
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Physical

  • The general examination occasionally reveals manifestations of associated conditions such as subacute bacterial endocarditis, trauma, or collagen-vascular disease.
  • Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
  • Neurologic findings exhibit considerable variability, depending on aneurysm characteristics.
    • Aneurysmal SAH may be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages, pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.
    • Giant aneurysms or dolichoectatic aneurysms may cause mass effects or distal thromboembolism with prominent focal deficits, optic atrophy or other cranial neuropathies, or brainstem compression.
  • Specific syndromes have been associated with particular aneurysmal locations.
    • Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, ACoA aneurysms are silent until they rupture. Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction. Neurological deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%).
    • Anterior cerebral artery: Aneurysms of this vessel, excluding ACoA, account for about 5% of all cerebral aneurysms. Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted.
    • Middle cerebral artery: Aneurysms of the middle cerebral artery, as shown below in the image and video, account for about 20% of aneurysms, typically at first or second division in the sylvian fissure. Aphasia, hemiparesis, hemisensory loss, anosognosia, or visual field defects may be noted. Cerebral aneurysms. CT angiography of a right middCerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.
      Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.
  • Posterior communicating artery: Aneurysms present at the junction of the termination of the ICA and PCoA account for 23% of cerebral aneurysms; they are directed laterally, posteriorly, and inferiorly. Pupillary dilatation, ophthalmoplegia, ptosis, mydriasis, and hemiparesis may result.
  • Internal carotid artery: Besides PCoA aneurysms, aneurysms of the ICA, shown below, account for about 4% of all cerebral aneurysms. Supraclinoid aneurysms may cause ophthalmoplegia due to compression of cranial nerve (CN) III or variable visual defects and optic atrophy due to compression of the optic nerve. Chiasmal compression may produce bilateral temporal hemianopsia. Hypopituitarism or anosmia may be seen with giant aneurysms. Cavernous-carotid aneurysms exert mass effects within the cavernous sinus, producing ophthalmoplegia and facial sensory loss. Rupture of these aneurysms typically produces a carotid-cavernous fistula, SAH, or epistaxis.Cerebral aneurysms. Sagittal multiplanar reformattCerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.
  • Basilar artery: Basilar tip aneurysms, shown in the image and the video below, are the most common in the posterior circulation, accounting for 5% of all aneurysms. Clinical findings usually are those associated with SAH, although bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction, respiratory difficulties, or neurogenic pulmonary edema. Cerebral aneurysms. Basilar tip aneurysm illustratCerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).
    Cerebral aneurysms. Volume-rendered CT angiography of a basilar tip aneurysm.
  • Vertebral artery or posterior inferior cerebellar artery: Aneurysms at these arterial segments typically result in ataxia, bulbar dysfunction, or spinal involvement.
  • False localizing signs: False localization may be associated with CN III palsy and hemiparesis in uncal herniation, CN VI palsy with elevated intracranial pressure, homonymous hemianopsia due to posterior cerebral artery compression along the tentorial edge, brainstem dysfunction associated with tonsillar herniation, and vasospasm in remote vessels.
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Causes

  • Congenital or familial inheritance
  • Atherosclerosis
  • Hypertension
  • Autosomal dominant inherited polycystic kidney disease
  • Vasculopathies
  • Arteriovenous malformations, shown below Cerebral aneurysms. Aneurysm associated with an arCerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI (left), 3D-time-of-flight MRI (middle), and conventional angiography (right).
  • Connective tissue disorders
  • Sickle cell anemia
  • Infections
  • Trauma
  • Neoplasms
  • Cigarette smoking
  • Illicit drug use
  • Alcohol
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Contributor Information and Disclosures
Author

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, 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.

Specialty Editor Board

Draga Jichici, MD, FRCP, FAHA  Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care Medicine (USA)

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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: 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, 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; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.
Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.
Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.
Cerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).
Cerebral aneurysms. Volume-rendered CT angiography of a basilar tip aneurysm.
Cerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI (left), 3D-time-of-flight MRI (middle), and conventional angiography (right).
Table 1. Clinical Condition at Presentation
GradeClinical Condition at Presentation
0Unruptured aneurysm
1Asymptomatic or minimal headache and slight nuchal rigidity
2Moderately severe or severe headache and nuchal rigidity; cranial neuropathy, no focal deficit
3Drowsiness, confusion, or mild focal deficit
4Stupor, moderate to severe hemiparesis
5Deep coma, decerebrate posturing, moribund appearance
Table 2. World Federation of Neurological Surgeons Scale
GradeGlasgow Coma Scale ScoreClinical Findings
I15No headache or focal signs
II15Headache, nuchal rigidity, no focal signs
III13-14Headache, nuchal rigidity, no focal signs
IV7-12Headache, rigidity, focal signs
V3-6Headache, rigidity, focal signs
Table 3. Fisher Grade
GradeCT Findings
1No blood detected
2Diffuse thin layer of subarachnoid blood
3Localized thrombus or thick layer of subarachnoid blood
4Intracerebral or intraventricular hemorrhage with diffuse or no subarachnoid blood
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