Cerebral Aneurysms Workup

Updated: Dec 06, 2018
  • Author: David S Liebeskind, MD, FAAN, FAHA, FANA; Chief Editor: Helmi L Lutsep, MD  more...
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Laboratory Studies

Lab studies that may be helpful for diagnosis include the following:

  • CBC with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk.

  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk.

  • Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial pressure.

  • Liver function tests: Identify hepatic dysfunction that may complicate clinical course.

  • Arterial blood gases: Assess blood oxygenation.


Imaging Studies

Advances in neuroimaging techniques have altered the diagnosis of cerebral aneurysms dramatically. Noninvasive angiographic methods, such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), allow for detection and characterization of aneurysms, further enhanced by postprocessing techniques that enable 3-dimensional evaluation of aneurysm morphology. Contemporaneous parenchymal imaging with CT scan or MRI yields a wealth of information that may assist surgical planning. However, minor aneurysmal hemorrhage may not be detected with noninvasive methods.

A study of 20 years of screening results of individuals with a positive family history of SAH found that the yield of long-term screening is substantial even after more than 10 years of follow-up and two initial negative screens. These data suggest that repeated screening should be considered in individuals with 2 or more first-degree relatives who had SAH or unruptured intracranial aneurysms. [5, 6]

CT scan

Aneurysmal SAH may be detected in 90-95% of cases. If CT scan result is negative and SAH is suspected, perform lumbar puncture (LP).

Noncontrast CT scan should be performed, as contrast may obscure detection of SAH.

Curvilinear calcification, aneurysmal thrombosis, or bone erosion may be characterized; however, bone structures also may produce artifacts.

Surrounding edema and an inflammatory reaction may be appreciated with contrast administration following the noncontrast study.

CTA may detect aneurysms greater than 3 mm, providing detailed evaluation of morphology such as relationship to the parent vessel and neck width.

CTA can detect more than 95% of aneurysms identified on conventional angiography. CTA may be superior to MRA because of shorter acquisition times, diminished motion artifacts, and detailed demonstration of other landmarks. However, bone and venous structures may complicate analysis.

Increasing use of CT perfusion in combination with CTA allows for reconstruction of multiphase CT angiographic images, potentially providing greater definition beyond standard CTA. [7]


Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and MRI in detection of SAH is controversial.

MRI may be impractical for patients in unstable condition. Flow voids may be seen extending from the parent vessel into the aneurysm.

Heterogeneous signal intensity adjacent to the aneurysm wall may be seen with thrombus of varying ages, although MRI is relatively insensitive to the presence of calcium.

Dolichoectatic and giant aneurysms are identified readily with MRI. Pulsation artifacts and the presence of turbulence may help to differentiate these aneurysms from other mass lesions, but slow and turbulent flow may preclude visualization on MRA.

MRA may reliably provide 3-dimensional imaging of aneurysms 4 mm or larger.

Phase-contrast techniques may facilitate detection of flow patterns and slow flow. Although phase-contrast MRA is preferable for large aneurysms, 3-dimensional time-of-flight techniques are preferable for small aneurysms. Source images should be inspected routinely in conjunction with the reconstructed views.


Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm location, size, and morphology may be evaluated in the acute or chronic setting with this modality.

Digital subtraction angiography with biplanar magnification views provides details that may be helpful in identifying an acutely ruptured aneurysm.

Aneurysmal irregularity, the presence of a daughter loculus, or focal spasm may be noted with acute rupture. Vasospasm may be depicted reliably and the collateral circulation may be demonstrated.

Perform 4-vessel angiography to identify remote vasospasm and the presence of multiple aneurysms. Acute angiography occasionally yields negative results (eg, due to thrombosis or vasospasm), in which case angiography should be repeated 1-3 weeks later. However, the risk and expense of this procedure may not be appropriate for screening of high-risk individuals.

A junctional dilatation of the terminal carotid artery at the origin of the PCoA may be noted in about 5-10% of patients. These infundibula or conical enlargements of less than 3 mm are unlikely to enlarge or rupture. However, overt aneurysms at the juncture of the terminal carotid artery with a persistent PCoA configuration may be more prone to rupture.

Further refinements in the characterization of cerebral aneurysms are expected following the recent introduction of 3-dimensional rotational angiography. Recent work has demonstrated that this technique may offer superior resolution and increased sensitivity for detection of small aneurysms. [8]

Other imaging studies

Transcranial Doppler ultrasonography: TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside. TCD has exhibited close correlation with angiography in the setting of vasospasm, typically manifesting 3-21 days following aneurysmal SAH.

Single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon-CT (XeCT): With these techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although these modalities are not employed routinely.

Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an unwitnessed loss of consciousness.


Other Tests

Other tests that may be helpful for diagnosis include the following:

  • ECG: Cardiac arrhythmias and myocardial ischemia may be evident. Aneurysmal SAH may be associated with several ECG changes, including peaked P waves, prolonged QT interval, and tall T waves.

  • Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of infectious or neoplastic aneurysms.

  • Evoked potentials and EEG: These functional neurophysiologic studies may be used to monitor cerebral aneurysm surgery or patients critically ill with aneurysmal SAH.



Lumbar puncture

LP may help to establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal SAH demonstrates hemorrhagic CSF with a xanthochromic supernatant, although these findings may be absent within the first few hours following aneurysmal rupture.

The opening pressure may be elevated.

WBC count may increase after a delay, reflecting a meningeal inflammatory reaction.

The protein may be elevated with normal or decreased glucose.

Cultures may reveal an infectious etiology.

Ventriculostomy: External drainage of CSF may assist in the management of hydrocephalus and cases with poor clinical grades.


Histologic Findings

Gross pathologic examination may reveal brownish pigmentation and fibrous adhesions of surrounding brain parenchyma. Aneurysm size may be diminished on postmortem examination, although a multilobular shape may be appreciated. A ruptured fundus may be visualized with calcifications of the aneurysm wall and intraluminal thrombus.

  • Microscopic examination reveals defects in the normal architecture of the vessel wall. The tunica media and internal elastic lamina may be absent or degenerated, with hemosiderin-laden phagocytes and lymphocytic infiltration.

  • Infectious aneurysms may exhibit an infected embolus adherent to a necrotic arterial wall. The intima and internal elastic lamina may be destroyed with an inflammatory infiltrate consisting of polymorphonuclear cells, lymphocytes, and macrophages.

  • Myofilament fragmentation and sarcolemmal destruction may be seen with vasospastic vessels.



Table 1. Clinical Condition at Presentation (Open Table in a new window)


Clinical Condition at Presentation


Unruptured aneurysm


Asymptomatic or minimal headache and slight nuchal rigidity


Moderately severe or severe headache and nuchal rigidity; cranial neuropathy, no focal deficit


Drowsiness, confusion, or mild focal deficit


Stupor, moderate to severe hemiparesis


Deep coma, decerebrate posturing, moribund appearance


Table 2. World Federation of Neurological Surgeons Scale (Open Table in a new window)


Glasgow Coma Scale Score

Clinical Findings



No headache or focal signs



Headache, nuchal rigidity, no focal signs



Headache, nuchal rigidity, no focal signs



Headache, rigidity, focal signs



Headache, rigidity, focal signs


Table 3. Fisher Grade (Open Table in a new window)


CT Findings


No blood detected


Diffuse thin layer of subarachnoid blood


Localized thrombus or thick layer of subarachnoid blood


Intracerebral or intraventricular hemorrhage with diffuse or no subarachnoid blood