Background Neuroimaging Gross Pathology Histopathology & Immunohistochemistry Differential Diagnosis

BACKGROUND AND CLINICAL INFORMATION: Head

Incidence: 1-6% in large autopsy series. 0.5 -1% in adults undergoing cerebral angiography. Multiple aneurysms are seen in 20-30% (depending on different studies) of cases, they are mostly seen in the middle cerebral artery. Ruptured aneurysm comprised about 80% of all non-traumatic subarachnoid hemorrhage.

Mortality: overall mortality is about 50-65%. The one-third rule: about 1/3 die within 72 hours, the other 1/3 has castrophic neurologic consequences although they survive.

Very rare in children. The mean age of patients with aneurysmal subarachnoid hemorrhage is around 50 years of age.

Associated conditions:

Increased incidence in patients with connective tissue or blood flow disorders such as autosomal dominant polycystic kidney disease (5-10% of asymptomatic adults with autosomal dominant polycystic kidney disease have saccular intracranial aneurysms), cerebral arteriovenous malformations, moyamoya disease, and coarctation of aorta, fibromuscular dysplasia, Ehlers-Danos syndrome type IV and type VI, neurofibromatosis type 1, and Marfan's syndrome.
Hypertension is considered an important factor in the formation of saccular aneurysms.
Use of cocaine will cause lead to a transient increase in blood pressure and may be associated with ruptured aneurysm.

Complications: The two most important complication of subarachnoid hemorrhage is ventricular dilatation and arterial spasm. Ventricular dilatation is resulted from impaired absorption of CSF in the arachnoid granulations.

NEUROIMAGING: Head

CT scan is very sensitive in detecting acute hemorrhage.

GROSS PATHOLOGY: Head

When hemorrhage due to ruptured aneurysm is suspected, the aneurysm should be dissected and the point of hemorrhage identified before fixation. Aneurysms are often multiple, and the offending lesion is not necesarily the one most obvious in the angiogram.

Locations:

Almost all saccular aneurysms arise at or very close to the point of bifurcation of intracranial arteries. Rupture of the aneurysm will cause a subarachnoid hemorrhage. The majority (>80%) are located in the anterior circulation.
40% (most common) are related to the intracranial portion of the internal carotid artery (usually at the junction of the internal carotid and posterior communicating arteries)
30% in the region of the anterior communicating artery
20% are on a middle cerebral artery mainly at the proximal point(s) of branching
5-10% are associated with the posterior cerebral arteries, with the basilar and vertebral arteries, or with other vessels in the posterior fossa.

Children: in contrast to adults, about 40-45% of aneurysms in children are found in the posterior cerebral circulation.

Size: 0.2-2 cm in diameter. About 5% may exceed 2.5 cm in diameter (giant aneurysm).

Morphology:

Many aneurysms are thin-walled, but fairly rigid berry (saccular) like poches. They have pale and opaque walls due to fibrosis. It is not uncommon to see aneurysms burried within the brain substance and do not protrude in an obvious fashion.
Yellow to orange discloration in the brain tissue adjacent to an intact aneurysm indicates previous bleeding without rupture.
Ruptured berry aneurysms that are burried within the brain substance may simulate intracerebral hemorrhage that rupture into the subdural space.

Rupture: Aneurysm that rupture are usually under 1 cm. Those greater than this rupture less frequently.

Giant aneurysms (>2.5 cm in diameter):

They may arise inthe posterior fossa, at the base of the cerebral hemisphere or within the lateral (sylvian) fissures from which they expand into the cerebral hemispheres.
They are frequently thrombosed and may be calcified. Although the blood clot may have be formed for a very long time, organization may be minimal and often litte macrophage invasion is seen.
Thrombosed giant aneurysm may not be seen in angiogram. They may suggest a space occupying lesion in CT or MRI scans.

Infarction: the arterial spasm resulted from subarachnoid hemorrhage may be severe and prolonged enough to cause areas of cerebral infarction which are often multiple and small.

HISTOPATHOLOGY AND IMMUNOHISTOCHEMISTRY: Head

Intracranial arteries, in contrast to the extracranial counterparts, have an attenuated tunica media and lack an external elastic lamina.

Rupture of larger arteries (500-700 micron in diameter) usually results in mortality. Rupture of smaller vessels (less than 300 micron in diameter) usually produce a hematoma that can be surgically removed. The most common rupture site is at or near the bifurcation of a vessel (59/61 cases) and than miliary aneurysm (2/61 cases).

DIFFERENTIAL DIAGNOSIS: Head

Atherosclerotic fusiform aneurysms: Most frequently seen in and the the supraclinoid segment of the internal carotid artery with or without extension into the middle cerebral artery, followed by the basilar artery (which may show an S-shaped distortion). They may compress the adjacent brain structures. Transient ischemic attacks or infarctions can be produced by small emboli originating in the walls of the aneurysm, thrombosis, or atherosclerotic obstruction. Infarction, due to the involvement of the paramedian penetrating arteries or emboli, in the cerebellum and brain stem are also seen. Hemorrhage may also occur.

NeuroLearn NeuroHelp Vascular For Comment: KarMing-Fung@ouhsc.edu

Background Neuroimaging Gross Pathology Histopathology & Immunohistochemistry Differential Diagnosis