Clinical Manifestations

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Aneurysms most often present subsequent to SAH. They also may manifest secondary to mass effect

(compression of adjacent structures) or cerebral is-chemic symptoms, or they may simply be detected as an incidental finding during a test done for other indications.

1. Subarachnoid Hemorrhage

Aneurysmal rupture normally gives rise to blood in and around the basal cisterns in the subarachnoid space (subarachnoid hemorrhage) but may hemorrhage into the ventricular system (intraventricular hemorrhage), brain parenchyma (intracerebral hemorrhage), or, rarely, the subdural space leading to subdural hemorrhage. This rupture presents clinically as the sudden onset of severe headache (often described as the ''worst headache of my life'') and is often associated with signs of meningeal irritation (such as nausea/vomiting, meningismus, photophobia, and phonophobia). Aneurysmal SAH often occurs during straining or exertion, such as with exercise, intercourse, or a bowel movement. SAH may also lead

Figure 11 Anterior circulation aneurysm. (Left) Axial noncontrasted CT scan revealing subarachnoid hemorrhage in basal cisterns and Sylvian fissure. Subarachnoid blood predominates in the left Sylvian fissure. (Right, top) Frontal view of angiogram after left ICA injection revealing large MCA bifurcation aneurysm. (Right, bottom) Same view angiogram postoperatively revealing aneurysm clip across aneurysmal neck with no residual aneurysm filling.

Figure 12 Posterior circulation aneurysm: angiograms after left vertebral artery injection. (Left, top) Lateral projection reveals basilar bifurcation aneurysm. (Left, bottom) Frontal view of same aneurysm. (Right) More superiorly projected frontal view provides optimal view of aneurysm.

to seizures. In more severe cases, SAH may lead to a decreased level of consciousness and various global and focal neurological deficits may be elicited during physical examination. Ophthalmologic examination may reveal unilateral or bilateral subhyaloid hemorrhages in nearly 25% of patients with SAH. These are venous in origin and are situated between the retina and vitreous membrane.

Symptoms preceding the major SAH, such as atypical headaches or neck stiffness, have been ascribed to small hemorrhages and are termed ''sentinel leaks'' or ''warning headaches.'' These symptoms occur in as many as 70% of patients, leading about half of these patients to seek medical attention. Many of these patients are misdiagnosed, which may have future catastrophic repercussions.

SAH may be complicated by cerebral vasospasm and ischemic stroke resulting from the delayed narrowing of intracranial vessels. The incidence of vasospasm begins to increase 3-5 days posthemorrhage, peaks between 7 and 10 days, and diminishes over 2 or 3 weeks. Clinically significant vasospasm occurs in 25-30% of patients, although angiographic evidence is seen in approximately 60-70% of cases.

The most significant predictor of the development of cerebral vasospasm following aneurysmal SAH is the amount and location of subarachnoid blood visualized by CT imaging as popularized by Fischer (Table VI). Approximately 50% of patients with symptomatic vasospasm develop infarction despite therapy. In addition, 15-20% of patients with symptomatic va-sospasm will develop a disabling stroke or die of progressive ischemia. Cerebral vasospasm remains the leading treatable cause of death and disability attributed to aneurysmal SAH.

SAH may also be complicated by hydrocephalus. Acute hydrocephalus occurs in 25% of patients with aneurysmal SAH, most often with intraventricular and/or blood in the ambient cisterns. Many patients develop chronic communicating hydrocephalus.

The most important predictor of the outcome of patients suffering from SAH is based on the patient's

Table VI

Fischer Grade Computed Tomographic Scan Classification of Subarachnoid Hemorrhage

Grade Description

1 No blood detected

2 Diffuse deposition or thin layer of blood, with all vertical layers of blood (interhemispheric fissure, insular cistern, and ambient cistern) < 1 mm thick

3 Localized clots or vertical layers of blood 1 mm or more in thickness (or both)

4 Diffuse or no subarachnoid blood but with intracerebral or intraventricular clots

Table VII

Hunt-Hess Clinical Grading Scale for Subarachnoid Hemorrhage Grade Clinical conditon

1 Asymptomatic or mild headache and mild nuchal rigidity

2 Cranial nerve palsy, nuchal rigidity, and moderate to severe headache

3 Drowsy, confused, or mild focal deficit

4 Stupor, moderate to severe hemiparesis, and early decerebrate posturing

5 Comatose and decerebrate posturing condition at presentation. Multiple grading systems have been proposed but the most widely utilized are the Hunt-Hess scale and the scale of the World Federation of Neurological Surgeons (Tables VII and VIII). The World Federation of Neurological Surgeons scale is based on the universally recognized Glasgow coma scale.

2. Mass Effect

Aneurysms, particularly large or giant, may compress adjacent structures and cause neurological deficits. Mass effect commonly causes headache or a third cranial nerve palsy from compression at the junction of the PCoA and the ICA. Other symptoms/signs may include visual field defects, trigeminal neuralgia, brain stem dysfunction, cavernous sinus syndrome (compression of structures traversing the cavernous sinus), seizures, or endocrinologic symptoms due to disruption of the hypothalamic-pituitary axis.

3. Cerebral Ischemia

Embolization of intraaneurysmal thrombus may lead to cerebral ischemic symptoms in the distribution of the cerebral vasculature occupied by the aneurysm. This is a rare presentation of an unruptured aneurysm.

4. Incidental Finding: The Asymptomatic Aneurysm

Widespread adoption of CT and MRI has increasingly led to the discovery of asymptomatic intracranial aneurysms. The discrepancy between the incidence of aneurysms as detected by autopsy and the incidence of SAH apparent in the preceding discussion of epide-

Table VIII

World Federation of Neurological Surgeons Clinical Grading Scale for Subarachnoid Hemorrhage

Table VIII

World Federation of Neurological Surgeons Clinical Grading Scale for Subarachnoid Hemorrhage


Glasgow coma scale

Motor deficit

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