In most patients, the neurologic manifestations do not point to the exact site of the aneurysm, but it can often be inferred from the location of the main clot on CT. A collection of blood in the anterior interhemispheric fissure indicates rupture of an anterior communicating artery aneurysm; in the sylvian fissure, a middle cerebral artery aneurysm; in the anterior perimesencephalic cistern, a posterior communicating or distal basilar artery aneurysm. In other instances clinical signs provide clues to its localization, as follows: (1) third-nerve palsy (ptosis, diplopia, dilatation of pupil, and divergent strabismus), indicates an aneurysm at the junction of the posterior communicating artery and the internal carotid artery—the third nerve passes immediately lateral to this point or at the posterior cerebral-posterior communicating artery junction; (2) transient paresis of one or both of the lower limbs at the onset of the hemorrhage suggests an anterior communicating aneurysm that has interfered with the circulation in the anterior cerebral arteries; (3) hemiparesis or aphasia points to an aneurysm at the first major bifurcation of the middle cerebral artery; (4) unilateral blindness indicates an aneurysm lying anteromedially in the circle of Willis (usually at the origin of the ophthalmic artery or at the bifurcation of the internal carotid artery); (5) a state of retained consciousness with akinetic mutism or abulia favors a location on the anterior communicating artery; (6) the side on which the aneurysm lies may be indicated by a unilateral preponderance of headache or by unilateral preretinal (subhyaloid) hemorrhage (Terson syndrome), the occurrence of monocular pain, or, rarely, lateralization of an intracranial sound heard at the time of rupture of the aneurysm. Sixth-nerve palsy, unilateral or bilateral, is usually attributable to raised intracranial pressure and is less often of localizing value.
Other clinical data may be of assistance in reaching a correct diagnosis. Levels of blood pressure of 200 mm Hg systolic are seen occasionally just after rupture, but usually the pressure is elevated only moderately and fluctuates with the degree of head pain. Nuchal rigidity is usually present but occasionally absent, and the main complaint of pain may be referable to the interscapular region or even the low back rather than to the head. Examination of the fundi frequently reveals smooth-surfaced, sharply outlined collections of blood that cover the retinal vessels—preretinal or subhyaloid hemorrhages (Terson syndrome); Roth spots are seen occasionally. Bilateral Babinski signs are found in the first few days following rupture if there is hydrocephalus. Fever up to 39°C (102.2°F) may be seen in the first week, but most patients are afebrile. Rarely, escaping blood enters the subdural space and produces a hematoma, evacuation of which may be lifesaving.
In summary, the clinical sequence of sudden severe headache, vomiting, collapse, relative preservation of consciousness with few or no lateralizing signs, and neck stiffness is diagnostic of subarachnoid hemorrhage caused by a ruptured saccular aneurysm. Vasospasm, hydrocephalus and particularly, rerupture follow and dominate prognosis in survivors.
Acute subarachnoid hemorrhage is associated with several characteristic responses in the systemic circulation, water balance, and cardiac function. The ECG changes include symmetrically large peaked T waves (“cerebral