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supraclinoid aneurysm near the anterior and middle cerebral bifurcation or the ophthalmic-carotid bifurcation Whether a small leak of blood from an aneurysm may serve as a warning sign of rupture ( warning leak ) has been disputed We have seen several cases where an acute and severe exertional or spontaneous headache was found to be associated with a small subarachnoid hemorrhage that was discovered by lumbar puncture; more often the headache is unrelated to hemorrhage and is attributable to migraine This latter thunderclap headache, which may be a variant of migraine, is discussed on page 160 A headache similar to that caused by subarachnoid hemorrhage may also be the re ection of pituitary apoplexy, cerebral venous thrombosis, hypertensive encephalopathy, intracranial hypotension, intracranial arterial dissection, and a condition characterized by diffuse cerebral vasospasm This last entity may be spontaneous or due to the ingestion of sympathomimetic or serotoninergic drugs (see further on, under Diffuse and Focal Cerebral Vasospasm The details of the CSF examination assume great importance in the diagnosis of subarachnoid hemorrhage and the exclusion of the disorders mentioned above Vasospasm Delayed hemiplegia and other focal de cits usually appear 3 to 12 days after rupture and rarely before or after this period These delayed syndromes and the focal narrowing of a large artery or arteries, seen on angiography, are referred to as vasospasm Fisher and coworkers have shown that spasm is most frequent in arteries surrounded by the largest collections of clotted subarachnoid blood The vasospasm appears to be a direct effect of blood or some blood product, possibly hematin or a platelet product, on the adventitia of the artery Areas of ischemic infarction in the territory of the vessel bearing the aneurysm, without thrombosis or other changes in the vessel, is the usual nding in such cases These ischemic lesions are often multiple and occur with great frequency, according to Hijdra and associates (in 57 of 176 prospectively studied patients and a comparable number in large series collected before more modern approaches to treatment became available) After a few days, arteries in chronic spasm undergo a series of morphologic changes The smooth muscle cells of the media become necrotic, and the adventitia is in ltrated with neutrophilic leukocytes, mast cells, and red blood corpuscles, some of which have migrated to a subendothelial position (Chyatte and Sundt) We favor the idea that these changes are caused by products of hemolyzed blood seeping inward from the pia-arachnoid into the muscularis of the artery The clinical features of cerebral vasospasm depend on the affected blood vessel but typically include a uctuating hemiparesis or aphasia and increasing confusion that must be distinguished from the effects of hydrocephalus (see below) In the past, an arteriogram was required to verify the diagnosis, although it is not often performed now because of the slight associated risk of worsening vascular spasm and the ease with which the condition can be recognized by its clinical presentation Severe vasospasm can be visualized with MRA and spinal CT techniques Transcranial Doppler measurements are an indirect and easier way of following, by observations of blood ow velocity, the caliber of the main vessels at the base of the brain Almost all patients have a greatly increased velocity of blood ow in the affected vessel that can be detected by this method in the days after hemorrhage However, progressive elevation of ow velocity in any one vessel (especially if over 175 cm/s) suggests that focal vasospasm is occurring There is a reasonable correlation between these ndings and the radio-.

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graphic appearance of vasospasm, but the clinical manifestations of ischemia depend on additional factors such as collateral blood supply and the cerebral perfusion pressure Hydrocephalus If a large amount of blood ruptures into the ventricular system or oods the basal subarachnoid space, it may nd its way into the ventricles through the foramina of Luschka and Magendie The patient then may become confused or unconscious as a result of acute hydrocephalus The clinical signs are greatly improved by draining the ventricles, either by external ventriculostomy or, in selected cases, by lumbar puncture A subacute hydrocephalus due to blockage of the CSF pathways by blood may appear after 2 to 4 weeks Anatomic-Clinical Correlations of Aneurysms 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 scan A collection of blood in the anterior interhemispheric ssure indicates rupture of an anterior communicating artery aneurysm; in the sylvian ssure, a middle cerebral artery aneurysm; in the anterior perimesencephalic cistern, a posterior communicating or distal basilar artery aneurysm; and so on In some instances clinical signs provide clues to its localization, as follows: (1) third nerve palsy (ptosis, diplopia, dilatation of pupil, and divergent strabismus), as stated above, usually 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; (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 rst major bifurcation of the middle cerebral artery; (4) unilateral blindness indicates an aneurysm lying anteromedially in the circle of Willis (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 (sometimes associated with paraparesis) favors a location on the anterior communicating artery, with ischemia of or hemorrhage into one or both of the frontal lobes or hypothalamus (with or without acute hydrocephalus); (6) the side on which the aneurysm lies may be indicated by a unilateral preponderance of headache or preretinal hemorrhage, 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 seldom of localizing value 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 due to a ruptured saccular aneurysm Other clinical data may be of assistance in reaching a correct diagnosis Almost all patients are hypertensive for one or several days following the bleed, but preceding hypertension is only slightly more common than in the general population Levels of 200 mmHg systolic are seen occasionally just after rupture, but usually the pressure is elevated only moderately and uctuates with the degree of head pain Spontaneous intracranial bleeding with normal blood pressure should also suggest ruptured aneurysm or arteriovenous malformation and, rarely, hemorrhage into a cerebral tumor 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.

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