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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-. asp.net ean 13 EAN - 13 ASP . NET Control - EAN - 13 barcode generator with free ...
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