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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
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(St Louis et al) As a rule, a cerebellar hematoma of less than 2 cm in diameter leaves most patients awake and infrequently leads to deterioration, therefore not requiring surgery Hematomas that are 4 cm or more in largest diameter, especially if located in the vermis, pose the greatest risk, and some surgeons have recommended evacuation of lesions of this size no matter what the clinical status of the patient In determining the need for surgical evacuation, we have been guided by the state of consciousness, the mass effect caused by the clot as visualized on CT scan (particularly the degree of compression of the quadrigeminal cistern, as pointed out by Taneda and colleagues), and the presence of hydrocephalus Often this requires daily or even more frequent CT scans The patient who is stuporous or displays arrhythmic breathing is best intubated and brought to the operating room within hours or sooner Once coma and pupillary changes supervene, few patients survive, even with surgery; however, rapid medical intervention with mannitol and hyperventilation, followed by surgical evacuation of the clot and drainage of the ventricles very soon after the onset of coma, has been successful in a few cases Patients who are only drowsy and those with hematomas of 2 to 4 cm in diameter pose the greatest dif culty in deciding about surgery If the level of consciousness is uctuating or if there is obliteration of the perimesencephalic cisterns, particularly if coupled with hydrocephalus, we believe that the risk of surgery is less than that of a sudden deterioration In only a very limited number of patients have we found it practical to perform only drainage of the enlarged ventricles, although some groups still favor this procedure and eschew a posterior fossa operation In our experience, evacuation of the clot has been more important than reduction of hydrocephalus
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Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
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This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemAnt communicating A
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orrhage, but one that is often disastrous Saccular aneurysms are also called berry aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches Their rupture causes a ooding of the subarachnoid space with blood under high pressure As a rule, the aneurysms are located at vessels bifurcations and branchings (Fig 34-22) and are generally presumed to result from developmental defects in the media and elastica An alternate theory holds that the aneurysmal process is initiated by focal destruction of the internal elastic membrane, which is produced by hemodynamic forces at the apices of bifurcations (Ferguson) As a result of the local weakness, the intima bulges outward, covered only by adventitia; the sac gradually enlarges and may nally rupture Saccular aneurysms vary in size from 2 mm to 2 or 3 cm in diameter, averaging 75 mm (Wiebers et al) Those that rupture usually have a diameter of 10 mm or more (by angiography), but rupture also occurs, albeit less often, in those of smaller size Aneurysms vary greatly in form Some are round and connected to the parent artery by a narrow stalk, others are broad-based without a stalk, and still others take the form of narrow cylinders The site of rupture is usually at the dome of the aneurysm, which may have one or more secondary sacculations A review of the subject by Schievink is recommended for further details In routine autopsies, the incidence of unruptured aneurysms is almost 2 percent excluding minor outpouchings of 3 mm or less Aneurysms are multiple in 20 percent of patients It has been estimated that 400,000 Americans harbor unruptured aneurysms and that there are an estimated 26,000 subarachnoid hemorrhages from them per year (Sahs et al) In childhood, rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years (average 49 years) Therefore they cannot be regarded as fully formed congenital anomalies; rather, they appear to develop over the years on the basis of either a developmental or acquired arterial defect
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