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higher rates, but it is clear that the cognitive problems improve over time in the majority of patients The use of Doppler insonation of the middle cerebral arteries is being studied to detect transient signals called HITs (high-intensity transients) as a manifestation of small emboli during surgery but, as in cerebral arteriography, the clinical importance of these emboli is not known The special stroke problems relating to prosthetic heart valves mainly infective endocarditis causing embolic strokes and anticoagulant-related cerebral hemorrhage are described in appropriate sections of this chapter
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INTRACRANIAL HEMORRHAGE
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This is the third most frequent cause of stroke Although more than a dozen causes of nontraumatic intracranial hemorrhage are listed in Table 34-9, primary or hypertensive ( spontaneous ) intracerebral hemorrhage, ruptured saccular aneurysm and vascular malformation, and hemorrhage associated with the use of anticoagulants or thrombolytic agents account for the majority Cerebrovascular amyloidosis and bleeding disorders account for a small number The small brainstem hemorrhages secondary to temporal lobe herniation and brainstem compression (Duret hemorrhages), hypertensive encephalopathy, and brain purpura might be included in this group, but they do not simulate a stroke
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Primary (Hypertensive) Intracerebral Hemorrhage
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This is the mundane spontaneous brain hemorrhage It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries In recent decades, with increased awareness of the need to control blood pressure, the proportion of hemorrhages attributable to causes other than hypertension has greatly increased; more than half such hemorrhages on our services now occur in Table 34-9 Causes of intracranial hemorrhage (including intracerebral, subarachnoid, ventricular, and subdural) 1 Primary (hypertensive) intracerebral hemorrhage 2 Ruptured saccular aneurysm 3 Ruptured AVM; less often, venous and dural vascular malformations 4 Cavernous angioma 5 Trauma including posttraumatic delayed apoplexy 6 Hemorrhagic disorders: leukemia, aplastic anemia, thrombocytopenic purpura, liver disease, complication of anticoagulant or thrombolytic therapy, hypo brinogenemia, hemophilia, Christmas disease, etc 7 Hemorrhage into primary and secondary brain tumors 8 Septic embolism, mycotic aneurysm 9 With hemorrhagic infarction, arterial or venous 10 With in ammatory and infectious disease of the arteries and veins 11 With arterial amyloidosis 12 Miscellaneous rare types: vasopressor drugs, cocaine, moyamoya, herpes simplex encephalitis, vertebral artery dissection, acute necrotizing hemorrhagic encephalitis (Hurst disease), tularemia, anthrax, etc
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normotensive individuals, and the hemorrhages more often than previously arise in locations that are not typical for hypertension Nevertheless, the hypertensive cerebral hemorrhage serves as a paradigm for understanding and managing the cerebral hemorrhage In order of frequency, the most common sites of a cerebral hemorrhage are (1) the putamen and adjacent internal capsule (50 percent); (2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension); (3) the thalamus; (4) a cerebellar hemisphere; and (5) the pons (see Weisberg et al) The vessel involved is usually a penetrating artery that originates from a larger trunk vessel About 2 percent of primary hemorrhages are multiple Rarely the bleeding is solely intraventricular, possibly from the choroid plexus The problem is one of bleeding that occurs within brain tissue; rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms and some vascular malformations The extravasation of blood forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues (Fig 34-20) Adjacent brain tissue is distorted and compressed If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers can be compromised, leading to coma and death in the manner described in Chap 17 Both the size and the location of the clot determine the degree of upper brainstem compression (Andrew et al) Rupture or seepage into the ventricular system may occur, and the CSF becomes bloody in these cases However, a hemorrhage of this type almost never ruptures through the cerebral cortex When the hemorrhage is small and located at a distance from the ventricles, the CSF may remain clear even on repeated examina-
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Figure 34-20 An unenhanced CT scan showing the typical picture of a massive primary (hypertensive) hemorrhage in the basal ganglia The third ventricle and ipsilateral lateral ventricle are compressed and displaced by the expanding mass (12 h after onset of stroke)
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