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Journal Article
Analysis of ischemic brain damage in cases of acute subdural hematomas.
Surgical Neurology 2003 June
BACKGROUND: Ischemic damage of the brain is one of the most important factors for the sequelae of acute subdural hematomas (ASDHs). However, ischemic damage is infrequently addressed in a systematic manner in the clinical setting.
METHODS: The analysis of ischemic brain damage was performed based on serial computed tomography (CT) scans in 80 patients with traumatic ASDHs. Single photon emission computed tomography (SPECT) for regional blood flow and/or magnetic resonance imaging (MRI) were also performed.
RESULTS: Follow-up CT scans showed ischemic brain damage in 19 patients and no significant damage in 35 patients. The remaining 26 patients progressively deteriorated to the point of brain death. The ischemic brain damage was seen most frequently in the territory of the anterior cerebral artery (13 cases), followed by the territory of the posterior cerebral artery (12 cases). The ischemic damages in the pallidum, the hypothalamus and the thalamus were demonstrated in 4, 8, and 4 cases, respectively. The ischemic damage in the underlying brain that was probably because of the direct compression of the hematoma was seen in only two cases.
CONCLUSIONS: Most of the ischemic brain damage noted in this study was because of arterial compression secondary to the brain shift and brain herniation, rather than the direct effect of the hematoma upon the underlying brain. Ischemic brain damage adversely affects outcome morbidity, and the difficulty in preventing ischemic damage in cases with marked brain shift leads to poor outcome in patients with ASDHs.
METHODS: The analysis of ischemic brain damage was performed based on serial computed tomography (CT) scans in 80 patients with traumatic ASDHs. Single photon emission computed tomography (SPECT) for regional blood flow and/or magnetic resonance imaging (MRI) were also performed.
RESULTS: Follow-up CT scans showed ischemic brain damage in 19 patients and no significant damage in 35 patients. The remaining 26 patients progressively deteriorated to the point of brain death. The ischemic brain damage was seen most frequently in the territory of the anterior cerebral artery (13 cases), followed by the territory of the posterior cerebral artery (12 cases). The ischemic damages in the pallidum, the hypothalamus and the thalamus were demonstrated in 4, 8, and 4 cases, respectively. The ischemic damage in the underlying brain that was probably because of the direct compression of the hematoma was seen in only two cases.
CONCLUSIONS: Most of the ischemic brain damage noted in this study was because of arterial compression secondary to the brain shift and brain herniation, rather than the direct effect of the hematoma upon the underlying brain. Ischemic brain damage adversely affects outcome morbidity, and the difficulty in preventing ischemic damage in cases with marked brain shift leads to poor outcome in patients with ASDHs.
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