A retrospective clinical and pathological review of 905 consecutive brain tumor cases (excluding pituitary adenoma and recurrent tumor) was conducted to identify cases in which intratumoral hemorrhage was confirmed grossly and/or pathologically. There were 132 cases so identified, for an overall tumor hemorrhage rate of 14.6%; of these, 5.4% were classified as macroscopic and 9.2% as microscopic. The presence of hemorrhage was correlated with the neurological presentation. The highest hemorrhage rate (70.0%) was found in patients with prior neurological history who experienced apoplectic deterioration (acute-on-chronic presentation). Only 57.1% of patients with acute deterioration in the absence of prior neurological symptoms had hemorrhages. The highest hemorrhage rate for primary brain tumors was 29.2% for mixed oligodendroglioma/astrocytoma, while the highest hemorrhage rate for any tumor type was 50% for metastatic melanoma. The clinical relevance of tumor hemorrhage is discussed.
✓ Cerebral blood flow (CBF), intracranial pressure (ICP), brain metabolism (CMRO2), systemic arterial pressure (SAP), and arterial blood gases were measured in comatose patients, most of whom had suffered a head injury. The patients were divided into two groups according to whether a mass lesion was or was not demonstrated by bilateral carotid angiography. In the majority of patients a control run measuring regional cerebral blood flow (rCBF) was followed by a test of cerebral autoregulation; hypertonic mannitol was then administered. During the control period there was marked and unpredictable variability in all of the parameters recorded. There was no correlation between ICP or CBF and neurological status or CMRO2 except at very high levels of ICP. Autoregulation was intact in some patients and defective in others, and there was no correlation between the status of autoregulation on the one hand and CBF or survival on the other. Mannitol increased CBF in nearly all patients, to twice the control value in a few, and CMRO2 increased with CBF in several patients. The change in CBF was independent of the initial ICP or the response of ICP to mannitol. Thus, the relationship of these parameters was unpredictable in acutely brain-damaged patients; the status of autoregulation was also unpredictable.
Acute spontaneous subdural hematoma is infrequent in association with rupture of intracranial saccular aneurysm. In the majority of cases, aneurysms of the middle cerebral artery along the convexity or of the anterior cerebral artery along the interhemispheric fissure are found to be the culprits. We present two recent cases of internal carotid-posterior communicating artery aneurysms causing acute subdural hematoma with little or no subarachnoid hemorrhage and discuss the possible mechanisms for this occurrence.
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