[Rupture of cerebral aneurysm in an acute stage resulting in hypotension].
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Biomedical subjects
Publications and source records attributed to M Taneda.
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An unusual case of delayed ischemia following rupture of an aneurysm of the left internal carotid artery is reported. Symptoms occurred twice after clipping the aneurysm and removing most of the subarachnoid blood on the left side the day after subarachnoid hemorrhage (SAH). Initial ischemia due to vasospasm occurred on the left side of the brain on the 8th day after SAH and responded favorably to induced hypervolemia. After complete recovery, a second episode due to vasospasm occurred on the 16th day after SAH on the right side of the brain from which the subarachnoid blood had not been removed. This caused a massive lesion and permanent severe neurological deficits. This case suggests that removal of subarachnoid blood may affect the severity and time course of vasospasm, and emphasizes the necessity of extensive removal of subarachnoid blood for prevention of severe delayed ischemic symptoms.
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An analysis of 251 patients who were hospitalized within 24 hours after rupture of the supratentorial aneurysms and were not comatose during the very early stage was carried out. The patients were divided into three groups in relation to timing and methods of surgery. In 64 patients of Group A, the operation was planned to be delayed more than 10 days from subarachnoid haemorrhage (SAH). In 91 patients of Group B, clipping of aneurysms was performed within 48 hours of SAH and subarachnoid blood clots were simultaneously removed while approaching the aneurysms. In 99 patients of Group C, clipping of aneurysms was performed within 48 hours of SAH and radical and extensive removal of any subarachnoid blood clot identified on the computerized tomographic scan was tried at the same time. The outcome at 3 months after SAH was the most favourable in Group C patients and the least favourable in Group A patients. Early operation combined with radical removal of subarachnoid clots minimizes the overall mortality and morbidity in patients with ruptured intracranial aneurysms by preventing rebleeding and probably by avoiding vasospasm.
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The authors review 15 patients with acute cerebellar infarction accompanied by obstructive hydrocephalus. These patients were among 1700 consecutive patients with acute cerebrovascular disease who were examined by angiography and also, except for the initial 320 cases. by computerized tomography (CT) scan. The CT scans were helpful in diagnosis and management of the patients. It demonstrated cerebellar mass lesions as being low density, isodense, or high density, according to the amount of hemorrhage into the infarcted area. Such cerebellar mass lesions caused acute compression of the posterior fossa. The clinical picture was determined mainly by the extent of the initially infarcted area in the vertebrobasilar territory and the speed of enlargement of the subsequently developing cerebellar mass lesion. Suboccipital decompressive surgery was performed in 10 patients and was generally beneficial. The postoperative prognosis depended mainly on the presence or absence of coexisting brain-stem infarction. Five patients who were managed conservatively died during the acute stage. Prompt and correct diagnosis of this illness is required to ensure adequate therapy.
The effect of removal of subarachnoid blood clots on the prevention of delayed ischemic deficit was evaluated in 239 consecutive patients with ruptured supratentorial non-giant aneurysms. All patients were hospitalized within 24 hours after subarachnoid hemorrhage (SAH) and were classified in Grades 1 to 4 according to the system of Hunt and Hess; classification was made immediately preoperatively in patients operated on within 48 hours after SAH, or 48 hours after SAH in patients for whom delayed operation was planned. Delayed ischemic deficit causing permanent disability or death occurred in 11 (25%) of 44 patients in whom surgery was planned to be delayed for 10 days or more, in 26 (27.7%) of 94 patients in whom the aneurysms were obliterated and blood clots adjacent to them were removed within 48 hours of SAH, and in 11 (10.9%) of 101 patients in whom the aneurysms were obliterated and extensive and aggressive removal of thick subarachnoid clots lying along the arteries (identified on computerized tomographic scan) was performed within 48 hours of SAH. Accordingly, early operation is an effective and reliable method to reduce the occurrence of severe delayed ischemic deficit only when subarachnoid blood clots are removed extensively and aggressively along the arteries within 48 hours of SAH.
A histopathological study on an autopsy case of 38-year-old female who had suffered from huge glioma and received radiation therapy as well as operation and chemotherapy was reported. The tumor mainly involved the right frontal lobe and partially invaded to the left cerebral hemisphere. Subarachnoidal dissemination of tumor cells was noticed in cerebellum, brain stem and spinal cord. Under the microscope the tumor was mainly consisted of astrocytic tumor cells, while oligodendrocytic ones and those with anaplastic or bizarre nuclei were observed among them. Though ependymomatous appearance was partially seen, no true rosette was found. From these findings the tumor was histologically diagnosed as anaplastic glioma. Simultaneously, there was massive coagulative necrosis which was limited to the irradiated area in the tumor tissue and surely attributable to irradiation. In addition, proliferation of gemistocytic astrocytes which was independent of glioma itself was widely observed in the field of irradiation. Another remarkable finding was spongiform degeneration which was located in the subpial area of brain stem including degenerative products of myelin sheaths and axons with neither inflammatory changes not gliosis. In some papers it is suggested that such a lesion has something to do with irradiation or chemotherapy. But in our case this lesion was found in non-irradiated area and no intramedullary injection of chemical agents was performed. Further, the distribution of this lesion was for the most part restricted to the domain of the pontine cistern which had been huge owing to stagnant hemorrhagic fluid. Therefore, it is highly probable that this lesion was caused by the abnormal pia-glial barrier.
Five cases of subdural hematoma from arterial rupture (SDH-AR) are described and other 39 reported cases are reviewed. The average age of the patient is 59 and male to female ratio is 2:1. Fifty two percent of the patients have history of recent head injuries most of which are trivial. A very few patient have initial loss of consciousness. Approximately half of the patients with history of head trauma have long lucid interval (average of 7 days). Those patients without history of head trauma have spontaneous onset of the symptoms and some of the have acute onset of headache and loss of consciousness, simulating cerebrovascular accident. Natural history of the SDH-AR is progressing deterioration of the symptoms, resulting in coma and death. Skull fracture is seldom demonstrated in the patients with SDH-AR. Angiography shows and extracerebral avascular mass over the cerebral convexity with marked midline shift. In 3 cases including our 2 cases, extravasation of the contrast medium from the cortical artery is observed and this is a useful finding for making diagnosis of this disease. Computerized tomography reveals high density extracerebral mass with remarkable mass effect. Craniotomy discloses subdural clot and spurting arterial rupture from a branch of the cortical artery around the Sylvian fissure. In some cases, subarachnoid hemorrhage is observed but in none of the cases, cerebral contusion or laceration is present. It is presumed that the mechanism of the arterial rupture is gliding movement of the brain within the skull upon injury, tearing an arterial twig with dural attachment. Hypertension, arteriosclerosis and brain atrophy may be important contributing factors to this mechanism. Pseudoaneurysm of the cortical artery caused by closed head injury is also associated with this mechanism and may explain delayed sudden onset of the symptoms in some patients with SDH-AR.
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Postoperative follow-up computerized tomographic (CT) scans were performed in 16 cases of acute epidural haematomas to assess the efficacy of surgical treatment. Particular attention was paid to postoperative intracerebral haematomas that were detected in four cases on the preoperative CT scans. The intracerebral haematomas were found to have enlarged in all four cases on CT scans performed immediately after removal of the epidural haematomas. In the other 12 patients in whom no apparent abnormalities other than epidural haematomas were detected on preoperative CT scans, postoperative CT scans did not show development of intracerebral bleeding. The results indicate that bleeding may be encouraged in areas of intracerebral haemorrhage when coexisting epidural haematomas are evacuated. The possible pathophysiology of enlargement of intracerebral haematomas after decompression is discussed.
The reliability of quantitative evaluation by doppler ultrasound with regard to the ophthalmic collateral blood flow in patients with carotid artery occlusion was estimated. The ultrasonic doppler flow signals of the ophthalmic collateral flow of 54 carotid occlusions were classified into four types and three degrees--high, moderate, and low reversed flow patterns--and were compared with the angiographic findings of the collateral flow classified into three grades--good, poor, and none. With the exception of three cases, the ultrasonic doppler flow patterns of the collateral flow correlated well with the angiographic findings in 54 occluded carotid arteries.