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Oligodendrogliomas

An Analysis of 63 Cases

Bryce Weir and Arthur R. Elvidge

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Bryce Weir, Ramon Erasmo, Jack Miller, John McIntyre, David Secord and Bruce Mielke

✓ This study investigates the relationship between vasospasm and repeated subarachnoid hemorrhages in 18 monkeys. Sixteen received weekly 4 cc injections of autogenous blood into the subfrontal subarachnoid space. The weekly mortality rate for 4 weeks was 6%, 33%, 20%, and 37% respectively. The over-all mortality was 75%. The degree of vasospasm did not correlate with the morbidity and mortality. Vasospasm was limited to the intradural cerebral vessels and was diffuse. It never lasted longer than a few hours, late vasospasm did not occur, and the degree of vasospasm did not alter with repeated occasions of “subarachnoid hemorrhage.” Immediate electrocardiogram abnormalities were related to the height of the cerebrospinal fluid pressure rise following the subarachnoid hemorrhage (injected blood). Pathological examination of the vessels shown to be in spasm was normal. The study suggests that the increased mortality associated with repeated subarachnoid hemorrhage is due to cumulative structural damage rather than a heightened vasospastic response to repeated hemorrhages.

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Bryce Weir

✓ In 23 patients with subdural hematomas the osmolality of the hematoma fluid was compared with that of venous blood and in 11 of these cases with lumbar cerebrospinal fluid. There was no significant difference in the osmolalities of these fluids. The electrophoretic pattern of the subdural hematoma fluid resembles that of serum in that it usually does not contain prealbumins. The hemoglobin breakdown products migrate with the alpha II and beta globulins and include methemoglobin, oxyhemoglobin, and bilirubin. It is suggested that the late onset of symptoms, which often occurs, is due to either progressive bleeding from the neovascular outer membrane, effusion through it of albumin and fluid, or recurrent bleeding from a venous stump. It is also possible that very little expansion in the size of the subdural hematoma occurs following the initial formation and that late decompensation results from dynamic changes in the compressed brain. This work provides no evidence either to support or refute the concept of an osmotic mechanism for hematoma expansion.

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Bryce Weir

✓ The records of 248 patients with supratentorial astrocytomas, Grades 3 and 4, treated surgically between 1960 and 1970 were analyzed. Abstracted clinical data were transferred to magnetic tape for computer analysis of postoperative survival factors using multiple chi square test and a step-wise multiple regression equation. All patients were followed, and only four were alive at the time of the study. It appeared that radiation therapy was the most important determinant of prolonged postoperative survival. The age of the patient was the only other factor of any significance.

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Bryce Weir

✓ A case of ectopia lentis (Marfan syndrome) with a cerebral subarachnoid cyst, a spinal extradural cyst connected to a lateral intrathoracic meningocele, and perineural cysts is presented. The association of these leptomeningeal cysts in this genetic disorder of connective tissue suggests a common pathogenesis.

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Bryce Weir, Pierre Band, Raul Urtasun, Gilles Blain, Don McLean, Fred Wilson, Bruce Mielke and Michael Grace

✓ Forty-one consecutive patients with supratentorial primary brain tumors (38 Grade III and IV astrocytomas, one giant-cell astrocytoma, and two cases with insufficient tissue for diagnosis) were randomly allocated within 2 weeks of surgery to one of three therapeutic groups. Group 1 (15 patients) received radiation therapy totaling 4000 to 4500 rads in 4 to 5 weeks. Group 2 (13 patients) received 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) 130 mg/sq m orally every 6 weeks. Group 3 (13 patients) received radiation therapy plus CCNU as for Groups 1 and 2. When the disease progressed, patients in Groups 1 and 2 were crossed over to receive CCNU and irradiation respectively. The median survival time in these groups was 188, 259, and 252 days, and the mean survival 263, 262, and 329 days. The median time from diagnosis to crossover (Groups 1 and 2) or to progression (Group 3) was 163, 99, and 220 days, and the mean time was 172, 108, and 231 days. There was no statistically significant difference between the means or medians in any of these situations.

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Bryce Weir, Michael Grace, John Hansen and Charles Rothberg

✓ Measurements were made at eight predetermined positions on 627 sets of angiograms from 293 patients with aneurysms. A ratio between the sum of the vessel diameters in the subarachnoid space to the sum in the base of skull and neck was calculated and plotted against time. Vasospasm has its onset in man about Day 3 after subarachnoid hemorrhage, is maximal at Days 6 to 8, and is gone by Day 12. There is a tendency for patients in poor clinical grades to have more vasospasm. The patients with most vasospasm have a significantly higher mortality than those with the least.

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Donald P. Boisvert, Thomas R. Overton, Bryce Weir and Michael G. Grace

✓ Regional cerebral blood flow (rCBF), angiographic cerebral arterial caliber, and cerebrospinal fluid (CSF) pressure were measured in rhesus monkeys to determine the effect of experimentally induced subarachnoid hemorrhage (SAH) on cerebral arterial responses to graded increases in blood pressure. These measurements were also performed in a control group of monkeys subjected to a mock SAH by injection of artificial CSF into the cerebral space.

Before subarachnoid injection of blood or artificial CSF, graded increases in mean arterial blood pressure (MABP) to a level 40% to 50% above baseline values had no effect on rCBF. The major cerebral arteries constricted and CSF pressure remained unchanged. Similar responses were observed after injection of artificial CSF. When MABP was increased in animals that had been subjected to subarachnoid injection of blood, rCBF increased and was associated with dilatation of the major cerebral arteries and moderate increases in CSF pressure. These results demonstrate that cerebral arterial responses to increases in blood pressure may be abnormal in the presence of subarachnoid blood. The manner in which abnormal cerebral arterial reactivity, changes in blood pressure, and vasospasm combine to determine the level of cerebral perfusion following SAH is postulated.

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Charles Rothberg, Bryce Weir, Thomas Overton and Michael Grace

✓ The pathophysiological responses to experimental subarachnoid hemorrhage (SAH) were investigated in 20 spontaneously breathing cynomolgus monkeys. Four different volumes of fresh autogenous blood were used: 1.0, 1.33, 1.67, and 2.0 cc/kg. Five other animals had injection of 1.67 cc/kg of mock cerebrospinal fluid. Cerebral blood flow (CBF) was measured using the xenon-133 clearance technique. Respiratory rate and tidal volume were monitored by way of a Vertek pneumotach. The reduction of CBF after the SAH became more pronounced with increasing volumes of subarachnoid blood. The CBF remained reduced despite a return to normal of the cerebral perfusion pressure. Increasing SAH volumes were associated with greater abnormalities in the respiratory pattern, consisting of apnea and hyperventilation. These larger volumes were also associated with hypoxemia. Morbidity and mortality increased with increasing volumes of SAH, and are believed to be the result of a combination of decreased CBF, respiratory center disturbances, and pulmonary diffusion defects.

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Bryce Weir

✓ The oncotic pressure of fluid from subdural heatomas and subdural hygromas was compared to that of simultaneously drawn venous blood in 20 patients. There was no significant difference in the oncotic pressure of fluid from subdural hematomas and venous blood; however, the oncotic pressure of fluid from subdural hygromas was significantly less than that of blood. This finding fails to support the Zollinger and Gross modification of Gardner's theory, that chronic subdural hematomas grow and produce symptoms after a latent interval because they attract fluid from the blood via dural vessels.