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L. M. Thomas, V. L. Roberts and E. S. Gurdjian

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John E. Coe, J. Robert Rivet and Thomas S. Hargest

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Increased Intracranial Pressure and Pulmonary Edema

Part 3: The Effect of Increased Intracranial Pressure on the Cardiovascular Hemodynamics of Chimpanzees

Thomas B. Ducker, Richard L. Simmons and Robert W. Anderson

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Robert C. Cantu, Thomas Souders and Robert S. Hepler

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Melville Roberts, Guy Owens, Juliet Vilinskas and David D. Thomas

✓ Seizures were induced in 12 monkeys rendered hemiparetic by middle cerebral artery occlusion. In a control group of five hemiparetic monkeys seizures were not induced. A mass spectrometer was used to monitor regional oxygen tension (pO2), carbon dioxide tension (pCO2) and the partial pressure of argon (pA) within the ischemic brains. Seisure activity resulted in a 74.3% mean increase in pO2 and 16.9% mean decrease in pCO2. The mean argon washout time was decreased 29.1%. The changes were transient and recovery from hemiparesis was no better in the experimental group than in the control group.

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John B. Thompson, Thomas H. Mason, Gerald L. Haines and Robert J. Cassidy

✓ In seven infants, nondepressed diastatic linear skull fractures occurred with extrusion of brain tissue into the subgaleal space. These patients exhibited a triad of clinical findings that should encourage early surgery. Craniotomy and duroplasty seem to offer the most satisfactory long-term results.

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Thomas D. Springer, Gerald Fishbone and Robert Shapiro

✓ An aneurysm at the origin of the superior cerebellar artery in a patient with a primitive hypoglossal artery is reported. Selective catheterization of the primitive artery is described with a brief discussion of the embryogenesis of carotid-basilar anastomoses. Associated findings in previously reported cases of persistent hypoglossal artery are briefly reviewed.

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Experimental cerebral oligemia and ischemia produced by intracranial hypertension

Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function

Lawrence F. Marshall, Felix Durity, Robert Lounsbury, David I. Graham, Frank Welsh and Thomas W. Langfitt

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

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Lawrence F. Marshall, David I. Graham, Felix Durity, Robert Lounsbury, Frank Welsh and Thomas W. Langfitt

✓ The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

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Lawrence F. Marshall, Frank Welsh, Felix Durity, Robert Lounsbury, David I. Graham and Thomas W. Langfitt

✓ The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.