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Biomedical subjects

L F Marshall

Publications and source records attributed to L F Marshall.

121 records · Page 7Linked to original sources
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 2: Brain morphology.

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.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism.

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.

Adenosine Triphosphate↗
PubMedDate not supplied

Pentobarbital therapy for intracranial hypertension in metabolic coma. Reye's syndrome.

In severe Reye's syndrome, with nonspecific intensive supportive therapy, the mortality rate approaches 75%. In many instances, death is due to uncontrolled cerebral edema and elevated intracranial pressure. (ICP). Pentobarbital therapy, sufficient to maintain a blood barbiturate level between 2.5 mg% and 4.0 mg%, was used to control ICP in seven patients with metabolic coma complicated by intracranial hypertension (intracranial pressure greater than 30 mm Hg for 30 min). The nadir of their neurological function was characterized by no response to deep pain, absent or abnormal oculocephalic responses, bilaterally dilated, unreactive pupils, and markedly irregular or absent respirations. Before barbiturate administration hyperventilation, steroids, mannitol, and other supportive therapies commonly used in Reye's syndrome were begun. After institution of pentobarbital therapy, the daily mannitol dose required to maintain the intracranial pressure below 20 mm Hg was significantly reduced (p less than 0.001), from 3.7 +/- 0.3 to 0.5 +/- 0.2 g/kg/day. All the patients survived, and six have no obvious neurological sequelae. Pentobarbital is a useful adjunct for intracranial pressure control in advanced metabolic coma.

Adolescent↗
PubMedDate not supplied

Alterations in behavior, brain electrical activity, cerebral blood flow, and intracranial pressure produced by triethyl tin sulfate induced cerebral edema.

The interrelationships between cerebral edema, intracranial pressure (ICP), and cerebral blood flow (CBF) were studied in acute and chronic triethyl tin sulfate treated rats. Prior to pentobarbital anesthesia behavioral observations were made. ICP and regional CBF were measured under steady state conditions and brain water content was determined by vacuum drying of the right cerebral hemisphere. Control and chronic animals were neurologically normal. There were two distinct acute groups: (1) acute low pressure (ALP) animals - alert but tetraperetic, and (2) acute high pressure (AHP) animals - deeply stuporous, with minimal pain response and gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and chronic animals. The interaction of increased pressure and edema (AHP) produced the greatest decrease in CBF, although deep white flows were significantly affected in all experimental groups. Chronic animals had significantly lower flow in four of seven regions compared to ALP animals despite no significant difference in ICP. Water content was significantly increased in all experimental groups with the greatest increase in the chronic animals. In the absence of any significant increase in ICP, cerebral edema appears to cause a significant reduction in cerebral blood flow and this reduction corresponds with the magnitude and location of the edema.

Acute Disease↗
PubMedDate not supplied

The influence of diurnal rhythms in patients with intracranial hypertension: implications for management.

Decompensation of brain injured patients during the night is common and has been attributed to the retention of CO2 during sleep. When CO2 is controlled, such nocturnal decompensation needs another explanation; consequently, the records of 21 consecutive patients with acute closed head injuries and increased intracranial pressure were reviewed. There were 185 separate episodes of intracranial hypertension (30 mm Hg or more for 10 minutes or more) in the 21 patients, 124 of which (67%) occurred between 4:00 a.m. and 9:00 a.m. (p less than 0.01). Intravenous pentobarbital (3 to 5 mg/kg) was effective in reducing the intracranial pressure (ICP) to normal levels during 104 of the 124 early morning episodes (84%), whereas mannitol was less effective (7 of 17; 41%). This suggests that an increase in brain blood volume directly related to diurnal rhythm is responsible for the increase in ICP. Severe bradycardia and systemic arterial hypertension were unreliable predictors of elevation in ICP. They preceded or accompanied less than one-fourth of the episodes.

Bradycardia↗
PubMedDate not supplied

Predictors of outcome following severe head trauma: follow-up data from the Traumatic Coma Data Bank.

Outcome as a function of employment status or return to school was evaluated in severely head-injured patients. A priori we selected the most salient demographic, physiological, neuropsychological and psychosocial outcome predictors with the aim of identifying which of there variables captured at baseline or 6 months would best predict employability at 6 or 12 months. Based on the patients evaluated at 6 months, 18% of former workers had returned to gainful employment and 62% of former students had returned to school. For those not back to work or school at 6 months, 31% of the former workers and 66% of the former students had returned by 12 months. Age, length of coma, speed for both attending and motor movements, spatial integration, and intact vocabulary were all significantly related to returning to work or school. The three most potent predictors for returning to work or school were intactness of the patient's verbal intellectual power, speed of information processing and age.

Activities of Daily Living↗
PubMedDate not supplied

Selected cases of poor outcome following a minor brain trauma: comparing neuropsychological and positron emission tomography assessment.

Neuropsychological residua are common particularly in the early stages following a minor traumatic brain injury (TBI), however, a minority of individuals complain of persistent deficits following months or years post-accident. Nine such cases are presented with little or no evidence of brain damage demonstrated according to non-functional neuroimaging (for example CT, MRI), yet their neuropsychological examinations were positive. Since the introduction of positron emission tomography (PET), which captures a functional approach, the question arose as to what extent the two techniques (i.e. PET and neuropsychological examination) are interrelated. All nine minor TBI cases revealed a corroboration between the positive neuropsychological findings confirmed on the PET. The PET procedure documented neuropathology which frequently was pronounced in the frontal and anteriotemporo-frontal regions. Moreover, no significant differences were evident between those five cases with reported loss of consciousness vs. those four cases without.

Adult↗