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E K Walsh

Publications and source records attributed to E K Walsh.

10 recordsLinked to original sources

Contribution of brain distortion and displacement to CSF dynamics in experimental brain compression.

The present study was designed to determine the contribution of brain distortion and displacement to changes in cerebrospinal fluid (CSF) dynamics [pressure-volume index (PVI), compliance (C), and outflow resistance (Ro)] during progressive brain compression and the effect of compression on brain mechanical properties. In 10 dogs measurements were made of CSF dynamics, brain elastic behavior, cerebral perfusion pressure, local cerebral blood flow, and suprainfratentorial intracranial pressure (ICP) during the incremental expansion of a supratentorial extradural balloon. PVI appeared more as a measure of the compressibility of the cerebral vascular compartment than of intracranial bulk compliance. Reciprocal changes in CSF dynamics behaved as expected when the balloon expanded predominantly supratentorially causing a moderate increase in ICP. A significant increase in ICP, however, caused a rise in PVI and a decrease in compliance. Under these conditions PVI alone could not differentiate between a falling cerebral perfusion pressure and an increasing suprainfratentorial ICP gradient. In contrast, the compliance decreased with balloon expansion while the outflow resistance showed an inverse correlation with compliance and a linear correlation with baseline ICP; Go, an elastic response parameter, consistently decreased, implying that C, Ro, and Go can be used as a trend of intracranial compensatory reserve during intracranial mass expansion.

Animals

Brain tissue elasticity and CSF elastance.

In the analysis of the pressure-volume relationship of the intracranial system, the concept of brain elastance, sometimes called tissue elastance or CSF elastance, is often used. It is generally designated as Ecsf and is calculated as the slope of the pressure-volume curve of the system. Variations in Ecsf are related to, for example, changes in the buffering capacity of the system which, however, could be influenced by the cerebral vascular volume, compressibility of the meningeal membranes, and compressibility of the subpial brain tissue. Our interest is in isolating the effect of controlled changes in the intracranial system with changes in the subpial tissue only. Here we discuss the measurement of brain tissue elasticity and describe two experimental conditions in which simultaneous measurements showed distinct differences between the behaviour of the system CSF elastance and brain tissue elastic behaviour.

Animals

Attenuation of decompressive hypoperfusion and cerebral edema by superoxide dismutase.

This study tested the hypothesis that ischemia-reperfusion injury initiated by the superoxide anion radical is a major component of postdecompression hypoperfusion and cerebral edema, and could be attenuated by superoxide dismutase (SOD). A supratentorial extradural balloon was placed in 20 fasting, lightly anesthetized, mechanically ventilated dogs and inflated in 0.5-ml increments (0.07 ml/sec) at 15-minute intervals. The end-point of balloon expansion was the onset of an isoelectric electroencephalogram, near-arrest of hemispheric cerebral blood flow (CBF) (measured by H2 clearance), and the appearance of a suprainfratentorial intracranial pressure gradient, which was held for 15 minutes. The in vivo development of brain edema was detected by measuring brain elastic response (BER) extradurally, and was correlated with postmortem measurement of brain water content (gravimetry); blood-brain barrier integrity was tested by Evans blue dye given after the insult. After decompression, the dogs were randomly assigned to one of four treatment groups: Group I received hyperventilation (PaCO2 28 +/- 1 mm Hg, mean +/- standard deviation); Group II received furosemide (2.4 mg/kg) and pentobarbital (10 mg/kg) every 8 hours; Group III received 20% mannitol in a 1.4-gm/kg bolus plus furosemide, 0.5 mg/kg; and Group IV received SOD, 15,000 U/kg every 15 minutes for 3 hours. At 4 hours of decompression Group IV had significantly greater recovery in local CBF and BER than Groups I, II, and III (p less than 0.05). The 24-hour survival rate was 20% for Group I, 60% for Group II, 80% for Group III, and 100% for Group IV. The survival rate appeared to correlate with a variable degree of postmortem intraparenchymal hemorrhages, blood-brain barrier disruption, and moderate to severe brain edema for Groups I, II, and III. In contrast, Group IV had the least brain edema (p less than 0.05) and Evans blue dye extravasation (p less than 0.05) and the fewest intraparenchymal hemorrhages. These data support the hypothesis that, under the experimental conditions described here, the superoxide anion plays a major role in the pathophysiology of postdecompression ischemic edema.

Animals

Brain tissue elastic behavior and experimental brain compression.

This study was designed to test the hypothesis that the progressive expansion of an extradural mass causes detectable changes in brain mechanical response properties, in particular the nonlinear elastic behavior, before any significant changes in intracranial cerebrospinal fluid pressure can be detected. In 10 chronically prepared and anesthetized dogs, incremental inflation (0.07 ml/s) of an extradural balloon caused 1) a progressive fall in the brain nonlinear elastic parameter (G0, mmHg/mm2), 2) nonsignificant changes in brain tissue elasticity (G0, mmHg/mm), 3) a disproportionate progressive rise in subpial tension, and 4) a progressive fall in local cerebral blood flow (H2 clearance), despite a modest decrease in cerebral perfusion pressure (extracranial). In previous brain compression experiments (Brain Res. 305: 141-143, 1984) we have shown that the compression site becomes compacted and stiffer (increased G0) and its nonlinear elastic parameter (G0) increases markedly. These earlier findings, coupled with the present observation of a loss in tissue nonlinearity distally to the compression site, are most likely the major mechanisms by which, with a rapidly expanding intracranial mass, tissue pressure gradients and brain displacement, including transtentorial herniation, develop.

Animals

On measurement of brain elastic response in vivo.

The elastic response behavior of brain tissue in vivo has been shown to be sensitive to the physiological environment of the brain and thus represents a useful parameter for identifying effects of controlled changes on the system. Here we describe a method for measuring brain elastic response using an epidural pressure-depth transducer and a minimum number of insertions. The method also serves to identify the nonlinear response of brain tissue.

Animals

Elastic behavior of brain tissue in vivo.

A measurement system and a test sequence have been developed to determine the in vivo elastic response of brain tissue in terms of a pressure-depth ratio. This parameter appears sensitive to changes in the tissue environment that may occur due to the influence of, e.g., anesthetic agents, hyperventilation, etc., and thus may be useful in evaluating such influences. The measurements are made with the dura-arachnoid membranes intact, thus maintaining the influence of the cerebrospinal fluid compartment on the response behavior of the brain tissue that comprises the subpial region. As an integral part of the test, the procedure also serves to determine the depth or position of the subpial region and thus assures that the subsequent pressure-depth measurements invole brain tissue response. Finally, some discussion is given to relating the measured pressure-depth ratio to the classical elastic modulus. Values of the pressure-depth ratio and the corresponding elastic modulus for seven dogs are given.

Animals