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Said H. Koozekanani, W. Michael Vise, Reza M. Hashemi and Robert B. McGhee

✓ Experimental spinal cord injuries were induced in dogs by dropping calibrated weights through a vented tube onto a small impounder resting on the surgically exposed cord. The motion of the impounder and the drop-mass were recorded by high-speed photography and the resulting data were compared to those obtained from a computer simulation of the dynamics of the injury mechanism. It is concluded that this method of inducing spinal cord injuries may yield markedly different degrees of cord compression depending upon the parameters of the animal material and apparatus even when the gm-cm of impact energy is maintained at a constant value. Some approaches to standardization of this injury model are suggested.

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Eric Zimmerman, John Grant, W. Michael Vise, David Yashon and William E. Hunt

✓ Two patients with bursting fractures of the atlas vertebra are presented. The use of a halo apparatus as an effective alternative to bedrest and cervical traction in these patients is discussed. Polytomography was helpful in establishing an accurate diagnosis.

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David Yashon, Alfred P. Magness II and W. Michael Vise

✓ The authors review the intraoperative use of elective hypotension to reduce the probability of hemorrhage, to increase pliability of the aneurysmal sac for ease of clip application, and to control hemorrhage. The optimum agent and techniques for lowering systemic blood pressure remain controversial, but trimethaphan, sodium nitroprusside, and halothane have been found most useful. When cerebral blood flow falls below the brain's capacity to autoregulate, distinct time-related alterations occur biochemically and histologically. The profile of prolonged reduced adenosine triphosphate (ATP), low phosphocreatine, low glucose, and elevated lactate and lactate/pyruvate ratio is associated with swelling of perivascular astrocytes and “blebbing” of vascular endothelial cells with subsequent cerebral damage. To prevent permanent alteration it is desirable to observe time constraints and to employ other means of protection such as hypothermia, although the authors believe the latter unnecessary for short hypotensive periods. It has been proposed, but not substantiated, that anesthetics which depress rate of cerebral oxygen consumption but do not affect cerebral ATP level protect the brain from hypotension. Several investigations suggest that halothane, a vasodiltor, satisfies the safety requirement. The most prominent contraindication to halothane, however, is elevation of intracranial pressure. At present hypotensive surgery for aneurysmorrhaphy is usually performed when intracranial pressure has returned to normal. Experimentally the electroencephalogram has been observed to show alterations prior to biochemical parameters for following brain vulnerability, so that it conceivably could be an effective monitoring technique during prolonged profound hypotension.

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W. Michael Vise, David Yashon and William E. Hunt

✓ Vascularity and blood-brain barrier (BBB) function within spinal cord were studied with fluorescent microscopy at 14 intervals following 300 gm-cm injuries to the thoracolumbar spinal cord in 32 dogs. Histochemical staining with formaldehyde brought out a yellow-green fluorescence of vascular origin that was unrelated to tracer dye. This fluorescence accumulated in perivascular sites and is possibly related to catecholamine elevation within damaged spinal cord. Intrinsic CNS mechanisms for catecholamine build-up (increased transport, increased synthesis, increased release) are reviewed as well as the pharmacological action of alpha methyl tyrosine. It is hypothesized that an intrinsic CNS source of norepinephrine build-up is unlikely and that elevation of circulating catecholamine levels following stress and trauma leads to the extravasation of this material across injured BBBs within contused spinal cord.

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David Yashon, W. Michael Vise, Richard C. Dewey and William E. Hunt

✓ The temperature of the spinal cord parenchyma during local hypothermia was recorded in 18 dogs with and without a 300 to 500 gm-cm spinal cord injury. Other variables included opening the dura, location of the inflow stream, and the use of alcohol bath cooling. In nontraumatized cord, the temperature varied between 5.4° and 23.5°C depending on the location of the inflow stream; the variable range of 10–15 minutes of perfusion to reach these levels was unexpected. Temperatures of the injured cord fell to those of the reservoir (1.0° to 3.8°C) within 2½ minutes. The fact that the temperature of nontraumatized areas two segments cephalad to the injury was also reduced showed the capacity of the cord for thermal conduction. Opening the dura or use of an alcohol bath had little effect on cord temperature. Lack of heat transport due to ischemia is postulated as the primary cause of the rapid reduction of temperature in the injured cord to that of the surrounding environment.