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  • Author or Editor: William E. Hunt x
  • By Author: Dewey, Richard C. x
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Carole A. Miller, Richard C. Dewey and William E. Hunt

✓ The authors describe a lumbar spine fracture that is characterized on anteroposterior x-ray views by separation of the pedicular shadows. It is almost invariably associated with posterior interlaminar herniation of the cauda equina through a dorsal dural split, and anterolateral entrapment or amputation of the nerve root. The fracture is unstable and requires internal fixation and fusion at the time of neurolysis. Fractures meeting these criteria should be explored as soon as the patient's condition permits. Myelography is usually unnecessary and may be contraindicated in some cases. The postulated mechanism of injury is hyperextension with vertical impaction and rupture of the ring made up of the lamina, pedicle, and vertebral body. The ring is fractured in several places in a manner similar to that seen in “Jefferson fracture” of C-1. The special anatomical relationships of the thoracolumbar junction and the plane of the lumbar facets are also discussed.

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Experimental cerebral hemodynamics

Vasomotor tone, critical closing pressure, and vascular bed resistance

Richard C. Dewey, Heinz P. Pieper and William E. Hunt

✓ Application of Burton's concept of the critical closing pressure to experimental data on brain-blood flow in the monkey suggests that perfusion pressure, not vascular bed resistance, is the primary variable affecting cerebral blood flow. Perfusion pressure for the cerebral circulation is the mean arterial pressure minus the critical closing pressure (MAP — CCP). Vasomotor tone and intracranial pressure are the major determinants of the critical closing pressure. Changes in either of these variables, therefore, affect perfusion pressure and flow. Data on brain-blood flow at fixed vasomotor tone obtained over wide pressure ranges show little change in vascular bed resistance despite significant changes in flow. The diameter of resistance vessels probably does not change significantly throughout the normal physiological range of cerebral blood flow. The limits of the critical closing pressure in the anesthetized monkey are from 10 to 95 mm Hg. Using these limits, and beginning with the average values for MAP and CCP in 11 awake monkeys breathing room air, the authors present theoretical flow curves in response to changes in intracranial pressure and mean arterial pressure that closely approximate the data reported in man.

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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.

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Calvin B. Early, Richard C. Dewey, Heinz P. Pieper and William E. Hunt

✓ Pressure-flow data are presented for the brain vascular bed in the rhesus monkey. These data are obtained at fixed levels of vasomotor tone. Resultant flow curves are called the “dynamic pressure-flow relationships” (DPFR). In the experimental model, arterial pressures are oscillated with a sinusoidal pump at frequencies exceeding the vasomotor response lag time. The resultant DPFR curves are discussed. A model is presented to show that changes in vasomotor tone cause a vertical shift of the DPFR. Changes in vascular bed resistance cause a change in the slope of the DPFR (▵P/▵F).