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Edward J. Kosnik and William E. Hunt

✓ Elevation of systemic arterial pressure in seven patients with intracranial arterial aneurysms has been shown to be effective in alleviating ischemic symptoms attributed to cerebral vasospasm. Autoregulation is at least partially lost in patients with cerebral hemodynamic crisis. Blood volume expansion was used to augment vasopressors in maintenance of systemic hypertension. The management of these cases is discussed. Caution in the use of this technique is advised, since the regimen is not without risk.

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David Yashon, George E. Locke and William E. Hunt

✓ Thirty-seven dogs were studied to establish the level of mean arterial pressure (MAP) causing cerebral tissue lactate (CTL) accumulation as a result of anaerobic metabolism and to assess the extent of preservation of aerobic metabolism afforded by autoregulation during oligemia. Specimens were removed prior to oligemia and at 5, 30, and 60 min following hypotension created by blood withdrawal. In four control animals, CTL averaged 4.83 (range 3.26 to 7.07) mMol/kg. At 60 min after induction of oligemic hypotension, 13 animals with a MAP of 30 and 40 mm Hg showed concentrations of CTL between 16.56 and 20.89. At a MAP of 50 mm Hg six animals showed a CTL concentration between 4.39 and 15.88; at a MAP of 60 mm Hg eight animals showed a CTL between 3.76 and 14.93; and at a MAP of 70 mm Hg six animals had a CTL between 2.43 and 4.27. At 5 min, at all mean arterial pressures the cerebral tissue lactate varied between 2.07 and 5.50. By 30 min the elevations were similar to those at 60 min. CTL elevation was independent of pre-oligemic MAP. In the canine brain there is a uniform incremental elevation of CTL between a MAP of 30 to 50 mm Hg directly related to the time of hypotension; there is variable intolerance to MAP in the range of 50 to 70 when related to a time longer than 5 min.

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William E. Hunt, John N. Meagher and James E. Barnes

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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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Edward J. Kosnik, William E. Hunt and Carole A. Miller

✓ The history, physical findings, and treatment of dural arteriovenous malformations are reviewed. The importance of completely identifying and obliterating the fistula, even at the expense of obliterating major venous sinuses, is emphasized. Failure of surgical treatment usually is the result of mistaking the more obvious dilated feeding vessels for the lesion itself.

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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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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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William E. Hunt, Bertha A. Bouroncle and John N. Meagher

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Stephen Hill, Edward Martin, E. C. Ellison and William E. Hunt

✓ Carcinoembryonic antigen (CEA) was measured in plasma and cerebrospinal fluid (CSF) in patients with neoplasms and non-neoplastic neurologic conditions of the central nervous system (CNS). Seventy-two control patients had a mean CEAcsf of 0.04 ng/cu cm, 31 patients with benign tumors had a mean CEAcsf of 0.03 ng/cu cm, and 21 patients with malignant CNS tumors had mean CEAcsf of 21.7 ng/cu cm. In the absence of intradural metastasis, the existence of non-CNS malignancies did not cause CEA to appear in the CSF. There was no relationship between the plasma and CSF levels of CEA. The CSF is normally free of CEA, and its detection is strongly suggestive of either primary or secondary intradural malignancy. The titres of CEA decline with effective therapy, and may be of use in monitoring treated patients for recurrence.