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Transmission of Increased Intracranial Pressure

I. Within the Craniospinal Axis

Thomas W. Langfitt, James D. Weinstein, and Neal F. Kassell

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Transmission of Increased Intracranial Pressure: II. Within the Supratentorial Space

Thomas W. Langfitt, James D. Weinstein, Neal F. Kassell, and L. John Gagliardi

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The Etiology of Acute Brain Swelling Following Experimental Head Injury

Thomas W. Langfitt, Howard M. Tannanbaum, and Neal F. Kassell

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Acute Brain Swelling in Neurosurgical Patients

Thomas W. Langfitt and Neal F. Kassell

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Glomus jugulare tumor presenting with increased intracranial pressure

Case report

David W. Beck, Neal F. Kassell, and Charles G. Drake

✓ The authors report a case of glomus jugulare tumor presenting with papilledema and visual loss. The tumor was extremely vascular with significant shunting of arterial blood into venous sinuses. There was no intracranial extension of tumor, and papilledema resolved after removal of the lesion.

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Early management of aneurysmal subarachnoid hemorrhage

A report of the Cooperative Aneurysm Study

Harold P. Adams Jr., Neal F. Kassell, James C. Torner, Donald W. Nibbelink, and Adolph L. Sahs

✓ The overall results are presented of early medical management and delayed operation among 249 patients studied during the period 1974 to 1977, treated within 3 days of subarachnoid hemorrhage (SAH) and evaluated 90 days after aneurysm rupture. The results included 36.2% mortality, 17.9% survival with serious neurological sequelae, and 46% with a favorable outcome. Of the patients admitted in good neurological condition, 28.7% had died and only 55.7% had a favorable recovery at 90 days after SAH. These figures represent the results despite effective reduction in early rebleeding by antifibrinolytic therapy and successful surgery in those patients reaching operation. Further therapeutic advances are needed for patients hospitalized within a few days after SAH.

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Influence of changes in arterial pCO2 on cerebral blood flow and metabolism during high-dose barbiturate therapy in dogs

Neal F. Kassell, Patrick W. Hitchon, Mary K. Gerk, Martin D. Sokoll, and Todd R. Hill

✓ In 13 dogs the response of the cerebral circulation to changes in PaCO2 ranging from 20 to 60 torr was studied before and after administration of high doses of sodium thiopental. Infusion of sufficient barbiturate to produce 30- to 60-second burst suppression in the electroencephalogram was associated with a profound degree of cerebral vasoconstriction, equivalent to that produced by hypocapnia with PaCO2 = 20 torr. Furthermore, once sodium thiopental was administered, no significant difference in cerebral blood flow (CBF) or vascular resistance (CVR) was noted between PaCO2 of 30 and 20 torr. However, changes of approximately 15% in CBF and 30% in CVR were noted between PaCO2 at 40 and 20 torr. These data suggest that hyperventilation of PaCO2 of less than 30 torr may not effectively increase the degree of cerebral vasoconstriction in these circumstances.

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Antifibrinolytic Therapy in Subarachnoid Hemorrhage

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The effects of gammahydroxybutyric acid on canine cerebral blood flow and metabolism

Kent W. Baumann, Neal F. Kassell, Julie Olin, and Thoru Yamada

✓ Gammahydroxybutyric acid has been proposed as an alternative to high-dose barbiturate therapy for protecting the brain after ischemic or traumatic insult. The cerebral and systemic metabolic and vascular effects of gammahydroxybutyrate and its lactone analogue, gammabutyrolactone, are addressed in this paper. In anesthetized normal dogs, gammahydroxybutyrate or gammabutyrolactone was infused intravenously at a rate of 1 gm/kg/hr. Cerebral blood flow (CBF) decreased progressively with increasing doses of either agent. Cerebral metabolic rate of oxygen (CMRO2) increased initially with gammahydroxybutyrate, but not following gammabutyrolactone. Reduction in CBF exceeded that of CMRO2 at all doses in both series.

The primary systemic effect noted was a severe, lethal metabolic acidosis resulting from infusion of gammabutyrolactone. Gammahydroxybutyrate did not cause a similar acidosis. The imbalance of the CBF-CMRO2 reduction following gammahydroxybutyrate administration suggests that it has no advantage over barbiturates in the management of patients with cerebral vascular insufficiency or intracranial hypertension.

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Cerebral and systemic circulatory effects of arterial hypotension induced by adenosine

Neal F. Kassell, David J. Boarini, Julie J. Olin, and James A. Sprowell

✓ In six dogs anesthetized with halothane and nitrous oxide, mean arterial pressure (MAP) was lowered to 40 mm Hg for an average of 90 minutes by intravenous infusion of adenosine. The hypotensive effect of the adenosine was potentiated by administering dipyridamole to block its intravascular inactivation. Blood flow to the brain, spinal cord, heart, kidneys, and skeletal muscle was measured six times in each animal using the radioactive microsphere technique. Determinations were made before, during, and 30 minutes after the hypotensive period.

During the hypotensive period, MAP was decreased 61% and was related to a proportional decrease in peripheral vascular resistance. Cardiac index decreased 14%. Total cerebral blood flow (CBF) decreased an average of 28% and cerebral vascular resistance decreased 53%. The reduction in CBF was heterogeneous; the cerebral cortex and corpus callosum were most affected and the brain stem least affected. No change occurred in the cerebral metabolic rate of oxygen usage (CMRO2). Left ventricle flow increased 147% and right ventricle flow increased 271%. Blood flow to the kidneys decreased 70%, and to the liver decreased to 6% of control. Jejunum blood flow increased 138% during recovery, while stomach flow varied but showed no statistical change. There was no tachyphylaxis, rebound hypertension, or toxicity associated with the adenosine-induced hypotension. These properties suggest that adenosine may be a useful agent for inducing arterial hypotension in neurosurgical patients.