Henry A. Shenkin

THE EFFECTS OF INCREASED INTRACRANIAL PRESSURE ON CEREBRAL CIRCULATORY FUNCTIONS IN MAN

The effect of increased intracranial pressure on cerebral blood flow has been the object of very few clinical studies. In accordance with the MonroeKellie-Cushing Doctrine, it would be presumed that increased intracranial pressure would increase cerebrovascular resistance and thereby decrease cerebral blood flow. However, Williams and Lennox (1) in 1939 concluded on the basis of cerebral arteriovenous oxygen differences that cerebral blood flow was practically unaffected by a rise in cerebrospinal fluid pressure. Courtice (2) also working with humans and using a similar technique came to a different conclusion: that there was a slowing of blood flow through the brain in certain types of brain tumor associated with increased intracranial pressure. More recently Ferris (3), using a plethysmographic meas-

THE BLOOD FLOW, VASCULAR RESISTANCE, AND OXYGEN CONSUMPTION OF THE BRAIN IN ESSENTIAL HYPERTENSION

The vascular bed of the brain should occupy a prominent place among the regions of interest to the clinical investigator who would seek to define the circulatory disturbances associated with hypertension. The vulnerability of cerebral arteries in chronic hypertensive disease has long been recognized. Statistical surveys demonstrate that about 15% of deaths in hypertension are the result of cerebrovascular lesions (1 to 3). Many hypertensive patients experience symptoms such as headache, dizziness, and tinnitus, which are probably referable to the brain. Furthermore it has been suggested :that some of the etiological factors in hypertension may be of cerebral origin. Knowledge of the cerebrovascular resistance and cerebral blood flow in human hypertension has been extremely limited. The well-recognized changes observed in retinal vessels, in the absence of more specific information, have been presumed to reflect similar phenomena in the cerebral vascular bed. Measurement of cerebral blood flow in this disease has been limited to studies of cerebral arteriovenous oxygen differences (4, 5) which become an index of blood flow only after cerebral metabolism can be measured or shown to be normal. The nitrous oxide method for the quantitative measurement of human cerebral blood flow (6, 7) found its first application to clinical disease in a study on five patients with various degrees of arterial hypertension (8). The present study represents a more complete investigation on 13 additional patients.

THE EFFECT OF BILATERAL STELLECTOMY UPON THE CEREBRAL CIRCULATION OF MAN

The role of the sympathetic nervous system in the intrinsic control of the cerebral circulation has always been controversial. Experiments heretofore have centered on the effects of stimulation of the cervical sympathetic nerves on changes in cerebral blood flow detected by instruments applied directly to the brain of animals. The results have generally agreed that cervical sympathetic stimulation causes only mild cerebral vasoconstriction. The marked effects of chemical agents (CO2 in particular) in affecting the cerebral circulation have led to the probably correct conclusion that the intrinsic control of the cerebral circulation in health is predominantly mediated via chemical agents in the blood and that neurogenic vasomotor control is at best only

Occlusion of the vertebral artery

The angiographic demonstration of an occluded vertebral artery in a patient with a brain-stem syndrome was first reported by Riechert in 1952, and similar cases have been described by various authors subsequently. The common site of the vertebral occlusion was in the area between the arch of the atlas and the junction of the vertebral arteries. Since routine brachial angiography has been initiated in this clinic, occlusion of the vertebral artery at this site has been noticed more frequently than expected. Despite good visualization of the vertebral artery, the injected contrast material sometimes stopped before the junction of the vertebral arteries, and the basilar artery was not demonstrated in a number of patients who did not have clinical evidence of vertebral or basilar artery occlusion. This observation has been mentioned by Sutton and Hoare (1951), and by Krayenbuhl and Ya,argil (1957a) and was considered by them to be due to technical failure or vascular spasm. This explanation did not seem satisfactory for many instances in which we encountered an apparent vertebral artery occlusion. Therefore a series of 150 consecutive brachial angiograms has been reviewed in order to determine the frequency with which occlusion of the vertebral artery with or without symptoms occurs, and if possible to elucidate further its clinical and physiological significance.