Bypass induced cerebral aneurysm.

The development of aneurysm after EC-IC bypass was studied in 6 cases by angiography. Increase in blood flow and alteration of slow pattern are contributing factors. It is suggested that the difference in structure between cortical arteries and scalp arteries enhances their sensitivity to transcranial pressure difference. High TCP gradients may induce post-operative aneurysm, and careful management of blood flow through the bypass is recommended.

Reflow into a thrombosed giant middle cerebral artery aneurysm after extracranial-intracranial bypass.

This report graphically illustrates the consequences of flow augmentation through extracranial-intracranial bypass grafts. Propagation of clot from a thrombosed middle cerebral artery aneurysm into the middle cerebral artery produced transient ischemic attacks. Superficial temporal artery-middle cerebral artery bypass was performed to augment cerebral blood flow. Postoperative angiography demonstrated filling of the aneurysm through improved collateral channels. The role of bypass operation in the presence of an aneurysm and its contribution to collateral blood flow and clot lysis are discussed.

Cortical artery aneurysm formation after extracranial to intracranial bypass surgery. Case report.

An aneurysm of the recipient cortical artery developed 13 months after an extracranial-intracranial bypass procedure. A high transcranial pressure gradient between the scalp and the cortical arteries may have contributed to this unusual complication.

Angiographic demonstration of postoperative cortical artery stenosis induced by Biemer temporary clips.

Five patients underwent cerebral revascularization operations during which Biemer clips were used to occlude temporarily a branch of the middle cerebral artery. Postoperative angiograms revealed stenoses at the sites where the clips were applied. Excessive clip closing forces may have caused significant endothelial injury, which then produced the stenoses. Clips that exert a minimal occlusive force would avoid this response and are recommended for temporary occlusion of cortical arteries.

Cortical artery pressure in normotensive and hypertensive aneurysm patients.

Cortical artery pressure (CAP) and systemic pressure (SP) were measured in eight normotensive and six hypertensive patients with anterior circulation aneurysms. In the hypertensive patients significant gradients developed between CAP and SP as these pressures were lowered. The relationship between CAP and SP was expressed by the best-fit equation CAP = 1.02 SP -9.27 in the normotensive patients and by CAP = 1.54 SP -65.60 in the hypertensive patients. In the latter, the cycle of decreasing and increasing pressures formed a hysteresis loop suggesting prolonged cortical vasoconstriction despite recovery of systemic pressure. Selective pressure measurements in the distal (D) and proximal (P) segments of the cortical arteries were also obtained. The D/P ratio describes the relative contribution of the collateral circulation to cortical artery pressure. In normotensive patients, the D/P ratio was maintained down to an SP of 48 mm Hg. In hypertensive patients this ratio decreased with lowered SP, and a critical closing pressure of 40 mm Hg was predicted for the distal circulation. These studies described the limited capacity of the cortical circulation to maintain perfusion pressure in hypertensive patients. These responses should be considered when assessing the risks associated with such procedures as carotid ligation or hypotensive anesthesia.

Cortical nicotinamide adenine dinucleotide (NADH) kinetics in patients undergoing extracranial-intracranial bypass.

Nicotinamide adenine dinucleotide (NADH) kinetics were measured in 76 cortical areas in 26 patients with transient ischemic attacks (TIAs) undergoing extracranial-intracranial bypass. Direct cortical stimulation was utilized to induce changes in surface fluorescence corresponding to a brief oxidation and reduction of mitochondrial NADH. Preoperative studies of cerebral blood flow in gray matter (CBF)g) demonstrated normal perfusion in 11 patients and ischemic changes ((CBF)g less than 43.5 ml/100 g/minute) in 15 patients. In 30 normally perfused areas within the craniotomy, the mean half-time for reduction (t1/2(red)) of cortical NAD was 21.5 +/- 2.6 seconds. In 39 ischemic areas, the mean t1/2(red) was 5.6 +/- 1.2 seconds. These rapid reduction rates were associated with supernormal overshoots of the base line indicative of a transient oxygen debt. Kinetic responses could not be elicited from 7 areas adjacent to foci of decreased attenuation on compound tomography. Bypass resulted in normalization of the t1/2(red) in 24 of 28 areas of ischemia. The dependence of NADH kinetics on blood flow through the graft was demonstrated in 15 of 19 areas of mild ischemia by the reapplication of a clip to the donor artery. It is concluded that persistent reversible abnormalities of cortical mitochondrial metabolism exit in a significant number of patients with a history of TIAs who are suitable candidates for bypass surgery. In such patients bypass may effectively augment the nutrient supply to meet the bioenergetic demands associated with increased electrophysiological activity.

Epidermoid tumor of the cerebellopontine angle: diagnostic value of computed tomographic metrizamide cisternography.

The extent of spread of an epidermoid tumor in the posterior fossa may be difficult to discern preoperatively. Conventional computed tomographic (CT) studies may not outline the tumor capsule, and the low attenuation of the tumor itself may not allow a distinction from cerebrospinal fluid. CT metrizamide cisternography was helpful in delineating the inferior pole of an epidermoid tumor, which could then be delivered through a transtentorial approach.

Reduced vascular trauma after temporary occlusion with modified Biemer and Yasargil clips.

The Biemer and Yasargil microvascular clips that are currently available commercially can traumatize the vascular endothelium. In an effort to resolve this problem, both clip designs were structurally modified by changing the length, width, and surface of the clip blades in various ways. Also, the occlusion force of the clips was set at either 15 or 30 g. Studies on the carotid arteries of 140 rats showed a correlation between the structural and mechanical alterations of the clips and the degree of endothelial trauma produced by temporary occlusion for 1 hour. The most favorable results were obtained with a Biemer clip that had long, wide, smooth blades and an occluding force of 15 g.

Aneurysmal bone cyst of the temporal bone presenting as a spontaneous intracerebral hemorrhage: case report.

An aneurysmal bone cyst originating from the squamous portion of the left temporal bone is reported. The lesion presented in a 62-year-old nonhypertensive man as a spontaneous, intraparenchymal left temporal lobe hematoma. No evidence of trauma, hermorrhagic diathesis, or concurrent systemic disease was found. Previous case reports of aneurysmal bone cysts of the skull are reviewed.

Neurogenic hypertension related to vascular compression of the lateral medulla.

Neurogenic hypertension may be reproduced consistently in experimental animals, although its clinical significance is unclear. An ectatic loop of the posterior inferior cerebellar (PICA) compressed the left vagus nerve root entry-exit zone in two patients with long-standing hypertension. When this loop was mobilized for occipital-PICA bypass, the hypertension resolved. These observations suggest that neurovascular compression of the area encompassing the nucleus tractus solitarius may be a sufficient cause of neurogenic hypertension in humans. The structural and functional relationships of these areas of the brain stem and their role in modulating blood pressure are reviewed.

Brain death. I. A status report of medical and ethical considerations.

Use of neurologic criteria to pronounce death, although accepted by many, has caused controversy among physicians, lawyers, legislators, philosophers, and theologians. The present work attempts to resolve this by accomplishing four objectives. (1) It summarizes scientific information that establishes the ability to determine the state of brain death with certainty on the basis of presently available clinical and laboratory criteria. (2) It shows that the concept of brain death is in accord with secular philosophy and the three major Western religions. (3) It documents the need for legislative recognition that death may be pronounced on the basis of neurologic criteria. (4) It reviews the present status of judicial and statutory law relating to the determination of death in the United States.

Oxidative metabolism in cerebral ischemia. Part 1. Measurement of oxygen extraction slopes of grey and white matter in vivo.

Regional oxidative metabolism was studied in vivo. Oxygen availability was monitored from polarographic electrodes in frontal cortical and subcortical tissue. The rate of oxygen extraction in these regions was estimated at frequencies of up to 3 measurements per minute. Transient ischemia of the frontal regions was induced and the resultant decay in the oxygen trace was analyzed kinetically. The oxygen extraction slopes (OES) were steeper in grey than in white matter. They were relatively insensitive to alterations of arterial blood gas concentrations within the physiological range. The slopes were predictably influenced by pharmacologic agents known to alter the rate of oxidative metabolism. Artifacts which may interfere with the OES measurments were considered. This method of estimating regional tissue oxygen extraction may be appropriate for studying aspects of focal CI.

Brain energetics and circulatory control after subarachnoid hemorrhage.

Ischemia-provoking factors such as vasospasm, decreased cerebral perfusion pressure, and intravascular thrombosis may be present after subarchnoid hemorrhage (SAH). When these factors were not present during controlled SAH, a primary depression of cerebral glycolysis associated with normal stores of energy-rich phosphates was found. Although cerebral blood flow usually changes in response to changes in cerebral metabolic needs, this influence on the circulation was not evident in the early hours after SAH. After 3 to 4 hours an erratic decrease in blood flow occurred, probably related to vasospasm, and there were measurable decreases in energy-rich phosphates similar to those occurring after more severe and prolonged ischemias. These findings are indicative of abnormally erratic vascular responses to metabolic cues and may play a role in producing the encephalopathy of SAH.