Heterogeneity of cerebral cavernous hemangiomas diagnosed by MR imaging.

The cavernous hemangioma (cavernoma) is increasingly recognized as a vascular malformation of the brain that may present with seizures, hemorrhage, or progressive neurological deficit. Since 1985 we have identified 13 cases of presumed cavernoma of the brain based on the findings on CT, selective angiography, and magnetic resonance (MR) imaging. In each case CT showed a high density lesion that was "occult" or "cryptic" on angiography. However, within all lesions MR revealed a complex internal structure consisting of reticulated patches of high and low intensity signal surrounded by a hypointense rim on T1- and T2-weighted pulse sequences. Of the nine operated cases, five resected specimens were compatible with pure arteriovenous malformations (AVMs), and the other four were mixtures of cavernoma with either AVM or venous angioma. Our experience strongly suggests that the above complex of radiographic findings is not at all specific for the cavernoma. We propose that the major common factor shared by such "cavernomatoid" malformations is low blood flow. We believe low flow lesions follow a relatively benign clinical course, and they readily lend themselves to surgical resection.

Intraoperative monitoring of evoked potentials with a spiral scalp electrode. Technical note.

Monitoring evoked potentials from the brain for prolonged periods during neurosurgical procedures ideally requires attached scalp electrodes that may be placed in a sterile field. The limitations of conventional surface and percutaneous electrodes in the operating room environment have led to the development of a disposable curved-needle electrode which is inherently self-retaining. Clinical results have demonstrated the advantages of this new electrode over other electrodes currently used for intraoperative neurophysiological monitoring.

Benign familial chorea: an association with intellectual impairment.

Twenty-four members of a family with benign familial chorea underwent testing for evidence of intellectual impairment. Lower verbal intelligence was found in affected individuals compared to unaffected family members, as were deficits in verbal abstract concept formation. These results challenge the notion that benign familial chorea uniformly spares the intellect in all kindreds.

Simultaneous measurement of local glucose utilization and blood flow in the rat brain: an autoradiographic method using two tracers labeled with carbon-14.

A simplified technique that uses two radionuclide tracers has been devised to measure local cerebral glucose utilization (ICGU) and local cerebral blood flow (ICBF) in the same rat. The method employs [14C]-2-deoxyglucose and [14C]iodoantipyrine to produce an autoradiogram before and another after extraction into chloroform of the [14C]iodoantipyrine from the brain sections. The chloroform-extracted autoradiogram yields ICGU, and the difference in tissue carbon-14 concentration between the two autoradiograms permits calculation of ICBF. The double-isotope technique provides values of ICGU and ICBF that are statistically indistinguishable from those derived from conventional single-isotope methods.

Experimental air embolism of the brain: an analysis of the technique in the rat.

Air embolization of the brain produces cerebral ischemia that can be focal and reversible. The method has previously been hampered by (1) lack of selective arterial injection of the embolus, (2) disruption of local hemodynamic relationships by ligation of major arterial channels, (3) excessive volume of the air embolus, and (4) uncontrolled bubble size. To minimize these factors, a technique was devised in the rat whereby a fine catheter was advanced through a branch of the external carotid artery into the internal carotid artery. Air emboli of 5 microliters were found to arrest blood flow and to attenuate electrical activity in the ipsilateral cerebral hemisphere for seconds to a couple of minutes. The duration of ischemia varied from region to region, and it tended to be prolonged by arterial hypotension. In the nonembolized hemisphere, CBF never declined abruptly (indicating no cross-over of air) although electrical activity was suppressed in two-thirds of the animals.

Cerebral ischemia produced by four-vessel occlusion in the rat: a quantitative evaluation of cerebral blood flow.

Cerebral ischemia was produced in the rat by simultaneous occlusion of the vertebral and carotid arteries according to the method of Pulsinelli and Brierley (Stroke 10: 267, 1979). Local cerebral blood flow (CBF) was determined by polarographic and autoradiographic techniques. Hydrogen-clearance measurements showed that mean CBF fell in four monitored regions of the hemispheres to between 0.11 and 0.18 ml/g/min, being least in deep rostal gray, intermediate in superficial gray, and greatest in deep caudal gray. However, individual animals had local CBF in excess of 0.20 and even 0.30 ml/g/min, and no animal showed zero CBF. When animals were rendered hypotensive (MABP of 50 Torr) during vascular occlusion, mean CBF ranged between 0.03 and 0.10 ml/g/min in the same regional order. With hypotension, total arrest of flow occurred. Autoradiographic data confirmed the above findings and indicated adequate CBF to the lower brainstem. During vascular occlusion, sufficient CBF may be present ot sustain cerebral tissue as in animals with a well developed spinal circulation or an inadvertently patent vertebral artery.

A comparison of short-latency auditory-evoked potentials in two strains of mice: possible neurophysiological correlates of susceptibility to audiogenic seizures?

The short-latency auditory-evoked response was recorded from adult (over 8 wk) and young (16-22 day) mice of the audiogenic seizure-prone DBA/2J (D2) and seizure-resistant C57BL/6J (C6) strains. An auditory complex made up of eleven peaks and troughs was found within the first 20 ms after click stimuli. The latencies of the potentials tended to be shorter in the C6 mice and in the adults of both strains. The ratio of amplitude differences of late to early peaks ('amplitude index') was much larger (P less than 0.01) in D2 mice. The data are consistent with greater neuronal recruitment to acoustic stimuli in the higher-order auditory centers of D2 mice.

Influence of factor VIII/von Willebrand factor protein (F VIII/vWF) and F VIII/vWF-poor cryoprecipitate on post-ischemic microvascular reperfusion in the central nervous system.

To test the hypothesis that plasma contains native constituents capable of impairing microcirculatory flow in zones of acute ischemic tissue damage, we performed 14C-antipyrine autoradiographic blood flow studies in splenectomized dogs subjected to 35 min of cerebrospinal fluid compression ischemia followed by 30 min of recirculation to the neuraxis. The animals were anticoagulated with heparin and were divided into 4 groups by exposure to various measures before induction of ischemia. Groups 1 and 2 served for comparison with the other groups and underwent, respectively, no glass-wool filtration and glass-wool filtration via an arteriovenous shunt. Post-ischemic brain blood flows in Group 1 were low and focal zones of greatly impaired reperfusion were present. In Group 2, post-ischemic brain blood flows were high and focal perfusion impairment did not occur. Group 3 received homologous purified factor VIII/von Willebrand factor protein (F VIII/vWF) after glass-wool filtration but before induction of ischemia; Group 4 received F VIII/vWF-poor cryoprecipitate at the same time point. The purpose of administering the plasma preparations was to check for the presence of activity that nullified the enhancement of post-ischemic reperfusion expected after exposure to glass-wool. The results indicate that activity deleterious to post-ischemic reperfusion primarily resides in the F VIII/vWF fraction of cryoprecipitate. The F VIII/vWF-poor cryoprecipitate infusate, containing 250 to 800-fold more protein than the F VIII/vWF fraction, produced an intermediate reduction of blood flow.

Prostaglandin I2 and indomethacin prevent impairment of post-ischemic brain reperfusion in the dog.

Twenty-seven heparinized dogs were exposed to 35 min of cerebrospinal fluid compression ischemia followed by 30 min of recirculation. The degree and distribution of post-ischemic reperfusion was then assessed by means of a 14C-antipyrine autoradiographic blood flow study. The animals were assigned to 5 groups by the administration of drugs as follows: 1) no additional drugs; 2) indomethacin 1.5 or 4 mg/kg prior to ischemia; 3) indomethacin 4 mg/kg 5 min after ischemia; 4) prostaglandin I2 (PGI2) infusion 30--180 ng/kg/min beginning 5 min after ischemia; and 5) indomethacin 4 mg/kg 5 min after ischemia plus PGI2 infusion 30--130 ng/kg/min beginning 5 min after ischemia. Animals receiving no additional drugs had relatively low post-ischemic blood flows with focal zones of greatly impaired reperfusion. Animals receiving either indomethacin or PGI2 after ischemia did not differ significantly from the no additional drug group. A significant enhancement of post-ischemic reperfusion occurred in animals receiving indomethacin prior to ischemia and those receiving the combination of indomethacin and PGI2 after ischemia. These observations implicate an imbalance in prostaglandin pathways at the blood-endothelial interface in the genesis of post-ischemic reflow impairment and suggest novel drug therapy for enhancing nutrient flow after ischemia.

Extracorporeal glass-wool filtration of whole blood enhances post-ischemic recovery of the cortical sensory evoked response.

In twenty dogs, anticoagulated with heparin 300 units/kg, the right cortical sensory evoked response (CSER) to contralateral median nerve stimulation was suppressed during 60 min ischemia induced by periodic infusion of 50 to 100 microliter increments of air via the right internal carotid artery. The post-ischemic recovery of the CSER was followed an additional 60 min in 19 of these animals divided into 2 groups. Ten dogs were subjected to glass-wool filtration of their blood by extracorporeal shunting from femoral artery to femoral vein for one hr prior to infusing air. Nine dogs did not receive glass-wool filtration. Post-ischemic recovery of CSER amplitude, a quantifiable electrophysiologic index of neuronal function, was significantly greater in the filtered group than in the non-filtered group. 14C-antipyrine autoradiographic blood flow studies were performed in 3 dogs. One was studied at the end of a 60 min ischemic CSER suppression period and showed severe flow disruption by air embolism. Two dogs, one from each group, were studied at the conclusion of the 60 min recovery period. In the filtered animal, cortical blood flow exceeded the threshold for CSER maintenance while cortical flow rates in the unfiltered animal fell below this threshold. The enhanced postischemic neuronal recovery in the filtered group as indicated by the CSER in attributed to the preservation of injury zone nutrient blood flow that is supported by collateral circulation.

Indomethacin prevents impaired perfusion of the dogs's brain after global ischemia.

Compression ischemia of the central nervous system (CNS) in heparinized dogs caused areas of diminished cerebral blood flow measured by 14C-antipyrine autoradiography. Intravenous infusion of indomethacin (1.5 or 4.0 mg/kg) approximately 1 hour before ischemia eliminated the circulatory defects. Prophylactic inhibition of prostaglandin synthetase may promote postischemic perfusion of the CNS by preventing vasoconstriction and by anti-hemostatic effects on blood.