Biomedical subjects
Publications and source records attributed to S J Peerless.
This statement for physicians redefines the use and importance of lumbar puncture to suspected stroke mechanisms. It also identifies neurologic conditions in which newer imaging techniques are safer and more effective diagnostic tools than lumbar puncture.
Barbiturate coma is still recommended for brain protection during periods of temporary focal ischaemia such as during carotid endarterectomy. We tested the hypothesis that a single dose of barbiturate given before a period of protracted severe focal ischaemia would protect against focal cerebral infarction. Sixteen cats had the proximal left middle cerebral artery (MCA) occluded. Eight cats received halothane alone titrated to keep their pulse and blood pressure within the normal range. Eight cats received, in addition to halothane, a bolus of thiopentone sufficient to produce an isoelectric EEG immediately prior to MCA occlusion. Six hours after the occlusions the animals were sacrificed and the brains scored histologically to assess both size and severity of ischaemia. There was no statistically significant difference in the size or severity of the infarcts between the groups. We conclude from this study that the extent of the histological injury was not reduced by a single prophylactic bolus of thiopentone given before prolonged focal cerebral ischaemia.
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The authors report their treatment of 66 infratentorial arteriovenous malformations (AVM's) in patients aged 5 to 69 years. Sixty-one of them presented with hemorrhage, three with headache, and two with focal neurological deficits. Five patients underwent surgical exploration only, one was treated with ventriculostomy, three had ligation of the AVM feeding arteries, four underwent intraoperative embolization, and two had pontine hematomas removed; complete excision was attempted in 51 patients and accomplished in 47. Twelve of the patients also had aneurysms (nine of which had ruptured). Of this series, 71% had a good result, 14% a poor result, and 15% died. Most of the operative morbidity was due to massive postoperative hemorrhage, probably related to inadequate hemostasis.
A randomized trial to determine whether bypass surgery would benefit patients with appropriate atherosclerotic lesions followed 1377 patients for almost five years, and found no benefit from surgery. This negative result has a number of potential implications for neuroradiologists including the expectation for other randomized trials to be carried out, such as for carotid endarterectomy, and the need for neuroradiologists to carry out trials for embolization of cerebral arteriovenous malformations and angioplasty of stenotic cervical or cranial vessels. We are reminded that, ultimately, the clinical outcome is the real measure of procedures, not pretty pictures.
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The effect of naloxone, opiate antagonist, was investigated on systemic arterial blood pressure(BP), cerebral blood flow (CBF), and cerebral oxygen consumption in the cat brain following occlusion of the middle cerebral artery(MCA). A total of 21 adult cats was studied under the anesthesia of alpha-chloralose (50 mg/kg). The left MCA was exposed and coagulated using transorbital approach under a operation microscope. Naloxone of 5 mg/kg was administrated intravenously within 30 minutes after MCA occlusion in early therapy group and 2.5 hours after the occlusion in delayed therapy group. Isotonic saline was administrated in the control group. The basal value of CBF in the intact animals was 54.0 +/- 5.9 (+/- SEM) ml/100g/min. Significant increases in mean BP of 13%, CBF of 12%, and CMRO2 of 16% were noted in the intact animals after naloxone administration. The CBF in MCA territory reduced to 24% after MCA occlusion and 85% in contralateral hemisphere. MCA occlusion had no significant effect on either mean BP or the difference in oxygen concentration between arterial and superior sagittal sinus blood. Naloxone increased these reduced CBF and mean BP significantly, but increase in oxygen consumption was not significant. There was no difference between early therapy group and delayed therapy group in pathological study. The effect of naloxone was temporary. Therapy of repeated or continuous naloxone administration appears to be effective during temporary focal cerebral ischemia.
A review of a series of 312 giant intracranial aneurysms treated at University Hospital in London, Ontario, showed that 93 of those aneurysms were located between the intracavernous portion and the bifurcation of the internal carotid artery. Sixty-five of those aneurysms were carotid ophthalmic, 12 were located in the internal carotid-posterior communicating-anterior choroidal artery regions and 16 involved the internal carotid artery bifurcation. For the majority, clinical presentation was related to the mass of the aneurysms and compression of surrounding structures such as visual pathways, ocular motor cranial nerves, the fifth nerve, and hypothalamic-pituitary axis. Fourteen patients presented with subarachnoid hemorrhage. Cerebral angiography, computed tomography and xenon inhalation studies of cerebral blood flow were the tools used to study the morphology of the aneurysm and dynamics of the circle of Willis.
Sixty-five carotid-cavernous fistulas were studied at University Hospital, London, Canada, from 1978 to 1982, 20 of which fulfilled the clinical and angiographic criteria of a spontaneous carotid-cavernous fistula. Of these 20 fistulas, 17 were unilateral, and three were bilateral. In 18 cases the angiographic findings were typical of an arteriovenous malformation (AVM), and in two a ruptured giant intracavernous aneurysm was found. These patients were treated according to whether they had a nonresolving or progressive cavernous sinus syndrome or deterioration of vision. The cavernous dural AVM's were treated with polyvinyl-alcohol and/or isobutyl-2-cyanoacrylate (IBCA) embolization of the external carotid artery blood supply. Two patients underwent postembolization surgical procedures. The detachable balloon technique was used to occlude the fistulas associated with the two giant ruptured intracavernous aneurysms and a small dural intracavernous AVM. Eight patients received no therapy; in two, spontaneous obliteration of the fistula occurred. Of the nine cavernous AVM's embolized with particles and/or IBCA, successful transvascular embolization was achieved in seven cases, and partial embolization followed by surgery in two cases. Successful balloon obliteration of the giant intracavernous ruptured aneurysm was obtained in two cases. In one patient, right hemiplegia with aphasia resulted from reflux of IBCA emboli through the artery of the foramen rotundum into the left middle cerebral artery.
Failure to obliterate intracranial aneurysms completely during initial surgery still occurs in spite of recent technical advances. Of the 115 reoperations reported in this series, 89% of the aneurysms were obliterated, and 84% of the patients had a satisfactory outcome. Twelve patients had poor results, three (2.6%) of whom were in poor condition before reoperation.
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In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.