Sydney J. Peerless

Treatment of Ischemic Deficits from Vasospasm with Intravascular Volume Expansion and Induced Arterial Hypertension

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.

Hunterian proximal arterial occlusion for giant aneurysms of the carotid circulation

Hunterian proximal artery occlusion was used in the treatment of 160 of 335 patients harboring giant aneurysms of the anterior circulation. One hundred and thirty-three of these aneurysms arose from the internal carotid arteries, 20 from the middle cerebral arteries, and seven from the anterior cerebral arteries. Ninety percent of the patients had satisfactory outcomes. The safety of internal carotid artery occlusion has been greatly enhanced by preoperative flow studies and by test occlusion with an intracarotid balloon to identify those patients who require preliminary extracranial-to-intracranial bypass, which was used in all of the middle cerebral occlusions. The anterior cerebral artery had magnificent leptomeningeal collateral flow that prevented infarction even without cross flow. Obliteration of the aneurysm by thrombosis was complete, or nearly so, in all but four patients whose treatment was completed. Analysis of poor outcome in 16 patients revealed that hemodynamic ischemic infarction was known to occur after only two of the carotid occlusions.

Are the results of the extracranial-intracranial bypass trial generalizable?

The dramatic results of the extracranial–intracranial (EC–IC) bypass trial have stimulated the vigorous discussion and debate that are essential to the pursuit of truth and the advancement of usefu...

Posterior Circulation Aneurysms

More than 1400 patients with aneurysms arising from the vertebral and basilar arteries have been operated upon in the neurosurgical unit at the University of Western Ontario in the past 35 years. The majority (1100) underwent surgical treatment since 1970 and, therefore, enjoyed the benefits of contemporary neuroradiology, anesthesiology, and the use of the operating microscope and microtechniques. Throughout this period, a system of pre- and postoperative management, anesthetic technique, and operative approach has evolved.

Extracranial-intracranial (EC/IC) bypass in the treatment of giant intracranial aneurysms.

Experience has now been gained in our service with the surgical treatment of 294 giant intracranial aneurysms: 106 on the anterior and 188 on the posterior circulation (8). In approximately half of these cases, treatment was by some form of ligation of the parent artery (Hunterian ligation), either in the neck or intracranially in 42%, with additional trapping in another 9%. In 40%, the neck of the giant aneurysm was clipped. In three cases, intraluminal thrombosis was induced with hair or wire and six aneurysms were wrapped with gauze or plastic. In 14 cases, the aneurysms were deemed to be inoperable. Literally every major intracranial and extracranial artery has been deliberately occluded by the principle of Hunterian ligation, including the carotid, basilar and vertebral (even bilaterally) and all their branches except PICA. Our experience suggests that most giant aneurysms will not require a bypass to supplement the collateral flow. Nevertheless, the EC/IC bypass technique has proved to be of value in carefully selected cases. This communication concerns a special group of 25 cases where EC/IC bypass was used to prevent infarction after occlusion of the parent artery. Subsequent to our initial communications in 1976 (1), 1977 (2,3,4) and 1978 (5), others have reported on their experience with the use of this technique (7,9,10). Extracranial-intracranial (EC/IC) bypass in the treatment of giant intracranial aneurysms

Trigeminal Neuralgia: A Comparison of the Results of Percutaneous Rhizotomy and Microvascular Decompression

Seventy-five patients were treated between March 1976 and June 1980 for classical idiopathic tic douloureux. Fifty-five patients underwent percutaneous trigeminal rhizotomy (PTR) and twenty-four had posterior fossa microvascular decompression (MVD) of the trigeminal nerve. Four patients had both procedures. In the PTR group, 4% were immediate failures, 42% had a delayed recurrence of pain, while 54% remained totally pain free with an average follow-up of 30 months. In the MVD group, 12% were immediate failures, 17% had a delayed recurrence of pain, and 71% have remained free of pain with a average follow-up of 28 months. Neither procedure can be regarded as ideal surgical treatment for patients with pain refractory to medical treatment. Percutaneous rhizotomy has an established place because of its safety, particularly in elderly patients. A high rate of recurrent pain is to be expected. Microvascular decompression has appeal in younger patients because of its non-destructive nature but the long term efficacy of the procedure is not known.

Magnetic resonance imaging of facial nerve neuromas

Facial nerve neuromas are uncommon tumors often confused with other tumors of the temporal bone and cerebellopontine angle. Radiologically, it may be impossible to differentiate an intracanalicu‐lar facial nerve neuroma from an acoustic neuroma. We present three case reports of facial nerve neuromas arising within the internal auditory canal to show the important magnetic resonance imaging features of these tumors. One tumor extended into the cerebellopontine angle, middle cranial fossa, and middle ear. Another filled the internal auditory canal and extended through the cerebellopontine angle to the brain stem. The third occurred in a patient who had neurofibromatosis as well as numerous other intracranial tumors. We feel that gadolinium‐enhanced magnetic resonance imaging provides the most useful information in the preoperative assessment of this disorder.

Angiographic study of vasospasm following subarachnoid hemorrhage in monkeys.

A model for producing chronic cerebral vasospasm in monkeys by injecting autologous blood into the basal cistern is described. Spasm/narrowing was observed by angiography one hour after SAH in 8 out of 10 monkeys and in 5 of these 8, spasm was observed both one and two weeks later. No narrowing of the vessels was observed in the control cases. In monkeys that showed spasm one week after SAH, narrowing of the extracranial vertebral arteries was also observed. Repeated injections of blood at intervals of one and two weeks caused intensification of spasm in the intracranial portion of vertebral arteries and the basilar arteries. It is suggested that cerebral vasospasm following SAH may in part be mediated by a central control mechanism acting through the sympathetic nervous system in that extracranial vessels remote from direct contact with blood showed reactive narrowing.

Correlation between somatosensory evoked potentials and neuronal ischemic changes following middle cerebral artery occlusion.

In an attempt to determine the usefulness of evoked potentials as a measure of focal cerebral ischemia, we examined somatosensory evoked potentials (SEPs) and morphological neuronal changes in cats following unilateral middle cerebral artery (MCA) occlusion. Fifteen adult cats underwent transorbital occlusion of the MCA under halothane anesthesia. In seven cats the ipsilateral SEPs were abolished after middle cerebral artery occlusion, and did not show any recovery after 6 hours. The same seven cats showed the greatest area of moderate and severe ischemic neuronal changes, ranging from 21 to 64% (mean 39 +/- 14%) of the total ipsilateral cortical area. The remaining eight cats showed a complete flattening or decreased amplitude of the SEP after occlusion, but demonstrated a considerable recovery in the amplitude of the primary cortical potential during the six hours of the study. All these cats had ischemic areas of less than 15% (mean 9 +/- 3%) of the total ipsilateral cortex. These results demonstrate that the disappearance of the SEP and their failure to recover correlate with the extent and degree of histological cerebral ischemia.

Treatment of giant cerebral aneurysms of the anterior circulation.

Giant intracranial aneurysms have been defined as those aneurysms over 2.5 cm (1 inch) in diameter (2), either saccular or fusiform in nature. The saccular variety are apparently an enlargement of the more commonplace berry aneurysms and arise at distal bifurcations of intracranial vessels. The fusiform variety, which are of less importance to the neurosurgeon, are, like the aneurysms of the abdominal aorta, atherosclerotic dilatations of the vessel wall. Giant intracranial aneurysms are unusual, amounting to only about 5% of all intracranial aneurysms (5). Giant aneurysms which arise from bifurcations grow from the neck and have a tendency gradually to incorporate the wall of the parent artery, as well as branch vessels, into the aneurysm. This makes clipping of the neck of these aneurysms more complex and even impossible in some instances. Also, these aneurysms tend to partially thrombose and they have a greater tendency toward marked atherosclerotic change at the base of the aneurysm, as well as in the proximal vessels (3). Friable intraluminal thrombus and atheromatous plaques which can be fractured with manipulation present further hazards to the neurosurgeon when dissecting and manipulating in the area. Instances of thromboembolism from the aneurysm, as well as fracture of the atherosclerotic plaque with dissection into the wall, and proximal vessel occlusion have been previously documented by ourselves and others (1). In our experience of nearly 300 giant intracranial aneurysms, the majority have presented with clinical syndromes associated with their mass effect. This has involved either hemisphere dysfuction, brain stem compression or combinations of hemisphere, brain stem and cranial nerve compression. The anatomical proximity of the carotid artery to the second and third cranial nerves, the basilar artery to the third, fourth, fifth and sixth cranial nerves, and the vertebral artery to the lower cranial nerves results in a frequent association of cranial nerve dysfunction with S. J. Peerless, C. G. Drake