Robert M. Crowell

The relation of cembral vasospasrn to the extent and location of subarachnoid blood visualized by CT scan: A prospective study

In 41 cases of verified ruptured saccular aneurysm, we prospectively predicted the presence or absence of delayed symptomatic cerebral vasospasm. CT criteria quantifying the extent and location of subarachnoid blood (developed in our previous retrospective study) were used in this prospective series of patients. Twenty-two patients had recognizable subarachnoid clots larger than 3×5 mm or layers of blood more than 1 mm thick (measured on reproduced images). In 20 of the 22 patients with severe significant clot or thick layer, severe vasospasm was correctly predicted and localized (2 false positives). In 19 patients with no blood, or diffuse blood, or blood outside the subarachnoid space, the absence of severe vasospasm was correctly predicted in 14 (5 false negatives). All of the false-positive and false-negative cases could be explained by inadequate CT technique. The data indicate that the extent and location of blood in the subarachnoid space determine the severity and location of vasospasm and that patients in jeopardy of developing symptomatic cerebral vasospasm can now be identified. Early preventive measures may now be assessed more accurately.

Differential regional vulnerability in transient focal cerebral ischemia.

Abstract not available.

Cervicocranial arterial dissection.

&NA; Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants. (Neurosurgery 29:89‐96, 1991)

Variability and reversibility of focal cerebral ischemia in unanesthetized monkeys.

To assess reversibility of focal cerebral ischemia, we performed a neurologic and pathologic study of 27 monkeys subjected to temporary middle cerebral artery occlusion. An implanted snare ligature occluded the artery in awake monkeys for 30 minutes, 4 hours, 8 hours, 16 hours, 24 hours, or permanently. Serial neurologic observations were made for 2 weeks, and systematic neuropathologic examination estimated extent of infarction. Deficits from ischemia were commonly reversible at 30 minutes and 4 hours, but were rarely reversible after 8 hours. Neurologic deficit and infarct size showed remarkable variability. Maximum irreversible infarction evolved in about 4 to 8 hours in most awake monkeys. Variability and reversibility of focal ischemia were probably related to variable collateral circulation. The results suggested that emergency surgical revascularization might help some cases of acute ischemic stroke.

Risks of surgical management for cavernous malformations of the nervous system.

OBJECTIVE As more information evolves regarding the natural history of cavernous malformations (CMs), the risks of operative intervention must be balanced against nonoperative management. In an attempt to better delineate the surgical risks for operable CMs, we undertook a retrospective analysis of 94 patients with 97 CMs surgically excised at the Massachusetts General Hospital. METHODS Data regarding surgical complications and outcome measures, including neurological status and seizure outcome, were analyzed. RESULTS The incidence of transient neurological morbidity was 20.6%, but only 4 of the 97 operations (4.1%) resulted in persistent disabling neurological complications and 2 (2.1 %) in nondisabling deficits. There was no operative mortality. Brain stem lesions (n=14) were associated with the highest incidence of neurological complications, both transient and persistent (odds ratio, 4.8; 95% confidence interval, 1.5-15.7). The overall neurological outcome was excellent or good in 89.7% of all lesions: 96.8% of lobar CMs (n=63), 64.2% of brain stem CMs (n=14), 87.5% of cerebellar CMs (n=8), 100% of cranial nerve CMs (n=4), and 75% of spinal cord CMs (n=8). Patients with brain stem and spinal cord CMs were in poorer preoperative neurological condition than were patients with CMs in other locations and therefore had a significantly reduced level of function after surgery (P < 0.01). There was improvement in 35.7% of the patients with brain stem lesions and 62.5% of the patients with spinal cord lesions after surgery. In the 38 patients presenting with seizures, 97% were seizure-free after surgery. CONCLUSION The risks of operative management of CMs varies based on location. When evaluating patients with operable CMs for surgery, the incidence of complications as well as final neurological outcome should be carefully weighed against the existing knowledge of the natural history of lesions managed expectantly.

Aneurysmal and Microaneurysmal “Angiogram-negative” Subarachnoid Hemorrhage

The source of bleeding remains obscure in most cases of subarachnoid hemorrhage (SAH) with a negative angiogram. From January 1, 1989, to July 1, 1993, 40 patients were admitted to the Massachusetts General Hospital with angiogram-negative SAH; 9 of these patients underwent surgical exploration. In seven of these explorations, an arterial source of the hemorrhage was discovered. These arterial sources included three anterior communicating artery complex lesions, two middle cerebral artery lesions, one internal carotid artery aneurysm arising at the origin of the posterior communicating artery, and one vertebral/posterior inferior cerebellar artery aneurysm. Three of these seven lesions had small aneurysmal sacs, but the other four were microaneurysms too small to accept a surgical clip. No source of hemorrhage could be found during surgery on one patient with a perimesencephalic pattern of blood. Two of the four patients with a microaneurysmal source of hemorrhage had two episodes of SAH. We propose that microaneurysms are the source of a significant percentage of nonperimesencephalic angiogram-negative SAH and suggest that these lesions may represent a forme fruste of saccular aneurysms. These findings lead us to propose a protocol for the management of angiogram-negative SAH based on the distribution of blood as seen on the patients first computed tomogram.

Use of Halifax interlaminar clamps for posterior C1-C2 arthrodesis

Eight patients with atlantoaxial instability secondary to trauma or rheumatoid arthritis were treated with posterior C1-C2 arthrodesis using the Halifax interlaminar clamp and autogenous bone graft or methylmethacrylate. Thus far, with an average follow-up of 6 months, satisfactory stability has been achieved with no instrument failure.

The anterior communicating artery has significant branches.

The anterior communicating artery was studied with the operating microscope in 10 autopsy cases. This \essel was present in all cases with reduplication in three. Arterial diameter ranged from 0.8 to 2.3 mm, with lengths of 5 to 10 mm. Branches of the anterior communicating artery were found in every case (range 3-13, average 5.4). Most branches were small (50-250 n), but at least one large branch (250-1000 /J) was imariably present. Small tentral branches ramified on the optic chiasm. Small and large dorsal branches distributed themselves to lamina terminalis, hvpothalamus, parolfactory areas, columns of fornix, and corpus callosum. Injury to these vessels caused by aneurysmal rupture or surgical manipulation may lead to serious clinical deficits.

Intravenous nitroglycerin in experimental cerebral vasospasm. A preliminary report.

Cerebral arteriospasm is a common complication of subarachnoid hemorrhage and is responsible for much of the brain damage which accompanies it. No pharmacologic agent has been found which regularly alleviates arteriospasm. We have evaluated the effect of continuous intravenous nitroglycerin infusion on the diameter of the basilar artery in dogs with cerebral vasospasm experimentally induced by subarachnoid blood injection. In 6 consecutive dogs, 10 minutes after beginning intravenous nitroglycerin at 100 ^ig/min and at other times during 120 minutes of infusion, the diameter of the basilar artery had increased from 75 ± 2% of control value to 114 ± 2% of control value (p < 0.001). In all 6 dogs, the basilar artery diameter during infusion was greater than the control value prior to creating subarachnoid hemorrhage. Intravenous nitroglycerin caused only a moderate (8%) decrease in blood pressure. Further investigation of the effects of nitroglycerin on cerebral vasospasm is warranted.

Patients in poor neurological condition after subarachnoid hemorrhage: early management and long-term outcome.

SummaryWe report management and outcome data on 118 patients that presented to our emergency room over a 4 year interval (1990–1994) in poor neurological condition after subarachnoid hemorrhage. All patients were treated following a strict protocol. After initial evaluation, patients underwent a head computerized tomography (CT) scan to try to understand the mechanism of coma. If CT did not show destruction of vital brain areas, a ventriculostomy was inserted and ICP measured. If ICP was less than 20 mm Hg, or if standard treatment of increased ICP was able to lower the ICP to a value less than 20 mmHg, patients were evaluated with cerebral angiogram to determine the location of the raptured aneurysm. The lesion was then treated by craniotomy for aneurysm clipping or endovascular obliteration. Postoperative monitoring for vasospasm with clinical exam and transcranial doppler studies was performed routinely. If vasospasm developed, this was managed aggressively with hypertensive, hypervolemic and hemodilutional therapy and, at times, endovascular treatment with angioplasty or papaverine. Outcome was measured at 1 year or more after treatment. Among patients who met criteria for aneurysm treatment, 47% had excellent or good neurologic outcome. There was a 30% mortality rate in these patients. In patients with high ICP, poor brainstem function or destruction of vital brain areas on CT, comfort measures only were offered and almost all died. It is concluded that an approach of early aneurysm obliteration and aggressive medical and endovascular management of vasospasm is warranted in patients in poor neurological conditions after subarachnoid hemorrhage.