Faculty Bibliography

The authors describe three cases of clinical cerebral ischemia associated with angiographic evidence of cerebral arterial luminal narrowing presenting 7, 14, and 52 weeks after subarachnoid hemorrhage (SAH) and aneurysm clipping. Delayed vasospasm, in its usual time setting 1 or 2 weeks after hemorrhage, did not occur symptomatically in these patients. No evidence for aneurysm clip migration or rebleed was present. All patients responded favorably to volume expansion and elevation of blood pressure. This unusual occurrence of a very delayed vasospasm may further the understanding of the vasospastic process. The symptomatic onset of arterial luminal narrowing months after SAH may suggest that a proliferative vasculopathy more accurately explains the observed vessel narrowing, rather than conventional active constriction of vascular smooth muscle.

There is continuing controversy about the benefits of decompressive craniectomy in the treatment of lesions causing increased intracranial pressure (ICP) and brain edema. Laboratory work has shown a decrease in ICP after craniectomy, but also a paradoxical enhancement in the formation of underlying cerebral edema, which may act to the detriment of the patient. Since Rengachary et al. advocated craniectomy for massive cerebral infarction and reported their group of three patients, we have managed five patients with acute supratentorial cerebral infarction who progressed to uncal herniation and impending death from raised ICP and brain stem compression. All were treated with frontotemporal craniectomy after conventional medical therapy failed to achieve a response. All patients survived and are walking, despite a paresis appropriate to their original stroke. Two have returned to work. Good results with supratentorial craniectomy after infarction show that this procedure is life-saving and can also give acceptable functional recovery.

The common vascular anomalies of cerebral aneurysm and arteriovenous malformation may exist independently, or together as part of a closely related hemodynamic pairing. Resection or embolization of an AVM may be followed by a decrease in local blood flow, and lead to regression of a suitably situated proximal aneurysm. However, aneurysms located outside the angioarchitecture of the AVM, which remain flow-unrelated to the malformation, will likely not regress, and may in fact enlarge. Two cases are presented which demonstrate these vascular relationships, in order to better understand the regional hemodynamics of these anomalies prior to surgical or endovascular treatment planning.

A review of 905 consecutive cases of pathologically confirmed brain tumour yielded 25 cases in which the initial presentation strongly suggested the diagnosis of occlusive cerebrovascular disease. Most of these 25 patients were admitted through the emergency department of our hospital and referred to the general medical service for investigation. Nineteen cases of transient ischemic attack and six cases of completed stroke were found in 12 cases of glioblastoma, seven of meningioma, two of metastatic renal cell carcinoma, and one case each of malignant astrocytoma, low-grade astrocytoma, oligodendroglioma, and metastatic squamous cell carcinoma. We document the clinical overlap between neoplastic and vascular syndromes, and stress the need for "tumour awareness" in the work-up of patients presenting to non-neurological practitioners with the clinical picture of occlusive cerebrovascular disease.

Acute spontaneous subdural hematoma is infrequent in association with rupture of intracranial saccular aneurysm. In the majority of cases, aneurysms of the middle cerebral artery along the convexity or of the anterior cerebral artery along the interhemispheric fissure are found to be the culprits. We present two recent cases of internal carotid-posterior communicating artery aneurysms causing acute subdural hematoma with little or no subarachnoid hemorrhage and discuss the possible mechanisms for this occurrence.

Tumors of mixed glial origin may present as low-grade neoplasms with distinct cell populations or as polymorphic malignant gliomas. Such cell populations are usually appropriate to the location of the tumor. A mixed tumor, with a cell population inappropriate to tumor location, is presented to discuss theories of glial differentiation and cellular heterogeneity. This mixed ependymoma-astrocytoma of the parietal cortex, ultrastructurally similar to subependymoma but anatomically separate from the subependymal cell matrix or ventricular surface, gives evidence for neoplastic differentiation into ependymal and astrocytic cell lines. This supports the idea of a common progenitor cell, the ependymoglia or tanycyte, in human cerebral cortex.