The question of whether unruptured intracranial vertebral artery dissections should be treated surgically or nonsurgically still remains unresolved. In this study, six consecutive patients with intracranial vertebral artery dissection presenting with brain-stem ischemia without subarachnoid hemorrhage (SAH) were treated non-surgically with control of blood pressure and bed rest, and five received follow-up review with serial angiography. No further progression of dissection or associated SAH occurred in any of the cases, and all patients returned to their previous lifestyles. In the serial angiograms in five patients, the findings continued to change during the first few months after onset. Four cases ultimately showed "angiographic cure," while fusiform aneurysmal dilatation of the affected vessel persisted in one case. In one patient, arterial dissection was visualized on the second angiogram despite negative initial angiographic findings. These results indicate that intracranial vertebral artery dissection presenting without SAH can be treated nonsurgically, with careful angiographic follow-up monitoring. Persistent aneurysmal dilatation as a sequela of arterial dissection seemed to form a subgroup of fusiform aneurysms of the posterior circulation. These aneurysms may be prone to late bleeding and may require surgical treatment.
Background and Purpose The purpose of this study is to demonstrate the magnetic resonance features of intracranial vertebrobasilar artery dissections and to determine the potential and limitations of magnetic resonance imaging in their diagnosis.Methods We studied five consecutive patients with angiographically verified intracranial vertebrobasilar artery dissection with magnetic resonance imaging (0.5 T) in regard to the shapes of the intramural hematoma and the chronological change of its signal intensity. We also estimated the sensitivity of magnetic resonance imaging for diagnosing dissection.Results We observed intramural hematoma in four patients on the first magnetic resonance scan and in all five patients during the course of the study. The shapes of the intramural hematomas were curvilinear, crescentic, "bamboo-cut," "bandlike," and spotty. The intensity of the intramural hematoma
An unusual, purely extramedullary hemangioblastoma of the spinal cord occurred in a 59-year-old female. Myelography revealed a filling defect at the Th6 level, and computed tomographic myelography demonstrated an extramedullary intradural isodense mass at the same level. The mass was homogeneously enhanced on postcontrast computed tomographic scans. T1-weighted magnetic resonance imaging showed an isointense mass, homogeneously enhanced by contrast medium. The tumor was removed en bloc.
The relationship between the thermosensitivity of cultured brain tumor cells and cytoskeleton was studied. C6 rat glioma cell line (C6 cells) and U-373-MG human glioblastoma cell line (MG cells) were used in monolayer culture. Survival rates at various temperatures were calculated by colony forming assay 10 days after heat treatment. Actin filaments, the main components of microfilaments, were observed by the 7-chloro-4-nitrobenzo-2-oxadiazole phallacidin staining and indirect immunofluorescence staining methods. Alpha-tubulins, the main components of microtubules, were also stained with an indirect immunofluorescence staining method. The morphological changes were investigated by scanning electron microscopy (SEM). Both the C6 cells and the MG cells showed moderate thermosensitivity on the survival curves. Actin filaments were revealed at stress fibers and the ruffles of the leading edge on both cell lines. Stress fibers were well developed in MG cells but were only minor in C6 cells. After heat treatment ruffles and stress fibers were disrupted. However, alpha-tubulins were not affected by heat treatment. SEM showed Swiss-cheese like change of cell surfaces due to many pores with disruption of ruffles and stress fibers after heat treatment. These results suggest that the cytoskeleton, especially microfilaments, may be damaged by hyperthermia.
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