ABSTRACT
Objective: To evaluate the clinical and angiographic data of cranial dural arteriovenous fistula in Thai patients and to determine the predisposing factors to aggressive symptoms. Methods: Retrospective review of 71 patients with cranial dural arteriovenous fistula who underwent cerebral angiography at Siriraj Hospital between July 2002 – February 2006. Their clinical manifestations were classified as benign or aggressive symptoms. The relationship between aggressive symptoms and the following factors were studied: gender, location of the fistula, classification according to venous drainage pattern, presence of cerebral sinus thrombosis, and shunt multiplicity. Linear-by-linear association and chi-square test were used to determine statistical significance. Results: Sixteen (22.5%) of 71 patients with cranial dural arteriovenous fistula had aggressive presenting symptoms. Factors that significantly correlate with aggressive symptoms were location of the fistula, retrograde leptomeningeal venous drainage, presence of cerebral sinus thrombosis, and multiplicity. Factor which was not significantly correlated with aggressive symptoms was gender. Conclusion: This study evaluated clinical data and angiographic features of cranial dural arteriovenous fistula in Thai patients. Predisposing factors to aggressive symptoms were location of the fistula, retrograde leptomeningeal venous drainage, presence of cerebral sinus thrombosis, and multiplicity.
ABSTRACT
An 18-year-old woman was admitted to our hospital because of headache and double vision. One year before, she had experienced similar symptoms which were ameliorated spontaneously. Before admission, she had been experiencing throbbing headaches for 20 days and double vision for 7 days, respectively. A brain magnetic resonance imaging (MRI) study, performed at another hospital 6 days before admission, showed no abnormality. On admission, she had paralysis of the left abducens nerve and papillaedema of the bilateral optic fundi. Magnetic resonance venography (MRV) revealed areas of signal loss expanding from the confluence of sinuses to the right transverse sinus, which confirmed the diagnosis of cerebral sinus thrombosis. Her symptoms improved dramatically with anticoagulation therapy. The present case suggests that the exploration of papillaedema of optic fundi is of paramount importance in the diagnosis of cerebral sinus thrombosis, and MRV can be definitely diagnostic despite the normal findings of conventional MRI.
ABSTRACT
OBJECTIVE: Although it is well known that cerebral sinus thrombosis or resection of large cerebral veins during surgery may cause venous hypertension, often leading to brain edema and intracerebral hemorrhage and the outcome is widely variable with symptoms from headache to coma, the pathophysiology of cerebral venous circulatory disturbance is poorly understood. The purpose of this study was to investigate the pathophysiological change of cerebral venous circulatory disturbance by measurement of intracranial pressure, regional cerebral blood flow and cerebral water content, and histological examination for extravasation of Evans blue dye and cerebral edema for 2 hours after occlusion of the superior sagittal sinus and diploic veins in cats. METHODS: Thirty five cats were divided into 4 groups: (1) control group, 5 cats with sham operation, (2) experiment group I, 10 cats with occlusion at the anterior 1/3 of the superior sagittal sinus, (3) experiment group II, 10 cats with occlusion at the middle 1/3 of the superior sagittal sinus, (4) experiment group III, 10 cats with occlusion at the posterior 1/3 of the superior sagittal sinus. RESULTS: The results were as follows: 1) After occlusion of the superior sagittal sinus, intracranial pressure was elevated with increased cerebral water content and regional cerebral blood flow was reduced in all experiment groups. The degree of their changes was the least in experiment group I, the most in experiment group III, and intermediate in experiment group II. 2) Extravasation of the Evans blue dye was not observed in any experiment groups 120 minutes after occlusion of the superior sagittal sinus. 3) On the histological examination, pericellular edematous change of the brain was observed in all experiment groups 120 minutes after occlusion of the superior sagittal sinus. The degree of edema also showed similar pattern in magnitude to that of changes of other parameters. CONCLUSION: These results suggest that occlusion of the middle or posterior 1/3 of the superior sagittal sinus could bring a significant harmful effect to the cerebral hemodynamics, leading to secondary brain injury and the hydrostatic edema is responsible for the cerebral swelling in early stage after occlusion of the superior sagittal sinus.