Spinal dural arteriovenous fistula with hematomyelia caused by intraparenchymal varix of draining vein.

BACKGROUND CONTEXT: Hemorrhage that results from spinal dural arteriovenous fistula (Type I arteriovenous malformation [AVM]) is uncommon. There are some reports of subarachnoid hemorrhage and subdural hematoma caused by Type I spinal AVM, but there are few reported cases of hematomyelia caused by spinal dural arteriovenous fistula. PURPOSE: To describe an interesting patient who had hematomyelia caused by a dural arteriovenous fistula (Type I spinal AVM). STUDY DESIGN: A case report. METHODS: We present a case of a 51-year-old man who presented acute onset epigastric pain, paraplegia, and sensory loss below his nipples. Magnetic resonance imaging and selective spinal angiogram demonstrated hematomyelia, subarachnoid hemorrhage, and spinal arteriovenous fistula fed by the right Th7 intercostal artery. By laminotomy of Th6-8, the varix-like draining vein and intramedurally hematoma were partially removed and the arterial supply was interrupted by coagulation of the right Th7 segmental artery. RESULTS: One month after surgery, he regained movement against gravity at the left ankle and toe but no functionally significant improvement. CONCLUSIONS: It must be kept in mind that spinal dural arteriovenous fistulas (Type I spinal AVM) has possibility of hematomyelia origin, despite the fact that it is extremely rare.

Reversible widespread ischemia after early reperfusion detected by initial diffusion-weighted magnetic resonance imaging.

We herein report the time-related dynamic changes according to the diffusion-weighted image (DWI) findings after a cerebral ischemic attack in a 63-year-old woman. At 2 weeks after undergoing a lower limb amputation due to diabetic atherosclerosis, she experienced a sudden loss of consciousness and right hemiparesis. Magnetic resonance image revealed left frontal and parietal areas with an increased signal on the DWI, and magnetic resonance angiography (MRA) showed the left middle cerebral artery to be occluded at the superior M2 branch. However, on the next day the lesion on DWI, except for the gray matter, was observed to have almost completely resolved, and MRA showed complete recanalization of the left superior M2 branch with diminished clinical symptoms. Although a few cases of reversible DWI-identified lesions have been described in the literature, the occurrence of large, reversed DWI lesions in the middle cerebral artery territory with severe apparent diffusion coefficient decreases, as seen in our case, are exceedingly rare.

Quantification of the regional cerebral blood flow and vascular reserve in moyamoya disease using split-dose iodoamphetamine I 123 single-photon emission computed tomography.

OBJECTIVES: We quantified the rCBF and regional vascular reserve (CVR) in adult patients with moyamoya disease before and after surgery using IMP I 123 SPECT. METHODS: The patient population included 5 adult patients with ages at presentation ranging between 23 and 42 years. One patient had stroke, whereas 4 patients had transient ischemic attacks. RESULTS: Before surgery, the mean resting rCBF and mean CVR in the frontal, parietal, and temporal lobes of the surgically treated hemisphere were 40.09, 39.50, and 36.9 mL/100 g per minute and 15.39%, 27.09%, and 28.92%, respectively. After surgery, the rCBF increased significantly (P = .0002, .0005, and .0062), but in a CVR evaluation, only the frontal lobe increased significantly (P = .0055). In the unaffected hemispheres, the mean resting rCBF significantly increased only in the frontal lobe (P = 038) and no significant increase in the CVR was observed after surgery. In 2 patients who showed steal phenomenon induced by acetazolamide administration, CVR significantly increased not only in the frontal lobe but also in the parietal and temporal lobe after surgery, although the CVR in these areas significantly decreased both before and after surgery in comparison to the mean CVR in all patients. CONCLUSIONS: The frontal lobe showed severe hemodynamic ischemia. The cerebral hemodynamics in patients with moyamoya disease improved after surgical intervention, especially in severely damaged patients. Split-dose (123)I-IMP SPECT was therefore found to be a useful diagnostic modality for quantifying the hemodynamics of moyamoya disease.

Aneurysmal embolization of a blisterlike aneurysm of the internal carotid artery: a case report and review of the literature.

BACKGROUND: Little is known regarding the optimal management of a ruptured blisterlike aneurysm of the ICA. Because of the high risk for intraoperative bleeding, direct surgical treatments of these fragile lesions have generally been associated with a poor outcome. We herein report a very rare case of a ruptured blisterlike aneurysm that was successfully treated with coil embolization in the late period. CASE DESCRIPTION: The patient was 21 years old when he had a Hunt and Hess grade IV subarachnoid hemorrhage. At the time of the hemorrhage, 3D-CTA demonstrated a minimal aneurysmal enlargement located in the left C2 portion of the ICA. Because of his poor neurological condition and the risk for a premature rupture during early surgery, delayed surgery was thus scheduled. Cerebral angiography, 13 days later, revealed the shape and size of the aneurysm to have changed in form from a blisterlike aneurysm to a saccular-type one. Initially, we planned to treat the aneurysm by trapping with bypass surgery on the 15th day. However, we instead performed coil embolization on the 19th day because a thick thrombus was found to cover the aneurysm at the time of surgery on the 15th day. CONCLUSION: This is the first report of a ruptured blisterlike aneurysm that was successfully treated with coil embolization in the late period of a subarachnoid hemorrhage after operative confirmation of thrombus formation around the aneurysm. Our findings suggest that coil embolization in the late period appears to be an effective option in the management of selective cases of ruptured blisterlike aneurysms.

Vitamin E prevents the neuronal cell death by repressing cyclooxygenase-2 activity.

The accumulation of damage caused by oxidative stress exacerbates cell death in many neurodegenerative diseases. We evaluated the mechanism of neuronal cell death raised by glutamate-induced toxicity, using the immortalized mouse hippocampal cell line HT-22. Our results showed that vitamin E prevented glutamate-induced cell death, accompanied by the decline of cyclooxygenase-2 expression confirmed by reverse transcriptase polymerase chain reaction and immunocytochemistry. Moreover, the neuroprotection was still effective even when vitamin E was supplied after glutamate treatment. The decline of cyclooxygenase-2 activity was also highly correlated with the neural protective effect against glutamate-induced toxicity. These results represent new insights about the timing of vitamin E supplementation after toxic stimulation and one mechanism by which vitamin E could prevent neuronal cell death by controlling cyclooxygenase-2 activity.

Retrospective analysis of neurological outcome after intra-arterial thrombolysis in basilar artery occlusion.

BACKGROUND: Basilar artery occlusion usually has a very poor outcome and is associated with a high mortality rate. Local intra-arterial thrombolysis may improve the clinical outcome and reduce mortality in the treatment of acute basilar artery occlusion. We evaluated the possible variables affecting recanalization and clinical outcome in patients with basilar artery occlusions undergoing thrombolytic therapy. METHODS: We analyzed retrospectively the clinical course and outcome of a series of 26 patients between 1998 and 2001. All patients who were examined within 24 hours after onset of symptoms underwent emergency cerebral angiography and subsequent intra-arterial thrombolysis. Three patients additionally received percutaneous transluminal angioplasty of underlying stenosis at the site of thrombosis. RESULTS: Outcome was good in 9 patients (34.6%) and poor in 17 (65.4%). Recanalization could be achieved in 24 patients (92.3%) and was not affected by age, sex, site of occlusion, etiology, thrombolytic drugs, or time interval. Good outcome was associated with younger age, good initial clinical condition, and no evidence of brain stem infarction. There was no association between the interval (greater or less than 6 hours) from the onset of symptoms until the end of thrombolysis and survival. CONCLUSIONS: We confirm that intra-arterial thrombolysis reduces mortality in basilar artery occlusion. Young patients (<75 years) without any infarct in brain stem before the start of treatment seem to be the ideal candidates for thrombolysis. Basilar artery thrombosis could and should be reopened, even late (after 6 hours) after symptom onset.