Isolated Hemangioblastoma of the Filum Terminale

The filum terminale is an exceptional location for isolated hemangioblastoma, and most commonly hemangioblastomas are present in patients with von Hippel-Lindau(VHL) syndrome. We describe here a case of hemangioblastoma of filum terminale not associated with VHL, presenting with the history of progressive back pain, particularly severe in recumbent posture, and recurrent bilateral sciatica. MRI and spinal angiography revealed a well-vasculized mass lesion in filum terminale. The tumor was resected surgically. Histological examination confirmed the hemangioblastoma diagnosis. We recommended that, although rare, hemangiblastoma of the filum terminale be included in the differential diagnosis of a patient with low back pain.

Analysis of Corticospinal Tract Injury by Using the Diffusion Tensor Imaging of 3.0 T Magnetic Resonance in Patients with Hypertensive Intracerebral Hemorrhage

OBJECTIVE: The purpose of this study is to identify correlations between diffusion tensor imaging(DTI) and motor improvement by quantifying and visualizing the corticospinal tract on DTI to predict motor impairment in patients with hypertensive intracerebral hemorrhage(ICH). METHODS: Fifteen normal subjects and 7 patients with hypertensive ICH were examined and the latter were treated surgically. DTI was performed with a 3.0 T MRI. The region of interest(ROI) from the posterior limbs of both internal capsules was measured on a fractional anisotropy(FA) map, and the ratios of ROIs were calculated. Tractography, 3-dimensional DTI was then constructed. Motor impairment was assessed on admission and 2weeks after stroke by the Motricity Index(MI). The FA ratio, tractography and score on MI were analyzed for correlations. RESULTS: The FA ratio from the initial DTI did not show a linear correlation with motor impairment. However, after 2weeks, patients with high FA ratios showed high degrees of motor recovery, regardless of the initial severity, and patients with low FA ratios showed low recovery rates. Otherwise, a relationship between the amount of hematoma and the degree of motor recovery could not be determined. On tractography, injury of the corticospinal tract could be visualized and estimated 3-dimensionally. CONCLUSION: FA ratio analysis and tractography constructed from DTI may be useful in understanding corticospinal tract injury and in predicting the recovery from motor impairment in patients.

Nitric Oxide-cGMP-Protein Kinase G Pathway Contributes to Cardioprotective Effects of ATP-Sensitive K+ Channels in Rat Hearts

Ischemic preconditioning (IPC) has been accepted as a heart protection phenomenon against ischemia and reperfusion (I/R) injury. The activation of ATP-sensitive potassium (KATP) channels and the release of myocardial nitric oxide (NO) induced by IPC were demonstrated as the triggers or mediators of IPC. A common action mechanism of NO is a direct or indirect increase in tissue cGMP content. Furthermore, cGMP has also been shown to contribute cardiac protective effect to reduce heart I/R-induced infarction. The present investigation tested the hypothesis that KATP channels attenuate DNA strand breaks and oxidative damage in an in vitro model of I/R utilizing rat ventricular myocytes. We estimated DNA strand breaks and oxidative damage by mean of single cell gel electrophoresis with endonuclease III cutting sites (comet assay). In the I/R model, the level of DNA damage increased massively. Preconditioning with a single 5-min anoxia, diazoxide (100muM), SNAP (300muM) and 8- (4-Chlorophenylthio)-guanosine-3', 5'-cyclic monophosphate (8-pCPT-cGMP) (100muM) followed by 15 min reoxygenation reduced DNA damage level against subsequent 30 min anoxia and 60 min reoxygenation. These protective effects were blocked by the concomitant presence of glibenclamide (50muM), 5-hydroxydecanoate (5-HD) (100muM) and 8- (4-Chlorophenylthio)-guanosine-3', 5'-cyclic monophosphate, Rp-isomer (Rp-8-pCPT-cGMP) (100muM). These results suggest that NO-cGMP-protein kinase G (PKG) pathway contributes to cardioprotective effect of KATP channels in rat ventricular myocytes.