Journal of the neurological sciences
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Cerebral microbleeds (CMBs) detected on T2*-weighted MRI gradient-echo have been associated with increased risk of cerebral infarction. We evaluated risk factors for these lesions in a cohort of first-time ischemic stroke patients. ⋯ Low HDL-C may be a risk factor of deep CMBs, including advanced PVH status, in elderly patients with acute ischemic stroke. Management of HDL-C levels might be a therapeutic target for the prevention of recurrence of stroke.
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Chronic demyelinated lesions and subsequent functional impairment are resulted from eventual failure of remyelination process as seen in multiple sclerosis. Activation of adenosine A1 receptor is reported to be effective on neural stem cells (NSCs) proliferation and oligodendrocytes differentiation. Therefore, this study attempted to investigate the effect of A1 receptor agonist N6-cyclohexyladenosine (CHA), on lysolecithin (LPC) induced demyelination and remyelination in rat optic chiasm. ⋯ I.c.v. treatment of animals with CHA during demyelination phase (days 0-13) reduced the extent of demyelination. During remyelination phase (days 14-28), CHA was able to increase remyelination in both electrophysiological and histopathological studies. The effects of CHA seem to be due to its protective effect on myelinating cells and its regenerative effect through potentiating endogenous neural progenitors.
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This study included 40 consecutive patients with athrothrombotic carotid occlusive disease (A-group) and 13 consecutive patients with moyamoya disease (M-group) who had an internal carotid artery occlusion and underwent EC-IC bypass. Flow velocity and diameter of the operated STA on duplex ultrasonography (STDU), as well as regional cerebral blood flow (rCBF) on single photon emission computed tomography (SPECT) were measured before, 14days after, and 3months after EC-IC bypass. The postsurgical changes in the ipsilateral STA mean flow velocity (MFV) were significantly higher (p=0.0030) and those in the rCBF in the MCA territory were relatively higher (p=0.0936) in the M-group than the A-group patients. ⋯ There were no significant differences in the postsurgical STA diameter and the ACZ reactivity between both groups. Changes in the STA MFV as well as the rCBF were higher in moyamoya disease than atherothrombotic carotid occlusive disease in the early phase after EC-IC bypass. The STA MFV is highly correlated with the rCBF after EC-IC bypass.
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The etiology of cerebral ischemia is undetermined in one-third of patients upon discharge. Occult paroxysmal atrial fibrillation (PAF) is considered a potential etiology. A high rate of PAF detection with 21-day mobile cardiac outpatient telemetry (MCOT) has been reported in two small studies. Optimal monitoring duration and factors predicting PAF have not been adequately defined. ⋯ MCOT frequently detects PAF in patients with cryptogenic stroke and TIA. Length of monitoring is strongly associated with detection of PAF, with an optimal monitoring period of at least 21 days. Of the predictors of PAF detection, the presence of premature atrial complexes on ECG held the strongest correlation with PAF.
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The present study, using a rodent model of closed-head diffuse traumatic brain injury (TBI), investigated the role of dysregulated aquaporins (AQP) 4 and 9, as well as hypoxia inducible factor -1α(HIF-1α) on brain edema formation, neuronal injury, and functional deficits. TBI was induced in adult (400-425 g), male Sprague-Dawley rats using a modified Marmarou's head impact-acceleration device (450 g weight dropped from 2m height). Animals in each treatment group were administered intravenous anti-AQP4 or -AQP9 antibodies or 2-Methoxyestradiol (2ME2, an inhibitor of HIF-1α) 30 min after injury. ⋯ Finally, compared to the non-treated TBI animals, AQP or HIF-1α inhibition significantly (p<0.01) improved neurobehavioral outcomes after TBI. Taken together, the present data supports a causal relation between HIF-AQP mediated cerebral edema, secondary neuronal injury, and tertiary behavioral deficits post-TBI. The data further suggests that upstream modulation of the molecular patho-trajectory effectively ameliorates both neuronal injury and behavioral deficits post-TBI.