ISRN Neurology最新文献

Asymptomatic intracranial abnormalities are increasingly becoming a focus of attention with the utilization of high-resolution imaging. The concurrence of tumor and aneurysm has been described, largely, by case reports and single-surgeon experiences. Recent papers have outlined the ethics of incidental findings and possible treatment algorithms. Incidental finding of an aneurysm occurs most commonly in patients with meningiomas, pituitary adenomas, and gliomas. Such an association may explain the mechanisms of aneurysm formation, growth, and rupture in acromegalic patients; however, insufficient data are available to link aneurysm with either glioma or meningioma.

Background. Mitoxantrone (MTX) and Rituximab (RTX) are successfully used for treatment of multiple sclerosis (MS) and can be combined to increase efficacy. Objective. We used MTX, RTX, and methylprednisolone in a single combined regiment and observed patients prospectively. Methods. We present results of observational pilot study of combined therapy of RTX and MTX in 28 patients with active MS. Therapeutic protocol consisted of two infusions within 14 days. First infusion was 1000 mg methylprednisolone (MP) IV, 1000 mg RTX IV, and 20 mg MTX IV. On day 14, 1000 mg MP IV and 1000 mg RTX IV were given. Patients were followed prospectively from 12 to 48 months. Results and Conclusion. There were no relapses among all 28 patients during the observation period. B-cell depletion of CD19+ and CD19+/CD27+ memory B-cell subpopulation in both compartments was confirmed in all patients at 6 months. We found a more rapid reconstitution of B cells in the CSF than in the peripheral blood and longstanding depression of CD19+CD27+ memory B-cell. Conclusion. Effectiveness of combined regimen of RTX and MTX could be related to longstanding depletion of CD19+CD27+ memory B-cell subset.

Objectives. To compare the outcome of early surgical intervention versus late surgical treatment in cases of neurogenic thoracic outlet syndrome (NTOS). Design. Prospective study. Settings. Secondary care (Al-Minia University Hospital, Egypt) from 2007 to 2010. Participants. Thirty-five patients of NTOS (25 women and 10 men, aged 20-52 years), were classified into 2 groups. First group (20 patients) was operated within 3 months of the onset and the second group (15 patients) was operated 6 months after physiotherapy. Interventions. All patients were operated via supraclavicular surgical approach. Outcomes Measures. Both groups were evaluated clinically and, neurophysiologically and answered the disabilities of the arm, shoulder, and hand (DASH) questionnaire preoperatively and 6 months after the surgery. Results. Paraesthesia, pain, and sensory nerve action potential (SNAP) of ulnar nerve were significantly improved in group one. Muscle weakness and denervation in electromyography EMG were less frequent in group one. The postoperative DASH score improved in both groups but it was less significant in group two (P < .001 in group 1 and P < .05 in group 2). Conclusions. Surgical treatment of NTOS improves functional disability and stop degeneration of the nerves. Early surgical treatment decreases the occurrence of muscle wasting and denervation of nerves compared to late surgery.

Astrocytes express the sodium-dependent glutamate transporters GLAST and GLT-1, which are critical to maintain low extracellular glutamate concentrations. Here, we analyzed changes in their expression and function following a mechanical lesion in the CA1 area of organotypic hippocampal slices. 6-7 days after lesion, a glial scar had formed along the injury site, containing strongly activated astrocytes with increased GFAP and S100 β immunoreactivity, enlarged somata, and reduced capability for uptake of SR101. Astrocytes in the scar's periphery were swollen as well, but showed only moderate upregulation of GFAP and S100 β and efficiently took up SR101. In the scar, clusters of GLT-1 and GLAST immunoreactivity colocalized with GFAP-positive fibers. Apart from these, GLT-1 immunoreactivity declined with increasing distance from the scar, whereas GLAST expression appeared largely uniform. Sodium imaging in reactive astrocytes indicated that glutamate uptake was strongly reduced in the scar but maintained in the periphery. Our results thus show that moderately reactive astrocytes in the lesion periphery maintain overall glutamate transporter expression and function. Strongly reactive astrocytes in the scar, however, display clusters of GLAST and GLT-1 immunoreactivity together with reduced glutamate transport activity. This reduction might contribute to increased extracellular glutamate concentrations and promote excitotoxic cell damage at the lesion site.

It has been suggested that children with autism are particularly deficient at imitating novel gestures or gestures without goals. In the present study, we asked high-functioning autistic children and age-matched typically developing children to imitate several types of gestures that could be either already known or novel to them. Known gestures either conveyed a communicative meaning (i.e., intransitive) or involved the use of objects (i.e., transitive). We observed a significant interaction between gesture type and group of participants, with children with autism performing known gestures better than novel gestures. However, imitation of intransitive and transitive gestures did not differ across groups. These findings are discussed in light of a dual-route model for action imitation.

Numerous cases of severe and life-threatening hyperammonemia (HA) related to the treatment of epileptic seizures with valproic acid (VPA) have been previously reported in the medical literature. The aim of this prospective, multicenter study was to verify the putative association between T1405 polymorphism and occurrence of VPA-induced HA in the cohort of 142 adult Caucasian patients with epilepsy treated with VPA for at least 1 year and with normal liver functions. The nonsynonymous T1405N polymorphism genotyping was performed by real-time TaqMan PCR genotyping. In addition to plasma ammonia level, concentrations of liver enzymes and total VPA were measured in plasma with standard laboratory methods. HA (defined as ammonia plasma level >65  μ mol/L) was observed in total of 11 (7.7%) of patients treated with VPA, and the carrier status for the investigated polymorphism was significantly (P = 0.009, odds ratio 5.4 with 95% confidence interval of 1.58-18.43) associated with the occurrence of HA. The results of this study support a notion that in the Caucasian patients with epilepsy undergoing VPA therapy, a T1405N (4217C > A, rs1047891) nonsynonymous variant was a significant risk factor for the occurrence of HA, even in patients with normal plasma levels of VPA.

Preclinical studies suggest that fluoxetine may have neuroprotective properties. In this pilot study forty-two patients with secondary or primary progressive MS were randomized to receive fluoxetine 20 mg twice daily or placebo for 2 years. Every 3 months the Expanded Disability Status Scale (EDSS), 9-hole peg test (9-HPT) and ambulation index (AI) were assessed. Brain MRI scans, Multiple Sclerosis Functional Composite, Fatigue Impact Scale, Guy's neurological disability Scale and SF-36 were performed at baseline, year 1 and year 2. Seven out of 20 (35%) patients in the fluoxetine group and 7 out of 22 (32%) patients in the placebo group had sustained progression on the EDSS, 9-HPT, or AI at 2 years. No differences were identified between the 2 treatment groups with respect to secondary clinical outcomes and T2 lesion load, grey matter volume and white matter volume. An unanticipated low rate of disability progression in the placebo group decreased the statistical power. At least 200 patients would have been needed to detect a 50% treatment effect. This trial shows that fluoxetine was generally well tolerated, but no assumptions can be made about a possible treatment effect. An adequately powered controlled trial of fluoxetine in progressive MS is still warranted. This trial is registered with Current Controlled Trials ISRCTN38456328.

Vitamin E exists in eight different forms, four tocopherols and four tocotrienols. It forms an important component of our antioxidant system. The structure of Vitamin E makes it unique and indispensable in protecting cell membranes. α -tocopherol, one of the forms of Vitamin E, is also known to regulate signal transduction pathways by mechanisms that are independent of its antioxidant properties. Vitamin E compounds reduce the production of inflammatory compounds such as prostaglandins. Swollen, dystrophic axons are considered as the hallmark of Vitamin E deficiency in the brains of rats, monkeys, and humans. The present work aimed to study the Vitamin E- ( α -tochopherol acetate-) induced alterations of enzymes involved in metabolism of Glutamate and GABA during developmental neurogenesis of cerebrum. Therefore, cytosolic and crude mitochondrial enzyme activities of glutamine synthetase, aspartate transaminase, alanine transaminase, GABA transaminase, succinic Semialdehyde dehydrogenase, glutamic dehydrogenase, and α -Ketoglutarate dehydrogenase were analysed. Vitamin E induced significant changes in these enzymes thus altering the normal levels of glutamate and GABA during developmental neurogenesis. Such changes are surely to disturb the expression and/or intensity of neurotransmitter signaling during critical periods of brain development.

Motor skill learning may induce behavioral and neurophysiological adaptations after intracerebral hemorrhage (ICH). Learning a new motor skill is associated with dendritic reorganization and requires protein synthesis and expression of MAP-2. The purpose of this study was to evaluate motor performance and expression of MAP-2 in the motor cortex of rats submitted to intracerebral hemorrhage model (ICH) and skill task training (SK) or unskilled training (US) during 4 weeks. The Staircase test was used for behavioral evaluation, and relative optical densities and morphometrical analysis were used to estimate MAP-2 immunoreactivity and parameters of brain tissue in both motor cortices. Results show that skill task training performed with the impaired forelimb was able to increase MAP-2 immunoreactivity in the motor cortex either in sham or in ICH groups in both cortices: ipsilesional [F (5,35) = 14.25 (P < 0.01)] and contralesional hemispheres [F (5,35) = 9.70 (P < 0.01)]. ICH alone also increased MAP-2 immunoreactivity despite the absence of functional gains. Behavioral evaluation revealed that ICH-SK group performed better than ICH and ICH-US animals in the Staircase test. Data suggest that motor skill training induces plastic modifications in both motor cortices, either in physiological or pathological conditions and that skill motor training produces higher brain plasticity and positive functional outcomes than unskilled training after experimental intracerebral hemorrhage.

The cause of Parkinson's disease (PD) remains elusive, but environmental chemical exposures have been postulated to be involved in the etiology of PD. We examined the association between the persistent organochlorine pesticides (OCPs) and PD in the North Indian population. This case control study included 70 PD and 75 control subjects in the age group of 50 to 85 years. Blood samples were collected and high-purity grade hexane and acetone (2 : 1 ratio) were used for extraction of organochlorine residues. OCPs (hexachlorocyclohexane (HCH), aldrin, dieldrin, endosulfan, pp'-Dichlorodiphenyldichloroethylene (pp'-DDE), op'-DDE, pp'- Dichlorodiphenyltrichloroethane (pp'-DDT), op'-DDT, pp'-dichlorodiphenyldichloroethane (pp'-DDD) and op'-DDD) were quantitatively estimated by using gas chromatography. The most frequently detected OCP was dieldrin, which was present in 9.3% of control and 61.4% of PD. The strongest predictor was β-hexachlorocyclohexane (β-HCH), which reported an odds ratio of 2.566, indicating that for every additional one unit of β-HCH, patients had 2.566 times more chances of presence of PD. This study indicates that increased level of β-HCH and dieldrin may be associated with the risk of PD.