Current Issue : July - September Volume : 2017 Issue Number : 3 Articles : 6 Articles
Background: Although previous studies found that aberrations in gray matter volume (GMV) and global functional\nconnectivity density (gFCD) are important characteristics of schizophrenia, to the best of our knowledge no study to date\nhas investigated the associations between the spatial distribution patterns of GMV and gFCD alterations. We investigated\npattern changes in gFCD and GMV among patients with schizophrenia and their associated spatial distributions.\nMethods: Ninety-five patients with schizophrenia and 93 matched healthy controls underwent structural and\nresting-state functional MRI scanning to assess gFCD and GMV.\nResults: We found that gFCD increased in the subcortical regions (caudate, pallidum, putamen, and thalami) and\nlimbic system (left hippocampus and parahippocampus), and decreased in the posterior parieto-occipito-temporal\ncortices (postcentral gyri, occipital cortex, temporo-occipital conjunction, and inferior parietal lobule), in patients with\nschizophrenia. By contrast, we found decreased GMV in brain regions including the frontal, parietal, temporal, occipital,\ncingulate cortices, and the insular, striatum, thalamus in these patients. Increased gFCD primarily occurred in subcortical\nregions including the basal ganglia and some regions of the limbic system. Decreased gFCD appeared primarily in the\ncortical regions. There were no statistically significant correlations between changes in gFCD and GMV, and their spatial\ndistribution patterns, in different regions.\nConclusions: Our findings indicate that gFCD and GMV are both perturbed in multiple brain regions in schizophrenia.\ngFCD and GMV consistently decreased in the cortical regions, with the exception of the Supplementary Motor Area\n(SMA). However, in the sub-cortical regions, the alterations of gFCD and GMV showed the opposite pattern, with\nincreased gFCD and decreased GMV simultaneously observed in these regions. Overall, our findings suggest that\nstructural and functional alterations appear to contribute independently to the neurobiology of schizophrenia....
Background: Combination therapy using acetylcholinesterase inhibitors (AChEIs) and cilostazol is of unknown\nefficacy for patients with Alzheimerââ?¬â?¢s disease (AD).\nMethods: We explored the therapeutic responses by using a caseââ?¬â??control study, which was conducted in Taiwan.\nWe enrolled 30 participants with stable AD who were receiving cilostazol (50 mg) twice per day as an add-on\ntherapy combined with AChEIs, and 30 participants as controls who were not receiving cilostazol as an add-on\ntherapy. The therapeutic responses were measured using neuropsychological assessments and analyzed in relation\nto cilostazol use, apolipoprotein E genotype, and demographic characteristics. Mini-mental state examination\n(MMSE) and clinical dementia rating sum of boxes (CDR-SB) were administered at the outset of the study and 12\nmonths later. Multiple logistic regression analysis was used to estimate the association between the therapeutic\nresponse and cilostazol use.\nResults: For the therapeutic indicator of cognition, Cilostazol use (adjusted odds ratio (aOR) = 0.17, 95% confidence\ninterval (CI) = 0.03ââ?¬â??0.80), initial CDR-SB score (aOR = 2.06, 95% CI = 1.31ââ?¬â??3.72), and initial MMSE score (aOR = 1.41,\n95% CI = 1.11ââ?¬â??1.90), but not age, sex, education, or ApoE Ã?µ4 status, were significantly associated with poor therapeutic\noutcomes. For the therapeutic indicator of global status, no significant association was observed between the\ncovariates and poor therapeutic outcomes.\nConclusions: Cilostazol may reduce the decline of cognitive function in stable AD patients when applied as an\nadd-on therapy....
Background: Neurocognitive dysfunction is a critical target symptom of schizophrenia treatment. A positive\ncorrelation between physical activity level and neurocognitive function has been reported in healthy individuals,\nbut it is unclear whether such a correlation exists in patients with schizophrenia and whether the relationship is\ndifferent according to inpatients or outpatients. This study aimed to examine the differences in the correlations\nbetween physical activity and multiple neurocognitive domains in inpatients and outpatients with schizophrenia\nand obtain suggestions for further study to facilitate this field.\nMethods: Twenty-nine patients with schizophrenia were examined (16 inpatients and 13 outpatients, 56.0 �± 11.4 years\nof age). Current symptoms were assessed using the Positive and Negative Symptom Scale and neurocognitive\nfunctions using Cognitrax, which yields a composite neurocognitive index (NCI) and 11 domain scores. After\ntesting, participants wore an HJA-750C accelerometer for one week to measure physical activity levels and\ndurations. Partial correlation analyses were performed between exercise and cognitive parameters.\nResults: In the outpatient group, higher physical activity was associated with faster Motor and Psychomotor\nSpeeds in outpatients. However, higher physical activity was associated with lower overall NCI, Attention score,\nand Memory scores in inpatients.\nConclusion: Although higher physical activity was associated with better neurocognitive functions of outpatients,\nin inpatients with non-remitted schizophrenia, higher physical activity was associated with worsening of several\ncognitive domains. In a future study examining the relationship between physical activity and neurocognitive\nfunction for facilitating this research field, separation between inpatients and outpatients are needed because the\nrelationship is different between inpatients and outpatients....
Purpose. Abnormal protein deposits including ...
Introduction. Status epilepticus is associated with neuronal breakdown. Radiological sequelae of status epilepticus include diffusion\nweighted abnormalities and T2/FLAIR cortical hyperintensities corresponding to the epileptogenic cortex. However, progressive\ngeneralized cerebral atrophy fromstatus epilepticus is underrecognized andmay be related to neuronal death.We present here a case\nof diffuse cerebral atrophy that developed during the course of super refractory status epilepticus management despite prolonged\nbarbiturate coma. Methods. Case report and review of the literature. Case. A 19-year-old male with a prior history of epilepsy\npresented with focal clonic seizures. His seizures were refractory tomultiple anticonvulsants and eventually required pentobarbital\ncoma for 62 days and midazolamcoma for 33 days. Serial brain magnetic resonance imaging (MRI) showed development of cerebral\natrophy at 31 days after admission to our facility and progression of the atrophy at 136 days after admission. Conclusion. This case\nhighlights the development and progression of generalized cerebral atrophy in super refractory status epilepticus. The cerebral\natrophy was noticeable at 31 days after admission at our facility which emphasizes the urgency of definitive treatment in patients\nwho present with super refractory status epilepticus. Further research into direct effects of therapeutic coma is warranted....
Cognitive impairment is a frequent non-motorsymptom of Parkinson�s disease\n(PD). In early disease stage, this takes the features of dysexecutive syndrome,\nand is mostly dependent on derangement of frontostriatal circuitries.\nIn advanced stages, worsening of dysexecutive symptoms is accompanied by\ndisorientation and memory deficit leading to dementia in 30% of cases, due to\nmultiple neurotransmitter derangement. Dysexecutive symptoms in the early\nstages of PD may benefit from dopamine replacement therapy (DRT). Conversely,\nsevere cognitive symptoms in more advanced stages are frequently\naggravated by DRT. In particular, pulsatile stimulation of dopaminergic receptors\nby orally administered levodopa (LD) plays a significant negative role\non cognitive and neuropsychiatric symptoms in advanced PD. The introduction\nof a gel of LD-carbidopa for continuous intestinal administration (LCIG)\nallows marked stabilization of plasma LD concentrations and provides benefit\non motor fluctuations and dyskinesia of significantly greater magnitude than\nconventional oral administration in advanced PD patients. The results from\nseveral preliminary studies suggest that efficacy of LCGI on motor symptoms\nmay be accompanied by good tolerability and potential benefit on several\nnon-motor symptoms, including cognitive impairment. Future studies with\nlonger observation period and larger cohorts are advised to confirm these preliminary\nobservations....
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