Journal of neurology, neurosurgery, and psychiatry
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
Multicenter StudyBrain lesion distribution criteria distinguish MS from AQP4-antibody NMOSD and MOG-antibody disease.
Neuromyelitis optica spectrum disorders (NMOSD) can present with very similar clinical features to multiple sclerosis (MS), but the international diagnostic imaging criteria for MS are not necessarily helpful in distinguishing these two diseases. ⋯ This study suggests that the brain MRI criteria for differentiating RRMS from NMOSD are sensitive and specific for all phenotypes.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
ReviewNeurodegeneration in multiple sclerosis and neuromyelitis optica.
Multiple sclerosis (MS) and neuromyelitis optica (NMO) are autoimmune demyelinating diseases of the central nervous system (CNS), having distinct immunological and pathological features. They have two pathogenic components, 'inflammation' and 'neurodegeneration', with different degrees of severity and pathogenetic mechanisms. The target antigen of autoimmunity in NMO is the water channel aquaporin-4 (AQP4), and antibodies directed against this antigen result in astrocyte damage. ⋯ Damage of the CNS tissue appears to be amplified by mechanisms that are in part shared by the two conditions and involve oxidative burst activation in microglia/macrophages, mitochondrial damage and axonal energy failure, Wallerian degeneration and meningeal inflammation. However, they appear to differ regarding the nature of the inflammatory response, the type and extent of cortical injury, and the type of astrocyte reaction and damage. Here, we provide a detailed comparison of the pathology between MS and NMO, which may help to define shared and disease-specific mechanisms of neurodegeneration in these diseases.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
ReviewNeuroendocrine abnormalities in Parkinson's disease.
Neuroendocrine abnormalities are common in Parkinson's disease (PD) and include disruption of melatonin secretion, disturbances of glucose, insulin resistance and bone metabolism, and body weight changes. They have been associated with multiple non-motor symptoms in PD and have important clinical consequences, including therapeutics. ⋯ We discuss pathophysiological mechanisms, clinical implications, and pharmacological and non-pharmacological interventions based on the current evidence. We also review recent advances in the field, focusing on the potential targets for development of neuroprotective drugs in Parkinson's disease and suggest future areas for research.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
Randomized Controlled TrialIVIG treatment of mild cognitive impairment due to Alzheimer's disease: a randomised double-blinded exploratory study of the effect on brain atrophy, cognition and conversion to dementia.
To determine the effect of intravenous immunoglobulin (IVIG) on brain atrophy and cognitive function in mild cognitive impairment (MCI) due to Alzheimer's disease (AD). ⋯ This exploratory study provides limited evidence that a short course of IVIG administered in the MCI stage of AD reduces brain atrophy, prevents cognitive decline in LMCI and delays conversion to AD dementia for at least 1 year; however, this effect of IVIG appears to wane by 2 years.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
Posterior lobules of the cerebellum and information processing speed at various stages of multiple sclerosis.
Cerebellar damage has been implicated in information processing speed (IPS) impairment associated with multiple sclerosis (MS) that might result from functional disconnection in the frontocerebellar loop. Structural alterations in individual posterior lobules, in which cognitive functioning seems preponderant, are still unknown. Our aim was to investigate the impact of grey matter (GM) volume alterations in lobules VI to VIIIb on IPS in persons with clinically isolated syndrome (PwCIS), MS (PwMS) and healthy subjects (HS). ⋯ GM volume decrease in posterior lobules (especially vermis VI) was associated with reduced IPS. Our results suggest a significant impact of posterior lobules pathology in corticocerebellar loop disruption resulting in automation and cognitive optimisation lack in MS.