An early diagnosis is not the same as a timely diagnosis of Parkinson's disease

referee-status: Indexed referee-response-35490: 10.5256/f1000research.15815.r35490, Matthew J. Farrer, Djavad Mowafhagian Centre for Brain, University of British Columbia, Vancouver, British Columbia, Canada, 18 Jul 2018, version 1, indexed referee-response-35489: 10.5256/f1000research.15815.r35489, Mayela Rodriguez-Violante, Movement Disorders Clinic, National Institute of Neurology and Neurosurgery, Mexico City, Mexico, 18 Jul 2018, version 1, indexed grant-information: This review was supported by grants from: Parkinson’s UK (G-1606), National Institute for Health Research University College Hospitals Biomedical Research Centre and Bart’s Charity (Preventative Neurology Grant). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. copyright-info: This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.This review was supported by grants from: Parkinson’s UK (G-1606), National Institute for Health Research University College Hospitals Biomedical Research Centre and Bart’s Charity (Preventative Neurology Grant)

Cerebral salt wasting syndrome: Review

Abstract Hyponatremia is the most frequent electrolyte disorder in critically neurological patients. Cerebral salt wasting syndrome (CSW) is defined as a renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. The pathogenesis of this disorder is still not completely understood. Sympathetic responses as well as some natriuretic factors play a role in this syndrome. Distinction between SIADH and CSW might be difficult. The essential point is the volemic state. It is necessary to rule out other intermediate causes. Treatment requires volume replacement and maintenance of a positive salt balance. Mineral corticoids may be useful in complicated cases

Colonic Oxidative and Mitochondrial Function in Parkinson’s Disease and Idiopathic REM Sleep Behavior Disorder

Objective. To determine potential mitochondrial and oxidative alterations in colon biopsies from idiopathic REM sleep behavior disorder (iRBD) and Parkinson’s disease (PD) subjects. Methods. Colonic biopsies from 7 iRBD subjects, 9 subjects with clinically diagnosed PD, and 9 healthy controls were homogenized in 5% w/v mannitol. Citrate synthase (CS) and complex I (CI) were analyzed spectrophotometrically. Oxidative damage was assessed either by lipid peroxidation, through malondialdehyde and hydroxyalkenal content by spectrophotometry, or through antioxidant enzyme levels of superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (Gpx1), and catalase (CAT) by western blot. The presence of mitochondrial DNA (mtDNA) deletions was assessed by long PCR and electrophoresis. Results. Nonsignificant trends to CI decrease in both iRBD (45.69±18.15; 23% decrease) and PD patients (37.57±12.41; 37% decrease) were found compared to controls (59.51±12.52, p: NS). Lipid peroxidation was maintained among groups (iRBD: 27.46±3.04, PD: 37.2±3.92, and controls: 31.71±3.94; p: NS). Antioxidant enzymes SOD2 (iRBD: 2.30±0.92, PD: 1.48±0.39, and controls: 1.09±0.318) and Gpx1 (iRBD 0.29±0.12, PD: 0.56±0.33, and controls: 0.38±0.16) did not show significant differences between groups. CAT was only detected in 2 controls and 1 iRBD subject. One iRBD patient presented a single mtDNA deletion