Complementary therapies are an essential component of the treatment of patients with Parkinson's disease. They aim to ameliorate disease symptoms in conjunction with dopamine substitution. Kinesiology trains about the effective use of physical, mental and emotional skills. Objectives of this pilot study were to demonstrate the efficacy of a standardised kinesiology programme in 20 patients with Parkinson's disease. They were on a stable drug regimen during the whole trial. Ten patients received two kinesiology sessions per week over a 6-week lasting interval. The remaining ten patients were only followed over the same time period without any kinesiology training. We scored disease symptoms, tested cognition and assessed instrumental movement performance at baseline and study end. Kinesiology improved disease symptoms, cognitive abilities and execution of simple but not complex movement series. We show a certain value of a standardised kinesiology programme as adjunct, complementary therapeutic approach in patients with Parkinson's disease.
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http://dx.doi.org/10.1007/s00702-019-02123-8 | DOI Listing |
PLoS One
January 2025
Institute of Psychiatry, Psychology & Neuroscience at King's College London, London, United Kingdom.
Fluctuation-related pain (FRP) affects more than one third of people with Parkinson's disease (PwP, PD) and has a harmful effect on health-related quality of life (HRQoL), but often remains under-reported by patients and neglected by clinicians. The National Institute for Health and Care Excellence (NICE) recommends The Parkinson KinetiGraphTM (the PKGTM) for remote monitoring of motor symptoms. We investigated potential links between the PKGTM-obtained parameters and clinical rating scores for FRP in PwP in an exploratory, cross-sectional analysis of two prospective studies: "The Non-motor International Longitudinal, Real-Life Study in PD-NILS" and "An observational-based registry of baseline PKG™ in PD-PKGReg".
View Article and Find Full Text PDFOper Neurosurg (Hagerstown)
September 2024
Department of Neurology, Washington University in St Louis, St Louis, Missouri, USA.
Background And Objectives: Surgical planning is critical to achieve optimal outcome in deep brain stimulation (DBS). The relationship between clinical outcomes and DBS electrode position relative to subthalamic nucleus (STN) is well investigated, but the role of surgical trajectory remains unclear. We sought to determine whether preoperatively planned DBS lead trajectory relates to adequate motor outcome in STN-DBS for Parkinson's disease (PD).
View Article and Find Full Text PDFAnn Clin Transl Neurol
January 2025
Department of Neurology, Movement Disorders Program, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Uniparental isodisomy (UPiD) can cause mixed phenotypes of imprinting disorders and autosomal-recessive diseases. We present the case of a 3-year-old male with a blended phenotype of TECPR2-related hereditary sensory and autonomic neuropathy (HSAN9) and Temple syndrome (TS14) due to maternal UPiD of chromosome 14, which includes a loss-of-function founder variant in the TECPR2 gene [NM_014844.5: c.
View Article and Find Full Text PDFNeurol Genet
December 2024
From the Division of Neurology (A.H.T., S.-Y.L.), Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Programa de Pós-Graduação em Ciências Médicas da Universidade Federal do Rio Grande do Sul (P.S.-A.), Clínica Santa María, Santiago, Chile; Departamento de Farmacologia (A.F.S.S.), Universidade Federal do Rio Grande do Sul; Serviço de Neurologia (A.F.S.S.), Hospital de Clínicas de Porto Alegre, Brazil; Institute of Neurogenetics (H.M., M.L.D., C.K.), University of Lübeck, Germany; Department of Biomedical Science (A.A.-A.), Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; The Michael J. Fox Foundation for Parkinson's Research (J.S., B.F.), New York; Department of Medical and Molecular Genetics (C.E.W.), Indiana University, Indianapolis; Department of Neuroscience and Brain Health (M.L.D.), Metropolitan Medical Center, Manila, Philippines; Centre for Preventive Neurology (S.D., M.T.P., A.J.N.), Wolfson Institute of Population Health, Queen Mary University of London, United Kingdom; Unidad de Trastornos del Movimiento (M.T.P.), Servicio de Neurología y Neurofisiología Clínica, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Spain; Laboratory of Neurogenetics (M.B.M.), National Institute on Aging, National Institutes of Health, Bethesda, MD; Department of Clinical and Movement Neurosciences (M.B.M., H.R.M.), UCL Queen Square Institute of Neurology, University College London, United Kingdom; Department of Neurology (R.N.A.), Columbia University Irving Medical Center, New York; Movement Disorders Division (R.N.A.), Neurological Institute, Tel Aviv Sourasky Medical Center and Tel Aviv School of Medicine, Tel Aviv University, Israel; Molecular Medicine Laboratory and Neurology Department (K.R.K.), Concord Clinical School, Concord Repatriation General Hospital, The University of Sydney; Translational Neurogenomics Group (K.R.K.), Genomic and Inherited Disease Program, Garvan Institute of Medical Research; and St Vincent's Healthcare Campus (K.R.K.), Faculty of Medicine, UNSW Sydney, Darlinghurst, New South Wales, Australia.
Background And Objectives: In the era of precision medicine, genetic test results have become increasingly relevant in the care of patients with Parkinson disease (PD). While large research consortia are performing widespread research genetic testing to accelerate discoveries, debate continues about whether, and to what extent, the results should be returned to patients. Ethically, it is imperative to keep participants informed, especially when findings are potentially actionable.
View Article and Find Full Text PDFPharmacol Res Perspect
February 2025
New Drug Development Center, Daegu, Korea.
Oxidation of dopamine can cause various side effects, which ultimately leads to cell death and contributes to Parkinson's disease (PD). To counteract dopamine oxidation, newly synthesized dopamine is quickly transported into vesicles via vesicular monoamine transporter 2 (VMAT2) for storage. VMAT2 expression is reduced in patients with PD, and studies have shown increased accumulation of dopamine oxidation byproducts and α-synuclein in animals with low VMAT2 expression.
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