Therapeutic Value of Exercise Training in Parkinson's Disease
Department of Clinical Neurosciences, King's College Hospital, London, United Kingdom. Medicine & Science in Sports & Exercise
(Impact Factor: 3.98).
12/1999; 31(11):1544-9. DOI: 10.1097/00008483-200005000-00012
The objective of this study was to investigate the influence of an intensive exercise training on motor disability, mood, and subjective well-being in parkinsonian patients.
The study was designed as an open long-term pilot trial over 20 wk. Sixteen slightly to moderately affected idiopathic parkinsonian patients (PD) were included. An intensive standardized exercise training was performed twice weekly over 14 wk in all patients. Evaluations were performed before the start of the study (exam. 1), after 7 wk (exam 2), 14 wk (exam 3), and 20 wk (exam 4/long-term effect). The test battery included: 1) basic motor test (BMT) [test for muscle strength, flexibility, and coordination]; 2) Unified Parkinson's Disease Rating Scale (UPDRS) and Columbia University Rating Scale (CURS) for PD-specific motor disability; and 3) registration of psychometric data by Mini Mental State (MMS) for dementia and the Adjective Mood Questionnaire of Zeersen (AMQZ) and Sickness Impact Profile (SIP) for subjective well-being.
UPDRS sigma score (P < 0.0001), CURS sigma score (P < 0.0001) and BMT 2 score (P < 0.0001) improved significantly by exercise training. Six weeks after termination of the training program, the majority of the patients had lost only minor components of their regained motor skills. There was no significant change in cognitive function during the study. The results of open interviews referring to subjective well-being were confirmed by the AMQZ and SIP. As an unexpected side effect, dyskinesias seemed to be better controlled.
Motor disability as well as mood and subjective well-being can be clearly improved by intensive sports activities in early to medium stage PD patients. A sustained ongoing benefit outlasting the active training period for at least 6 wk can be achieved but the exact duration of this benefit is open.
Available from: Pei Zhang
- "Exercise reduces the level of systemic inflammation by increasing the release of adrenaline, cortisol, growth hormone, prolactin, and other factors that have immunomodulatory effects and decreasing expression of toll-like receptors at the surface of monocytes, which have been suggested to be involved in mediating systemic inflammation [97–99]. Many results of the present research synthesis support the fact that the patients with PD improve their physical performance, activities of daily living [100, 101], and the effect of pharmacologic therapy  through exercise. The transcriptional coactivator PGC1α controls muscle plasticity and suppresses chronic systemic inflammation via repressing FOXO3 activity, increasing vascularization, ROS detoxification, and mitochondrial and metabolic gene expression . "
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ABSTRACT: Metabolic syndrome is becoming commoner due to a rise in obesity rates among adults. Generally speaking, a person with metabolic syndrome is twice as likely to develop cardiovascular disease and five times as likely to develop diabetes as someone without metabolic syndrome. Increasing oxidative stress in metabolic syndrome and Parkinson's disease is mentioned in the comprehensive articles; however, the system review about clear relation between metabolic syndrome and Parkinson's disease is deficient. In this review, we will focus on the analysis that the metabolic syndrome may be a risk factor for Parkinson's disease and the preventions that reduce the incident of Parkinson's disease by regulating the oxidative stress.
Available from: Micaela Morelli
- "However, recent meta-analysis studies have suggested that the effects of physical activity in PD patients, although clinically significant, are often small and involve a limited number of motor symptoms (Lima et al. 2013). Nevertheless , physical activity seems to impact both motor impairment and motor complications, as an amelioration of LID has been reported in patients undergoing intensive physical training (Reuter et al. 1999, 2000). Importantly, physical activity seems not to affect the pharmacokinetics of L-DOPA (Goetz et al. 1993; Reuter et al. 2000). "
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ABSTRACT: Dopamine replacement therapy in Parkinson's disease is associated with several unwanted effects, of which dyskinesia is the most disabling. The development of new therapeutic interventions to reduce the impact of dyskinesia in Parkinson's disease is therefore a priority need. This review summarises the key molecular mechanisms that underlie dyskinesia. The role of dopamine receptors and their associated signaling mechanisms including DARPP-32, ERK, mTOR, MSK-1 and Histone H3 are summarised, along with an evaluation of the role of cannabinoid and nicotinic acetylcholine receptors. The role of synaptic plasticity, and animal behavioural results on dyskinesia are also evaluated. The most recent therapeutic advances to treat Parkinson's disease are discussed, with emphasis on the possibilities and limitations of non pharmacological interventions such as physical activity, deep brain stimulation, transcranial magnetic field stimulation and cell replacement therapy. The review suggests new prospects for the management of Parkinson's disease-associated motor symptoms, especially the development of dyskinesia.This article is protected by copyright. All rights reserved.
Available from: Nicola Simola
- "Therefore, the performance of movement might itself play a role in the emergence of abnormal motor responses caused by DRT. Interestingly, studies in both dopamine-denervated experimental animals and PD patients provide support to this view, by showing that physical activity may influence the severity of abnormal motor responses triggered by repeated administration of dopaminergic drugs (Reuter et al., 1999, 2000; Frazzitta et al., 2012; Aguiar et al., 2013). Moreover, recent evidence obtained in an experimental model of abnormal motor responses in hemiparkinsonian rats has provided a direct demonstration of an important role of movement performance in the emergence of these untoward effects (Simola et al., 2009; Frau et al., 2013). "
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ABSTRACT: Abnormal involuntary movements (AIMs) and dyskinesias elicited by drugs that stimulate dopamine receptors in the basal ganglia are a major issue in the management of Parkinson's disease (PD). Preclinical studies in dopamine-denervated animals have contributed to the modeling of these abnormal movements, but the precise neurochemical and functional mechanisms underlying these untoward effects are still elusive. It has recently been suggested that the performance of movement may itself promote the later emergence of drug-induced motor complications, by favoring the generation of aberrant motor memories in the dopamine-denervated basal ganglia. Our recent results from hemiparkinsonian rats subjected to the priming model of dopaminergic stimulation are in agreement with this. These results demonstrate that early performance of movement is crucial for the manifestation of sensitized rotational behavior, indicative of an abnormal motor response, and neurochemical modifications in selected striatal neurons following a dopaminergic challenge. Building on this evidence, this paper discusses the possible role of movement performance in drug-induced motor complications, with a look at the implications for PD management.
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