Respiratory Dysfunction in Parkinson'S Disease

Torsney, KM; Forsyth, Duncan R.

doi:10.4997/jrcpe.2017.108

Cited by 74 publications

(57 citation statements)

References 30 publications

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“…However, a restrictive pattern of pulmonary dysfunction has been a consistent finding, reported in up to 94% of cases in different studies. This has been attributed to a combination of factors including increased rigidity of the respiratory muscles and chest wall, and reduced lung volumes because of kyphoscoliosis . The response to levodopa in patients with restrictive deficits has been variable, with improved pulmonary function demonstrated in some studies but not in others.…”

Section: Studies Of Pulmonary Function In Pdmentioning

confidence: 99%

“…For example, the term “sensory dyspnea” has been used in PD to refer to the feeling of inability to take a breath in the absence of observable abnormal breathing. These observations lead to further questions regarding the contribution to the genesis of dyspnea of subjective sensory and perceptual changes, such as the threshold for dyspnea and the perception of respiratory load, which have so far received limited attention and warrant further investigation …”

Section: Future Studiesmentioning

confidence: 99%

“…This has been attributed to a combination of factors including increased rigidity of the respiratory muscles and chest wall, and reduced lung volumes because of kyphoscoliosis. 38 The response to levodopa in patients with restrictive deficits has been variable, with improved pulmonary function demonstrated in some studies but not in others. In general, these studies have focused on ventilatory capacity and lung volumes, and there is a striking lack of studies evaluating central ventilatory responses as a potential mechanism for dyspnea.…”

Section: Studies Of Pulmonary Function In Pdmentioning

confidence: 99%

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Brainstem Ventilatory Dysfunction: A Plausible Mechanism for Dyspnea in Parkinson's Disease?

et al. 2020

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Dyspnea is an under‐recognized and debilitating symptom that is reported in up to 40% of patients with Parkinson's disease and may have multiple origins. Despite its frequency, it is poorly researched, and there is a general lack of understanding of the pathophysiology of dyspnea and respiratory dysfunction in PD. Consequently, a number of PD patients are labelled as having “unexplained dyspnea.” Studies to date have focused mainly on evaluating ventilatory capacity and lung volumes, and little is known about the effects of the disease on the medullary and pontine ventilatory control centers within the brainstem. This is of particular relevance in view of neuropathological studies demonstrating early involvement of the dorsal medulla and other brainstem structures by the disease process. The possibility that impaired brainstem ventilatory control is a contributory mechanism for dyspnea and could be a premotor manifestation in some PD patients therefore warrants further attention. This review focuses on clinical, pathological, and experimental evidence for the involvement of brainstem respiratory centers in PD. We highlight the need for further research, particularly in PD patients with unexplained dyspnea. © 2020 International Parkinson and Movement Disorder Society

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Section: Studies Of Pulmonary Function In Pdmentioning

confidence: 99%

Section: Future Studiesmentioning

confidence: 99%

Section: Studies Of Pulmonary Function In Pdmentioning

confidence: 99%

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Brainstem Ventilatory Dysfunction: A Plausible Mechanism for Dyspnea in Parkinson's Disease?

et al. 2020

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“…The lungs are one of the most sensitive organs in the body; however, few studies have described the negative changes and impact on the lungs during the development of PD (Baille et al, 2018;Seccombe et al, 2011;Torsney & Forsyth, 2017).…”

Section: Impairment Of Lung Properties In Pd Micementioning

confidence: 99%

“…Breathing problems are recognized as a cause of morbidity and mortality in patients with Parkinson's disease (PD), caused by neural damage in specific regions of the ventral medulla that are responsible for rhythm generation and chemoreception, such as the preBötzinger complex (preBötC) and retrotrapezoid nucleus (RTN), respectively (Baille et al., ; Benarroch, Schmeichel, Low, & Parisi, ; Owolabi, Nagoda, & Babashani, ; Seccombe et al., ; Torsney & Forsyth, ). Previous studies have also found that PD patients showed a reduction of pulmonary volumes and stiffening of respiratory muscles, indicating an impairment directly in the lung, ribcage and/or the muscles responsible for breathing (Baille et al., ; LeWitt et al., ; Owolabi et al., ; Seccombe et al., ).…”

Section: Introductionmentioning

confidence: 99%

Respiratory disturbances in a mouse model of Parkinson's disease

Oliveira

Moriya

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Clinical reports have described and suggested central and peripheral respiratory abnormalities in Parkinson's disease (PD) patients; however, these reports have never addressed the occurrence of these abnormalities in an animal model. What is the main finding and its importance?A mouse model of PD has reduced neurokinin‐1 receptor immunoreactivity in the pre‐Bӧtzinger complex and Phox2b‐expressing neurons in the retrotrapezoid nucleus. The PD mouse has impairments of respiratory frequency and the hypercapnic ventilatory response. Lung collagen deposition and ribcage stiffness appear in PD mice. Abstract Parkinson's disease (PD) is a neurodegenerative motor disorder characterized by dopaminergic deficits in the brain. Parkinson's disease patients may experience shortness of breath, dyspnoea, breathing difficulties and pneumonia, which can be linked as a cause of morbidity and mortality of those patients. The aim of the present study was to clarify whether a mouse model of PD could develop central brainstem and lung respiratory abnormalities. Adult male C57BL/6 mice received bilateral injections of 6‐hydroxydopamine (10 μg μl−1; 0.5 μl) or vehicle into the striatum. Ventilatory parameters were assessed in the 40 days after induction of PD, by whole‐body plethysmography. In addition, measurements of respiratory input impedance (closed and opened thorax) were performed. 6‐Hydroxydopamine reduced the number of tyrosine hydroxylase neurons in the substantia nigra pars compacta, the density of neurokinin‐1 receptor immunoreactivity in the pre‐Bӧtzinger complex and the number of Phox2b neurons in the retrotrapezoid nucleus. Physiological experiments revealed a reduction in resting respiratory frequency in PD animals, owing to an increase in expiratory time and a blunted hypercapnic ventilatory response. Measurements of respiratory input impedance showed that only PD animals with the thorax preserved had increased viscance, indicating that the ribcage could be stiff in this animal model of PD. Consistent with stiffened ribcage mechanics, abnormal collagen deposits in alveolar septa and airways were observed in PD animals. Our data showed that our mouse model of PD presented with neurodegeneration in respiratory brainstem centres and disruption of lung mechanical properties, suggesting that both central and peripheral deficiencies contribute to PD‐related respiratory pathologies.

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Vigorous Aerobic Exercise in the Management of Parkinson Disease: A Systematic Review

Rodríguez

Albillos-Almaraz

López-Aguado

et al. 2020

PM&R

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Objective To summarize the findings from studies examining the effects of vigorous‐intensity aerobic exercise in the management of Parkinson disease. Type Systematic review. Literature Survey PubMed/MEDLINE, EMBASE, Scopus, Web of Science, Cochrane Library, SPORTDiscus, and ScienceDirect databases were searched up to May 2020. Reference lists of the included articles were also searched for additional studies. Searches were restricted to English language. Methodology Seven papers, including six studies, five randomized controlled trials and one controlled trial, were identified. The studies examined the effects of vigorous‐intensity aerobic exercise in participants with Parkinson disease. Studies in which the minimal intensity required was ≥77% of maximum heart rate, 60% of heart rate reserve or 64% of maximal oxygen uptake met the inclusion criteria. Method appraisal showed a mean score of 5.3 in the Physiotherapy Evidence Database (PEDro) scale. Synthesis No statistically significant differences were found between vigorous‐intensity aerobic exercise and moderate/low‐intensity aerobic exercise for the main outcomes (disease severity and motor function). Only one study concluded a significant higher aerobic fitness in favor of the group that exercised at vigorous intensity compared to the moderate intensity group. Conclusions Vigorous‐intensity aerobic exercise has not shown statistically significant improvements in motor and nonmotor impairments in individuals with Parkinson disease as compared to moderate/low‐intensity aerobic exercise. Hence, the current evidence is too limited to allow recommendations for clinical practice.

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Respiratory Dysfunction in Parkinson'S Disease

Cited by 74 publications

References 30 publications

Brainstem Ventilatory Dysfunction: A Plausible Mechanism for Dyspnea in Parkinson's Disease?

Brainstem Ventilatory Dysfunction: A Plausible Mechanism for Dyspnea in Parkinson's Disease?

Respiratory disturbances in a mouse model of Parkinson's disease

Vigorous Aerobic Exercise in the Management of Parkinson Disease: A Systematic Review

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