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Respiratory Muscle Performance and the Perception of Dyspnea in Parkinson's Disease

Published online by Cambridge University Press:  02 December 2014

Paltiel Weiner ,
Rivka Inzelberg ,
Avi Davidovich ,
Puiu Nisipeanu ,
Rasmi Magadle ,
Noa Berar-Yanay  and
Ralph L. Carasso
Paltiel Weiner
Affiliation:
Department of Medicine, Hillel Yaffe Medical Center, Hadera, Israel
Rivka Inzelberg
Affiliation:
Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel
Avi Davidovich
Affiliation:
Department of Medicine, Hillel Yaffe Medical Center, Hadera, Israel
Puiu Nisipeanu
Affiliation:
Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel
Rasmi Magadle
Affiliation:
Department of Medicine, Hillel Yaffe Medical Center, Hadera, Israel
Noa Berar-Yanay
Affiliation:
Department of Medicine, Hillel Yaffe Medical Center, Hadera, Israel
Ralph L. Carasso
Affiliation:
Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel
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Abstract

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Background:

Pulmonary and respiratory muscle function impairment are common in patients with Parkinson's disease (PD). However, dyspnea is not a frequent complaint among these patients, although it is well documented that the intensity of dyspnea is related to the activity and the strength of the respiratory muscles.

Patients and Methods:

We studied pulmonary function, respiratory muscle strength and endurance and the perception of dyspnea (POD) in 20 patients with PD (stage II and III Hoehn and Yahr scale) before and after their first daily L-dopa dose. Respiratory muscle strength was assessed by measuring the maximal inspiratory and expiratory mouth pressures (PImax and PEmax), at residual volume (RV) and total lung capacity (TLC) respectively. The POD was measured while the subject breathed against progressive load and dyspnea was rated using a visual analog scale.

Results:

Respiratory muscle strength and endurance were decreased and the POD was increased during the off medication period compared to normal subjects. There was a nonsignificant trend to an increase in PImax, PEmax and endurance after L-dopa intake. The POD of PD patients decreased (p<0.05) following medication, although, it remained increased (p<0.01) as compared to the normal subjects. Even if patients had spirometry data showing a mild restrictive pattern, before medication, both forced vital capacity (FVC) and forced expiratory volume (FEV)1 remained almost identical after L-dopa intake.

Conclusions:

Patients with PD have higher POD, compared to normal subjects and this increased perception is attenuated when the patients are on dopaminergic medication. The change in the POD is not related to changes in respiratory muscle performance or pulmonary functions. A central effect or a correction of uncoordinated respiratory movements by L-dopa may contribute to the decrease in POD following L-dopa treatment.

Résumé:

RÉSUMÉ:Introduction:

L'altération de la fonction pulmonaire et des muscles respiratoires est fréquente chez les patients atteints de la maladie de Parkinson (MP). Cependant, ces patients se plaignent rarement de dyspnée, bien qu'il soit bien connu que l'intensité de la dyspnée est reliée à l'activité et à la force des muscles respiratoires. Patients et

Méthodes:

Nous avons étudié la fonction pulmonaire, la force des muscles respiratoires, ainsi que l'endurance et la perception de la dyspnée (PD) chez 20 patients atteints de MP (stage II et III à l'échelle de Hoehn et Yahr) avant et après la première prise de L-dopa de la journée. La force des muscles respiratoires a été évaluée par la mesure buccale des pressions inspiratoires et expiratoires maximales (Plmax et PEmax), au VR et à la CT respectivement. La PD a été mesurée pendant que le sujet respirait contre une charge progressive. Il évaluait sa dyspnée au moyen d'une échelle visuelle analogue.

Résultats:

La force des muscles respiratoires et l'endurance étaient diminuées et la PD était augmentée pendant la période sans effet médicamenteux par rapport à des sujets normaux. On a observé une tendance non significative à l'augmentation des Plmax, PEmax et de l'endurance après la prise de L-dopa. La PD a diminué (p(0.05), tout en demeurant plus élevée comparée à celle des sujets normaux (p(0.01). Même si on observait un patron légèrement restrictif à la spirométrie des patients avant la prise du médicament, le CVF et la VEMS sont demeurés presque inchangés après.

Conclusions:

Les patients atteints de la MP ont plus de PD comparés aux sujets normaux et cette perception augmentée est atténuée quand les patients sont sous médication dopaminergique. Le changement de la PD n'est pas relié aux changements de performance des muscles respiratoires ou à la fonction pulmonaire. Un effet central ou une correction des mouvements respiratoire incoordonnés par la L-dopa peuvent contribuer à la diminution de la PD suite à l'administration de L-dopa.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 29 , Issue 1 , February 2002 , pp. 68 - 72
Copyright
Copyright © Canadian Neurological Sciences Federation 2002

References

1. Marsden, CD. Parkinson’s disease. J Neurol Neurosurg Psychiatry 1994; 57:672–681.Google Scholar
2. Obenour, WH, Stevens, PM, Cohen, AA, et al. The causes ofabnormal pulmonary function in Parkinson’s disease. Am Rev Respir Dis 1972; 105:382–387.Google Scholar
3. Lilker, ES, Woolf, CR. Pulmonary function in Parkinson’s syndrome:the effect of thalamotomy. Can Med Assoc J 1968; 99:752–757.Google Scholar
4. Vincken, WG, Gauthier, SG, Dollfuss, RE, et al. Involvement ofupper-airway muscles in extrapyramidal disorders: a cause of airflow limitation. N Engl J Med 1984; 311:438–442.CrossRefGoogle ScholarPubMed
5. Sabate, M, Rodriguez, M, Mendez, E, et al. Obstructive and restrictivepulmonary dysfunction increases disability in Parkinson’s disease. Arch Phys Med Rehabil 1996; 77:29–34.Google Scholar
6. Tzelepis, GE, McCool, FD, Fridman, JH, et al. Respiratory muscledysfunction in Parkinson’s disease. Am Rev Respir Dis 1988; 138:266–271.Google Scholar
7. Estenne, M, Hubert, M, DeTroyer, A. Respiratory muscleinvolvement in Parkinson’s disease. N Engl J Med 1984; 311:1516.Google Scholar
8. De Bruin, FFC, De Bruin, VMS, Lees, AJ, et al. Effects of treatmenton airway dynamics and respiratory muscle strength in Parkinson’s disease. Am Rev Respir Dis 1993;148:1576–1580.CrossRefGoogle Scholar
9. Neu, HC, Connolly, JJ, Schwertley, FW, et al. Obstructive respiratory dysfunction in parkinsonian patients. Am Rev Respir Dis 1967;95:33–47.Google ScholarPubMed
10. Ebmeier, KP, Calder, SA, Crawford, JR, et al. Mortality and causes ofdeath in idiopathic Parkinson’s disease: results from the Aberdeen whole population study. Scott Med J 1990; 35:173–175.Google Scholar
11. Saltin, B, Landin, S. Work capacity, muscle strength and SDHactivity in both legs of hemiparetic patients and patients with Parkinson’s disease. Scand J Clin Lab Invest 1975; 35:531–538.Google Scholar
12. Carter, JH, Nutt, JG, Woodward, WR. The effect of exercise onlevodopa absorption. Neurology 1992;42:2042–2045.CrossRefGoogle Scholar
13. Killian, KG, Campbell, EJM. Dyspnea and exercise. Ann RevPhysiol 1983;445:465–479.Google Scholar
14. Killian, KG, Jones, NL. The use of exercise testing and othermethods in the investigation of dyspnea. Clin Chest Med 1984;5:99–108.Google Scholar
15. Killian, KJ, Gandevia, SC, Summers, E. Effect of increased lungvolume on perception of breathlessness, effort, and tension. J Appl Physiol 1984; 57:686–691.CrossRefGoogle Scholar
16. Hoehn, MM, Yahr, MD. Parkinsonism: onset, progression andmortality. Neurology 1967;17:427–442.Google Scholar
17. Fahn, S, Elton, RL. Members of the UPDRS DevelopmentCommittee. Unified Parkinson’s Disease Rating Scale. In: Fahn, S, Marsden, CD, Goldstein, M, Calne, DB, eds. Recent Development in Parkinson’s Disease. 2nd Ed. New York: Macmillan 1987:153–163.Google Scholar
18. Black, LF, Hyatt, RE. Maximal respiratory pressures: normal valuesand relationship to age and sex. Am Rev Respir Dis 1969;99:696–702.Google Scholar
19. Nickerson, BG, Keens, TG. Measuring ventilatory muscle endurancein humans as sustainable inspiratory pressure. J Appl Physiol 1982;52:768–772.Google Scholar
20. Martyn, JB, Moreno, RH, Pare, PD, et al. Measurement of inspiratorymuscle performance with incremental threshold loading. Am Rev Respir Dis 1987;135:919–923.CrossRefGoogle Scholar
21. Kikuchi, Y, Okabe, S, Tamura, G, et al. Chemosensitivity andperception of dyspnea in patients with a history of near-fatal asthma. N Engl J Med 1994;330:1329–1334.Google Scholar
22. el-Manshawi, A, Killian, KJ, Summers, E, et al. Breathlessnessduring exercise with and without resistive load. J Appl Physiol 1986;61:896–905.CrossRefGoogle Scholar
23. Lyall, RA, Reuter, I, Mills, J, et al. Effects of acute subcutaneousapomorphine on respiratory muscle strength in Parkinson’s disease. Mov Disord 1998;13(suppl 2):148.Google Scholar
24. Paulson, GD, Tarfrate, RH. Some “minor” aspects of parkinsonism, especially pulmonary function. Neurology 1970;20(2):14–19.CrossRefGoogle Scholar
25. Bogaard, JM, Hovestadt, A, Meerwaldt, J, et al. Maximal expiratoryand inspiratory flow-volume curves in Parkinson’s disease. Am Rev Respir Dis 1989;139:610–614.Google Scholar
26. American Thoracic Society. Dyspnea. mechanism, assessment, andmanagement: a consensus statement, Am J Respir Crit Care Med 1999;159:321–349.Google Scholar
27. Schwartzstein, RM, Simon, PM, Weiss, JW, et al. Breathlessnessinduced by dissociation between ventilation and chemical drive. Am Rev Respir Dis 1989;139:1231–1237.Google Scholar
28. Schwartzstein, RM, Manning, HL, Weiss, JW, et al. Dyspnea: asensory experience. Lung 1990;168:185–199.Google Scholar
29. Flash, T, Inzelberg, R, Schechtman, E, et al. Kinematic properties ofupper limb trajectories in Parkinson’s disease. Exp Neurol 1992;118:215–226.Google Scholar