Hostname: page-component-848d4c4894-2pzkn Total loading time: 0 Render date: 2024-05-08T20:20:41.614Z Has data issue: false hasContentIssue false

Electrogastrography in Patients with Parkinson’s Disease

Published online by Cambridge University Press:  02 December 2014

T. Naftali
Affiliation:
Department of Neurology, Meir General Hospital Kfar Saba and the Sackler Faculty of Medicine, Tel-Aviv University, Israel
N. Gadoth
Affiliation:
Department of Neurology, Meir General Hospital Kfar Saba and the Sackler Faculty of Medicine, Tel-Aviv University, Israel
M. Huberman
Affiliation:
Department of Gastroenterology, Meir General Hospital Kfar Saba and the Sackler Faculty of Medicine, Tel-Aviv University, Israel
B. Novis
Affiliation:
Department of Gastroenterology, Meir General Hospital Kfar Saba and the Sackler Faculty of Medicine, Tel-Aviv University, Israel
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Impaired gastrointestinal motility in Parkinson’s disease may affect absorption of levodopa and contribute to the disabling response fluctuations (RF). In this study gastric myoelectric activity was recorded with electrogastrography in patients with PD and correlated with the duration, severity and the presence of RF.

Method:

Electrogastrography (EGG) was performed in 36 patients with PD of which 22 were men. The mean age was 67 years (48-81), mean duration of disease was 7.07 years (1-20), and mean duration of treatment with levodopa was 5.07 years (1-20). Gastric dysrrythmia was diagnosed when either preprandial or postprandial dysrrythmia for more than 30% of the recording period was detected.

Results:

The EGG was abnormal in 24 of 36 patients. Significant association was found between preprandial dysrrythmia and duration of disease (P=0.002); duration of levodopa treatment (P=0.003), severity of 86RF (P=0.001), but not with age (P=0.076). Out of 18 patients with RF, 17 had at least one pattern of dysrrythmia. In 11 out of the 18 patients without RF, the EGG was normal while the remaining seven had at least one pattern of dysrrythmia.

Conclusion:

Abnormal EGG was quite common in this group of patients with PD, particularly in those with RF. The most common pattern of abnormality was preprandial dysrrythmia, which was positively associated with disease duration and length of levodopa treatment. Although frequently asymptomatic, preprandial dysrrythmia leading to impaired gastric emptying may contribute to irregular absorption of levodopa from the small intestine and contribute to disabling response fluctuations.

Résumé:

RÉSUMÉ:Introduction:

Une altération de la motilité gastro–intestinale dans la maladie de Parkinson (MP) peut perturber l’absorption de la lévodopa et contribuer aux fluctuations motrices (FM) observées. Dans cette étude, l’activité myoélectrique gastrique a été enregistrée au moyen de l’électrogastrographie (ÉGG) chez des patients atteints de MPet les données recueillies ont été corrélées à la durée, à la sévérité et à la présence de FM.

Méthode:

Trente–six patients, 22 hommes et 14 femmes, atteints de MP ont subi une ÉGG. L’âge moyen des patients était de 67 ans (48 à 81 ans), la durée moyenne de la maladie était de 7,07 ans (1 à 20 ans) et la durée moyenne du traitement par la lévodopa était de 5,07 ans (1 à 20 ans). On posait un diagnostic de dysrythmie gastrique quand l’enregistrement démontrait une dysrythmie pendant 30% ou plus de la période d’enregistrement, soit en période préprandiale ou postprandiale.

Résultats:

L’ÉGG était anormal chez 24 des 36 patients. Une association significative a été observée entre la dysrythmie préprandiale et la durée de la maladie (p = 0,002), la durée du traitement par la lévodopa (p = 0,014), la sévérité de la FM (p = 0,047). Aucune association avec l’âge n’a été observée (p = 0,1). Parmi les 18 patients ayant des FM, 17 avaient des signes de dysrythmie. Chez 11 des 18 patients sans FM, l’ÉGG était normal alors que les 7 autres avaient des signes de dysrythmie.

Conclusion:

Un enregistrement ÉGG anormal était fréquemment observé dans ce groupe de patients atteints de la MP, particulièrement chez ceux qui ont des FM. Le tableau le plus fréquent était une dysrythmie préprandiale associée de façon positive à la durée de la maladie et du traitement par la lévodopa. Bien qu’elle soit fréquemment asymptomatique, la dysrythmie préprandiale entraînant une altération de la vidange gastrique peut contribuer à une absorption irrégulière de la lévodopa au niveau de l’intestin grêle et contribuer aux FM invalidantes.

Type
Original Articles
Copyright
Copyright © The Canadian Journal of Neurological 2014

References

1. Djaldetti, R, Baron, J, Ziv, I, Melamed, E. Gastric emptying inParkinson’s disease: patients with and without response fluctuations. Neurology 1996; 46:10511054.Google Scholar
2. Soykan, I, Lin, Z, Bennett, JP, McCallum, RW. Gastric myoelectricalactivity in patients with Parkinson’s disease: evidence for a primary gastric abnormality. Dig Dis Sci 1999;44:927931.CrossRefGoogle ScholarPubMed
3. Krygowska Wajs, A, Lorens, K, Thor, P, Szezudlic, A, Konturek, S. Gastric electromechanical dysfunction in Parkinson’s disease. Func Neurol 2000;15:4146.Google ScholarPubMed
4. Bassotti, G, Maggio, D, Battaglia, E. Manometric investigation ofanorectal function in early and late stage Parkinson’s disease. J Neurol Neurosurg Psychiat 2000;68:768770.Google Scholar
5. Qualman, SJ, Haupt, HM, Yang, P, Hamilton, SR. Esophageal Lewybodies associated with ganglion cell loss in achalasia. Similarity to Parkinson’s disease. Gastroenterology 1984; 87:848856.CrossRefGoogle Scholar
6. Wakabayashi, K, Takahashi, H, Takeda, S, Ohama, E, Ikuta, F. Parkinson’s disease: the presence of Lewy bodies in Auerbach’s and Meissner’s plexuses. Acta Neuropathol 1988;76:217221.Google Scholar
7. Kupsky, WJ, Grimes, MM, Sweeting, J, Bertsch, R, Cote, LJ. Parkinson’s disease and megacolon: concentric hyaline inclusions (Lewy bodies) in enteric ganglion cells. Neurology 1987;37:12531255.Google Scholar
8. Edwards, LL, Quigley, EMM, Pfeiffer, RF. Gastrointestinaldysfunction in Parkinson’s disease: frequency and pathophysiology. Neurology 1992;42:726732.Google Scholar
9. Rivera-Calimlim, L, Dujovne, CA, Bianchine, JR, Lasagna, L. L-dopaabsorption and metabolism by the human stomach. J Clin Invest 1970;49:79a.Google Scholar
10. Kurlan, R, Nutt, JG, Woodward, WR, et al. Duodenal and gastricdelivery of levodopa in Parkinsonism. Ann Neurol 1988; 23:589595.Google Scholar
11. Berstad, A, Hausken, T, Giljia, OH, et al. Ultrasonography of thehuman stomach. Scand J Gastroenterol (Suppl.) 1996; 220:7582.Google Scholar
12. Azpiroz, F. Gastric neurology: evolving concepts and techniques. Eur J Gastroenterol Hepatol, 1998;10:733735 CrossRefGoogle ScholarPubMed
13. Poitras, P, Picard, M, Dery, R, et al. Evaluation of gastric emptyingfunction in clinical practice. Dig Dis Sci 1997; 42:21832189.CrossRefGoogle ScholarPubMed
14. Sanders, KM. A case for interstitial cells of Cajal as pacemakers andmediators of neurotransmission in the gastrointestinal tract. Gastroenterol 1996; 111:492515.Google Scholar
15. Hamilton, JW, Bellaahsene, BE, Reichelderfer, M, Webster, J, Bass, P. Human electrogastrograms: Comparison of surface and mucosal recordings. Dig Dis Sci, 1986; 31:3339.Google Scholar
16. Smout, AJPM, Van der Schee, EJ, Grashuis, JL. What is measured inelectrogastrography? Dig Dis Sci, 1980;25:179187.Google Scholar
17. Mintchev, MP, Stickel, A, Bowes, KL. Comparative assessment ofpower dynamics of gastric electrical activity. Dig Dis Sci 1997; 42:11541157.Google Scholar
18. Chen, JZ, McCallum, RW. Electrogastrography: measurements,analysis and prospective applications. Med Biol Eng Comput 1991; 29:339350.Google Scholar
19. Bortolotti, M. Electrogastrography: a seductive promise, onlypartially kept. Am J Gastroenterol 1998; 93 (10):17911794.Google Scholar
20. Levanon, D, Zhang, M, Chen, JDZ. Efficiency and efficacy of theelectrogastrogram. Dig Dis Sci 1998;43:10231030.CrossRefGoogle Scholar
21. Chase, TN, Fabbrini, G, Juncos, JL, Mouradian, MM. Motor responsecomplications with chronic levodopa therapy. In: Streifler, MB, Korczyn, AD, Melamed, E, Youdim, MBH (Eds.) Advanced Neurology Vol 53: Parkinson’s Disease: Anatomy, Pathology and Therapy. New York: Raven Press, 1990:377381.Google Scholar
22. Sage, JL, Trooskin, S, Sonsalla, PK, Heikkila, R, Duvoisin, RC. Longterm duodenal infusion of levodopa for motor fluctuations inParkinsonism. Ann Neurol 1988; 24:8789.Google Scholar
23. Hardoff, R, Sula, M, Tamir, A, et al. Gastric emptying time and gastricmotility in patients with Parkinson’s disease. Mov Disord 2001;16:10411047.Google Scholar