Aktuelle Neurologie 2007; 34: S6-S10
DOI: 10.1055/s-2007-970907
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Gastrointestinale Störungen bei Morbus Parkinson

Gastrointestinal Disturbances in Patients with Parkinson's DiseaseT.  Müller1 , O.  Götze2 , D.  Woitalla1
  • 1Neurologische Klinik, St. Josef-Hospital, Ruhr-Universität Bochum
  • 2Medizinische Klinik I, St. Josef-Hospital, Ruhr-Universität Bochum
Further Information

Publication History

Publication Date:
04 March 2008 (online)

Zusammenfassung

Schon James Parkinson beschrieb gastrointestinale Dysfunktionen wie vermehrtes Speichelaufkommen, Schluckstörungen und chronische Obstipation. Parkinsonpatienten berichten auch über typische dyspeptische Beschwerden wie Übelkeit, Völlegefühl, frühes Sättigungsgefühl, epigastrische Beschwerden, Erbrechen, Sodbrennen und Meteorismus. Diese können auch von der gastrointestinalen Motilität mit verursacht werden. Eine reduzierte Magenentleerung wird sogar als ein prämotorisches Symptom des Morbus Parkinson diskutiert, da eine Verlangsamung der Magenentleerung auch bei unbehandelten Parkinsonpatienten gezeigt werden konnte und ebenso im Bereich des die intestinale motorische Funktion steuernden enterischen Nervensystems Lewy-Körperchen gehäuft gefunden wurden. Unklar sind die Effekte, die die Therapie mit Levodopa auf die gastrointestinale Motilität ausübt. Zu diskutieren sind neben einem Serotoninmangel, einerseits durch verminderte Aufnahme von Tryptophan oder Abbau von Levodopa zu Dopamin in gastrointestinalen serotonergen neuronalen Zellen. Dies hat vor dem Hintergrund der 5-HT-Rezeptor-gesteuerten Peristaltik einen hypothetischen Einfluss auf die häufige Manifestation einer chronischen Obstipation bei mit Levodopa behandelten Parkinsonpatienten.

Abstract

Even James Parkinson described gastrointestinal symptoms, such as increased saliva in the mouth, dysphagia and chronic constipation. Patients with Parkinson's disease (PD) also complain about typical dyspeptic symptoms such as nausea, fullness, early satiety epigastric pain, vomiting heartburn and meteorism. These symptoms may also result from reduced gastrointestinal motility. Delayed gastric emptying is even discussed as premotor symptom of PD. This was even shown in untreated PD patients and may result from increased appearance of lewy bodies in the enteric nervous system. The impact of levodopa application on gastrointestinal motility is not well studied, levodopa itself delays gastric emptying. However, long-term levodopa application may hypothetically also impact duodenal, jejunal and caecal motility due to decreased tryptophane uptake, which is the metabolic precursor of 5-HT, or the metabolism of levodopa in 5-HT metabolising gastrointestinal neuronal cells. Both may hypothetically cause decreased gastrointestinal 5-HT levels, which may support onset of chronic constipation, since 5-HT stimulates gastrointestinal motility. Constipation is frequent in levodopa treated PD patients.

Literatur

  • 1 Parkinson J. An Essay on the Shaking Palsy. London; Sherwood Neely and Jones 1817
  • 2 Muller T. Drug treatment of non-motor symptoms in Parkinson's disease.  Expert Opin Pharmacother. 2002;  3 381-388
  • 3 Quigley E M. Gastrointestinal dysfunction in Parkinson's disease.  Semin Neurol. 1996;  16 245-250
  • 4 Braak H, Rub U, Gai W P, Del Tredici K. Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen.  J Neural Transm. 2003;  110 517-536
  • 5 Braak H, de Vos R A, Bohl J, Del Tredici K. Gastric alpha-synuclein immunoreactive inclusions in Meissner's and Auerbach's plexuses in cases staged for Parkinson's disease-related brain pathology.  Neurosci Lett. 2006;  396 67-72
  • 6 Przuntek H, Müller T, Riederer P. Diagnostic staging of Parkinson's disease: conceptual aspects.  J Neural Transm. 2004;  111 201-216
  • 7 Goetze O, Wieczorek J, Müller T. et al . Impaired gastric emptying of a solid test meal in patients with Parkinson's disease using 13C-sodium octanoate breath test.  Neurosci Lett. 2005;  375 170-173
  • 8 Goetze O, Nikodem A B, Wiezcorek J. et al . Predictors of gastric emptying in Parkinson's disease.  Neurogastroenterol Motil. 2006;  18 369-375
  • 9 Hardoff R, Sula M, Tamir A. et al . Gastric emptying time and gastric motility in patients with Parkinson's disease.  Mov Disord. 2001;  16 1041-1047
  • 10 Loeffler D A, Camp D M, Conant S B. Complement activation in the Parkinson's disease substantia nigra: an immunocytochemical study.  J Neuroinflammation. 2006;  3 29
  • 11 Sulzer D. alpha-synuclein and cytosolic dopamine: stabilizing a bad situation.  Nat Med. 2001;  7 1280-1282
  • 12 Kurlan R, Rothfield K P, Woodward W R. et al . Erratic gastric emptying of levodopa may cause „random” fluctuations of parkinsonian mobility.  Neurology. 1988;  38 419-421
  • 13 Müller T, Erdmann C, Muhlack S. et al . Inhibition of catechol-O-methyltransferase contributes to more stable levodopa plasma levels.  Mov Disord. 2006;  21 332-336
  • 14 Müller T, Russ H. Levodopa, motor fluctuations and dyskinesia in Parkinson's disease.  Expert Opin Pharmacother. 2006;  7 1715-1730
  • 15 Müller T, Erdmann C, Bremen D. et al . Impact of gastric emptying on levodopa pharmacokinetics in Parkinson disease patients.  Clin Neuropharmacol. 2006;  29 61-67
  • 16 Woitalla D, Götze O, Kim J I. et al . Levodopa availability improves with progression of Parkinson's disease.  J Neurol. 2006;  253 1221-1226
  • 17 Nyholm D. Pharmacokinetic optimisation in the treatment of Parkinson's disease: an update.  Clin Pharmacokinet. 2006;  45 109-136
  • 18 Müller T, Erdmann C, Muhlack S. et al . Pharmacokinetic behaviour of levodopa and 3-O-methyldopa after repeat administration of levodopa/carbidopa with and without entacapone in patients with Parkinson's disease.  J Neural Transm. 2006;  113 1441-1448
  • 19 Nissinen E, Tuominen R, Perhoniemi V, Kaakkola S. Catechol-O-methyltransferase activity in human and rat small intestine.  Life Sci. 1988;  42 2609-2614
  • 20 Muhlack S, Woitalla D, Welnic J. et al . Chronic levodopa intake increases levodopa plasma bioavailability in patients with Parkinson's disease.  Neurosci Lett. 2004;  363 284-287
  • 21 Müller T, Werne B, Fowler B, Kuhn W. Nigral endothelial dysfunction, homocysteine, and Parkinson's disease [letter].  Lancet. 1999;  354 126-127
  • 22 Gershon M D. Review article: serotonin receptors and transporters - roles in normal and abnormal gastrointestinal motility.  Aliment Pharmacol Ther. 2004;  20, Suppl 7 3-14
  • 23 Müller T, Muhlack S. Acute levodopa intake and associated cortisol decrease in patients with Parkinson disease.  Clin Neuropharmacol. 2007;  30 101-106
  • 24 Nicholson S L, Brotchie J M. 5-hydroxytryptamine (5-HT, serotonin) and Parkinson's disease - opportunities for novel therapeutics to reduce the problems of levodopa therapy.  Eur J Neurol. 2002;  9, Suppl 3 1-6
  • 25 Wade P R, Cowen T. Neurodegeneration: a key factor in the ageing gut.  Neurogastroenterol Motil. 2004;  16, Suppl 1 19-23
  • 26 Singaram C, Ashraf W, Gaumnitz E A. et al . Dopaminergic defect of enteric nervous system in Parkinson's disease patients with chronic constipation.  Lancet. 1995;  346 861-864
  • 27 Takahashi H, Wakabayashi K. The cellular pathology of Parkinson's disease.  Neuropathology. 2001;  21 315-322
  • 28 Wakabayashi K, Takahashi H, Takeda S. et al . Parkinson's disease: the presence of Lewy bodies in Auerbach's and Meissner's plexuses.  Acta Neuropathol (Berl). 1988;  76 217-221
  • 29 Wakabayashi K, Takahashi H, Takeda S. et al . Lewy bodies in the enteric nervous system in Parkinson's disease.  Arch Histol Cytol. 1989;  52, Suppl 191-194
  • 30 Wakabayashi K, Takahashi H, Ohama E, Ikuta F. Parkinson's disease: an immunohistochemical study of Lewy body-containing neurons in the enteric nervous system.  Acta Neuropathol (Berl). 1990;  79 581-583

Prof. Dr. Thomas Müller

Neurologische Klinik, St. Josef-Hospital, Ruhr-Universität Bochum

Gudrunstraße 56

44791 Bochum

Email: thomas.mueller@ruhr-uni-bochum.de

    >