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Zentrale Schmerzverarbeitung bei Morbus Parkinson

Epidemiologie, Physiologie und experimentelle Befunde zur Schmerzverarbeitung

Central pain processing and Parkinson’s disease

Epidemiology, physiology, and experimental results issuing pain processing

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Zusammenfassung

Der Morbus Parkinson (MP) geht mit einer Degeneration der dopaminergen Neurone in der Substantia nigra (SN) und einer daraus resultierenden Minderfunktion der nigrostriatalen Verbindungen mit den Basalganglien im Zentrum einher. Neben den motorischen Symptomen lassen sich bei einer beträchtlichen Anzahl an Parkinson-Patienten verschiedene Typen von Schmerz, beispielsweise dystoniebedingte muskuloskeletale Schmerzen oder zentrale Schmerzen, sowie Auffälligkeiten in der Schmerzverarbeitung beobachten, die sich möglicherweise in einer erhöhten Schmerzsensibilität manifestieren. Die genauen Ursachen hierfür sind jedoch unklar.

Der vorliegende Artikel gibt daher einen Überblick über einschlägige Studien, die die Anomalien in der Schmerzverarbeitung beim MP größtenteils mittels elektrophysiologischer [Elektroenzephalogramm (EEG), sympathische Hautreaktion (SSR)] und psychophysikalischer Methoden [quantitative sensorische Testung (QST), RIII-Reflexschwelle] untersuchen.

Auf Grundlage der Literatursichtung werden im Dopaminmangel begründete Dysfunktionen der endogenen Schmerzhemmung unter Beteiligung der Basalganglien, besonders des Striatums, aber auch mesolimbischer Areale als wichtige pathophysiologische Mechanismen der Auffälligkeiten in der Schmerzverarbeitung beim MP postuliert.

Abstract

Parkinson’s disease (PD) is caused by degeneration of the dopaminergic neurons in the substantia nigra (SN) and a resulting dysfunction of the nigrostriatal pathways including the basal ganglia. Beside motor symptoms, different types of pain (e.g., dystonic musculoskeletal pain or central pain) occur in a considerable number of patients. In addition, abnormalities in pain processing have been observed in PD patients, which may present as increased pain sensitivity. The pathophysiological mechanisms involved in disturbed pain processing of PD, however, are still poorly understood.

The present article gives an overview of the relevant experimental studies, investigating the abnormalities of pain processing in PD by means of electrophysiological [electroencephalography (EEG), sympathetic skin response (SSR)] and psychophysical methods [quantitative sensory testing (QST), RIII reflex threshold].

Based on a review of the literature, it is postulated that dysfunction in endogenous pain inhibition caused by dopaminergic deficiency in the basal ganglia, especially in the striatum, but also in mesolimbic areas is a main pathophysiological mechanism involved in nociceptive abnormalities in PD.

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Literatur

  1. Altier N, Stewart J (1999) The role of dopamine in the nucleus accumbens in analgesia. Life Sci 65:2269–2287

    Article  PubMed  CAS  Google Scholar 

  2. Barnes C, Fung S, Adams W (1979) Inhibitory effects of substantia nigra on impulse transmission from nociceptors. Elsevier, New York, S 207–215

  3. Beiske A, Loge J, Rønningen A, Svensson E (2009) Pain in Parkinson’s disease: prevalence and characteristics. Pain 141:173–177

    Article  PubMed  CAS  Google Scholar 

  4. Borsook D, Upadhyay J, Chudler E, Becerra L (2010) A key role of the basal ganglia in pain and analgesia – insights gained through human functional imaging. Mol Pain 6:27

    Article  PubMed  Google Scholar 

  5. Brefel-Courbon C, Payoux P, Thalamas C et al (2005) Effect of levodopa on pain threshold in Parkinson’s disease: a clinical and positron emission tomography study. Mov Disord 20:1557–1563

    Article  PubMed  Google Scholar 

  6. Chen KJ, Lin RT, Liu CK et al (2006) Relationship between event-related potentials and frontal-subcortical dysfunction in Parkinson’s disease. Parkinsonism Relat Disord 12:453–458

    Article  PubMed  CAS  Google Scholar 

  7. Chudler E, Dong W (1995) The role of the basal ganglia in nociception and pain. Pain 60:3–38

    Article  PubMed  CAS  Google Scholar 

  8. Coffeen U, Ortega-Legaspi J, Gortari P et al (2010) Inflammatory nociception diminishes dopamine release and increases dopamine D2 receptor mRNA in the rat’s insular cortex. Mol Pain 6:75

    Article  PubMed  Google Scholar 

  9. Cole L, Farrell M, Gibson S, Egan G (2010) Age-related differences in pain sensitivity and regional brain activity evoked by noxious pressure. Neurobiol Aging 31:494–503

    Article  PubMed  Google Scholar 

  10. Djaldetti R, Shifrin A, Rogowski Z et al (2004) Quantitative measurement of pain sensation in patients with Parkinson disease. Neurology 62:2171–2175

    Article  PubMed  CAS  Google Scholar 

  11. Ford B (2010) Pain in Parkinson’s Disease. Mov Disord 25:98–103

    Article  Google Scholar 

  12. Gao HR, Shi TF, Yang CX et al (2010) The effect of dopamine on pain-related neurons in the parafascicular nucleus of rats. J Neural Transm 117:585–591

    Google Scholar 

  13. García-Larrea L, Peyron R, Laurent B, Mauguière F (1997) Association and dissociation between laser-evoked potentials and pain perception. NeuroReport 8:3785–3789

    Article  PubMed  Google Scholar 

  14. Gerdelat-Mas A, Simonetta-Moreau M, Thalamas C et al (2007) Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study. J Neurol Neurosurg Psychiatry 78:1140–1142

    Google Scholar 

  15. Hagelberg N, Martikainen I, Mansikka H et al (2002) Dopamine D2 receptor binding in the human brain is associated with the response to painful stimulation and pain modulatory capacity. Pain 99:272–279

    Article  Google Scholar 

  16. Iannetti G, Hughes N, Lee M, Mouraux A (2008) Determinants of laser-evoked EEG responses: pain perception or stimulus saliency? J Neurophysiol 100:815–828

    Google Scholar 

  17. Jääskeläinen S, Rinne J, Forssell H et al (2001) Role of the dopaminergic system in chronic pain – a fluorodopa-PET study. Pain 90:257–260

    Article  PubMed  Google Scholar 

  18. Kornhuber J, Quack G, Danysz W et al (1995) Therapeutic brain concentration of the NMDA receptor antagonist amantadine. Neuropharmacology 34:713–721

    Article  PubMed  CAS  Google Scholar 

  19. LeBars D, Dickinson AH, Besson JM (1979) Diffuse noxious inhibitory control (DNIC). Effect on dorsal horn convergent neurones in rats. Pain 6:283–304

    Article  CAS  Google Scholar 

  20. Lin M (1981) Activation of striatal dopamine receptors induces pain inhibition in rats. J Neural Transm 51:213–222

    Google Scholar 

  21. McHaffie M, Stanford T, Stein B et al (2005) Subcortical loops through the basal ganglia. Trends Neurosci 28:401–407

    Article  PubMed  CAS  Google Scholar 

  22. Mylius V, Engau I, Teepker M et al (2009) Pain sensitivity and descending inhibition of pain in Parkinson’s disease. J Neurol Neurosurg Psychiatry 80:24–28

    Google Scholar 

  23. Pertovaara A, Martikainen I, Hagelberg N et al (2004) Striatal dopamine D2/D3 receptor availability correlates with individual response characteristics to pain. Eur J Neurosci 20:1587–1592

    Article  PubMed  Google Scholar 

  24. Redgrave P, Coizet V (2007) Brainstem interactions with the basal ganglia. Parkinsonism Relat Disord 13:301–305

    Article  Google Scholar 

  25. Schestasky P, Kumru H, Valls-Solé J et al (2007) Neurophysiologic study of central pain in patients with Parkinson’s disease. Neurology 69:2162–2169

    Article  Google Scholar 

  26. Tassorelli C, Armentero MT, Greco R et al (2007) Behavioral responses and Fos activation following painful stimuli in a rodent model of Parkinson’s disease. Brain Res 1176:53–61

    Article  PubMed  CAS  Google Scholar 

  27. Tiede W, Magerl W, Baumgärtner U et al (2010) Sleep restriction attenuates amplitudes and attentional modulation of pain-related evoked potentials, but augments pain ratings in healthy volunteers. Pain 148:36–42

    Article  PubMed  Google Scholar 

  28. Tinazzi M, Del Vesco C, Defazio G et al (2008) Abnormal processing of the nociceptive input in Parkinson’s disease: a study with CO2 laser evoked potentials. Pain 136:117–124

    Article  PubMed  Google Scholar 

  29. Tinazzi M, Recchia S, Simonetto S et al (2009) Hyperalgesia and laser evoked potentials alterations in hemiparkinson: Evidence for an abnormal nociceptive processing. J Neurol Sci 276:153–158

    Google Scholar 

  30. Ungless M, Magill P, Bolam J (2004) Uniform inhibition of dopamine neurons in the ventral tegmental area by aversive stimuli. Science 303:2040–2042

    Article  PubMed  CAS  Google Scholar 

  31. Wu Q, Garcia-Larrea L, Mertens P et al (1999) Hyperalgesia with reduced laser evoked potentials in neuropathic pain. Pain 80:209–214

    Article  PubMed  CAS  Google Scholar 

  32. Yarnitsky D, Arendt-Nielsen L, Bouhassira D et al (2010) Recommendations on terminology and practice of psychophysical DNIC testing. Eur J Pain 14:339

    Article  PubMed  Google Scholar 

  33. Zgaljardic DJ, Borodb JC, Foldib NS et al (2006) An examination of executive dysfunction associated with frontostriatal circuitry in Parkinson’s disease. J Clin Exp Neuropsychol 28:1127–1144

    Google Scholar 

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Danksagung

Das Projekt „Schmerz und Morbus Parkinson – Nozizeption, Schmerzverarbeitung und Schmerzkommunikation bei Parkinson-Patienten“ wird von der Deutschen Stiftung Neurologie (DSN) gefördert.

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Der korrespondierende Autor gibt für sich und seine Koautoren an, dass kein Interessenkonflikt besteht.

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Authors and Affiliations

  1. Physiologische Psychologie, Institut für Psychologie, Otto-Friedrich-Universität Bamberg, Markusplatz 3, 96045, Bamberg, Deutschland

    J.A. Priebe & S. Lautenbacher

  2. Neurologische Klinik, Klinikum Bamberg, Sozialstiftung Bamberg, Bamberg, Deutschland

    P. Rieckmann

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  1. J.A. Priebe
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  2. P. Rieckmann
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  3. S. Lautenbacher
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Correspondence to J.A. Priebe.

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Priebe, J., Rieckmann, P. & Lautenbacher, S. Zentrale Schmerzverarbeitung bei Morbus Parkinson. Schmerz 26, 647–654 (2012). https://doi.org/10.1007/s00482-012-1222-9

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  • DOI: https://doi.org/10.1007/s00482-012-1222-9

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