Skip to main content
Log in

Das vaskuläre Parkinson-Syndrom

Vascular parkinsonian syndrome

  • Übersichten
  • Published:
Der Nervenarzt Aims and scope Submit manuscript

Zusammenfassung

In der vorliegenden Übersicht soll deutlich gemacht werden, dass ein vaskuläres Parkinson-Syndrom (VPS) im engeren Sinne eine seltene und klinisch nicht immer von der idiopathischen Parkinson abgrenzbare Erkrankung ist. Im klinischen Sprachgebrauch wird der Terminus VPS allerdings auch für andere Störungsbilder verwendet, die nicht zuletzt aufgrund der unterschiedlichen therapeutischen Implikationen von einem VPS differenziert werden sollten. Die Differenzialdiagnose des VPS umfasst in erster Linie die subkortikale arteriosklerotische Enzephalopathie, bei der eine Parkinson-artige Gangstörung nicht mit weiteren Kardinalsymptomen eines Parkinson-Syndroms verbunden ist sowie die Koexistenz eines neurodegenerativen Parkinson-Syndroms mit einer subkortikalen vaskulären Enzephalopathie. Ein akutes oder subakutes VPS entsteht in der Regel kontralateral zu Hirninfarkten, die den externen Teil des Globus pallidus, den ventrolateralen Teil des Thalamus und (seltener) die Substantia nigra betreffen. Chronische VPS mit schleichendem Beginn entstehen auf dem Boden bilateraler lakunärer subkortikaler Infarkte mit Beeinträchtigung thalamokortikaler Projektionen. Progressionsneigung und Dopa-Responsivität kommen bei akuten und chronischen VPS vor und erschweren die Differenzialdiagnose zu einem degenerativen Parkinson-Syndrom.

Summary

The present review shows that vascular parkinsonian syndrome (VPS) fulfilling stringent diagnostic criteria for parkinsonism is a rare disease that cannot always be distinguished from neurodegenerative parkinsonism on clinical grounds. Thus VPS needs to be differentiated from other disturbances, which have distinct phenomenological and therapeutical features including isolated gait disturbances associated with subcortical arteriosclerotic encephalopathy and neurodegenerative parkinsonism complicated by comorbid vascular encephalopathy. Acute or subacute VPS is usually caused by contralateral infarctions involving the external globus pallidus, ventrolateral thalamus, and, less often, the substantia nigra. Chronic VPS with insidious onset is related to bilateral subcortical infarctions affecting thalamocortical projections. Differentiation from degenerative parkinsonism is difficult in cases of VPS that display a progressive course and response to levodopa.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Subscribe and save

Springer+ Basic
$34.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or eBook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Abb. 1
Abb. 2

Literatur

  1. Critchley M (1929) Arteriosclerotic parkinsonism. Brain 52:23–83

    Google Scholar 

  2. Winikates J, Jankovic J (1999) Clinical correlates of vascular parkinsonism. Arch Neurol 56:98–102

    Article  PubMed  Google Scholar 

  3. Fenelon G, Gray F, Wallays C et al. (1995) Parkinsonism and dilatation of the perivascular spaces (état crible) of the striatum: a clinical, magnetic resonance imaging, and papathological study. Mov Disord 10:754–760

    Article  PubMed  Google Scholar 

  4. Kim JS (1992) Delayed onset hand tremor caused by cerebral infarction. Stroke 23:292–294

    PubMed  Google Scholar 

  5. Mark MH, Sage JI, Walters AS et al. (1995) Binswanger’s disease presenting as levodopa-responsive parkinsonism: clinicopathologic study of three cases. Mov Disord 10:450–454

    Article  PubMed  Google Scholar 

  6. Murrow RW, Schweiger GD, Kepes JJ et al. (1990) Parkinsonism due to a basal ganglia lacunar state: clinicopathologic correlation. Neurology 40:897–900

    PubMed  Google Scholar 

  7. Tolosa ES, Santamaria J (1984) Parkinsonism and basal ganglia infarcts. Neurology 34:1516–1518

    PubMed  Google Scholar 

  8. Zijlmans JC, Daniel SE, Hughes AJ et al. (2004) Clinicopathological investigation of vascular parkinsonism, including clinical criteria for diagnosis. Mov Disord 19:630–640

    Article  PubMed  Google Scholar 

  9. Sudarsky L (2001) Gait disorders: prevalence, morbidity and etiology. Adv Neurol 87:11–18

    PubMed  Google Scholar 

  10. Fitzgerald PM, Jankovic J (1989) Lower body parkinsonism: evidence for vascular etiology. Mov Disord 4:249–260

    Article  PubMed  Google Scholar 

  11. Hughes AJ, Daniel SE, Blankson S et al. (1993) A clinicopathological study of 100 cases of Parkinson’s disease. Arch Neurol 50:140–148

    PubMed  Google Scholar 

  12. Bathia KP, Marsden CD (1994) The behavioural and motor consequences of focal lesions of the basal ganglia in man. Brain 117:825–834

    PubMed  Google Scholar 

  13. Reider-Groswasser I, Bornstein NM, Korczyn AD (1995) Parkinsonism in patients with lacunar infarcts of the basal ganglia. Eur Neurol 35:46–49

    PubMed  Google Scholar 

  14. Boiten J, Lodder J (1992) Large striatocapsular infarct: clinical presentation and pathogenesis in comparison with lacunar and cortical infarcts. Acta Neurol Scand 86:298–303

    PubMed  Google Scholar 

  15. Weiller C, Ringelstein EB, Reiche W et al. (1990) The large striatocapsular infarct. A clinical and pathophysiological entity. Arch Neurol 47:1085–1091

    PubMed  Google Scholar 

  16. Chung CS, Caplan LR, Yamamoto Y et al. (2000) Striatocapsular haemorrhage. Brain 123:1850–1862

    Article  PubMed  Google Scholar 

  17. Peralta C, Werner P, Holl B et al. (2004) Parkinsonism following striatal infarcts: incidence in a prospective stroke unit cohort. J Neural Transm 111:1473–1483

    Article  PubMed  Google Scholar 

  18. Foltynie T, Barker R, Brayne C (2002) Vascular Parkinsonism: a review of the precision and frequency of the diagnosis. Neuroepidemiology 21:1–7

    Article  PubMed  Google Scholar 

  19. Baloh RW (1995) White matter lesions and disequilibrium in older people. Arch Neurol 52:970–979

    PubMed  Google Scholar 

  20. Masdeu JC, Wolfson L, Lantos G et al. (1989) Brain white-matter changes in the elderly prone to falling. Arch Neurol 46:1292–1296

    PubMed  Google Scholar 

  21. Van Zagten M, Lodder J, Kessels F (1998) Gait Disorder and Parkinsonian signs in patients with stroke related to small deep infarcts and white matter lesions. Mov Disord 13:89–95

    Article  PubMed  Google Scholar 

  22. Yamanouchi H, Nagura H (1997) Neurological signs and frontal white matter lesions in vascular parkinsonism. Stroke 28:965–969

    PubMed  Google Scholar 

  23. Tison F, Duche B, Loiseau P (1993) Vascular hemi-parkinson disease. Rev Neurol 149:565–567

    PubMed  Google Scholar 

  24. Zijlmans JC, Katzenschlager R, Daniel SE et al. (2004) The L-dopa response in vascular parkinsonism. J Neurol Neurosurg Psychiatry 75:545–547

    Article  PubMed  Google Scholar 

  25. Volkmann J (2004) Morbus Parkinson—Indikationen und Auswahl des Zielpunktes. In: Krauss JK, Volkmann J (Hrsg) Tiefe Hirnstimulation. Steinkopff, Darmstadt, S 258–268

  26. Bäzner H, Schanz J, Blahak C et al. (2005) Differential pattern of hand-tapping compromise in vascular versus idiopathic parkinsonism: a study based on computerized movement analysis. Mov Disord 20:504–508

    Article  PubMed  Google Scholar 

  27. Durif F, Pollak P, Hommel M et al. (1992) Relationship between levodopa-independent symptoms and central atrophy evaluated by magnetic resonance imaging in Parkinson’s disease. Eur Neurol 32:32–36

    PubMed  Google Scholar 

  28. Piccini P, Pavese N, Canapicchi R et al. (1995) White matter hyperintensities in Parkinson’s disease. Arch Neurol 52:191–194

    PubMed  Google Scholar 

  29. Ebersbach G, Sojer M, Valldeoriola F et al. (1999) Comparative analysis of gait in Parkinson’s disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy. Brain 122:1349–1355

    Article  PubMed  Google Scholar 

  30. Ebersbach G, Sojer M, Müller J et al. (2002) Gleichgewichtsstörungen bei idiopathischer Parkinson-Erkrankung. Nervenarzt 73:162–165

    Article  PubMed  Google Scholar 

  31. Bonnet AM, Loria Y, Saint-Hilaire MH et al. (1987) Does long-term aggravation of Parkinson’s disease result from nondopaminergic lesions? Neurology 37:1539–1542

    PubMed  Google Scholar 

  32. Gerschlager W, Bencsits G, Pirker W et al. (2002) [123I]beta-CIT SPECT distinguishes vascular parkinsonism from Parkinson’s disease. Mov Disord 17:518–523

    Article  PubMed  Google Scholar 

  33. Lorberboym M, Djaldetti R, Melamed E et al. (2004) 123I-FP-CIT SPECT imaging of dopamine transporters in patients with cerebrovascular disease and clinical diagnosis of vascular parkinsonism. J Nucl Med 45:1688–1693

    PubMed  Google Scholar 

  34. Katzenschlager R, Zijlmans J, Evans A et al. (2004) Olfactory function distinguishes vascular parkinsonism from Parkinson’s disease. J Neurol Neurosurg Psychiatry 75:1749–1752

    Article  PubMed  Google Scholar 

Download references

Interessenkonflikt

Der korrespondierende Autor versichert, dass keine Verbindungen mit einer Firma, deren Produkt in dem Artikel genannt ist, oder einer Firma, die ein Konkurrenzprodukt vertreibt, bestehen.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to G. Ebersbach.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Ebersbach, G., Poewe, W. Das vaskuläre Parkinson-Syndrom. Nervenarzt 77, 139–147 (2006). https://doi.org/10.1007/s00115-005-1978-6

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00115-005-1978-6

Schlüsselwörter

Keywords

Navigation