Nervenheilkunde 2011; 30(04): 259-262
DOI: 10.1055/s-0038-1627799
Fortbildung Kaiserslautern
Schattauer GmbH

Untersuchung der Okulomotorik als differenzialdiagnostisches Instrument bei Parkinson-Syndromen

Oculomotor changes as differential diagnosis in Parkinsonian syndromes
E. H. Pinkhardt
1   Klinik für Neurologie, Universitätsklinik Ulm
,
J. Kassubek
1   Klinik für Neurologie, Universitätsklinik Ulm
› Author Affiliations
Further Information

Publication History

Eingegangen am: 22 September 2010

angenommen am: 05 October 2010

Publication Date:
23 January 2018 (online)

Zusammenfassung

Okulomotorikstörungen kommen in der Gruppe Parkinson-Syndrome vor und sind eng mit der zugrunde liegenden Neuropathologie der jeweiligen Erkrankung verknüpft. Durch eine geräteunterstützte Untersuchung der Augenbewegungen (Videookulografie) ist es möglich, diese oft subtilen Differenzen im Muster der okulomotorischen Störungen aufzuzeigen. Dabei können für einzelne Entitäten spezifische Veränderungen herausgefiltert werden, die, über neurowissenschaftliche Erkenntnisse bezüglich der spezifischen Funktionsänderungen der funktionellen Netzwerke hinaus, klinisch in der teilweise schwierigen Differenzialdiagnose in frühen Erkrankungsstadien hilfreich sein können.

Summary

Oculomotor abnormalities can be observed in nearly all Parkinsonian syndromes. These oculomotor deficits are closely related to the underlying neuropathology of the particular disease entity. Using video-oculography (VOG) it is possible to elicit different causes of apparently similar oculomotor changes that may help in the early differential diagnosis within the group of Parkinsonian syndromes.

 
  • Literatur

  • 1 Williams DR, Lees AJ. How do patients with parkinsonism present? A clinicopathological study. Intern Med J 2009; 39 (01) 7-12.
  • 2 Williams DR, Lees AJ. What features improve the accuracy of the clinical diagnosis of progressive supranuclear palsy-parkinsonism (PSP-P)?. Mov Disord 2010; 25 (03) 357-62.
  • 3 Poewe W. Treatments for Parkinson disease – past achievements and current clinical needs. Neurology 2009; 72 (Suppl. 07) S65-73.
  • 4 Dickson DW. et al. Neuropathological assessment of Parkinson’s disease: refining the diagnostic criteria. Lancet Neurol 2009; 08 (12) 1150-7.
  • 5 Dickson DW, Rademakers R, Hutton ML. Progressive supranuclear palsy: pathology and genetics. Brain Pathol 2007; 17 (01) 74-82.
  • 6 Foulds P. et al. Parkinson disease: Progress towards a molecular biomarker for Parkinson disease. Nat Rev Neurol 2010; 06 (07) 359-61.
  • 7 Anderson T. et al. Oculomotor function in multiple system atrophy: clinical and laboratory features in 30 patients. Mov Disord 2008; 23 (07) 977-84.
  • 8 Leigh RJ, Zee DS. The neurology of eye movements. 4th ed.. Oxford: Oxford University Press; 2006
  • 9 Eggert T. Eye movement recordings: methods. Dev Ophthalmol 2007; 40: 15-34.
  • 10 van der Geest JN, Frens MA. Recording eye movements with video-oculography and scleral search coils: a direct comparison of two methods. J Neurosci Methods 2002; 114 (02) 185-95.
  • 11 Amador SC. et al. Dissociating cognitive deficits involved in voluntary eye movement dysfunctions in Parkinson’s disease patients. Neuropsychologia 2006; 44 (08) 1475-82.
  • 12 Armstrong IT. et al. Control of saccades in Parkinson’s disease. Brain Cogn 2002; 49 (02) 198-201.
  • 13 Briand KA. et al. Control of voluntary and reflexive saccades in Parkinson’s disease. Exp Brain Res 1999; 129 (01) 38-48.
  • 14 Chan F. et al. Deficits in saccadic eye-movement control in Parkinson’s disease. Neuropsychologia 2005; 43 (05) 784-96.
  • 15 Vidailhet M. et al. Eye movements in parkinsonian syndromes. Ann Neurol 1994; 35 (04) 420-6.
  • 16 Kimmig H. et al. What is pathological with gaze shift fragmentation in Parkinson’s disease?. J Neurol 2002; 249 (06) 683-92.
  • 17 MacAskill MR, Anderson TJ, Jones RD. Adaptive modification of saccade amplitude in Parkinson’s disease. Brain 2002; 125 (Pt 7): 1570-82.
  • 18 Blekher T. et al. Multiple step pattern as a biomarker in Parkinson disease. Parkinsonism Relat Disord 2009; 15 (07) 506-10.
  • 19 Blekher T. et al. Test-retest reliability of saccadic measures in subjects at risk for Huntington disease. Invest Ophthalmol Vis Sci 2009; 50 (12) 5707-11.
  • 20 Tusa RJ, Ungerleider LG. Fiber pathways of cortical areas mediating smooth pursuit eye movements in monkeys. Ann Neurol 1988; 23 (02) 174-83.
  • 21 Pinkhardt EH. et al. Comparison of smooth pursuit eye movement deficits in multiple system atrophy and Parkinson’s disease. J Neurol 2009; 256 (09) 1438-46.
  • 22 Pierrot-Deseilligny C. et al. Decisional role of the dorsolateral prefrontal cortex in ocular motor behaviour. Brain 2003; 126 (Pt 6): 1460-73.
  • 23 Mosimann UP. et al. Saccadic eye movement changes in Parkinson’s disease dementia and dementia with Lewy bodies. Brain 2005; 128 (06) 1267-76.
  • 24 van Stockum S. et al. Don’t look now or look away: two sources of saccadic disinhibition in Parkinson’s disease?. Neuropsychologia 2008; 46 (13) 3108-15.
  • 25 Salman MS, Sharpe JA, Lillakas L, Steinbach MJ. Square wave jerks in children and adolescents. Pediatr Neurol 2008; 38 (01) 16-9.
  • 26 Crevits L. et al. Antisaccadic effects of a dopamine agonist as add-on therapy in advanced Parkinson’s patients. Neuropsychobiology 2000; 42 (04) 202-6.
  • 27 Gibson JM, Kennard C. Quantitative study of “onoff” fluctuations in the ocular motor system in Parkinson’s disease. Adv Neurol 1987; 45: 329-33.
  • 28 Vermersch AI. et al. Sequences of memory-guided saccades in Parkinson’s disease. Ann Neurol 1994; 35 (04) 487-90.
  • 29 Rivaud-Pechoux S. et al. Improvement of memory guided saccades in parkinsonian patients by high frequency subthalamic nucleus stimulation. J Neurol Neurosurg Psychiatry 2000; 68 (03) 381-4.
  • 30 Sauleau P. et al. Subthalamic stimulation improves orienting gaze movements in Parkinson’s disease. Clin Neurophysiol 2008; 119 (08) 1857-63.
  • 31 Temel Y, Visser-Vandewalle V, Carpenter RH. Saccadic latency during electrical stimulation of the human subthalamic nucleus. Curr Biol 2008; 18 (10) R412-4.
  • 32 Yugeta A. et al. Effects of STN stimulation on the initiation and inhibition of saccade in Parkinson disease. Neurology 2010; 74 (09) 743-8.
  • 33 Harrison J, Henderson L, Kennard C. Abnormal refractoriness in patients with Parkinson’s disease after brief withdrawal of levodopa treatment. J Neurol Neurosurg Psychiatry 1995; 59 (05) 499-506.
  • 34 Ozawa T. et al. The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations. rain 2004; 127 (Pt 12): 2657-71.
  • 35 Bhidayasiri R, Riley DE, Somers JT, Lerner AJ, Buttner-Ennever JA, Leigh RJ. Pathophysiology of slow vertical saccades in progressive supranuclear palsy. Neurology 2001; 57 (11) 2070-7.
  • 36 Pinkhardt EH. et al. Differential diagnostic value of eye movement recording in PSP-parkinsonism, Richardson’s syndrome, and idiopathic Parkinson’s disease. J Neurol 2008; 255 (12) 1916-25.
  • 37 Revesz T, Sangha H, Daniel SE. The nucleus raphe interpositus in the Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy). Brain 1996; 119 ( Pt 4): 1137-43.
  • 38 Ludolph AC. et al. Tauopathies with parkinsonism: clinical spectrum, neuropathologic basis, biological markers, and treatment options. Eur J Neurol 2009; 16 (03) 297-309.
  • 39 Williams DR. et al. Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson’s syndrome and PSP-parkinsonism. Brain 2005; 128 (Pt 6): 1247-58.
  • 40 Rivaud-Pechoux S. et al. Longitudinal ocular motor study in corticobasal degeneration and progressive supranuclear palsy. Neurology 2000; 54 (05) 1029-32.