Journal of Neurology

, Volume 241, Issue 7, pp 421–426 | Cite as

Saccadic lateropulsion in Wallenberg's syndrome may be caused by a functional lesion of the fastigial nucleus

  • Christoph Helmchen
  • Andreas Straube
  • Ulrich Büttner
Original Communication


One of the clinical oculomotor hallmarks of lateral medullary infarction (Wallenberg's syndrome) is the so-called saccadic lateropulsion. In man and in animals, cerebellar lesions lead to dysmetric saccades and underline the importance of cerebellar control on saccadic accuracy. In order to study the lesion site responsible for saccadic lateropulsion we prospectively examined 12 patients with Wallenberg's syndrome who did not show a cerebellar lesion on CT or MRI. All patients consistently showed hypermetric saccades to the ipsilateral side and hypometric contralateral saccades comparable with the effects of cerebellar lesions in monkeys on saccadic accuracy. Based on the most recent experiments involving recordings from saccade-related neurons in the deep cerebellar nuclei of monkeys (oculomotor region of fastigial nucleus), we hypothesize that saccadic lateropulsion in lateral medullary infarction is essentially identical with cerebellar saccadic dysmetria and results from a disruption of afferent olivocerebellar climbing fibres that gives rise to functional disinhibition of the cerebellar cortex and to increased inhibition of the deep cerebellar nuclei.

Key words

Wallenberg's syndrome Saccadic lateropulsion Saccadic dysmetria Fastigial nucleus Climbing fibres 


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Copyright information

© Springer-Verlag 1994

Authors and Affiliations

  • Christoph Helmchen
    • 1
  • Andreas Straube
    • 1
  • Ulrich Büttner
    • 1
  1. 1.Neurologische KlinikLudwig-Maximilians-Universität München, Klinikum GroßhadernMünchenGermany

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