Poster Abstracts

3186 Unexpected lower facial weakness in the lateral medullary syndrome – probable role of aberrant corticobulbar fibres

Abstract

Background Lateral medullary infarction classically results in the ‘Wallenberg syndrome’, characterised by an ipsilateral Horner’s syndrome, loss of pain and temperature in the ipsilateral face and contralateral body, vertigo, dysphagia and dysphonia. Contralateral motor weakness is uncommon but can occur with caudal extension in the ‘Babinski-Nageotte’ syndrome. Isolated, ipsilateral facial weakness is exceedingly rare. Similarly, only a few cases with contralateral facial sensory loss have been described. The presence of these two signs together in lateral medullary infarction has not been reported before.

Case Presentation We present the case of a 47-year-old gentleman presenting with an acute left Horner’s syndrome, left ocular lateropulsion and central nystagmus, in combination with left lower facial weakness sparing the frontalis and reduced pain and temperature sensation in the right face, arm and leg. MRI of the brain revealed diffusion restriction consistent with acute infarction in the left lateral medulla. There was no midbrain or pontine involvement.

Discussion Ipsilateral lower facial weakness in lateral medullary infarction is postulated to occur secondary to involvement of an aberrant bundle of corticobulbar fibres that decussate in the medulla before ascending to the contralateral facial nerve nucleus in the pons. Contralateral sensory loss in the face is thought to occur secondary to involvement of the ventral trigeminothalamic tract in the medulla after its decussation.

Conclusion Our case demonstrates that lower facial weakness with contralateral sensory loss can occur secondary to lateral medullary infarction. This highlights the complex organisation of the sensorimotor pathways in the brainstem.

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