Lateral medullary (Wallenberg) syndrome Overview
Lateral medullary (Wallenberg) syndrome is an ischaemic infarct of the lateral medulla, most commonly due to occlusion of the posterior inferior cerebellar artery (PICA) or a vertebral artery lesion compromising PICA flow.
It is a classical posterior‑circulation brainstem stroke with a characteristic mix of cranial‑nerve, long‑tract and cerebellar/vestibular signs.
In the emergency department it should be managed as an acute stroke because of reperfusion considerations and early risks such as airway compromise and aspiration from bulbar dysfunction (NICE NG128).
Anatomy and pathophysiology (why the pattern occurs) The clinical features reflect infarction of structures in the lateral medulla and adjacent pathways supplied by PICA:
- Spinal trigeminal nucleus/tract → ipsilateral facial pain and temperature loss.
- Spinothalamic tract → contralateral body pain and temperature loss.
- Nucleus ambiguus (cranial nerves IX, X) → dysphagia, hoarseness, reduced gag reflex and impaired airway protection.
- Vestibular nuclei and inferior cerebellar peduncle → vertigo, nystagmus, nausea and ipsilateral ataxia.
- Descending sympathetic fibres → ipsilateral Horner’s syndrome.
- Nearby cochlear/vestibular pathways → tinnitus or variable hearing disturbance.
Typical clinical features
- Crossed sensory deficits with ipsilateral loss of facial pain/temperature and contralateral loss from the body.
- Bulbar signs including dysphagia, hoarseness and decreased gag reflex due to nucleus ambiguus involvement; these create a high aspiration and airway‑protection risk.