Clinical meaning
Lateral medullary syndrome (Wallenberg syndrome) results from infarction of the lateral medulla oblongata, most commonly caused by occlusion of the posterior inferior cerebellar artery (PICA) or, more frequently, the ipsilateral vertebral artery. The lateral medulla contains several critical neural structures packed into a small area, and their ischemic injury produces a characteristic and predictable constellation of crossed neurological findings.
Structures affected and their clinical manifestations include: (1) Nucleus ambiguus -- contains motor neurons of cranial nerves IX and X; damage causes ipsilateral palatal paralysis (uvula deviates AWAY from the lesion side), vocal cord paralysis (hoarseness/dysphonia), and pharyngeal weakness (dysphagia with aspiration risk -- the most dangerous complication). (2) Vestibular nuclei -- damage causes vertigo, nystagmus (typically horizontal or rotatory), nausea, and vomiting. (3) Inferior cerebellar peduncle -- carries cerebellar input; damage causes ipsilateral limb ataxia (difficulty with coordination, past-pointing on finger-to-nose testing). (4) Spinothalamic tract -- carries contralateral pain and temperature sensation ascending to the thalamus; damage causes CONTRALATERAL loss of pain and temperature sensation in the body (trunk and limbs). (5) Spinal trigeminal nucleus and tract -- carries ipsilateral facial pain and temperature sensation; damage causes IPSILATERAL loss of pain and temperature sensation on the face. (6) Descending sympathetic tract (hypothalamospinal tract) -- damage causes ipsilateral Horner syndrome (miosis, partial ptosis, anhidrosis on the affected side of the face).
The hallmark of Wallenberg syndrome is the 'crossed' sensory deficit: ipsilateral face and contralateral body loss of pain and temperature, with preserved touch and proprioception (which travel in the dorsal columns, not the lateral medulla). This crossing pattern is virtually pathognomonic.