Neuroscience · Year 2 · from Neuroscience

Case 1: Lateral Medullary Syndrome (Wallenberg Syndrome)

Patient Presentation

Demographics: 58-year-old male

Chief Complaint: Sudden dizziness, difficulty swallowing, and facial numbness

History of Present Illness: A 58-year-old man with a history of hypertension and hyperlipidemia suddenly developed severe vertigo while at work. He describes the room spinning and immediate nausea and vomiting. He also noticed numbness on the left side of his face and difficulty swallowing, with liquids coming out of his nose. He reports that his voice sounds hoarse. He feels off-balance and tends to fall to the left. His left eye appears smaller than usual according to his coworker. He denies limb weakness, headache, or change in consciousness.

Physical Examination:

  • Vital signs: BP 175/105, HR 78, RR 16
  • General: Alert, nauseated, dysphonic
  • Neurological:
  • Mental status: Alert, oriented, normal cognition
  • Cranial nerves:
  • Left Horner syndrome (miosis, ptosis, anhidrosis)
  • Nystagmus (direction-changing)
  • Decreased sensation to pain and temperature on LEFT face (V1-V3)
  • Absent left gag reflex; left palate droop; left vocal cord weakness (hoarseness)
  • Tongue midline
  • Motor: 5/5 strength in all extremities
  • Sensory: Decreased pain and temperature on RIGHT body (arm, trunk, leg); normal on left body; light touch and proprioception intact bilaterally
  • Coordination: Left-sided limb ataxia (finger-to-nose dysmetria); truncal ataxia with falling toward left
  • Gait: Wide-based, falls to left

Workup:

  • CT head: No hemorrhage
  • MRI brain with DWI: Acute infarct in left lateral medulla
  • MR angiography: Left vertebral artery occlusion
  • CT angiography (neck): Left vertebral artery dissection
  • Echocardiogram: Normal; no cardioembolic source

Diagnosis: Left lateral medullary syndrome (Wallenberg syndrome) secondary to vertebral artery dissection

Treatment:

  • Antiplatelet therapy (aspirin) initiated; anticoagulation considered for dissection
  • NPO initially with video swallow evaluation; modified diet after improvement
  • Speech therapy for dysphagia
  • Physical therapy for vestibular rehabilitation and ataxia
  • Aggressive secondary prevention (statin, blood pressure control)
  • Spontaneous improvement in swallowing over 2-3 weeks
  • Persistent mild ataxia and sensory symptoms at 6 months

Clinical Pearl: Lateral medullary syndrome results from occlusion of the vertebral artery or its branch (PICA), affecting structures in the lateral medulla. The classic findings include ipsilateral facial sensory loss (descending trigeminal tract), ipsilateral Horner syndrome (descending sympathetic fibers), ipsilateral cerebellar ataxia (inferior cerebellar peduncle), dysphagia and hoarseness (nucleus ambiguus), vertigo and nystagmus (vestibular nuclei), and CONTRALATERAL body pain/temperature loss (spinothalamic tract). Notably, motor pathways are spared because the pyramids are located medially. This "crossed" sensory pattern (ipsilateral face, contralateral body) is the hallmark of a lateral brainstem lesion.


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