Lateral Medullary (Wallenberg) Syndrome: Clinical Features, Imaging, and Acute Management
Clinical Features
Lateral medullary syndrome presents with a characteristic constellation of symptoms resulting from infarction of the lateral medulla, most commonly due to posterior inferior cerebellar artery (PICA) occlusion. 1, 2
Classic Triad
- Ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) 3, 4
- Ipsilateral ataxia and limb incoordination 1, 3
- Crossed hemisensory disturbance: ipsilateral facial pain/numbness with contralateral body pain and temperature loss 3, 5
Additional Cranial Nerve Deficits
- Vertigo, nystagmus, and severe disequilibrium from vestibular nucleus involvement 1, 6, 2
- Dysphagia and dysarthria when cranial nerves IX and X nuclei are affected 1, 2, 5
- Ipsilateral facial sensory loss if the spinal trigeminal nucleus is involved 1, 5
- Hoarseness and loss of gag reflex ipsilaterally 2, 5
Important Clinical Caveat
Presentation variability is the rule rather than the exception—not all patients exhibit the complete classic triad. 3 Atypical presentations may include additional cranial nerve palsies (CN VI, CN VII) when adjacent pontine structures are involved. 4
Recommended Imaging
First-Line Imaging
MRI brain with diffusion-weighted imaging (DWI) is the mandatory initial study—CT scanning should NOT be routinely ordered as posterior fossa ischemic strokes are difficult to detect on CT with sensitivity as low as 10%. 1, 7
Imaging Protocol Details
- MRI brain without contrast is the preferred modality 1
- Thin-section coronal DWI detects nearly 25% more acute brainstem infarcts than standard axial DWI 1, 7
- 3.0 Tesla scanners are preferred over 1.5 Tesla for superior signal-to-noise ratio and spatial resolution 7
Vascular Imaging
Add MRA or CTA of the head and neck to evaluate for vertebral artery dissection, which is strongly associated with lateral medullary infarction and must be identified urgently. 3 These modalities provide approximately 94% sensitivity and 95% specificity for detecting vertebral artery stenosis. 8
Acute Management
Immediate Supportive Care
Keep the patient nil per os (NPO) and perform an immediate swallowing assessment—dysphagia occurs when cranial nerves IX and X nuclei are affected and aspiration risk is high. 1 If oral intake is unsafe, provide nutrition via nasogastric, nasoduodenal, or percutaneous endoscopic gastrostomy (PEG) tubes. 1
Do not postpone PEG placement if dysphagia persists beyond 7–10 days, as early intervention supports recovery. 1
Acute Stroke Therapy
- Initiate antiplatelet therapy with aspirin in all eligible patients, as early antithrombotic administration before discharge is a recognized quality-of-care indicator for stroke treatment 1
- Manage blood pressure cautiously during the acute phase, avoiding aggressive reduction unless pressures are severely elevated, to preserve cerebral perfusion 1
Thromboprophylaxis
Provide deep-vein thrombosis prophylaxis using intermittent pneumatic compression devices or anticoagulant medication. 1
Secondary Prevention
- Implement aggressive modification of vascular risk factors, including control of hypertension, diabetes, and hyperlipidemia, to reduce recurrence risk 1
- Advise and support smoking cessation as part of comprehensive secondary prevention 1
- Continue long-term antiplatelet therapy after the acute episode to maintain secondary stroke protection 1
Prognosis
The small size of these infarcts and lack of hemorrhagic transformation suggest favorable prognosis with optimal therapy. 1, 3 Most patients show massive improvement with early hospitalization and treatment, though recovery timelines vary. 2
Critical Pitfall to Avoid
Never rely on CT as the initial imaging modality—it misses the majority of posterior circulation infarcts and will delay diagnosis and appropriate acute stroke intervention. 1, 7 The association between lateral medullary infarction and vertebral artery dissection underscores the need for urgent vascular imaging in all cases. 3