Lateral Medullary Syndrome (Wallenberg Syndrome)

Overview

Lateral medullary syndrome (LMS), or Wallenberg syndrome, results from infarction of a wedge-shaped area of the lateral medulla lying posterior to the inferior olivary nucleus, along with portions of the inferior cerebellum. It is one of the most classic and recognizable brainstem stroke syndromes.

Vascular Anatomy & Etiology

The lateral medulla is supplied by the posterior inferior cerebellar artery (PICA) in its proximal segment, which arises from the vertebral artery (VA). Contrary to tradition, most cases are caused by intracranial vertebral artery occlusion, not PICA occlusion directly.

Among 130 consecutive cases of pure lateral medullary infarction, the breakdown was:

Large vessel atherosclerotic steno-occlusive disease: 50%
Arterial dissection: 15% (more common with caudal lesions; spontaneous VA dissection is a frequent cause)
Small vessel disease: 13%
Cardioembolism: 5%

Other rarer causes include cocaine abuse, neck manipulation (chiropractic), trauma, demyelination, metastases, radionecrosis, and vascular malformation rupture.

Clinical Features

The syndrome results from damage to multiple structures packed into the lateral medulla. The key is understanding which side each finding appears on:

Classic Signs (organized by structure)

Structure Damaged	Sign/Symptom	Laterality
Spinal trigeminal nucleus & tract	Pain & temperature loss - face	Ipsilateral
Spinothalamic tract	Pain & temperature loss - trunk & limbs	Contralateral
Nucleus ambiguus (CN IX, X)	Dysphagia, dysarthria, hoarseness, palatal/vocal cord paralysis, diminished gag reflex	Ipsilateral
Descending sympathetic fibers	Horner syndrome (miosis, ptosis, anhidrosis)	Ipsilateral
Vestibular nuclei	Vertigo, nausea, vomiting, nystagmus	Present
Inferior cerebellar peduncle (restiform body) & cerebellum	Limb ataxia, gait ataxia, lateropulsion (falling/toppling toward lesion side)	Ipsilateral
Nucleus tractus solitarius	Loss of taste	Present
Utricular nucleus (otolithic pathways)	Vertical diplopia, skew deviation, ocular tilt reaction, environmental tilt ("floor-on-ceiling" phenomenon)	Present

The Hallmark Crossed Sensory Pattern

Ipsilateral face + contralateral body pain/temperature loss = the crossed hemianesthesia that clinches the diagnosis. This "alternating hemianalgesia" is pathognomonic of a lateral medullary location.

Identifying Clinical Triad

The triad of ipsilateral Horner syndrome + ipsilateral ataxia + contralateral hypoalgesia clinically identifies lateral medullary infarction with high specificity.

What is Spared

Because the pyramids, medial lemniscus, and hypoglossal nucleus lie in the medial medulla, LMS typically spares:

Motor power (no hemiparesis - this is key; presence of hemiparesis suggests medial extension or a different lesion)
Vibration and joint position sense
Tongue movements

Eye Signs (Detailed)

Eye findings in LMS are varied and highly characteristic:

Nystagmus - almost invariable; direction-changing nystagmus with gaze positions suggests brainstem origin.

Skew deviation - hypotropia on the side of the lesion (type 2 skew deviation per Brandt & Dieterich), caused by otolithic vestibular nuclei damage.

Ocular tilt reaction - ipsilateral head tilt + disconjugate ocular torsion (exocyclodeviation of the ipsilateral eye).

Ocular ipsipulsion (lateropulsion) - saccades deviate toward the side of the lesion due to damage to climbing fibers from the contralateral inferior olivary nucleus to the dorsal vermis. Hypometric saccades toward the lesion side; hypermetric saccades in the opposite direction.

Internuclear ophthalmoplegia fragment may occur.

Rostral vs. Caudal Lesion Differences

Rostral lesions	Caudal lesions
Severe dysphagia and hoarseness	Marked vertigo, nystagmus, gait ataxia
Facial paresis	Ipsilateral sensory symptoms in upper extremities
-	More often due to arterial dissection

Lesions extending more ventromedially may cause contralateral (rather than ipsilateral) facial sensory changes. Nausea, vomiting, and Horner syndrome occur regardless of lesion level.

Rare Manifestations

As catalogued in Localization in Clinical Neurology:

Wild arm ataxia (lateral cuneate nucleus involvement)
Central pain with allodynia
Contralateral hyperhidrosis with ipsilateral anhidrosis
Inability to sneeze OR paroxysmal sneezing
Loss of taste (nucleus tractus solitarius)
Autonomic dysfunction - tachycardia, BP lability
Ondine's curse (failure of automatic breathing) - from nucleus ambiguus + adjacent reticular formation involvement
Transient urinary retention
Body lateropulsion without limb ataxia (lateral vestibulospinal tract)
Opalski syndrome - LMS + ipsilateral hemiparesis (lesion extends just below the pyramidal decussation)
Pure sensory stroke variant
Central hypoventilation

Fragmentary (Partial) Syndromes

Partial syndromes are common at onset. The smallest infarctions may cause only lateropulsion + mild ipsilateral limb ataxia, or isolated vertigo. While vertigo is the most frequent feature, isolated vertigo alone is insufficient to diagnose LMS.

Prognosis & Complications

Most cases recover substantially in the first days and weeks.
Sudden death from respiratory or cardiac arrest has been reported even without cerebellar swelling or basilar thrombosis, emphasizing the need for monitoring.
Dysphagia is a major functional morbidity - aspiration pneumonia is a key risk.
Cerebellar swelling (when inferior cerebellum is infarcted) can cause obstructive hydrocephalus and brainstem herniation, requiring neurosurgical decompression.

Comparison: Lateral vs. Medial Medullary Syndrome

Feature	Lateral (Wallenberg)	Medial
Motor	Spared	Contralateral hemiparesis (pyramid)
Sensory	Crossed (face ipsilateral, body contralateral) pain/temp	Contralateral loss of position/vibration (medial lemniscus)
Tongue	Normal	Ipsilateral weakness (CN XII)
Horner	Ipsilateral	Absent
Dysphagia	Yes (CN IX/X)	No
Artery	VA > PICA	Anterior spinal artery or VA perforators

Sources:

Localization in Clinical Neurology, 8e, Chapter 15 (pp. 921-925)
Adams and Victor's Principles of Neurology, 12th ed., p. 816
Harrison's Principles of Internal Medicine 22E, p. 3477

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