Wallenberg syndrome
Lateral medullary stroke produces the largest SVV tilts in clinical practice — and a complete ocular tilt reaction to go with them.
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Wallenberg syndrome — lateral medullary infarction — produces the largest SVV tilts in clinical practice. A bucket test takes ninety seconds and can change a discharge to an admission.
The typical patient: an older adult with vascular risk factors, sudden onset of vertigo within the last six hours. On examination there is hoarseness, dysphagia, ipsilateral Horner's syndrome, and the crossed sensory pattern — facial sensory loss on the lesion side, body sensory loss on the opposite side.
Critically: the head impulse test is normal. The semicircular canal reflex pathway runs lateral and dorsal to the lesion. This is the dissociation that separates Wallenberg from peripheral neuritis.
The SVV tilts ipsilesionally — toward the affected side — typically eight to fifteen degrees. Direction follows the pontine decussation rule: Wallenberg sits below the decussation, so the tilt is ipsiversive.
Why so large? A peripheral lesion removes one vestibular nerve. Wallenberg removes the entire vestibular nuclear complex on that side — the central neurons that integrate canal and otolith inputs. The asymmetry signal reaching the rest of the brainstem is correspondingly larger, and central compensation works less well because the compensating circuitry itself is damaged.
The complete ocular tilt reaction usually accompanies the SVV tilt: head tilt, ocular counter-roll, and skew deviation, all on the lesion side.
The bedside diagnostic shortcut: a large ipsiversive SVV tilt with a normal head impulse test in an acutely vertiginous patient is a posterior circulation stroke until proven otherwise. The combination is highly specific.
Time course. SVV magnitudes decay over weeks, but residuals at six months are common. Wallenberg patients often have persistent lateropulsion well after the acute presentation has resolved.
Expected SVV signature
| Feature | Finding |
|---|---|
| Direction | Ipsilesional (toward the affected medulla) |
| Magnitude | Typically 8–15°; sometimes >15° |
| OTR triad | Complete: head tilt, ocular counter-roll, skew — all ipsiversive |
| Time course | Maximal at onset; decays over weeks but residuals common at 6 months |
| Variability | Low — precise but tilted |
The lateral medullary infarct affects the vestibular nuclei on the lesion side[2]. Because this is below the pontine decussation, the SVV tilts toward the lesion — the same direction as a peripheral vestibular lesion, but with larger magnitude.
Why so large?
A unilateral peripheral lesion removes one vestibular nerve. A lateral medullary stroke removes the entire vestibular nuclear complex on that side — first-order central neurons integrating canal and otolith inputs. The asymmetry signal reaching the rest of the brainstem is correspondingly larger, and central compensation takes longer to develop because the compensating circuitry itself is partially damaged.
Companion findings
The classic Wallenberg constellation:
- Vertigo, nystagmus (often torsional, beating away from the lesion)
- Ipsilateral Horner’s syndrome
- Ipsilateral facial sensory loss (CN V), contralateral body sensory loss (spinothalamic)
- Ipsilateral palatal and pharyngeal weakness (CN IX, X) — hoarseness, dysphagia
- Ipsilateral limb ataxia (inferior cerebellar peduncle)
- Lateropulsion — the patient’s body falls toward the lesion side
Why SVV is the diagnostic shortcut
In an acutely vertiginous patient, a large ipsiversive SVV tilt with intact horizontal head impulse testing should raise immediate concern for a posterior circulation stroke. The combination is highly specific for a brainstem (rather than peripheral) origin. The bedside bucket test takes 90 seconds and may be the difference between admitting the patient and discharging them with ‘benign vertigo’.
In the first hours of a Wallenberg event, the SVV tilt may dominate the picture before the cranial nerve signs are obvious. A grossly tilted SVV in a patient without the expected audiovestibular peripheral pattern — preserved HIT, no nystagmus suppression with fixation — warrants posterior fossa imaging.