Wallenberg’s syndrome (lateral medullary syndrome)

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86 Wallenberg’s syndrome (lateral medullary syndrome)

Instruction

Examine this patient’s cranial nerves.

Salient features

History

• Severe nausea, vomiting, nystagmus (involvement of the lower vestibular nuclei)

• Limb ataxia (involvement of the inferior cerebellar peduncle)

• Intractable hiccups, dysphagia (ninth and tenth cranial nerve involvement).

Examination

• Ipsilateral involvement of fifth, sixth, seventh and eighth cranial nerves

• Bulbar palsy: impaired gag, sluggish palatal movements

• Horner syndrome.

Proceed as follows:

• Tell the examiner that you would like to check for the following:

• Cerebellar signs on the same side

• Pain and temperature sensory loss on the opposite side (dissociated sensory loss).

• The main features of this syndrome is ipsilateral Horner syndrome and contralateral loss of pain and temperature sensation.

• Wallenberg syndrome is an infarction of the lateral portion of the medullary tegmentum. The most common cause is occlusion of the intracranial vertebral artery.

• Neuroimaging: MRI is preferred because CT provides less complete visualization of the brainstem, owing to artefacts related to the skull. MRI with diffusion-weighted imaging is the most sensitive test available to detect acute infarcts.

Diagnosis

This patient has lateral medullary syndrome (lesion) caused by a stroke (aetiology) and has dysphagia (functional status).

Advanced-level questions

Which vessel is occluded?

Any of the following five vessels:

• Posterior inferior cerebellar artery

• Vertebral artery

• Superior, middle or inferior lateral medullary arteries.

How may these patients present?

With sudden onset of vertigo, vomiting and ipsilateral ataxia, with contralateral loss of pain and temperature sensations.

Where is the lesion in lateral medullary syndrome?

It results from infarction of a wedge-shaped area of the lateral aspect of the medulla and inferior surface of the cerebellum. The deficits are from involvement of one side of the nucleus ambiguus, trigeminal nucleus, vestibular nuclei, cerebellar peduncle, spinothalamic tract and autonomic fibres.

What is the medial medullary syndrome?

It is caused by occlusion of the lower basilar artery or vertebral artery. Ipsilateral lesions result in paralysis and wasting of the tongue. Contralateral lesions result in hemiplegia and loss of vibration and joint position sense.

Mention a few other eponymous syndromes with crossed hemiplegias

• Weber syndrome: contralateral hemiplegia with ipsilateral lower motor neuron lesion of the oculomotor nerve. The lesion is in the midbrain

• Millard–Gubler syndrome: contralateral hemiplegia with lower motor neuron lesion of the abducens nerve. The lesion is in the pons

• Foville syndrome: as Millard–Gubler syndrome with gaze palsy.

What is Benedikt syndrome?

It causes cerebellar signs on the side opposite the third nerve palsy (which is produced by damage to the nucleus itself or to the nerve fascicle). It is caused by a midbrain vascular lesion causing damage to the red nucleus, interrupting the dentatorubrothalamic tract from the opposite cerebellar signs.

Further reading

Savitz SI, Caplan LR. Vertebrobasilar disease. N Engl J Med. 2005;352:2618. classic article

Achille LF Foville (1799–1878), a Parisian neurologist.

Auguste LJ Millard (1830–1915) and Adolphe Marie Gubler (1821–1879), Parisian physicians.

Adolf Wallenburg (1862–1949), a German neurologist, described this syndrome in 1895.

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