Wallenberg Syndrome — Cause, Clinical Features and Treatment

Definition. Wallenberg syndrome is the lateral medullary syndrome — infarction of the dorsolateral medulla, often with the inferior cerebellum. Despite the name “PICA syndrome”, the commonest vessel involved is the vertebral artery (about 80%), with PICA occlusion accounting for the remainder.

Causes in the elderly. Atherothrombosis of the vertebral artery (commonest), cardioembolism (atrial fibrillation), vertebral artery dissection — which may follow neck manipulation, trauma or even trivial neck rotation and should be suspected when there is neck or occipital pain — vasculitis, and hypercoagulable states.

Clinical features — the crossed sensory loss. Loss of pain and temperature sensation on the IPSILATERAL face (spinal trigeminal nucleus and tract) with loss of pain and temperature on the CONTRALATERAL body (spinothalamic tract), while touch, vibration and proprioception are preserved. This dissociated, crossed pattern is the diagnostic signature.

Other ipsilateral features. Horner’s syndrome — ptosis, miosis, anhidrosis (descending sympathetic fibres); cerebellar ataxia and lateropulsion (inferior cerebellar peduncle) — the body is pulled towards the side of the lesion; vertigo, nystagmus, nausea and vomiting (vestibular nuclei); intractable hiccups; and dysphagia, hoarseness, absent gag reflex and ipsilateral palatal weakness (nucleus ambiguus).

The key negative and the practical dangers. There is NO hemiparesis — the pyramidal tract lies medially and is spared. This is the single most useful discriminator from a hemispheric stroke. Two dangers dominate management: severe dysphagia out of proportion to the rest of the deficit, with a very high aspiration risk, and rarely Ondine’s curse (loss of automatic respiration), which is life-threatening.

Diagnosis and treatment. MRI with DWI is the investigation of choice — CT frequently misses posterior fossa infarcts; add CT or MR angiography of the vertebrobasilar system to identify occlusion or dissection. Treatment: thrombolysis if within the window, stroke-unit care, and above all aspiration prevention — nil by mouth, formal swallow assessment, nasogastric feeding and early speech-and-language therapy. Secondary prevention with an antiplatelet (or anticoagulation for cardioembolism), high-intensity statin, and blood pressure and glycaemic control. Treat intractable hiccups (baclofen, chlorpromazine or gabapentin) and central post-stroke pain (amitriptyline or pregabalin); vestibular rehabilitation and physiotherapy for lateropulsion. Prognosis is generally good, with recovery over weeks to months.

AHA/ASA 2026 Acute Ischaemic Stroke Guideline — posterior circulation stroke. Two points are directly relevant. First, thrombolysis is recommended for any disabling deficit within 4.5 hours regardless of NIHSS score — important because posterior circulation strokes such as Wallenberg systematically score low on the NIHSS despite causing severe disability and dysphagia. Second, endovascular thrombectomy is now recommended for basilar artery occlusion (following the ATTENTION and BAOCHE trials), the condition to which progressive vertebrobasilar disease may lead. The guideline also contains updated recommendations on dysphagia screening and management, the dominant practical problem in this syndrome.