Makindo Medical Notes

An anterior (medial) medullary infarct is a brainstem stroke of the medial medulla, usually due to occlusion of the anterior spinal artery or paramedian branches of the vertebral artery. It classically produces a triad of contralateral hemiparesis, contralateral loss of vibration and joint position sense, and ipsilateral hypoglossal palsy. Recognising this pattern helps distinguish it from the more common lateral medullary (Wallenberg) syndrome.

🧬 Vascular Anatomy & Pathophysiology

• The medial medulla is supplied by the anterior spinal artery and small paramedian branches of the vertebral arteries.
• Occlusion causes infarction of:
  • Corticospinal tract → contralateral limb weakness.
  • Medial lemniscus → contralateral loss of vibration and proprioception.
  • Hypoglossal nucleus or exiting XII nerve fibres → ipsilateral tongue weakness.
• Atherosclerosis of the vertebral artery, cardioembolism, or vertebral dissection may underlie the event, especially in younger patients.

📌 Clinical Features (Classic Triad)

• Contralateral hemiparesis (arm and leg) – often pyramidal distribution; face may be relatively spared.
• Contralateral loss of vibration and joint position sense – due to medial lemniscus involvement.
• Ipsilateral hypoglossal palsy – tongue deviates towards the lesion on protrusion, with dysarthria and swallowing difficulty.

Additional/variant features:

• Ataxia from involvement of descending cerebellar pathways.
• Respiratory or cardiovascular instability in extensive lesions.
• Usually no Horner’s syndrome or spinothalamic sensory loss – those point more to lateral medullary infarction.

🩻 Imaging

• MRI with DWI is the modality of choice, often showing a “V-shaped” or paramedian lesion in the medial medulla on axial images.
• CTA/MRA should assess vertebral arteries and the origin of the anterior spinal artery for stenosis, occlusion, or dissection.
• CT head is frequently normal early or may show only subtle changes; MRI is often needed for confirmation.

💊 Management

• Acute management follows usual hyperacute stroke protocols – assess for IV thrombolysis and/or thrombectomy according to timing and imaging.
• Secondary prevention as per ischaemic stroke: antiplatelet or anticoagulation (if cardioembolic), statin, BP and risk-factor control, smoking cessation.
• Rehabilitation focuses on bulbar function (swallow, speech), limb weakness, and gait/balance training.
• Monitor for respiratory compromise and aspiration risk; early SALT and nutrition input are often needed.

🧑‍⚕️ Teaching Pearls

• Think “medial medulla = XII + pyramids + medial lemniscus” → tongue, power, and dorsal-column sensation.
• Crossed signs (ipsilateral cranial nerve, contralateral body) are a big clue to a brainstem lesion.
• Differential includes lateral medullary syndrome, high cervical cord lesions, and internal capsule strokes – the tongue sign helps localise.