Cerebellar Ischaemic Stroke

Learning objectives

Causes of Cerebellar Infarcts Clinical presentation Diagnosis and management Role of surgical intervention

About

• Cerebellar signs may not just be due to cerebellar disease but also its connections to the brainstem
• Less than 5 % of all strokes. Prognosis more benign than initially seen as smaller infarcts now diagnosed more.
• Even small amounts of cerebellar oedema can acutely increase intracranial pressure (ICP) or directly compress the brainstem.
• Localised swelling results from both cytotoxic and vasogenic edema
• Very small cerebellar infarcts (diameter <2 cm) are a frequent finding on MRI.

Blood supply

• Superior cerebellar artery: May also supply lateral midbrain/pons. The SCA territory is in the superior and tentorial surface of the cerebellum. It comes off the basilar artery.
• Anterior inferior cerebellar artery: May also supply lateral pons. Comes of the basilar artery.
• Posterior inferior cerebellar artery: May also supply lateral medulla. Comes of the ipsilateral vertebral artery and supplies lateral medulla and inferior surface of the cerebellum. The PICA and AICA are in balance, if one is smaller the other larger and vice versa.
• Venous drainage by the superior and inferior cerebellar veins. They drain into the superior petrosal, transverse and straight dural venous sinuses.

Aetiology

• Vertebrobasilar atherosclerosis with artery to artery embolism
• Cardioembolism - AV, LV aneurysm, Endocarditis, STEMI
• Aorta/Subclavian atherosclerosis with artery to artery embolism
• Post Cardiac catheterisation

Clinical

• Vomiting, headache, Horner's syndrome
• Ipsilateral limb ataxia, vertigo, nystagmus, past pointing,
• Local oedema with coma and upgoing plantars
• Head or neck pain consider vertebral artery dissection.
• Look for AF and MI and other embolic causes

Differentials

• Labyrinthitis
• Alcohol - it is not unique for a person with a cerebellar stroke to spend a night with the police as a "drunk" until patient doesn't sober up !
• Drug toxicity - anticonvulsants

Complications

• Coma with Brainstem (pontine) compression and acute hydrocephalus due to obstruction of the IVth ventricle.
• Coma is most reliable clinical sign.
• Aspiration, DVT/PE, Respiratory arrest

Investigations

• FBC, U&E, LFTs, Glucose, Lipids, ECG, CXR
• CT may show evolved large infarct and hydrocephalus but can be normal early on
• MRI: Positive DWI and increased signal on T2-weighted axial and coronal sections
• MRA/CTA may show vertebrobasilar disease

Management

• ABC, Admit to HASU or ITU as needed. Comatose may need airway protection and intubated and ventilated. Coma usually develops post admission depending on onset time.
• Alteplase may be considered if NIHSS > 3 / disabling stroke suspected
• Aspirin 300 mg given if not thrombolysed or post lysis if CT no blood
• Prophylactic suboccipital decompression of large cerebellar infarcts before brainstem compression, although not tested rigorously in a clinical trial, is practiced at most stroke centers.
• External ventricular drainage may be considered

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