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Cerebellar Strokes

Learning objectives

  • Anatomy of Cerebellum and its connections
  • Clinical presentation of cerebellar strokes
  • Management of cerebellar strokes


  • The cerebellum contains as many neurons as the entire cerebrum. Its primary role is the coordinating motor function with other parts of the brain. It is composed of a core of white matter surrounded by grey matter. The cerebellum also consists of a cortex covered in grey matter folded into folia with deep fissures. Anatomically it is closely related to the IVth ventricle and contains 4 deep nuclei called the dentate, emboliform, globose and fastigial.
  • The cerebellum receives sensory input as well as input from the motor and premotor cortex and returns feedback to these same centres. As such the cerebellar hemispheres deal with ipsilateral movement and function. Cerebellar hemispheres communicate via inferior, middle and superior cerebellar peduncles. Inferiorly lie the cerebellar tonsils which are important in Arnold-Chiari malformations. The cerebellum is separated from the pons by the fourth ventricle. Histologically the important functional cell is the Purkinje cell which lies between the molecular and deep granular layer of cells. The purkinje cells communicate with the deep cerebellar nuclei.
  • The cerebellum is composed of a midline vermis and two lateral cerebellar hemispheres. It is composed of anterior and posterior lobes and flocculomodular lobe. The vermis is concerned with midline and truncal position and receives input from the spinal cord. Dysfunction is noted by postural instability and gait ataxia. Processing occurs in the cerebellar hemisphere and output is via the superior cerebellar peduncle which decussates in the midbrain and whose fibres pass to the motor nuclei of the thalamus and from there back to the motor and premotor cortex.

Cerebellar peduncles

  • The cerebellum attaches to the posterior aspect of the brainstem by 3 large tracts, the superior, middle and inferior cerebellar peduncles. Do not confuse these with the cerebral peduncle.
  • Superior cerebellar peduncle (brachium conjunctivum) contains efferent fibres from the cerebellum to other centres.
  • Middle cerebellar peduncle (brachium pontis) has afferent fibres from the cerebral cortex. The cerebellar hemispheres receive input from the contralateral motor and premotor cortices by fibres which have decussated in the pons and enter the cerebellum via the middle cerebellar peduncle. The middle peduncle brings input from pontine nuclei.
  • Inferior cerebellar peduncle receives input from the spinal cord.

Cerebellar Anatomy:The cerebellum is composed of three lobes

  • Anterior lobe (lobules I-V according to the revised Larsell classification): anterior lobe is separated from the posterior lobe by the primary fissure, which is easily identified in the axial and midsagittal plane as the deepest and thickest fissure in the superior part of the vermis
  • Posterior lobe (lobules VI-IX): There are two prominent fissures within the posterior lobe of the cerebellum; the posterior superior fissure and the great horizontal fissure. The posterior superior fissure runs parallel and posterior to the primary fissure in the superior surface of the cerebellum. The great horizontal fissure runs together with the posterior superior fissure in the midline. More laterally, it slopes inferiorly in the posterior surface of the cerebellum. Lobule VI is easily recognized as the area in between the primary fissure and the posterior superior fissure
  • Flocculonodular lobe (lobule X) : composed of the nodulus in the midline and the flocculus in the cerebellar hemispheres.

Vascular Supply

  • Superior Cerebellar Artery: The SCA territory is in the superior and tentorial surface of the cerebellum. It comes off the basilar artery.
  • Anterior Inferior Cerebellar Artery : Comes of the basilar artery.
  • Posterior Inferior Cerebellar Artery: 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.

Cerebellar Infarction

  • Cerebellar signs may not just be due to cerebellar disease but also due to vascular damage to its connections to the brainstem via the cerebellar peduncles
  • Cerebellar strokes cause less than 5 % of all strokes. Prognosis more benign than initially seen as smaller infarcts now diagnosed more.
  • However even small amounts of cerebellar oedema or haemorrhage can acutely increase intracranial pressure (ICP) or directly compress the brainstem with hydrocephalus.
  • Localised swelling results from both cytotoxic and vasogenic edema
  • Very small cerebellar infarcts (diameter <2 cm) are a frequent finding on MRI. With an increasing scientific interest in cerebral microinfarcts, very small infarcts in the cerebellum have been referred to as lacunar infarcts, as junctional, border zone or watershed infarcts, as nonterritorial infarcts, as very small territorial or end zone infarcts, or simply as (very) small cerebellar infarcts


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


  • 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


  • Labyrinthitis
  • Alcohol - its not unique for a person with a cerebellar stroke to spend a night in the drunk tank or the drunk person to be admitted as stroke
  • Drug toxicity - anticonvulsants


  • 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


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


  • Admit to HASU or ITU as needed. ABC. 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 practised at most stroke centers.
  • External ventricular drainage may be considered

    Learning objectives

    • Causes of Cerebellar haemorrhage
    • Clinical presentation
    • Diagnosis and management
    • Role of surgical intervention


  • Some may need urgent neurosurgical input with clot evacuation and urgent neurosurgery


  • Cause of acute usually non transient vertigo with other symptoms


  • Midline lesions can damage deep cerebellar nuclei
  • Hemispheric (better prognostically) The more lateral the bleed the better


  • Hypertensive rupture of small penetrating vessels
  • Amyloid angiopathy, Cocaine
  • AV malformations, Tumours with haemorrhage
  • Anticoagulants / Coagulopathies
  • Spinal surgery, Spontaneous intracranial hypotension


  • Abrupt onset of nausea, vertigo, headache, vomiting
  • Ipsilateral cerebellar signs and VI and VII nerve lesions
  • (Truncal) Ataxic gait unable to walk usually
  • Coma and pupillary abnormalities suggest compression
  • Neck stiffness and pain
  • Coma, loss of corneal reflexes, pinpoint pupils
  • Extensor plantars, Cheyne stokes


  • Swelling and pressure on brainstem causing coma with increased pressure and reduced perfusion of brainstem
  • Obstructing CSF flow due to compression of the ventricle leading to hydrocephalus
  • Death due to the above


  • FBC, Coagulation Screen, U&E, LFTs
  • ECG and CXR if needed
  • Urgent CT head is usually diagnostic. Measure maximal diameter of bleed and look for hydrocephalus. Look for brainstem distortion and blood in ventricles.
  • MRI may be performed if stable especially if there is suspect structural lesion


  • Correct any coagulopathy e.g. Octaplex or similar for warfarin. Cautiously control any high BP.
  • Admit stroke Unit and manage as any haemorrhagic stroke if not for surgery. Escalate in any change in condition. For those with significant coma, brainstem signs then end of life care may be indicated. Take expert advice.
  • Ventriculostomy is indicated in patients with haemorrhage and hydrocephalus.
  • Suboccipital craniotomy with clot evacuation is indicated in patients with reduced LOC and a large clot usually > 3-4 cm in diameter
  • Consider Mannitol 1 g/kg as a bridge to surgical treatment in those with evidence of increased pressure.
  • Refer to neurosurgeons as there can be profound benefits from timely surgery in those where brainstem compression or hydrocephalus is imminent. However if patient is awake with a near normal GCS(14/15) and the bleed is less than 3 cm and no sign of hydrocephalus then these patients may be managed conservatively with an option to operate with any deterioration.
  • Do not forget the role of good Multidisciplinary stroke unit care and rehabilitation.

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