Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Causes of Stroke

Introduction

Cerebellar ischemic stroke occurs when there is an interruption of blood flow to the cerebellum, leading to ischaemia and infarction of cerebellar tissue. Cerebellar signs may not only be due to cerebellar disease but also involve its connections to the brainstem. Although cerebellar strokes account for less than 5% of all strokes, prompt recognition and management are crucial due to potential life-threatening complications such as brainstem compression and hydrocephalus.

About

• Cerebellar strokes constitute less than 5% of all strokes.
• Advances in imaging have led to increased diagnosis of smaller cerebellar infarcts, revealing a more benign prognosis in many cases.
• Even small amounts of cerebellar edema can acutely increase intracranial pressure (ICP) or directly compress the brainstem.
• Localized swelling results from both cytotoxic and vasogenic edema.
• Small cerebellar infarcts (diameter < 2 cm) are a frequent finding on MRI.

Blood Supply

The cerebellum is supplied by three main arteries, each with distinct territories and potential involvement of adjacent brainstem structures:

• Superior Cerebellar Artery (SCA): Supplies the superior aspect of the cerebellum and parts of the midbrain and pons. It arises from the basilar artery.
• Anterior Inferior Cerebellar Artery (AICA): Supplies the anterior inferior portion of the cerebellum and lateral pons. It also arises from the basilar artery.
• Posterior Inferior Cerebellar Artery (PICA): Supplies the posterior inferior cerebellum and lateral medulla. It originates from the ipsilateral vertebral artery. The PICA and AICA territories may vary inversely in size depending on individual anatomy.

Venous drainage occurs via the superior and inferior cerebellar veins, which empty into the superior petrosal, transverse, and straight dural venous sinuses.

Aetiology

• Large Artery Atherosclerosis: Vertebrobasilar atherosclerosis can lead to artery-to-artery embolism or in situ thrombosis.
• Cardioembolism: Emboli originating from the heart due to atrial fibrillation, left ventricular aneurysm, infective endocarditis, or myocardial infarction (especially ST-elevation MI).
• Arterial Dissection: Vertebral artery dissection, often associated with neck trauma or manipulation.
• Procedural Causes: Post cardiac catheterization or other vascular interventions can lead to embolic events.
• Other Causes: Hypercoagulable states, vasculitis, and less commonly, paradoxical emboli via a patent foramen ovale.

Clinical Features can vary but commonly includes:

• Vertigo and Dizziness: Sudden onset, often severe, and may be accompanied by nausea and vomiting.
• Headache: Occipital headache is common due to involvement of the posterior circulation.
• Ataxia: Ipsilateral limb ataxia leading to uncoordinated movements and difficulty walking (gait ataxia).
• Nystagmus: Abnormal eye movements, typically horizontal or vertical nystagmus.
• Dysarthria and Dysphagia: Difficulty speaking and swallowing due to involvement of cranial nerve nuclei.
• Horner's Syndrome: Ipsilateral ptosis, miosis, and anhidrosis resulting from disruption of sympathetic pathways.
• Diplopia: Double vision due to cranial nerve involvement.
• Altered Level of Consciousness: May progress to coma in cases of mass effect from edema.
• Positive Babinski Sign: Upgoing plantar reflex indicating corticospinal tract involvement.
• Neck Pain: May suggest vertebral artery dissection, especially if associated with head or neck trauma.
• Cardiac Findings: Evidence of atrial fibrillation or recent myocardial infarction as potential embolic sources.

Differential Diagnosis

• Labyrinthitis: Inflammation of the inner ear causing vertigo and balance disturbances.
• Vestibular Neuritis: Viral infection affecting the vestibular nerve.
• Alcohol Intoxication: Acute alcohol ingestion can cause ataxia and impaired coordination; important to differentiate, especially in unresponsive patients.
• Drug Toxicity: Medications such as anticonvulsants (e.g., phenytoin) can cause cerebellar symptoms.
• Multiple Sclerosis: Demyelinating lesions in the cerebellum presenting with ataxia and other neurological signs.
• Posterior Fossa Tumors: Mass lesions can mimic stroke symptoms due to compression of cerebellar structures.

Complications

• Hydrocephalus: Obstruction of the fourth ventricle leading to accumulation of cerebrospinal fluid (CSF) and increased intracranial pressure.
• Brainstem Compression: Edema and swelling can compress the brainstem, leading to respiratory arrest and death.
• Coma: A reliable clinical sign of worsening condition due to brainstem involvement.
• Aspiration Pneumonia: Due to impaired swallowing and reduced consciousness.
• Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE): Resulting from immobility and reduced consciousness.
• Respiratory Arrest: Due to involvement of respiratory centers in the brainstem.

Investigations

• Laboratory Tests: Full blood count (FBC), urea and electrolytes (U&E), liver function tests (LFTs), glucose, lipid profile, coagulation studies.
• Electrocardiogram (ECG): To detect atrial fibrillation or other arrhythmias.
• Chest X-ray (CXR): To assess for cardiac enlargement or pulmonary pathology.
• Computed Tomography (CT) Scan: May show cerebellar infarction or hemorrhage; early CT can be normal, but essential to rule out hemorrhage before thrombolysis.
• Magnetic Resonance Imaging (MRI): More sensitive than CT, especially with diffusion-weighted imaging (DWI) to detect acute infarcts.
• Magnetic Resonance Angiography (MRA) or Computed Tomography Angiography (CTA): To visualize vertebrobasilar circulation and identify arterial occlusions or dissections.
• Echocardiography: Transthoracic (TTE) or transesophageal (TEE) to identify cardiac sources of emboli.

Management: Early recognition and treatment are critical to prevent complications:

• Initial Stabilization:
  • Airway, breathing, circulation (ABC) assessment; secure airway if necessary.
  • Admit to a high-dependency unit (HDU) or intensive care unit (ICU) for monitoring.
  • Frequent neurological assessments to detect signs of deterioration.
• Thrombolytic Therapy:
  • Consider intravenous thrombolysis with alteplase if within the therapeutic window (typically within 4.5 hours of symptom onset) and no contraindications.
  • National Institutes of Health Stroke Scale (NIHSS) score > 3 or disabling stroke symptoms support consideration for thrombolysis.
• Antiplatelet Therapy:
  • Aspirin 300 mg should be administered if thrombolysis is not given or after ruling out hemorrhage on imaging.
• Management of Increased Intracranial Pressure:
  • Monitor for signs of increased ICP; elevate head of bed to 30 degrees.
  • Consider osmotherapy with mannitol or hypertonic saline in acute settings.
  • Neurosurgical consultation for potential decompressive surgery.
• Surgical Intervention:
  • Suboccipital decompressive craniectomy may be performed prophylactically or urgently in cases of large cerebellar infarcts with mass effect.
  • External ventricular drainage (EVD) may be necessary if hydrocephalus develops.
• Supportive Care:
  • Maintain adequate oxygenation and blood pressure within target ranges.
  • Prevent complications such as aspiration pneumonia, DVT/PE with prophylactic measures.
  • Physical therapy, occupational therapy, and speech therapy as part of rehabilitation.
• Secondary Prevention:
  • Address modifiable risk factors: hypertension, diabetes, hyperlipidemia, smoking cessation.
  • Initiate anticoagulation if atrial fibrillation is confirmed and after hemorrhagic transformation is ruled out.
  • Lipid-lowering therapy with statins.

Prognosis

The prognosis of cerebellar ischemic stroke varies depending on the size of the infarct, timely recognition, and management of complications:

• Small cerebellar infarcts may have a benign course with good recovery.
• Large infarcts with mass effect carry a high risk of deterioration and mortality if not promptly managed.
• Early surgical intervention has been associated with improved outcomes in cases of significant edema and brainstem compression.

References

• Neurology textbooks such as "Adams and Victor's Principles of Neurology" for detailed descriptions of cerebellar strokes.
• American Heart Association/American Stroke Association guidelines for management of acute ischemic stroke.
• Edlow JA, Newman-Toker DE, Savitz SI. A new diagnostic approach to the adult patient with acute dizziness. J Emerg Med. 2008;45(2):141-158.
• Voetsch B, DeWitt LD, Pessin MS, Caplan LR. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 2004;61(4):496-504.