Cerebellar infarction

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Mechanism

• Strokes are usually due to atherosclerotic disease or embolic events.

  • Less common causes are trauma, tumor, arterial dissection, migraine, fibromuscular dysplasia or vasculitis. As you might expect, these other causes are relatively more common in young patients with cerebellar infarcts.

• Embolic cerebellar strokes are more likely to be bilateral and involve other regions, and are more likely to be hemorrhagic.

Anatomical Distribution

• There have been several case series of cerebellar stroke. They have divided the groups slightly differently, but generally sort them according to vessel as follows:

  • Superior cerebellar artery territory (SCA) – middle region
  • Anterior inferior cerebellar artery territory (AICA) – middle region
  • Posterior inferior cerebellar artery (PICA) – proximal region

Epidemiology and Demographics

Infarcts in the cerebellum are relatively uncommon, representing about 1.5% (0.6-4.2% in different studies) of all strokes. Identification is important however, because patients may present with vertigo suggestive of a benign disorder, and because postinfarct edema can sometimes result in life-threatening brain stem compression. Up to half of all cerebellar infarcts may be asymptomatic or misdiagnosed as a benign vertiginous syndrome. Cerebellar infarcts are more common than cerebellar hemorrhages, accounting for 85% of all cerebellar strokes.

Risk Factors

Risk factors for cerebellar stroke are similar to those for usual strokes:

• Hypertension (HTN) (45-48%)
• Diabetes Mellitus (DM) (16-23%)
• Coronary Artery Disease (CAD) (25%)
• Smoking (36-38%)
• Hyperlipidemia (11-14%)
• Atrial Fibrillation (AF) (12-23%)
• Male gender – 2-3 more common in men than women
• Increased age – mean age 65

Natural History, Complications and Prognosis

• Prognosis correlates to a large extent on size of infarct. Prognosis is often generally fair in patients who do not develop postinfarct edema.

  • Likelihood of significant postinfarct edema and brain stem compression correlate with size of infarct and location.

• Prognosis is better in patients with higher levels of consciousness on presentation.
• In one series of 282 patients, postinfarct outcomes were:

  • Independent 69%
  • Dependent 21%
  • Bedridden 4%
  • Vegetative state 1%
  • Death 5%

History and Symptoms

• The clinical manifestations in cerebellar stroke, and to some extent the mechanism, can be described based on the vascular distribution of the stroke. There are some generalities that are discussed below regarding the likelihood of particular signs and symptoms depending on the vessel involved. Note that SCA and PICA strokes are most common.

Superior cerebellar artery territory (SCA) – middle region

• Limb ataxia very common (73%)
• Gait disturbance usually present (67%) – usually sudden and severe; patients tend to fall to the side of the cerebellar lesion (ipsilateral axial lateropulsion)
• Headache (often posterior) in a subset (40%); vertigo in a subset (37%), with nystagmus in 50%
• Vomiting common in patients with vertigo, but also present in a subset without vertigo
• Dysarthria common
• Prognosis better than PICA infarcts, with mass effect, hydrocephalus and brain stem compression only in 7%
• Embolic source relatively common, accounting for up to two-thirds of all cases (70%) in one study.

Anterior inferior cerebellar artery territory (AICA) – middle region

• Uncommon compaired to SCA and PICA infarcts
• Vestibular signs usually present
• Dysmetria common
• Horner’s syndrome (meiosis, ptosis and anhydrosis)
• Facial sensory impairment
• Contralateral pain and temperature sensory loss in the limbs
• Also may have headache, vertigo and gait imbalance
• Less common features include dysphagia, severe facial palsy, deafness, lateral gaze palsy
• Commonly due to atherosclerosis of the basilar artery

Posterior inferior cerebellar artery (PICA) – proximal region

• Commonly present with vertigo (78%), headache (often posterior) (64%) and gait imbalance (75%)
• Vertigo is usually sudden, and often associated with vomiting. Nystagmus present in 75%.
• Gait imbalance usually sudden and severe; patients tend to fall toward the side of the cerebellar lesion (ipsilateral axial lateropulsion)
• Limb ataxia occurs in half (50%)
• Severe cerebellar mass effect in 30%, resulting in hydrocephalus in 20%, resulting in death in 10%
• Commonly caused by both embolic and arterial disease
• Lateral medullary syndrome of Wallenberg present completely in a third (33%), but most show some aspects of:

  • Ipsilateral hand ataxia
  • Horner’s syndrome
  • Palatal weakness
  • Facial hypesthesia to pain and temperature
  • Contralateral hypesthesia to pain and temperature in the limbs and trunk
  • Note that the lateral medullary syndrome of Wallenberg may also be seen less commonly in other cerebellar strokes with different vascular distributions

Other adjacent areas may also be affected

• Brainstem infarct – facial palsy, trigeminal involvement, ocular motor abnormalities, motor weakness, and sensory loss
• Occipitotemporal infarct – visual field defects, cortical blindness, memory loss

Pseudotumor Cerebellar Infarcts

In any distribution, significant postinfarct edema and brain stem compression may occur. Aqueduct or fourth ventricle obstruction can cause obstructive hydrocephalus and acute intracranial hypertension. Cerebellar swelling can also cause tonsillar herniation through the foramen magnum.

• Described by Menzies in 1893
• Likelihood correlates with size of infarct and location.
• Complete (versus partial) infarct in a particular vessel’s distribution usually is present in these patients
• PICA infarcts are more likely to have this effect
• May develop anytime 12 hours to 10 days after the stroke (mean 2-5 days)
• Clinically patients develop lethargy and coma. Early signs might include contralateral or bilateral hemiplegia suggestive of brain stem infarction, or 6th nerve palsy, suggestive of lateral pontine compression by the adjacent swollen cerebellar hemisphere.
• Surgery is indicated once consciousness changes.

  • Ventricular drainage or suboccipital craniectomy to open the dura mater.
  • Recovery rates with surgery may be as high as 63%.

MRI

• MRI is the gold standard for stroke identification and localization, and shows increased signal on T2-weighted axial and coronal sections.

CT

• CT effectively images most cerebellar infarcts, somewhat impaired by bone shadowing.

References

1. Kase, CS, et al. Cerebellar infarction: 66 cases. Stroke 1993;24:76.
2. Chaves, CJ, et al. Cerebellar infarctions in the NEMC posterior circulation stroke registry. Neurology 1994;44:1385.
3. Tohgi, H, et al. Cerebellar infarction: 293 cases. Stroke 1993;24:1697.
4. Amarenco, P. Spectrum of cerebellar infarctions. Neurology 1991;41:973.
5. Amarenco, P, et al. Territorial and nonterritorial cerebellar infarcts in 115. Stroke 194;25:105.
6. Barinagarrementeria, F, et al. Cerebellar infarction in young patients. Stroke 1997;28:2400.
7. Chaves, CH, et al. Cerebellar hemorrhagic infarction. Neurology 1996;46:346.

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