Neurosurgery notes/Cerebellar infarction

Cerebellar infarction

View Details
logo
Parent item
Occlusion syndrome
Numbers
  • Relatively rare
    • 0.6% of all CTs obtained for any reason
    • 80% of patients developing signs of brainstem compression will die, usually within hours to days.
Classified as involving the
  • PICA distribution (cerebellar tonsil and/or inferior vermis),
  • Superior cerebellar artery distribution (superior hemisphere or superior vermis),
  • Other indeterminate patterns.
Clinical features
  • Sudden onset, without premonitory symptoms.
  • Early
    • The first 12 hrs after onset were characterized by lack of progression.
    • Clinical features due to the intrinsic cerebellar lesion (ischemic infarction or hemorrhage)
    • Symptoms
      • Dizziness or vertigo
      • Nausea/vomiting
      • Loss of balance, often with a fall and inability to get up
      • Headache (infrequent)
    • Signs
      • Truncal and appendicular ataxia
      • Nystagmus
      • Dysarthria
  • Later
    • Develop increased pressure within the posterior fossa (due to cerebellar edema or mass effect from clot), with brainstem compression (particularly posterior pons).
    • Clinical findings generally increase between 12 and 96 hrs following onset.
    • Compression of the Sylvian aqueduct can cause acute hydrocephalus with attendant increased ICP.
Imaging studies
  • CT scan:
    • May be normal very early in these patients.
    • Subtle findings of a tight posterior fossa:
      • Compression or obliteration of basal cisterns or 4th ventricle or hydrocephalus.
  • MRI: (including DWI)
    • More sensitive for ischemia, especially in the posterior fossa.
Surgical indications
  • Having the following symptoms: (Findings proceed in the approximate following sequence if there is no intervention) AND
    • Abducens (VI) nerve palsy
    • Loss of ipsilateral gaze (compression of VI nucleus and lateral gaze center)
    • Peripheral facial nerve paresis (compression of facial colliculus)
    • Confusion and somnolence (may be partly due to developing hydrocephalus)
    • Babinski sign
    • Hemiparesis
    • Lethargy
    • Small but reactive pupils
    • Coma
    • Posturing → flaccidity
    • Ataxic respirations
  • If there is no response to medical therapy.
  • Suboccipital craniectomy for cerebellar infarction
    • Similar to patients with cerebellar hemorrhage
    • The operation of choice is a suboccipital decompression to include enlargement of the foramen magnum.
      • The dura is then opened and the infarcted cerebellar tissue usually exudes “like toothpaste” and is easily aspirated.
    • Avoid using ventricular drainage alone
      • Cause upward cerebellar herniation
      • Does not relieve the direct brainstem compression.
  • Lateral medullary syndrome (LMS)
    • Often accompany a cerebellar infarct.
    • Signs are usually present from the onset (dysphagia, dysarthria, Horner syndrome, ipsilateral facial numbness, crossed sensory loss…)
    • There is no place for surgical decompression
      • Represents primary brainstem ischemia and not compression.