• malignant cerebral infarction = extensive infarction with large space-occupying edema
    • occurs in up to 10% of patients with supratentorial infarcts 
    • it is traditionally associated with a high mortality rate (up to 80%)  [Hacke, 1996]
  • occurs mainly in cases of ICA and MCA occlusions or with posterior circulation strokes (mainly cerebellar infarctions)
  • it is characterized by a development of edema within 24 h, clinical deterioration usually in < 72h, sometimes later (e.g., in case of collateral circulation failure and development of infarction in the penumbra
  • early surgical decompression reduces mortality and increases the number of younger patients with a favorable outcome according to randomized controlled trials (RCTs)

Predictors of malignant infarction

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Clinical features

  • the initial severe neurological deficit with hemiplegia, deviation of eyes and head, high NIHSS, nausea, vomitus
  • the posterior circulation infarction is associated with impaired consciousness, oculomotor dysfunction, altered brainstem reflexes, ataxia, and dysmetria
  • progressive impairment of consciousness and conus symptoms due to craniocaudal deterioration
  • Cushing’s triad is present in advanced stages of intracranial hypertension
    • hypertension
    • bradycardia
    • respiratory disorders
      • hypo-, hyperventilation
      • Cheyne-Stokes breathing
      • apneic pauses
  • cardiovascular lability
  • cerebellar infarctions are associated with an increased risk of brainstem compression and hydrocephalus development

Diagnostic evaluation

Blood tests

  • tests should exclude extracerebral causes of clinical deterioration
  • a basic metabolic panel including hepatic enzymes
  • minerals, including phosphate
  • coagulation and blood count
  • toxicology and ASTRUP should be considered in the presence of impaired consciousness not fully explained by structural changes on CT

Imaging methods

  • look for expansive behavior of ischemia and a midline shift on CT
  • repeat brain CT within the first 48h in high-risk patients [AHA/ASA 2014 I/C]
  • use MRI for early detection of large DWI lesions
    • prediction of fulminant course within 6 h: DWI lesion > 80-89 mL
    • prediction of fulminant course beyond 14 h: DWI lesion > 145 mL
Malignant ischemia

Malignant infarction in MCA and ACA territory
Malignant infarction in MCA territory
Cerebellar malignant infarction causing hydrocephalus

Others methods

  • EEG excludes nonconvulsive status epilepticus (unless NCCT correlates with the severe clinical condition)
  • TCD / TCCD can be used to monitor blood flow
    • occlusion detection (TIBI criteria)
    • signs of intracranial hypertension
  • ICP monitoring

Differencial diagnosis

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Medical therapy

  • routine intensive care for acute stroke patients see here
  • consider transport to a hospital capable of performing acute decompressive craniectomy
  • antiedema therapy
    • osmotic therapy Mannitol / NaCl 10% (AHA/ASA 2019 IIa/C-LD)
    • there are no data on the benefit of hypothermia, barbiturates, and corticosteroids in stroke patients and they are therefore not recommended
    • therapy should be initiated only in patients with developing edema; prophylactic administration of osmotherapy is not recommended
  • the effect of conservative treatment in malignant ischemia is usually insufficient and not clearly demonstrated


  • preferred in younger patients
  • with developing malignant ischemia, don’t wait for the effect of drug therapy (as it has only minimal impact)
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Clinical trials

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Malignant cerebral infarction