Cortical Hyperintensity T2/FLAIR

Cortical Hyperintensity T2/FLAIR
Karen L. Salzman, MD
DIFFERENTIAL DIAGNOSIS
Common
  • Cerebral Ischemia-Infarction, Acute
  • Cerebral Contusion
  • Hypotensive Cerebral Infarction
  • Status Epilepticus
  • Herpes Encephalitis
Less Common
  • Diffuse Astrocytoma, Low Grade
  • Acute Hypertensive Encephalopathy, PRES
  • Vasculitis
  • Oligodendroglioma
  • Anaplastic Oligodendroglioma
  • Hypoxic-Ischemic Encephalopathy, NOS
  • DNET
  • Pleomorphic Xanthoastrocytoma
  • Tuberous Sclerosis Complex
  • Cerebritis
  • Hypoglycemia
Rare but Important
  • MELAS (Acute Presentation)
  • Creutzfeldt-Jakob Disease (CJD)
  • Dysplastic Cerebellar Gangliocytoma
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
  • Vast majority of cortical lesions are related to ischemia & trauma
  • Remainder of lesions much less common and include primarily tumors & infections
  • DWI may help differentiate lesions
Helpful Clues for Common Diagnoses
  • Cerebral Ischemia-Infarction, Acute
    • T2 hyperintensity in a typical vascular distribution (ACA, MCA, PCA)
    • Wedge-shaped, involves gray matter (GM) & white matter (WM)
    • DWI restriction
  • Cerebral Contusion
    • T2 hyperintensity in inferior frontal & temporal lobe GM & subcortical WM
    • Blood products nearly always present
    • CT: Patchy superficial hemorrhages with surrounding edema
    • History of trauma
  • Hypotensive Cerebral Infarction
    • “Border zone” or watershed infarct related to insufficient cerebral blood flow
    • T2 hyperintense cortically based, wedge-shaped lesions at border zone between vascular territories
    • Edematous gyri with local mass effect
    • May involve basal ganglia (BG) & thalamus
    • DWI positive acutely
  • Status Epilepticus
    • T2 hyperintensity in GM &/or subcortical WM with mild mass effect
    • May focally involve hippocampus or corpus callosum
    • DWI positive acutely; variable enhancement
  • Herpes Encephalitis
    • T2 hyperintensity in the limbic system & temporal lobes; DWI positive
    • Subtle blood products, patchy enhancement common
    • Typically bilateral, but asymmetric
    • Acute onset, often with fever; may present with seizures
Helpful Clues for Less Common Diagnoses
  • Diffuse Astrocytoma, Low Grade
    • Infiltrating T2 hyperintense WM mass
    • May extend to involve cortex
    • No enhancement typical
  • Acute Hypertensive Encephalopathy, PRES
    • Patchy cortical/subcortical PCA territory lesions in a patient with severe acute/subacute hypertension (HTN)
    • Parietooccipital T2 hyperintense cortical lesions in 95%
    • DWI: Usually normal
    • Variable patchy enhancement
    • Diverse causes, clinical entities with HTN
  • Vasculitis
    • Multiple small areas of T2 hyperintensity in deep & subcortical WM, often bilateral
    • GM involvement common
    • DWI positive in acute setting
    • Variable enhancement
  • Oligodendroglioma
    • Calcified T2 hyperintense frontal mass
    • Slowly growing but diffusely infiltrating cortical/subcortical mass
    • Variable enhancement
  • Anaplastic Oligodendroglioma
    • Calcified frontal lobe mass involving cortex/subcortical WM, ± enhancement
    • May appear discrete, but always infiltrative
    • Difficult to differentiate from oligodendroglioma
  • Hypoxic-Ischemic Encephalopathy, NOS
    • Bilateral cortical involvement common
    • Deep gray nuclei often involved
    • DWI positive in acute setting
  • DNET
    • Well-demarcated, wedge-shaped “bubbly” cortical mass
    • Temporal & parietal lobes most common
    • May remodel overlying bone
    • Typically a young patient with longstanding seizures
  • Pleomorphic Xanthoastrocytoma
Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on Cortical Hyperintensity T2/FLAIR

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