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

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Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on Cortical Hyperintensity T2/FLAIR

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