T2 Hyperintense Basal Ganglia



T2 Hyperintense Basal Ganglia


Karen L. Salzman, MD



DIFFERENTIAL DIAGNOSIS


Common



  • Hypoxic-Ischemic Encephalopathy, NOS



    • Hypotensive Cerebral Infarction


    • HIE, Term


  • Neurofibromatosis Type 1


  • ADEM


  • CO Poisoning


  • Vasculitis



    • Systemic Lupus Erythematosus


    • Hemolytic Uremic Syndrome


    • Infectious Vasculitis


Less Common



  • Drug Abuse


  • Gliomatosis Cerebri


  • Osmotic Demyelination Syndrome


  • Encephalitis (Miscellaneous)


Rare but Important



  • Creutzfeldt-Jakob Disease (CJD)


  • Acute Hypertensive Encephalopathy, PRES


  • Metabolic, Inherited



    • Leigh Syndrome


    • Wilson Disease


    • MELAS


    • MERRF


    • Glutaric Aciduria Type 1


  • Huntington Disease


ESSENTIAL INFORMATION


Key Differential Diagnosis Issues



  • Basal ganglia (BG) are paired deep gray nuclei & include caudate nuclei, putamen, & globus pallidus (GP)


  • Lentiform nucleus: Putamen & GP


  • Corpus striatum: Caudate, putamen, & GP


  • Symmetric BG lesions suggest a toxic/metabolic process or hypoxia


  • DWI may help differentiate BG lesions


Helpful Clues for Common Diagnoses



  • Hypoxic-Ischemic Encephalopathy, NOS



    • Includes anoxia, hypoxia, near drowning, & cerebral hypoperfusion injury


    • T1 & T2 hyperintense BG & cortical lesions


    • DWI restriction if acute


  • Hypotensive Cerebral Infarction



    • Infarct resulting from insufficient cerebral blood flow to meet metabolic demands


    • May be isolated to BG


    • Border zone between major arterial territories typical


    • DWI restriction if acute


  • HIE, Term



    • Involvement of BG & thalamus typically seen with profound insult


    • T1 & T2 hyperintensity in BG & thalamus


    • Ventrolateral thalamus typically involved


    • DWI restriction if acute


  • Neurofibromatosis Type 1



    • Focal areas of increased signal intensity (FASI) characteristic, BG typical


    • May also see FASI in brainstem


  • ADEM



    • Multifocal white matter (WM) & BG lesions following infection/vaccination


    • Bilateral, asymmetric T2 hyperintensities


  • CO Poisoning



    • Bilateral, symmetric GP T2 hyperintensity


    • May also involve putamen, thalamus, WM


  • Vasculitis



    • Heterogeneous group of CNS disorders characterized by nonatheromatous inflammation & blood vessel wall necrosis


    • Angiography: Multifocal areas of smooth or mildly irregular stenosis alternating with dilatations


    • T2 hyperintensity in BG & WM


    • DWI restriction if acute


  • Systemic Lupus Erythematosus



    • CNS involvement in up to 75% of cases, typically multifocal ischemia


    • True vasculitis of CNS is rare in SLE


    • Small multifocal WM lesions ± BG


  • Hemolytic Uremic Syndrome



    • May cause vasculitis or hypertensive encephalopathy (PRES)


    • BG involvement typical in patients with neurological complications of HUS


  • Infectious Vasculitis



    • Bacterial meningitis: Infarct due to vascular involvement seen in 25%


    • Tuberculous meningitis: Skull base vessels most commonly involved


    • Lenticulostriate artery involvement common


Helpful Clues for Less Common Diagnoses



  • Drug Abuse



    • Young/middle-aged patient with stroke


    • May cause stroke &/or vasculitis


    • T2 hyperintensities or hemorrhage in BG



  • Gliomatosis Cerebri



    • Diffusely infiltrating glial tumor involving 2 or more lobes, frequently bilateral


    • Typically hemispheric WM with BG or thalami (75%)


    • Often infiltrates beyond BG into WM


  • Osmotic Demyelination Syndrome



    • 50% in pons (CPM) & 50% extra-pontine sites (EPM): BG & cerebral WM


    • Symmetric hyperintensity in BG, WM


  • Encephalitis (Miscellaneous)



    • Many pathogens, most commonly viruses


    • Abnormal T2 hyperintensity of gray matter ± WM or deep gray nuclei


    • West Nile encephalitis: Symmetric BG, thalami, mesial temporal lobe, brainstem, & cerebellum T2 hyperintensities


    • Japanese encephalitis: High signal foci in WM, brainstem, BG, thalami bilaterally


    • Epstein-Barr virus: Symmetric BG, thalami, cortex, or brainstem T2 hyperintensities


    • Mycoplasma: May cause acute bilateral striatal necrosis


Helpful Clues for Rare Diagnoses

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Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on T2 Hyperintense Basal Ganglia

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