T1 Hyperintense Basal Ganglia



T1 Hyperintense Basal Ganglia


Karen L. Salzman, MD



DIFFERENTIAL DIAGNOSIS


Common



  • Physiologic Calcification, Brain


  • Neurofibromatosis Type 1


  • Hepatic Encephalopathy


  • Hyperalimentation


Less Common



  • Hypoxic-Ischemic Encephalopathy, NOS



    • HIE, Term


    • Hypotensive Cerebral Infarction


  • CO Poisoning


  • Kernicterus


  • Wilson Disease


Rare but Important



  • Endocrine Disorders



    • Hypothyroidism


    • Hyperparathyroidism


    • Hypoparathyroidism


    • Pseudohypoparathyroidism


    • Pseudopseudohypoparathyroidism


  • Hypoglycemia


  • Hallervorden-Spatz Syndrome


  • Fahr Disease


  • Encephalitis (Miscellaneous)



    • Japanese Encephalitis


    • HIV, Congenital


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


  • BG T1 hyperintensity is usually symmetric, related to calcification (Ca++) or other mineralization


Helpful Clues for Common Diagnoses



  • Physiologic Calcification, Brain



    • Commonly affects GP more than putamen


    • Seen as normal variant in aging brain


    • Typically in patients older than 30 years


  • Neurofibromatosis Type 1



    • Focal areas of increased signal intensity (FASI) characteristic, T2 hyperintense


    • FASI occur in deep gray nuclei, GP most common


    • T1 hyperintensity in GP, thought to be related to FASI &/or mineralization


    • T1 hyperintensity increases with age, but may resolve by adulthood


  • Hepatic Encephalopathy



    • GP & substantia nigra (SN) hyperintensity


    • History of liver disease


  • Hyperalimentation



    • Abnormal manganese metabolism in patients undergoing parenteral feeding


    • T1 hyperintensity in GP & SN


Helpful Clues for Less Common Diagnoses



  • Hypoxic-Ischemic Encephalopathy, NOS



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


    • T1 & T2 hyperintense BG & cortical lesions


    • DWI restriction if acute


  • HIE, Term



    • Cerebral hypoperfusion injury


    • Several patterns of injury related to infant development, severity & duration of insult


    • T1 & T2 hyperintense BG & thalamus with profound insult


    • May involve posterior mesencephalon, hippocampi, & peri-Rolandic cortex


  • Hypotensive Cerebral Infarction



    • Insufficient cerebral blood flow


    • Border zone between major arterial territories typical


    • May be isolated to BG or thalami


    • T1 hyperintensity related to blood or pseudolaminar necrosis


  • CO Poisoning



    • Bilateral, symmetric GP T2 hyperintensity


    • May also involve putamen, thalamus, white matter (WM)


    • If hemorrhagic necrosis, T1 hyperintense


  • Kernicterus



    • T1 & T2 hyperintensity in GP in a neonate


    • Acute: T1 & (subtle) T2 hyperintensity in GP, hippocampi, SN


    • MR changes may be reversible with exchange transfusion in some cases


  • Wilson Disease



    • Children: T1 hyperintensity in GP


    • Children & adults: Symmetric T2 hyperintensity or mixed intensity in putamina, GP, caudate, & thalami


    • Characteristic “face of the giant panda” sign at midbrain level & T2 hyperintense WM tracts



Helpful Clues for Rare Diagnoses

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Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on T1 Hyperintense Basal Ganglia

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