Globus Pallidus Lesion(s)



Globus Pallidus Lesion(s)


Karen L. Salzman, MD



DIFFERENTIAL DIAGNOSIS


Common



  • Hypoxic-Ischemic Encephalopathy, NOS


  • HIE, Neonate


  • CO Poisoning


  • Neurofibromatosis Type 1


Less Common



  • Drug Abuse


  • Hyperalimentation


  • Hepatic Encephalopathy


  • Leigh Syndrome


  • Cyanide Poisoning


  • Kernicterus


  • Hypothyroidism


  • Fahr Disease


Rare but Important



  • Neurodegeneration with Brain Iron Accumulation (NBIA)


  • Hallervorden-Spatz Syndrome


  • Maple Syrup Urine Disease


  • Methylmalonic Acidemia


  • Wilson Disease


ESSENTIAL INFORMATION


Key Differential Diagnosis Issues



  • Globus pallidus (GP) are paired deep nuclei within the basal ganglia (BG) with lateral & medial segments


  • Lentiform nucleus = putamen & GP


  • Corpus striatum = caudate, putamen, & GP


  • Majority of GP lesions are symmetric indicating a toxic/metabolic process or hypoxia


  • Lesions may be differentiated based on patient age or T1/T2 signal abnormality


Helpful Clues for Common Diagnoses



  • Hypoxic-Ischemic Encephalopathy, NOS



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


    • Occurs in adult or child, pattern depends on severity of insult


    • T1 & T2 hyperintense BG & cortical lesions; may affect only GP


  • HIE, Neonate



    • Acquired condition related to cerebral hypoperfusion


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


    • Involvement of BG & thalamus typically seen with profound insult


    • T1 & T2 hyperintensity in BG & thalamus


    • Ventrolateral thalamus typically involved


  • CO Poisoning



    • Bilateral, symmetric GP T2 hyperintensity


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


    • If hemorrhagic necrosis, T1 hyperintense


    • Chronic: T2 hyperintensity in centrum semiovale, internal/external capsules, & corpus callosum often seen


  • Neurofibromatosis Type 1



    • Focal areas of increased signal intensity (FASI) characteristic


    • FASI: T2 hyperintensities within deep nuclei, most commonly affecting GP


    • May be present within brainstem


    • FASI are transient & rarely enhance


Helpful Clues for Less Common Diagnoses



  • Drug Abuse



    • Methylenedioxymethamphetamine (a.k.a. MDMA, “Ecstasy”) causes bilateral GP ischemia from prolonged vasospasm


    • Heroin: GP ischemia &/or toxic leukoencephalopathy, hypoxic brain injury


    • MDMA & heroin: T2 hyperintense GP


    • Heroin inhalation: Symmetric WM T2 hyperintensity


  • Hyperalimentation



    • Abnormal manganese metabolism in patients undergoing parenteral feeding


    • T1 hyperintensity in GP & substantia nigra (SN), related to manganese


  • Hepatic Encephalopathy



    • T1 hyperintensity in GP & SN


    • History of liver disease


  • Leigh Syndrome



    • Symmetric T2 hyperintense lesions with onset in infancy/early childhood


    • Lesions primarily in brainstem, BG & WM; putamen > GP


  • Cyanide Poisoning



    • Bilateral T2 hyperintense GP


    • May involve cerebellar cortex


    • Causes hemorrhagic necrosis


  • Kernicterus



    • T1 & T2 hyperintensity in GP in a neonate


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



    • Chronic: T2 hyperintensity in GP & dentate nucleus


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


  • Hypothyroidism



    • T1 hyperintensity & T2 hypointensity in BG & SN related to calcification (Ca++)


    • Diffuse WM T2 hyperintensity in Hashimoto thyroiditis


  • Fahr Disease



    • Bilateral symmetric BG Ca++ on CT


    • GP most common site


    • Putamen, caudate, thalami, cerebellum, cerebral WM may also be involved


Helpful Clues for Rare Diagnoses

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Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on Globus Pallidus Lesion(s)

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