Corpus Callosum Splenium Lesion



Corpus Callosum Splenium Lesion


Karen L. Salzman, MD



DIFFERENTIAL DIAGNOSIS


Common



  • Diffuse Axonal Injury (DAI)


  • Multiple Sclerosis


  • Status Epilepticus


  • Drug Toxicity, NOS


Less Common



  • Transient Metabolic Derangement


  • Encephalitis (Miscellaneous)


  • Hypoxic-Ischemic Encephalopathy, NOS


  • Alcoholic Encephalopathy


  • Neoplasms


  • PML


  • Hypoglycemia


Rare but Important



  • X-Linked Adrenoleukodystrophy


  • Acute Hypertensive Encephalopathy, PRES


  • ADEM


  • White Matter Disease with Lactate


  • Enlarged Perivascular Spaces


  • Systemic Lupus Erythematosus


ESSENTIAL INFORMATION


Key Differential Diagnosis Issues



  • Corpus callosum (CC) has 4 named parts: Rostrum, genu, body, & splenium


  • Splenium is most likely portion to be affected by various pathologies



    • Possibly related to posterior pericallosal artery vascular supply


  • Splenium lesions may have similar imaging appearance, history often key to diagnosis


  • Many etiologies may cause a reversible T2 hyperintense lesion



    • Pathophysiology for reversible lesions is thought to be cytotoxic edema


Helpful Clues for Common Diagnoses



  • Diffuse Axonal Injury (DAI)



    • Punctate hemorrhages at gray-white interfaces, corpus callosum (CC), deep gray matter, & upper brainstem typical


    • CC involved in 20%; 75% involve splenium & undersurface of posterior body


    • T2*/GRE & SWI typically shows multiple additional lesions


  • Multiple Sclerosis



    • Callososeptal T2 hyperintensities characteristic


    • Focal splenium lesion less common


    • CC almost always involved, callosal striations seen early


    • May have characteristic incomplete ring or horseshoe enhancement


  • Status Epilepticus



    • T2 hyperintensity in supratentorial gray matter &/or subcortical white matter (WM) with mild mass effect typical


    • May focally involve hippocampus or CC splenium


  • Drug Toxicity, NOS



    • Multiple drugs have been associated with a reversible splenium lesion



      • Anti-epileptic agents, metronidazole, sympathomimetic-containing diet pills


    • Focal T2 hyperintensity, DWI positive


    • Metronidazole encephalopathy may also affect dentate, brainstem, & WM


Helpful Clues for Less Common Diagnoses



  • Transient Metabolic Derangement



    • Focal T2 hyperintense splenium lesion, DWI positive


    • Typically reversible


  • Encephalitis (Miscellaneous)



    • Multiple infectious agents may cause focal T2 hyperintense splenium lesion



      • Influenza type A, rotavirus, E. coli, measles, mumps, adenovirus, herpes, varicella, EBV, West Nile, salmonella


    • Typically reversible & DWI positive


  • Hypoxic-Ischemic Encephalopathy, NOS



    • Most common in deep gray nuclei


    • DWI positive acutely


    • Focal splenium lesion less common


  • Alcoholic Encephalopathy



    • Marchiafava-Bignami: Sudden onset of altered mental status, seizures, dysarthria, ataxia, hypertonia, pyramidal signs



      • T2 hyperintense CC (middle layers) virtually pathognomonic


    • Toxic leukoencephalopathy with demyelination, rare complication, often involves splenium & periventricular WM


    • Superior vermian atrophy common


  • Neoplasms



    • Lymphoma & glioblastoma (GBM) classically cross CC splenium or genu


    • Enhancing WM mass with CC extension


    • Lymphoma: Homogeneous enhancement


    • GBM: Heterogeneous enhancement



  • PML



    • Occurs in immunosuppressed or immunocompromised patients


    • T2 hyperintensity in subcortical & deep WM, crosses CC splenium & genu


    • Involves subcortical U-fibers


  • Hypoglycemia



    • Severe parietooccipital edema &/or infarcts in a newborn


    • T2 hyperintensity in occipital & parietal lobes; commonly affects splenium


    • DWI positive


    • May be reversible if treated early

Aug 7, 2016 | Posted by in NEUROLOGY | Comments Off on Corpus Callosum Splenium Lesion

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