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
Helpful Clues for Rare Diagnoses

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