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Cytotoxic Lesion of the Corpus Callosum

Summary

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  • Rare, reversible white matter lesion affecting the corpus callosum
  • Characterised by transient oedema without infarction or necrosis
  • Typically associated with various metabolic, infectious, or toxic etiologies1

Pathophysiology

  • Exact mechanism unclear, but thought to involve:
    • Cytokine-mediated inflammatory response
    • Excitotoxicity due to glutamate release
    • Oxidative stress and mitochondrial dysfunction
  • Lesions predominantly affect oligodendrocytes and myelin
  • Reversible oedema without true infarction or necrosis

Demographics

  • Can affect all age groups, but more common in adults
  • Slight male predominance reported in some studies
  • Associated conditions include:
    • Alcohol abuse and withdrawal
    • Malnutrition
    • Infections (e.g., influenza)
    • Metabolic disturbances (e.g., hyponatremia)
    • Drug toxicity (e.g., antiepileptics, chemotherapy)

Diagnosis

  • Clinical presentation:
    • Altered mental status
    • Seizures
    • Dysarthria
    • Gait disturbances
  • Laboratory findings:
    • Often nonspecific
    • May reflect underlying etiology (e.g., hyponatremia, elevated liver enzymes)
  • Diagnosis primarily based on characteristic imaging findings

Imaging

  • MRI is the modality of choice:
    • T2-weighted and FLAIR: Hyperintense lesions in corpus callosum
    • DWI/ADC: Restricted diffusion in acute phase
    • T1-weighted: Hypointense to isointense lesions
    • Contrast enhancement: Usually absent
  • Typical distribution:
    • Splenium most commonly affected
    • Can involve entire corpus callosum in severe cases
  • Key features:
    • Symmetric, oval-shaped lesions
    • No mass effect
    • Reversible nature (resolution on follow-up imaging)

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  • 40-year-old patient with longterm epilepsy had his anti-epileptic medication changed following an increase in seizure frequency.
  • CT showed low density in the splenium of the corpus callosum.
  • On MRI, there was T2-hyperintensity and diffusion restriction in the same region.

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  • A 50-year-old patient underwent a suboccipital decompression due to a posterior fossa haematoma.
  • The presence of deep microhaemorrhages suggested that the haemorrhage was a consequence of hypertension.
  • The symmetrical diffusion restriction within the splenium of the corpus callosum was compatible with a CLOCC.

Treatment

  • Treat the underlying cause; the lesion is typically reversible and resolves on follow-up

Differential diagnosis

Differential Diagnosis Differentiating Feature
Multiple Sclerosis Lesions typically ovoid and periventricular; less likely to involve entire corpus callosum
Acute Disseminated Encephalomyelitis More widespread brain involvement; usually monophasic
Ischaemic Stroke Arterial ischaemia usually unilateral (venous ischaemia could be bilateral); diffusion restriction more pronounced and persistent
Posterior Reversible Encephalopathy Syndrome Predominantly affects posterior cerebral regions; often spares corpus callosum
Marchiafava-Bignami Disease Primarily affects alcoholics; involves entire corpus callosum more uniformly
Wernicke Encephalopathy Involves mammillary bodies, thalami, and periaqueductal gray matter
Viral Encephalitis Often involves temporal lobes; may have meningeal enhancement
Vasculitis Multiple infarcts of different ages; vessel wall enhancement may be seen

  1. Lebecque et al. Cytotoxic Lesion of the Corpus Callosum Caused by Puumala Hantavirus Infection. 2019. Journal of the Belgian Society of Radiology - Open in new tab. ↩