Thin Corpus Callosum
Susan I. Blaser, MD, FRCPC
DIFFERENTIAL DIAGNOSIS
Common
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Normal Variant
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Immature Brain
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Encephalomalacia
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Multiple Sclerosis
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White Matter Injury of Prematurity
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Callosal Dysgenesis
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Callosectomy/Callosotomy
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Obstructive Hydrocephalus
Less Common
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Hypomyelination
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Injury (Any Cause)
Rare but Important
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Susac Syndrome
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Holoprosencephaly
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Inherited Metabolic Disorders
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Hereditary Spastic Paraplegia with Thin
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Corpus Callosum (HSP-TCC)
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
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Diffuse corpus callosum (CC) thinning can be normal
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Newborn (immature brain)
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Abnormally thin CC can be inherited or acquired
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Broad spectrum of congenital malformations, inherited metabolic disorders can all result in thin CC
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Check history for trauma, surgery, ischemia-infarction
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Thin CC, normal signal hyperintensity
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Normal variant, immature brain
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Secondary to hemispheric white matter (WM) volume loss
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Dysgenesis
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Thin CC, abnormal signal intensity
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Hypomyelination or demyelinating disease (chronic MS, Susac syndrome)
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Injury (trauma, ischemia, radiation, toxic-metabolic insult)
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Obstructive hydrocephalus
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Helpful Clues for Common Diagnoses
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Normal Variant
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Focal thinning of corpus callosum at “isthmus” (junction between posterior body, splenium) is normal
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Sagittal section slightly off-midline can make corpus callosum appear mildly thinned
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Immature Brain
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Hemispheric WM in newborn unmyelinated, corpus callosum thin and hypointense on T1WI
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As myelination progresses, corpus callosum thickens, becomes hyperintense on T1WI
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Corpus callosum splenium at 4 months
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Corpus callosum genu at 6 months
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By 8 months, corpus callosum essentially like an adult’s
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Encephalomalacia
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Holohemispheric WM volume loss, regardless of etiology, causes diffuse corpus callosum thinning
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Focal WM loss can cause focal corpus callosum thinning
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Multiple Sclerosis
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Look for T2/FLAIR hyperintense lesions along callososeptal interface
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Ependymal “dot-dash” sign along callosoventricular border occurs early
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Longstanding MS with decreased hemispheric WM volume results in thinned corpus callosum
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White Matter Injury of Prematurity
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Corpus callosum thinning secondary to periventricular white matter infarction
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Posterior corpus callosum disproportionately affected
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Callosal Dysgenesis
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Hypoplasia or absence of part or all of corpus callosum
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Rostrum, splenium most likely deficient
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Remnants vary in size, shape, and configuration
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Most common abnormality associated with other malformations
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Chiari 2 malformation
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Heterotopias
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Interhemispheric lipoma
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Cephaloceles
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Callosectomy/Callosotomy
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History important!
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Surgical disruption
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Look for surgical changes of craniotomy, ventriculostomy
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Obstructive Hydrocephalus
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Causes 2 kinds of corpus callosum abnormalities: Stretching and intrinsic signal abnormality
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As lateral ventricles enlarge, corpus callosum is stretched, appears thinned
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Look for associated signal abnormality in corpus callosum (sagittal T2WI/FLAIR best)
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Post-shunt decompression may show corpus callosum thinning, signal abnormality
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Can appear bizarre, causing horizontal hyperintense “streaks” in corpus callosum on axial imaging
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Can extend into periventricular WM
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Theories: Impingement of corpus callosum against falx cerebri with resulting ischemia or axonal stretch
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Helpful Clues for Less Common Diagnoses
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Hypomyelination
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Undermyelination, delayed myelin maturation
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Diminished/absent WM myelination for age
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Can be primary or secondary to other pathology
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Injury (Any Cause)
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Trauma (e.g., axonal injury, radiation-induced leukoencephalopathy)
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Ischemia
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Helpful Clues for Rare Diagnoses
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Susac Syndrome
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M < F
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Classic triad
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Encephalopathy (headache, confusion, memory loss)
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Vision problems (retinal artery occlusions)
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Hearing loss
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Always involves corpus callosum
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Central > callososeptal interface lesions
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Middle callosal “holes” (subacute/chronic)
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Holoprosencephaly
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Many variants; often affect corpus callosum
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Inherited Metabolic Disorders
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Focal or diffuse atrophy
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Focal: X-linked adrenoleukodystrophy
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Diffuse: Many
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Hereditary Spastic Paraplegia with Thin Corpus Callosum (HSP-TCC)
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HSP-TCC is 1 of many hereditary spastic paraplegias
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Autosomal recessive with SPG11 gene mutations on chromosome 15q13-15
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Progressive neurodegenerative disorder
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Clinical
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Slow ↑ spastic paraparesis
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Adolescent-onset cognitive decline
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Pseudobulbar dysfunction
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Imaging
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Thin corpus callosum (especially genu, body) with progressive atrophy
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Cerebral, cerebellar atrophy often associated
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Image Gallery
![]() (Left) Axial DWI MR in a newborn shows extensive diffusion restriction of the left hemisphere following perinatal stroke. Acute axonal degeneration of the corpus callosum
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