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Corpus Callosum Impingement Syndrome e84adf32-bae3-47d5-b368-489f413f6aea
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a25c450b-3d34-4f64-bba3-cc0834813df6 Miral D. Jhaveri, MD, MBA
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Brain 2188842b-0f05-4580-9c01-5ee89586a08f 4 06/09/20 Corpus Callosum Impingement Syndrome Brain, Diagnosis, Anatomy-Based Diagnoses, Ventricles and Cisterns, Hydrocephalus, Corpus Callosum Impingement Syndrome Corpus Callosum Impingement Syndrome | STATdx Corpus Callosum Impingement Syndrome DX true
Brain
Diagnosis
Anatomy-Based Diagnoses
Ventricles and Cisterns
Hydrocephalus
Corpus Callosum Impingement Syndrome

title: "Corpus Callosum Impingement Syndrome" docid: "e84adf32-bae3-47d5-b368-489f413f6aea" authors:

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  • "Brain"
  • "Diagnosis"
  • "Anatomy-Based Diagnoses"
  • "Ventricles and Cisterns"
  • "Hydrocephalus"
  • "Corpus Callosum Impingement Syndrome"

KEY FACTS

  • Terminology

    • Corpus callosum impingement syndrome (CCIS)
    • Corpus callosum (CC)
    • Callosal injury from longstanding obstructive hydrocephalus

  • Imaging

    • Acute - Following ventricular decompression in longstanding obstructive hydrocephalus - Swollen and hyperintense body of CC - Diffuse or focal hyperintense areas in CC
    • Chronic - Encephalomalacic foci, shrunken and atrophic-appearing CC
    • No hemorrhage, restricted diffusion, or enhancement

  • Top Differential Diagnoses

    • Acute phase: CC swollen with T2/FLAIR hyperintensity - Tumors involving CC, tumefactive demyelination, transient cytotoxic splenial lesion, ischemia/infarct, diffuse axonal injury
    • Chronic phase: CC atrophy with cystic changes - Multiple sclerosis, postsurgical, enlarged perivascular spaces, Marchiafava-Bignami disease, Susac syndrome

  • Pathology

    • Exact mechanism for callosal lesions unknown

  • Clinical Issues

    • CC injury does not appear to produce any clinically recognizable symptomatology
    • CCIS is uncommon sequel of severe chronic hydrocephalus
    • Longstanding cases: Atrophic CC and signal abnormality, may persist after ventricular decompression

  • Diagnostic Checklist

    • Consider CCIS in patient treated with ventricular decompression for longstanding obstructive hydrocephalus
    • CC signal change, although dramatic, should not be mistaken for other pathologies

TERMINOLOGY

  • Abbreviations

    • Corpus callosum impingement syndrome (CCIS)
    • Corpus callosum (CC)

  • Definitions

    • Callosal injury from longstanding obstructive hydrocephalus

IMAGING

  • General Features

    • Best diagnostic clue

      - Diffuse &/or focal T2/FLAIR hyperintensity in CC

    • Location

      - Isthmus, body of CC, splenium generally spared

    • Size

      - Variable

    • Morphology

      - Ill-defined or focal lesions

  • CT Findings

    • Thinning and upward displacement of CC
    • Postventricular decompression or shunting - Acute: Swollen, hypodense body of CC - Chronic: Atrophy, cystic changes in body of CC

  • MR Findings

    • T1WI

      - Severe hydrocephalus with upward bowing and thinning of CC
- Following ventricular decompression, swollen hypointense body of CC

    • T2WI

      - Acute
        - Following ventricular decompression
        - Swollen, hyperintense body of CC
        - Diffuse or focal hyperintense areas
        - May see periventricular white matter (WM) hyperintensities
- Chronic
        - Encephalomalacic foci, shrunken and atrophic-appearing CC

    • FLAIR

      - More sensitive to evaluate CC and periventricular WM

    • T2* GRE

      - No hemorrhage

    • DWI

      - No restricted diffusion

    • T1WI C+

      - No enhancement

    • DTI: Fiber disruption in body of CC

  • Imaging Recommendations

    • Best imaging tool

      - MR

    • Protocol advice

      - Add sagittal T2/FLAIR

DIFFERENTIAL DIAGNOSIS

  • Acute Phase: Corpus Callosum Swollen With T2/FLAIR Hyperintensity

    • Tumors involving CC - Lymphoma: Uniform enhancement, restricted diffusion - Glioblastoma: Central necrosis, irregular enhancement
    • Tumefactive demyelination - Often incomplete, horseshoe-shaped enhancement
    • Transient cytotoxic splenial lesion - Round or boomerang-shaped diffusion restriction in CC splenium, diverse etiologies
    • Ischemia/infarct - Diffusion restriction in CC likely due to "acute wallerian degeneration"
    • Diffuse axonal injury (DAI) - Signal loss on SWI, ↑ T2, diffusion restriction
    • Interstitial edema (obstructive hydrocephalus) - ↑ T2/FLAIR signal along CC ventricular surface - Look for additional abnormal signal of frontal and occipital periventricular WM

  • Chronic Phase: Corpus Callosum Atrophy With Cystic Changes

    • Multiple sclerosis - "Burned-out" chronic lesions
    • Postsurgical - Small CC "holes" common after shunt - Corpus callosotomy
    • Enlarged perivascular spaces - Follow CSF on all sequences - When CC involved, adjacent brain often involved
    • Marchiafava-Bignami disease - Rare complication of chronic alcoholism - T2-hyperintense CC (middle layers)
    • Susac syndrome - Encephalopathy, visual changes, hearing loss - Multifocal supratentorial WM lesions + CC

PATHOLOGY

  • General Features

    • Etiology

      - Exact mechanism for callosal lesions unknown
- Mechanical compression
        - Severe obstructive hydrocephalus
        - CC compressed against free inferior margin of falx
        - Pressure necrosis
- Ventricular decompression associated edema
- Compromised venous drainage
- Traction-induced arterial compromise, demyelination

  • Gross Pathologic & Surgical Features

    • Chronic impingement of CC associated with callosal thinning, cystic changes

  • Microscopic Features

    • Loss of callosal axons

CLINICAL ISSUES

  • Presentation

    • Most common signs/symptoms

      - Signs/symptoms related to obstructive hydrocephalus
- CCIS does not appear to produce any clinically recognizable symptoms

  • Demographics

    • CCIS uncommon sequela of severe chronic hydrocephalus
    • MR CC signal change in 8.3% of patients following shunt insertion for obstructive hydrocephalus

  • Natural History & Prognosis

    • Ventricular decompression may reverse CC signal change
    • Longstanding cases: Atrophic CC and signal abnormality, may persist after ventricular decompression
    • No long-term neurologic sequel from callosal damage

  • Treatment

    • None for CC signal abnormality

DIAGNOSTIC CHECKLIST

  • Consider

    • CCIS in patient treated with ventricular decompression for longstanding obstructive hydrocephalus

  • Image Interpretation Pearls

    • CC signal change, although dramatic, should not be mistaken for other pathologies

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References

Selected References

  1. Su S et al: Post-shunting corpus callosal signal change and review of the literature. J Clin Neurosci. 72:466-8, 2020
  2. Oon SF et al: Corpus callosum impingement syndrome: a callosal or colossal problem? Can J Neurol Sci. 44(6):728-9, 2017
  3. Ferrara JM: Signal hyperintensity of the callosum after ventriculoperitoneal shunting. Neurology. 84(15):1609-10, 2015
  4. Lane JI et al: Corpus callosal signal changes in patients with obstructive hydrocephalus after ventriculoperitoneal shunting. AJNR Am J Neuroradiol. 22(1):158-62, 2001

Images

Selected Images

Sagittal T1 MR in a patient with longstanding severe obstructive hydrocephalus demonstrates markedly dilated lateral ventricle with upward displacement and thinning of the corpus callosum (CC) . Note the shunt catheter , which was placed immediately before the scan. Sagittal T1 MR in a patient with longstanding severe obstructive hydrocephalus demonstrates markedly dilated lateral ventricle with upward displacement and thinning of the corpus callosum (CC) . Note the shunt catheter , which was placed immediately before the scan.

Sagittal T1 MR in the same patient 7 days after placement of the shunt catheter shows patchy areas of low signal in the CC . Lateral ventricles are now decompressed, and there is no mass effect on the CC. Sagittal T1 MR in the same patient 7 days after placement of the shunt catheter shows patchy areas of low signal in the CC . Lateral ventricles are now decompressed, and there is no mass effect on the CC.

Axial FLAIR MR in the same patient 7 days following placement of the shunt catheter demonstrates ill-defined hyperintensities in the body of the CC as well as in the periventricular white matter . Note decompressed lateral and 3rd ventricles. Axial FLAIR MR in the same patient 7 days following placement of the shunt catheter demonstrates ill-defined hyperintensities in the body of the CC as well as in the periventricular white matter . Note decompressed lateral and 3rd ventricles.

Axial FLAIR MR in the same patient 1 month after placement of the shunt shows mild decrease in the hyperintensities in the CC as well as the periventricular white matter with further decompression of the lateral and 3rd ventricles. Axial FLAIR MR in the same patient 1 month after placement of the shunt shows mild decrease in the hyperintensities in the CC as well as the periventricular white matter with further decompression of the lateral and 3rd ventricles.

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