Enhance document processing in scrapers
- Updated pediatric multiple sclerosis article reference ID. - Improved document_to_markdown.py to handle differential diagnoses, tables, anatomy, and cases more effectively. - Added logging for cached entries of DDX, Tables, Anatomy, and Cases. - Adjusted file pattern matching to process all JSON files by default. - Fixed document ID extraction logic for various data types.
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Ross
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---
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title: "Abnormal Shape/Configuration of Corpus Callosum"
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docid: "238ca32d-6bc6-4f5a-81b1-6601dd605856"
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authors:
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- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
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value: "Luke L. Linscott, MD"
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breadcrumbs:
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-
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name: "Pediatrics"
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slug: "pediatrics"
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treeNodeId: "a915965c-d436-44cf-ae65-2f22e7246ea4"
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-
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name: "Differential Diagnosis"
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slug: "differential-diagnosis"
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treeNodeId: "9e45b379-de58-40ea-b8b0-9877f7ebe994"
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-
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name: "Brain"
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slug: "brain"
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treeNodeId: "0ad2e6d5-5dc7-4db0-a2f9-de0cf62fd0de"
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-
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name: "Abnormal Shape/Configuration of Corpus Callosum"
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slug: "abnormal-shapeconfiguration-of-cor-"
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treeNodeId: null
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category: "Pediatrics"
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documentVersionId: "bea8db40-78a1-4745-a1f7-c18bbf5f3f30"
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imageCount: 53
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lastUpdated: "08/16/19"
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pageDescription: "Abnormal Shape/Configuration of Corpus Callosum"
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pageKeywords: "Pediatrics, Differential Diagnosis, Brain, Abnormal Shape/Configuration of Corpus Callosum"
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pageTitle: "Abnormal Shape/Configuration of Corpus Callosum | STATdx"
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enhancedTitle: "Abnormal Shape/Configuration of Corpus Callosum"
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type: "DDX"
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references: true
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breadcrumbs:
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- "Pediatrics"
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- "Differential Diagnosis"
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- "Brain"
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- "Abnormal Shape/Configuration of Corpus Callosum"
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---
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# ESSENTIAL INFORMATION
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- ## Key Differential Diagnosis Issues
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- Clinical features to consider
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- Normal corpus callosum (CC) varies in thickness & shape
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- Associated anomalies portend worse prognosis
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- If not congenital anomaly, clinical history is crucial
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- Prior surgical history, prematurity etc.
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- Corpus callosotomy, shunt placement, endoscopic 3rd ventriculostomy
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- Imaging features to consider
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- Isolated callosal dysgenesis is not common → additional malformations in > 50%
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- Malformations of cortical development
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- Noncallosal midline anomalies
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- Abnormal brainstem or cerebellum
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- Look for parenchymal abnormalities to identify etiology
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- White matter (WM) volume loss, prior infarction, diffuse axonal injury
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- Ventricular abnormalities are common
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- Colpocephaly → CC agenesis/dysgenesis, Chiari 2
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- Enlarged, angular ventricles → periventricular leukomalacia
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- Modality considerations
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- CT: Helpful to distinguish cellular vs. inflammatory
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- ↑ density → cellular mass, hemorrhage
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- ↓ density → edema, inflammation
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- MR: Best spatial & contrast resolution
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- Sagittal imaging is critical for evaluation of CC
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- 3D acquisitions allow multiplanar reconstructions
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- ## Helpful Clues for Common Diagnoses
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- **Normal Variant**
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- Immature CC is thin
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- Gradually thickens with progressive myelination
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- Size, shape, & thickness of normal CC vary
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- Splenium & genu are largest parts of CC
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- Normal narrowing at junction of body & splenium ("isthmus")
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- Dorsal surface of fully developed, normally myelinated CC is often "wavy"
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- **Thin Corpus Callosum**
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- Many causes (congenital, acquired)
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- All may result in focal or diffuse callosal thinning
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- **Periventricular leukomalacia**
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- Premature infant is at greatest risk
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- Acute findings: US → ↑ periventricular WM echogenicity
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- MR: Diffusion restriction, ↑ T1, ↓ T2
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- Subacute findings: Cavitation, periventricular cysts
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- Chronic findings: ↓ volume of periventricular WM
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- Thin posterior body & splenium are most common
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- Ventricular enlargement shows angular margins
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- **Hypoxic-ischemic encephalopathy**
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- Loss of cerebral WM → thin CC
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- May occur with profound or partial prolonged injury
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- Profound: Often perirolandic → posterior body CC
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- Partial prolonged: Watershed injury → entire CC
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- **Chronic cerebral infarction**
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- Axonal loss → focal/diffuse thinning of CC
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- **Obstructive hydrocephalus**
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- Look for obstructing lesion (e.g., tumor, aqueductal stenosis) or sequelae of prior hemorrhage/infection
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- Acute: CC stretched, bowed upward
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- Chronic: Thinned, irregular (sequela of CC impingement against falx & chronic WM injury from hydrocephalus)
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- **Chemotherapy & radiation therapy**
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- WM injury with volume loss
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- e.g., chronic methotrexate toxicity
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- **Postsurgical Defects**
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- **Corpus c****allosotomy**
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- Surgical disruption for intractable epilepsy
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- Isolated callosotomy or part of functional hemispherotomy
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- Often imaged in postoperative setting to detect residual neuronal connections across midline
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- Best seen on sagittal or coronal MR
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- **Ventricular drainage catheter tract**
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- Small defect in paramidline CC
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- Typically with overlying WM parenchymal tract & postoperative skull focus
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- May see hypointense intracranial catheter ± hyperintense fluid-filled extracranial components
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- **Endoscopic 3rd ventriculostomy**
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- Small defect in CC represents scope tract, typically with overlying WM parenchymal tract & postoperative skull focus
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- ## Helpful Clues for Less Common Diagnoses
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- **Callosal Agenesis**
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- Absent WM bridging cerebral hemispheres
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- Absent septum pellucidum
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- Absent cingulate gyrus with vertically oriented parasagittal sulci radiating to high-riding 3rd ventricle
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- Lateral ventricles: Colpocephaly, upturned frontal horns
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- Probst bundles (WM tracts that would have formed CC) lie along medial aspects of lateral ventricles
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- **Primary Callosal Dysgenesis**
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- Absence of 1 or all segments
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- Rostrum & splenium are most likely to be deficient
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- Remnants vary in size, shape, configuration
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- Look for other associated malformations
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- "Micro" CC: Small but well formed, often syndromic
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- "Mega" CC: Megalencephalic (bulky WM) vs. small to normal brain (syndromic)
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- **Chiari 2 Malformation**
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- Constellation of intracranial findings secondary to open neural tube defect (e.g., myelomeningocele)
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- Small posterior fossa, towering cerebellum that wraps around dorsal brainstem, small elongated 4th ventricle, vermian/tonsillar extension into upper cervical spine, "beaked" tectum, scalloped clivus
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- Degree of callosal dysgenesis is highly variable
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- Correlates with severity of hydrocephalus
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- **Neoplasm**
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- **Glioblastoma**
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- Common in adults, uncommon in children
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- "Butterfly" glioma crosses CC
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- Central necrosis + thick, irregular rim enhancement
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- **Lymphoma**
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- NECT: Hyperdense
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- Strong, uniform enhancement
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- **Pericallosal Lipoma**
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- 40-50% occur in interhemispheric fissure
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- Almost always located in subarachnoid space; blood vessels & cranial nerves course through lipoma
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- 2 morphologic types
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- Bulky, mass-like ("tubulonodular" type)
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- Thin, dorsal to body/splenium ("curvilinear" type)
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- Midline lipomas may be part of more general midline developmental disorder; CC is often deficient
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- **Neurofibromatosis Type 1 (NF1)**
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- Patients with NF1 have ↑ CC volume
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- Sometimes markedly so & qualitatively evident
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- Nonenhancing lesions of NF1 can occur in CC
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- If focal lesions of CC enhance, suggest low-grade tumor
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- **Holoprosencephaly**
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- Alobar
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- CC absent
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- "Pancake" anterior cerebral tissue
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- Monoventricle with large dorsal "cyst"
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- Semilobar
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- Frontal lobe fusion/hypoplasia; caudate head fusion
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- Splenium may be present
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- Lobar
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- Genu sometimes present; GM often crosses with genu
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- Absent anterior midline falx & fissure
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- Middle interhemispheric variant (a.k.a. syntelencephaly)
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- Splenium & genu present, body deficient
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- Middle CC body "dips"
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- GM crosses midline in expected location of CC body
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- ± bilateral perisylvian polymicrogyria
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- ## Helpful Clues for Rare Diagnoses
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- **Hypomyelination**
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- Primary pathologic hypomyelination is rare
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- e.g., Pelizaeus-Merzbacher, *TUBB4A* disorders
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- **Inherited Metabolic Leukodystrophies**
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- **Metachromatic leukodystrophy**
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- Entire CC affected, genu & splenium worst
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- **X-linked adrenoleukodystrophy**
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- Most commonly involves splenium
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- **Alexander disease**
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- Frontal lobe & genu involvement
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- **Krabbe disease**
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- Central WM + deep gray nuclei (especially thalamus)
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## References
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# Selected References
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1. [Al-Hashim AH et al: Corpus callosum abnormalities: neuroradiological and clinical correlations. Dev Med Child Neurol. 58(5):475-84, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26661037%5Bpmid%5D)
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1. [Edwards TJ et al: Clinical, genetic and imaging findings identify new causes for corpus callosum development syndromes. Brain. 137(Pt 6):1579-1613, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24477430%5Bpmid%5D)
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1. [Battal B et al: Corpus callosum: normal imaging appearance, variants and pathologic conditions. J Med Imaging Radiat Oncol. 54(6):541-9, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=21199431%5Bpmid%5D)
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1. [Bourekas EC et al: Lesions of the corpus callosum: MR imaging and differential considerations in adults and children. AJR Am J Roentgenol. 179(1):251-7, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12076946%5Bpmid%5D)
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## Images
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### Selected Images
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**Normal Variant**
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*Midline sagittal T1 MR in a normal term neonate shows a thin, unmyelinated corpus callosum (CC) <img src='/img/arrows/CS.png'/>. The CC will gradually thicken as it myelinates from posterior to anterior. Note that the entire pituitary gland normally shows T1 shortening <img src='/img/arrows/CO.png'/> in the 1st few weeks of life.*
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**Normal Variant**
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*Midline sagittal T1 MR in a normal term neonate shows a thin, unmyelinated corpus callosum (CC) <img src='/img/arrows/CS.png'/>. The CC will gradually thicken as it myelinates from posterior to anterior. Note that the entire pituitary gland normally shows T1 shortening <img src='/img/arrows/CO.png'/> in the 1st few weeks of life.*
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**Normal Variant**
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*Midline sagittal T1 MR in a 13 year old with headaches shows a normal variant morphology of the CC with relative thinning of the posterior body <img src='/img/arrows/CS.png'/>. This should not be mistaken for a sign of white matter (WM) volume loss.*
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**Periventricular Leukomalacia**
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*Axial FLAIR MR in a 7 year old with a history of prematurity & periventricular leukomalacia (PVL) shows severe WM volume loss <img src='/img/arrows/CO.png'/> with relatively little signal abnormality. Also note the angular margins <img src='/img/arrows/CC.png'/> of the expanded ventricular occipital horns, consistent with PVL related to extreme prematurity.*
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**Periventricular Leukomalacia**
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*Midline sagittal T1 MR in the same patient shows marked thinning of the posterior body & splenium of the CC <img src='/img/arrows/CS.png'/> due to WM volume loss. This is the most common area of CC involvement in PVL.*
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**Hypoxic-Ischemic Encephalopathy**
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*Axial T2 MR in a 9 year old with a history of hypoxic-ischemic encephalopathy (HIE) at birth shows extensive gliosis & encephalomalacia causing WM volume & signal abnormality in a watershed distribution <img src='/img/arrows/CS.png'/>. This results in marked CC thinning.*
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**Hypoxic-Ischemic Encephalopathy**
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*Midline sagittal T1 MR in the same patient shows marked thinning of the CC <img src='/img/arrows/CS.png'/> secondary to WM loss as a consequence of the remote HIE injury.*
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**Obstructive Hydrocephalus**
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*Midline sagittal T2 MR in a neonate with posthemorrhagic hydrocephalus shows a stretched & thinned CC <img src='/img/arrows/CO.png'/>. Note the enlarged lateral <img src='/img/arrows/CS.png'/>, 3rd <img src='/img/arrows/BS.png'/>, & 4th <img src='/img/arrows/BO.png'/> ventricles as well as thin T2 hypointensity <img src='/img/arrows/CC.png'/> along the brainstem, consistent with hemosiderin deposition.*
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**Obstructive Hydrocephalus**
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*Midline sagittal T1 MR in the same patient 1 year after shunting shows a thinned & dysmorphic CC <img src='/img/arrows/CS.png'/> as well as numerous thin, pencil-like gyri (stenogyria) <img src='/img/arrows/CO.png'/>.*
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**Corpus Callosotomy**
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*Coronal FLAIR MR shows changes of a left functional hemispherotomy with a WM disconnection <img src='/img/arrows/CS.png'/> & insular decortication <img src='/img/arrows/CO.png'/>. Corpus callosotomy may be performed in isolation or as part of a more extensive functional hemispherotomy, as in this patient.*
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**Corpus Callosotomy**
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*Coronal T2 MR shows absence of the midline CC <img src='/img/arrows/CS.png'/> with persistent paramidline callosal tissue <img src='/img/arrows/CC.png'/>, consistent with an isolated surgical callosotomy.*
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**Ventricular Drainage Catheter Tract**
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*Paramidline sagittal T1 MR in a 12 year old with Chiari 2 malformation shows a ventricular shunt catheter tract <img src='/img/arrows/CS.png'/> in the anterior body of the CC. Note the caudal migration of the cerebellum & brainstem <img src='/img/arrows/CO.png'/>, consistent with Chiari 2.*
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**Endoscopic 3rd Ventriculostomy**
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*Paramidline sagittal T2 MR in a teenager with a history of a prior endoscopic 3rd ventriculostomy shows a linear defect <img src='/img/arrows/CS.png'/> in the parasagittal body of the CC. The defect represents the site of surgical access for the scope to enter the 3rd ventricle.*
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**Callosal Agenesis**
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*Coronal T2 MR in a 4 year old with callosal agenesis shows widely spaced upturned lateral ventricular frontal horns <img src='/img/arrows/CC.png'/>, a high-riding 3rd ventricle <img src='/img/arrows/CS.png'/>, & bilateral Probst bundles <img src='/img/arrows/WS.png'/>. Also note the extensive periventricular gray matter (GM) heterotopia <img src='/img/arrows/CO.png'/>.*
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**Callosal Dysgenesis**
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*Midline sagittal T1 MR in a 5 month old with isolated callosal dysgenesis shows a very short & thin CC <img src='/img/arrows/WO.png'/> with no evident rostrum or splenium. Isolated callosal dysgenesis is uncommon. Associated anomalies should be carefully sought.*
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**Callosal Dysgenesis**
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*Midline sagittal T1 MR in a 7 year old with multiple anomalies shows a short, thin, & dysmorphic CC with a poorly formed splenium <img src='/img/arrows/CS.png'/> & rostrum <img src='/img/arrows/CO.png'/>.*
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**Chiari 2 Malformation**
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*Midline sagittal T2 MR in a child with a repaired myelomeningocele & Chiari 2 malformation (with beaked tectum <img src='/img/arrows/CO.png'/>, small 4th ventricle <img src='/img/arrows/CC.png'/>, & scalloped clivus <img src='/img/arrows/WS.png'/>) shows a thinned & dysmorphic CC <img src='/img/arrows/CS.png'/>.*
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**Glioblastoma**
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*Coronal T2 MR in a 10 year old with glioblastoma shows mass-like infiltrative signal <img src='/img/arrows/CS.png'/> crossing the midline through an expanded CC. Infiltrative high-grade glial neoplasms should be considered whenever such a finding is encountered, as they commonly spread along WM tracts, such as the CC.*
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**Lymphoma**
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*Midline sagittal T2 MR shows expansion & increased signal in the rostrum & anterior genu of the CC <img src='/img/arrows/CO.png'/>, consistent with tumor infiltration/edema in this patient with CNS lymphoma.*
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**Pericallosal Lipoma**
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*Midline sagittal T1 MR in a 4 month old shows a T1-hyperintense lipoma <img src='/img/arrows/CS.png'/> along the dorsal CC with associated absence of the splenium <img src='/img/arrows/CO.png'/>.*
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**Neurofibromatosis Type 1**
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*Midline sagittal T1 MR in a 15 year old with neurofibromatosis type 1 (NF1) shows diffuse marked thickening of the entire CC, a finding that can be seen in NF1. Look for associated findings of NF1, such as nonenhancing signal abnormalities of the globus pallidus & medial cerebellum, optic pathway gliomas, & plexiform neurofibromas.*
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**Holoprosencephaly**
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*Midline sagittal T2 MR shows absence of the CC in a patient with alobar holoprosencephaly. There is continuity of frontal WM & GM across the midline with a large dorsal cyst <img src='/img/arrows/CO.png'/> that communicates with a monoventricle <img src='/img/arrows/CS.png'/>. Note the lack of a vermian primary fissure due to associated rhombencephalosynapsis.*
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**Holoprosencephaly**
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*Midline sagittal T1 MR in a 2 year old with semilobar holoprosencephaly shows absence of a normal CC & extension of cortical GM <img src='/img/arrows/CS.png'/> across the midline.*
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**Holoprosencephaly**
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*Midline sagittal T1 MR in a teenager with the middle interhemispheric variant of holoprosencephaly shows an intact CC anteriorly <img src='/img/arrows/CO.png'/> & posteriorly <img src='/img/arrows/CC.png'/> but abnormal extension of GM <img src='/img/arrows/CS.png'/> across the midline in the expected location of the CC body. The abnormal body of the CC typically "dips" down toward the interthalamic adhesion.*
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**Holoprosencephaly**
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*Coronal T2 MR in the same patient with syntelencephaly shows abnormal GM <img src='/img/arrows/WS.png'/> crossing the midline along the CC WM <img src='/img/arrows/CS.png'/>. Also note the azygous internal carotid artery (ICA) <img src='/img/arrows/CO.png'/>.*
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**Metachromatic Leukodystrophy**
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*Coronal T2 MR in a 13-year-old female patient with metachromatic leukodystrophy shows symmetric extensive WM signal abnormality <img src='/img/arrows/CS.png'/> with preservation of the subcortical WM <img src='/img/arrows/CC.png'/>. Note the marked thinning of the CC <img src='/img/arrows/CO.png'/>.*
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**X-Linked Adrenoleukodystrophy**
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*Axial FLAIR MR in a 14-year-old male patient with X-linked adrenoleukodystrophy (ALD) shows symmetric increased FLAIR signal intensity <img src='/img/arrows/CO.png'/> that crosses the splenium <img src='/img/arrows/CS.png'/> of the CC. This is the most common distribution of signal abnormality in X-linked ALD.*
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### Additional Images
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**Normal Variant**
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*Midline sagittal 3D SSFP MR with a close-up view of the corpus callosum shows normal "wavy" dorsal surface. Note the focal thinning along the posterior body <img src='/img/arrows/WS.png'/>, a common normal finding.*
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**Normal Variant**
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*Midline sagittal T1 MR shows a normal neonatal corpus callosum <img src='/img/arrows/WS.png'/>, thin due to an age-appropriate lack of myelin. The cingulate gyrus <img src='/img/arrows/WC.png'/> is normal.*
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**Periventricular Leukomalacia**
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*Midline sagittal T1 MR shows diffuse thinning of the posterior corpus callosum <img src='/img/arrows/WS.png'/>, greater than typically seen. The thinning of the corpus callosum is secondary to loss of commissural fibers, damaged by periventricular leukomalacia.*
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**Periventricular Leukomalacia**
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*Axial T2 MR in the same child shows marked loss of the right periventricular parenchyma <img src='/img/arrows/BO.png'/> at the site of a prior grade 4 hemorrhage. The posterior white matter loss correlates with the focal corpus callosum atrophy <img src='/img/arrows/CS.png'/>.*
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**Periventricular Leukomalacia**
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*Midline sagittal T1 MR shows marked callosal thinning <img src='/img/arrows/WO.png'/> in a child whose hydrocephalus follows unilateral grade 4 intraventricular hemorrhage. Note the more severe callosal volume loss posteriorly <img src='/img/arrows/WC.png'/>.*
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**Chronic Cerebral Infarction**
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*Midline sagittal T1 MR shows thinning <img src='/img/arrows/WO.png'/> of the body & splenium of the corpus callosum following neonatal parietooccipital ischemia & gliosis from a combination of hypoxic ischemic encephalopathy & hypoglycemia.*
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**Chronic Cerebral Infarction**
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*Coronal T2 MR shows parietal ulegyria <img src='/img/arrows/WO.png'/> & marked thinning of the posterior corpus callosum <img src='/img/arrows/WC.png'/>.*
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|
||||
|
||||
**Obstructive Hydrocephalus**
|
||||
*Midline sagittal T2 MR shows mild stretching & thinning of the corpus callosum due to hydrocephalus. There is obstruction of the aqueduct of Sylvius by a tectal glioma <img src='/img/arrows/BO.png'/>.*
|
||||
|
||||
|
||||
**Chemotherapy & Radiation Therapy**
|
||||
*Coronal FLAIR MR shows thinning & gliosis of the corpus callosum <img src='/img/arrows/WO.png'/> & surrounding white matter following therapy for acute lymphoblastic leukemia (ALL).*
|
||||
|
||||
|
||||
**Postsurgical Defects**
|
||||
*Midline sagittal T1 MR shows a focal defect at the junction of the genu & body of the corpus callosum <img src='/img/arrows/WO.png'/>, which had been the site of a prior surgical approach to this child's suprasellar tumor <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Corpus Callosotomy**
|
||||
*Paramidline sagittal T1 MR in a 7 year old with intractable epilepsy shows near-complete absence of the corpus callosum <img src='/img/arrows/CS.png'/> due to surgical discontinuity.*
|
||||
|
||||
|
||||
**Corpus Callosotomy**
|
||||
*Midline sagittal T2 MR in an 11 year old with intractable epilepsy who had undergone an isolated corpus callosotomy shows absence of the corpus callosum <img src='/img/arrows/CS.png'/> but presence of a cingulate gyrus <img src='/img/arrows/CO.png'/>. The presence of a cingulate gyrus would not be expected with congenital agenesis of the corpus callosum.*
|
||||
|
||||
|
||||
**Callosal Agenesis**
|
||||
*Midline sagittal T1 MR shows complete absence of the corpus callosum with associated absence of the cingulate gyrus. Note the radial arrangement of parasagittal gyri/sulci <img src='/img/arrows/WS.png'/>, which point toward the 3rd ventricle.*
|
||||
|
||||
|
||||
**Callosal Agenesis**
|
||||
*Axial T1 MR in a patient with callosal agenesis shows parallel lateral ventricles with colpocephaly <img src='/img/arrows/BS.png'/>, resulting in a typical tear-drop shape.*
|
||||
|
||||
|
||||
**Primary Callosal Dysgenesis**
|
||||
*Midline sagittal T1 MR shows only a residual genu <img src='/img/arrows/WC.png'/> of the corpus callosum with absence of the body & splenium as well as truncation of the rostrum.*
|
||||
|
||||
|
||||
**Primary Callosal Dysgenesis**
|
||||
*Midline sagittal T1 MR in a child with severe microcephaly shows a short, thick corpus callosum <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Chiari 2 Malformation**
|
||||
*Midline sagittal T1 MR shows an abnormal corpus callosum with an absent rostrum, small deformed genu, thick body <img src='/img/arrows/WO.png'/>, & absent splenium in this child with a Chiari 2 malformation due to a myelomeningocele. Note the prominent massa intermedia <img src='/img/arrows/WS.png'/>, inferiorly beaked tectum <img src='/img/arrows/WC.png'/>, & caudally displaced elongated 4th ventricle with flattening of the fastigium <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
**Chiari 2 Malformation**
|
||||
*Axial T2 MR shows a prominent massa intermedia <img src='/img/arrows/WC.png'/> & colpocephalic lateral ventricles with periventricular white matter deficiency in Chiari 2. The genu <img src='/img/arrows/WO.png'/> of the corpus callosum, usually seen on axial images, is absent.*
|
||||
|
||||
|
||||
**Chiari 2 Malformation**
|
||||
*Midline sagittal T2 MR in a 15 month old with Chiari 2 malformation shows a severely thinned & dysmorphic corpus callosum <img src='/img/arrows/CS.png'/>. Note the typical Chiari 2 features, including a small posterior fossa with caudal herniation of the brainstem & cerebellum, clival scalloping <img src='/img/arrows/CC.png'/>, elongated 4th ventricle <img src='/img/arrows/WS.png'/>, & beaked tectum <img src='/img/arrows/BS.png'/>.*
|
||||
|
||||
|
||||
**Glioblastoma**
|
||||
*Coronal T1 C+ MR shows a classic "butterfly" glioblastoma multiforme of the corpus callosum <img src='/img/arrows/WS.png'/>. Central necrosis with an irregular rind of enhancing tumor is typical.*
|
||||
|
||||
|
||||
**Lymphoma**
|
||||
*Axial T1 C+ MR shows a primary CNS lymphoma involving the splenium of the corpus callosum. There is avid, solid enhancement of the tumor <img src='/img/arrows/BS.png'/> with extension into the adjacent parenchymal white matter.*
|
||||
|
||||
|
||||
**Lymphoma**
|
||||
*Coronal oblique T1 C+ MR in an 11 year old with CNS lymphoma shows bifrontal areas of enhancement <img src='/img/arrows/CS.png'/>, which corresponded to hyperdense areas on CT (not shown). Note the abnormally thickened corpus callosum <img src='/img/arrows/CO.png'/> that is infiltrated by a nonenhancing tumor.*
|
||||
|
||||
|
||||
**Pericallosal Lipoma**
|
||||
*Midline sagittal T1 MR shows a large pericallosal lipoma with severe dysgenesis of the corpus callosum <img src='/img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Pericallosal Lipoma**
|
||||
*Axial FLAIR MR shows a large midline lipoma. Two smaller lipomatous masses <img src='/img/arrows/WO.png'/> protrude into the lateral ventricles.*
|
||||
|
||||
|
||||
**Holoprosencephaly**
|
||||
*Axial T1 MR in a patient with holoprosencephaly shows the lack of a midline fissure. White matter <img src='/img/arrows/WC.png'/> is in continuity across the midline. The small basal ganglia <img src='/img/arrows/WO.png'/> approximate each other. Note the monoventricle <img src='/img/arrows/CS.png'/> communicating with a dorsal cyst <img src='/img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
**Holoprosencephaly**
|
||||
*Midline sagittal T1 MR shows both white & gray matter <img src='/img/arrows/WO.png'/> crossing midline anterior & posterior to the "dip" <img src='/img/arrows/WC.png'/> in the corpus callosum, where only gray matter traverses. This is a middle interhemispheric variant of holoprosencephaly (syntelencephaly).*
|
||||
|
||||
|
||||
**Holoprosencephaly**
|
||||
*Axial T1 MR in the same patient shows gray & white matter traversing the midline <img src='/img/arrows/WO.png'/> in the expected location of the splenium. Gray matter also protrudes <img src='/img/arrows/WC.png'/> into the ventricular system. The septum pellucidum is absent.*
|
||||
|
||||
@@ -409,9 +409,6 @@ breadcrumbs:
|
||||
|
||||
*Axial FLAIR MR shows peripheral, confluent areas of hyperintensity predominantly involving the subcortical white matter (WM) in this child with ADEM. The bilateral but asymmetric pattern is typical of ADEM.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows peripheral, confluent areas of hyperintensity predominantly involving the subcortical white matter (WM) in this child with ADEM. The bilateral but asymmetric pattern is typical of ADEM.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows marked, irregular enhancement of nearly all lesions. As ADEM is a monophasic illness, enhancement of the majority of lesions is typical; all lesions have a similar time course. Enhancement of multiple sclerosis (MS) lesions is more variable.*
|
||||
|
||||
|
||||
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@@ -180,7 +180,7 @@ breadcrumbs:
|
||||
**Aging Brain, Normal**
|
||||
*Axial NECT shows typical basal ganglia (BG) Ca⁺⁺ in this 75-year-old man who presented after minor trauma. Note the location within the globus pallidus (GP) <img src='/img/arrows/CS.png'/>, typical for normal aging brain. Physiologic Ca⁺⁺ is typically seen in adults over 30 years.*
|
||||
|
||||
|
||||
|
||||
**Aging Brain, Normal**
|
||||
*Axial NECT shows typical basal ganglia (BG) Ca⁺⁺ in this 75-year-old man who presented after minor trauma. Note the location within the globus pallidus (GP) <img src='/img/arrows/CS.png'/>, typical for normal aging brain. Physiologic Ca⁺⁺ is typically seen in adults over 30 years.*
|
||||
|
||||
|
||||
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|
||||
|
||||
- 95% with clinically definite MS have positive MR findings
|
||||
|
||||
a5089f2b-fbb1-4100-b013-c093925fe15e
|
||||
4f257a7a-e9b9-4b8e-81ab-2922fcef8a3b
|
||||
|
||||
## References
|
||||
|
||||
|
||||
Reference in New Issue
Block a user