Cord Lesion, T2 Hyperintense, Central
Lubdha M. Shah, MD
DIFFERENTIAL DIAGNOSIS
Common
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Syringomyelia
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Multiple Sclerosis, Spinal Cord
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Acute Transverse Myelitis, Idiopathic
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Infarction, Spinal Cord
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Type I DAVF
Less Common
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Acute Disseminated Encephalomyelitis, Spinal Cord
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Viral Myelitis
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Cavernous Malformation, Spinal Cord
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Astrocytoma, Spinal Cord
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Central Spinal Cord Syndrome
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Radiation Myelopathy
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
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T2 hypointensity ± susceptibility artifact on gradient echo recalled sequences to indicate hemorrhagic products
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Abnormal enlarged flow voids along the surface of the cord suggest a vascular lesion
Helpful Clues for Common Diagnoses
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Syringomyelia
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Expanded cord with dilated or beaded cystic cavity & surrounding gliosis/myelomalacia
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Contrast important to exclude tumor in complex cavitary lesion
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Primary: Associated basilar invagination, Chiari 1 or 2 malformation
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Secondary: Seen in 25% of cord injury
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Extensive MR signal change in superior spinal cord parenchyma is ancillary sign of disease advancement in clinically progressive post-traumatic syringomyelia
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“Cloak-like” pain & temporary sensory loss with preservation of position sense, proprioception, light touch
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Multiple Sclerosis, Spinal Cord
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Peripheral T2 hyperintensity with central enhancement (acute/subacute) classic
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< 2 vertebral segments in length
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< 1/2 cross-sectional area of cord, usually dorsolateral aspect
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Cord atrophy
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Cervical cord most often involved
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May occur in any portion of cord
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Up to 33% may have isolated cord lesions
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90% have intracranial lesions
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Oligoclonal bands in CSF in 90%
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Acute Transverse Myelitis, Idiopathic
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Both halves of the cord result in bilateral motor, sensory, & autonomic dysfunction
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Defined sensory level
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CSF pleocytosis or elevated IgG index
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Long cord segment involvement (> 2 vertebral segments) with > 2/3 of cross-sectional area of cord
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Central T2 hyperintensity with patchy eccentric enhancement
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Infarction, Spinal Cord
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Focal T2 hyperintensity in slightly expanded cord
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Gray matter, adjacent white matter, or cross-sectional cord may be involved
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Classically, the anterior horn cells show T2 hyperintensity
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Focal hemorrhage seen as T1 hyperintensity/T2 hypointensity
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Adjacent anterior vertebral body infarction
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Thoracic cord most frequently involved because of arterial border zone
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Restricted diffusion on DWI
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Acute onset of myelopathy; motor signs predominantly
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Type I DAVF
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Enlarged T2 hyperintense distal cord with dilated pial veins
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Intradural, extramedullary flow voids at level of conus
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“Flame-shaped” edema spares cord periphery
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Venous hypertension from pial vessel engorgement results in reduced tissue perfusion & cord ischemia
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80% patients are men in 5th or 6th decade presenting with progressive lower extremity weakness
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Acute myelopathy due to venous thrombosis: Foix-Alajouanine syndrome
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Helpful Clues for Less Common Diagnoses
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Acute Disseminated Encephalomyelitis, Spinal Cord
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Multifocal white matter lesions with little mass effect or vasogenic edema
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Punctate, ring-shaped, or fluffy enhancement
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Concomitant supratentorial involvement is characteristic
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Cranial nerve involvement with ADEM to help differentiate from MS
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Autoimmune process producing inflammatory reaction
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Delay between clinical onset and appearance of imaging findings
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Viral Myelitis
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Either immune-mediated or direct viral invasion
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Echovirus, Coxsackie, CMV, varicella-zoster, HSV, EBV, hepatitis
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Central T2 hyperintensity with variable enhancement
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Enlarged edematous cord with segmental continuous involvement
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Central T1 hypointensity is higher than CSF
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Cavernous Malformation, Spinal Cord
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Well-defined lesion with hemorrhage of various ages
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Speckled signal with peripheral T2 hypointense rim (hemosiderin)
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Enhancement absent/minimal
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No edema, unless acute hemorrhage
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50% thoracic, 40% cervical, 10% conus
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Astrocytoma, Spinal Cord
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T2 hyperintense enhancing infiltrating mass, expanding cord
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Usually < 4 segments, holocord with pilocytic astrocytoma
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Cervical > thoracic cord
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Diffuse or partial enhancement
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Central Spinal Cord Syndrome
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Diffuse disruption axons, especially within lateral columns of cervical cord (corticospinal tracts); central gray matter intact
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Most common mechanism may be direct compression of cord by buckling of ligamenta flava into an already narrowed spinal canal
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MR & pathology indicate that intramedullary hemorrhage is not a necessary feature, probably uncommon
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