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