Transverse myelitis MRI
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Julinka Auta Fernandes
Overview
- Magnetic resonance imaging (MRI) is the preferred imaging modality in suspected transverse myelitis. Its immediate purposes are to exclude an extra-axial compressive lesion, identify and characterize an intrinsic spinal cord lesion, and provide imaging clues to the underlying cause.[2][3]
- There is no single pathognomonic MRI finding for transverse myelitis. MRI findings must be interpreted with the clinical syndrome and the remainder of the diagnostic evaluation.[2]
- A normal initial spinal MRI does not exclude transverse myelitis, particularly when imaging is obtained early. When the clinical syndrome remains strongly suggestive and objective evidence of inflammation is not yet demonstrated, repeat MRI is appropriate.[2]
| Clinical point: A compressive lesion is an alternative diagnosis and may require urgent surgical or other cause-specific management. It must be excluded before a noncompressive inflammatory myelopathy is classified as transverse myelitis. |
Recommended initial MRI evaluation
The American College of Radiology (ACR) rates MRI of the cervical and thoracic spine without and with intravenous contrast, and MRI of the brain without and with intravenous contrast, as usually appropriate initial imaging for an adult with acute or subacute sensorimotor symptoms below a spinal cord level when transverse myelitis is suspected.[4]
| Component | Recommended approach and purpose |
|---|---|
| Spinal coverage | Obtain cervical and thoracic spinal MRI without and with intravenous gadolinium-based contrast material unless contrast is contraindicated. When feasible—particularly when lesion localization is uncertain or an inflammatory demyelinating cause is suspected—coverage should extend through the entire spinal cord, including the conus medullaris.[4][5] |
| Spinal sequences | Include sagittal and axial T2-weighted images to determine lesion level, longitudinal extent, cross-sectional distribution, and cord swelling. Axial T2-weighted images should cover each abnormal level and, when feasible, the full cord because small lesions may be missed on sagittal images alone.[5] |
| Precontrast and postcontrast imaging | Obtain T1-weighted images before and after intravenous gadolinium-based contrast material. Enhancement may provide evidence of active inflammation and may help distinguish inflammatory lesions from neoplastic, infectious, and other mimics; however, enhancement is neither required nor specific for transverse myelitis.[2][5] |
| Brain MRI | Brain MRI without and with intravenous contrast is part of the recommended initial imaging assessment. It may demonstrate additional central nervous system lesions that refine etiologic classification and recurrence-risk assessment, but it does not independently confirm transverse myelitis.[4][6] |
| Problem-solving sequences | Diffusion-weighted imaging (DWI) and susceptibility-sensitive sequences may be added when spinal cord infarction, hemorrhage, or another vascular mimic is suspected. These sequences are adjunctive and are not diagnostic of transverse myelitis.[5] |
MRI findings and interpretation
| Finding | Interpretation |
|---|---|
| Extra-axial compression | Evaluate for spinal cord compression from degenerative disc disease or spinal stenosis, tumor, epidural abscess, epidural hematoma, or another structural lesion. Demonstration of a causative compressive lesion argues against a diagnosis of inflammatory transverse myelitis and requires urgent cause-specific evaluation.[2][3] |
| Intramedullary T2 signal abnormality | The typical abnormality is one or more areas of increased T2-weighted signal within the spinal cord. Signal intensity, margin, location, and longitudinal and axial extent are variable; no pattern alone confirms transverse myelitis. |
| Cord swelling | Focal or longitudinal cord expansion may be present during the acute phase. Swelling is nonspecific and should prompt careful assessment for inflammatory, infectious, neoplastic, and vascular causes.[5] |
| Contrast enhancement | Enhancement may be absent or may appear patchy, nodular, linear, or ring-like. Its presence supports disruption of the blood–spinal cord barrier and may satisfy the imaging component of objective inflammation in the Transverse Myelitis Consortium Working Group framework, but it is not specific for transverse myelitis.[2][5] |
| Lesion length | Longitudinally extensive transverse myelitis (LETM) describes a spinal cord lesion extending across three or more contiguous vertebral segments. Lesion length is an etiologic clue rather than a diagnosis: both long and short lesions require clinical and laboratory correlation.[6][5] |
| Axial distribution | Central versus peripheral location, gray-matter versus white-matter predominance, percentage of cord cross-section involved, and associated swelling may help narrow the differential diagnosis. These features should not be used in isolation to assign a cause.[5] |
| Normal or equivocal MRI | A normal early examination does not exclude transverse myelitis. Reassess image quality, anatomic coverage, and timing; repeat imaging is warranted when the clinical syndrome persists or evolves.[2] |
Sequence of MRI assessment
- Perform urgent spinal MRI to exclude an extra-axial compressive lesion and other structural emergencies.
- Characterize any intrinsic cord abnormality on sagittal and axial images, documenting level, length, axial location, cord swelling, enhancement, and associated findings.
- Obtain brain MRI as part of the initial etiologic imaging assessment.[4]
- If the initial MRI is normal or equivocal but the clinical syndrome remains compatible with transverse myelitis, repeat spinal MRI. The Transverse Myelitis Consortium Working Group framework specifies repeat assessment for objective inflammation within 2 to 7 days after symptom onset when initial criteria are not met.[2]
- Obtain further follow-up MRI when symptoms worsen, new neurologic deficits emerge, the initial study was technically limited, or imaging evolution is needed to clarify the differential diagnosis.[5]
Limitations
- MRI supports diagnosis, excludes urgent mimics, and helps determine etiology; it does not replace clinical localization or establish transverse myelitis by itself.
- Neither absence of a visible cord lesion nor absence of enhancement excludes transverse myelitis.
- Lesion length, enhancement pattern, and axial distribution overlap among inflammatory, infectious, vascular, neoplastic, metabolic, and other causes of myelopathy.
- No validated MRI sensitivity or specificity threshold is available that can confirm or exclude transverse myelitis across all clinical settings; therefore, a sensitivity-and-specificity comparison table is not appropriate for this page.
References
- ↑ Gaillard F. Transverse myelitis MRI. Radiopaedia via Wikimedia Commons. Licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License. The displayed image was cropped from the original. Accessed October 1, 2026.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology. 2002;59(4):499-505. doi:10.1212/WNL.59.4.499. PubMed identifier: 12236201.
- ↑ 3.0 3.1 Peckham M, Hutchins TA, Amrhein TJ, et al. ACR Appropriateness Criteria® Myelopathy: 2026 Update. Journal of the American College of Radiology. 2026;23(9):1870-1883. doi:10.1016/j.jacr.2026.06.003. PubMed identifier: 42340276.
- ↑ 4.0 4.1 4.2 4.3 Kalnins A, Lewis LM, Soderlund KA, et al. ACR Appropriateness Criteria® Demyelinating Diseases. Journal of the American College of Radiology. 2026;23(6):1183-1214. doi:10.1016/j.jacr.2026.02.003. PubMed identifier: 41762178.
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 Jarius S, Aktas O, Ayzenberg I, et al.; Neuromyelitis Optica Study Group (NEMOS). Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD)—revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part I: Diagnosis and differential diagnosis. Journal of Neurology. 2023;270(7):3341-3368. doi:10.1007/s00415-023-11634-0. PubMed identifier: 37022481.
- ↑ 6.0 6.1 Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis. Neurology. 2011;77(24):2128-2134. doi:10.1212/WNL.0b013e31823dc535. PubMed identifier: 22156988.
