Transverse myelitis diagnostic study of choice
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D., Julinka Auta Fernandes
Overview
There is no single gold-standard or independently confirmatory diagnostic study for transverse myelitis. The diagnosis is based on a compatible acute or subacute spinal cord syndrome, exclusion of spinal cord compression, and objective evidence of spinal cord inflammation on magnetic resonance imaging (MRI) or cerebrospinal fluid (CSF) examination.[1]
MRI of the spinal cord is the diagnostic imaging study of choice. It should be performed urgently to exclude an extra-axial compressive lesion and to detect and characterize an intrinsic spinal cord abnormality.[2]
Diagnostic Study of Choice
Study of choice
There is no single diagnostic study that independently confirms transverse myelitis.[1] However, urgent MRI of the spinal cord is the diagnostic imaging study of choice in a patient presenting with an acute or subacute myelopathic syndrome.[2]
- MRI of the clinically relevant spinal region should be performed as soon as possible.[2]
- For initial imaging of acute myelopathy, MRI without intravenous contrast and MRI without and with intravenous gadolinium-based contrast material are both considered appropriate. Noncontrast MRI can be used when gadolinium cannot be administered.[2] When inflammatory myelitis is suspected and contrast can be administered safely, precontrast and postcontrast imaging helps demonstrate enhancement.[3]
- Imaging should include sagittal and axial acquisitions.[3]
- Imaging of the entire spinal cord, including the conus medullaris, should be considered when the neurological level is uncertain, symptoms involve multiple levels, or neuromyelitis optica spectrum disorder (NMOSD) or myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is suspected.[3]
- Brain MRI should be obtained during the etiologic evaluation to identify abnormalities supporting multiple sclerosis or another inflammatory demyelinating disorder.[3]
- When NMOSD or MOGAD is suspected, the French NOMADMUS expert consensus supports MRI of the brain, optic nerves, and spinal cord, including the cauda equina nerve roots, without and after gadolinium administration at initial diagnosis.[4]
The principal purposes of spinal MRI are to:
- Exclude spinal cord compression and other structural emergencies.[2]
- Detect an intramedullary spinal cord lesion.[2]
- Determine the craniocaudal extent and axial distribution of the lesion.[3]
- Identify spinal cord swelling and gadolinium enhancement.[3]
- Evaluate for vascular, neoplastic, infectious, and other alternative causes of myelopathy.[3]
- Identify imaging patterns that may guide testing for an underlying inflammatory demyelinating disorder.[3]
If MRI cannot be performed, computed tomography (CT) myelography may be considered to evaluate for spinal canal compression. Routine CT of the spine is not an adequate substitute for MRI when assessing intrinsic spinal cord inflammation.[2]
The comparison of various diagnostic studies for transverse myelitis
Transverse myelitis is a heterogeneous clinical syndrome rather than a single etiologic disease.[1] MRI, CSF examination, and disease-specific antibody testing answer different diagnostic questions and should be interpreted together with the clinical presentation.[3] The table below summarizes their roles; it does not represent a head-to-head diagnostic-accuracy study or provide a single sensitivity or specificity estimate applicable to every cause of transverse myelitis.
| Diagnostic study | Sensitivity | Specificity | Principal role |
|---|---|---|---|
| Spinal MRI | Varies with etiology, timing, and imaging technique | Varies with etiology and imaging pattern | Imaging study of choice; excludes compression and detects and characterizes an intrinsic spinal cord lesion.[2] A normal initial study does not exclude every form of inflammatory myelitis.[5] |
| CSF examination | Varies with etiology and the CSF marker assessed | Inflammatory findings are not specific to a single etiology | Assesses inflammation and helps investigate infectious and inflammatory causes; results require clinical and imaging correlation.[3] |
| Brain MRI | Not applicable as an isolated test for transverse myelitis | Not applicable as an isolated test for transverse myelitis | Identifies accompanying lesions that may support multiple sclerosis or another demyelinating disorder.[3] |
| Serum aquaporin-4 immunoglobulin G (AQP4-IgG) and myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG) testing | Assay- and disease-dependent | Assay- and disease-dependent | Helps identify NMOSD or MOGAD when the clinical presentation is compatible; antibody results must be interpreted using the relevant disease-specific criteria.[6][7] |
| CT myelography | Not established as a test for inflammatory transverse myelitis | Not established as a test for inflammatory transverse myelitis | Alternative for evaluating spinal canal compression when MRI cannot be performed; limited for evaluating intrinsic spinal cord inflammation.[2] |
No diagnostic study should be selected solely on the basis of an isolated sensitivity or specificity value; test selection depends on the clinical question and suspected underlying cause.[2]
Diagnostic results
No individual MRI finding is independently confirmatory of transverse myelitis. Findings that may support inflammatory myelitis, when interpreted with the clinical and CSF findings, include:[8]
- An intramedullary T2-weighted hyperintense spinal cord lesion corresponding to the clinical syndrome.[3]
- Focal or longitudinally extensive spinal cord involvement.[3]
- Spinal cord swelling during the acute phase.[3]
- Intramedullary gadolinium enhancement.[3]
- An axial and longitudinal lesion distribution compatible with an inflammatory demyelinating disorder.[3]
Lesion length or enhancement pattern alone should not be used to assign an etiology. Longitudinally extensive lesions may occur in NMOSD and MOGAD but can also occur with infectious, vascular, systemic autoimmune, metabolic, and neoplastic disorders.[3]
A normal initial spinal MRI does not completely exclude inflammatory myelitis. MRI-negative myelitis has been documented in MOGAD, and abnormalities may become apparent on follow-up imaging.[5] If clinical suspicion remains high, repeat MRI should be considered. Under the Transverse Myelitis Consortium Working Group criteria, when objective evidence of inflammation is absent at presentation, repeat MRI and lumbar puncture should be performed within 2–7 days.[1]
Sequence of Diagnostic Studies
The following is a practical diagnostic sequence. After urgent spinal imaging has excluded compression, CSF evaluation, brain MRI, and etiologic blood tests can be coordinated according to the clinical presentation rather than treated as a rigid sequence.[1]
- Urgent spinal MRI to exclude an extra-axial compressive lesion and identify an intrinsic spinal cord abnormality.[2]
- CSF examination after a compressive lesion has been excluded, to evaluate for pleocytosis, an elevated immunoglobulin G index, intrathecal immunoglobulin synthesis, and relevant infectious causes.[3]
- Brain MRI to evaluate for accompanying abnormalities suggestive of multiple sclerosis or another inflammatory demyelinating disorder.[3]
- Targeted etiologic investigations, including serum AQP4-IgG and MOG-IgG testing when clinically indicated. Cell-based assays and the appropriate disease-specific diagnostic criteria should be used when evaluating suspected NMOSD or MOGAD.[3]
- Repeat spinal MRI and CSF examination when the initial evaluation is nondiagnostic but clinical suspicion for inflammatory myelitis remains high; repeat MRI and lumbar puncture within 2–7 days are recommended by the Consortium criteria when initial evidence of inflammation is absent.[1]
Name of Diagnostic Criteria
The principal published transverse-myelitis-specific criteria are the Transverse Myelitis Consortium Working Group proposed diagnostic criteria for idiopathic acute transverse myelitis. All inclusion criteria and none of the exclusion criteria should be present for classification as idiopathic acute transverse myelitis.[1]
| Inclusion criteria | Exclusion criteria for idiopathic acute transverse myelitis |
|---|---|
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If objective inflammation is not demonstrated at symptom onset, the Consortium criteria recommend repeating MRI and lumbar puncture within 2–7 days.[1]
The exclusion criteria above apply to classification as idiopathic acute transverse myelitis. Identification of infection, systemic autoimmune disease, multiple sclerosis, NMOSD, MOGAD, or another defined cause may instead indicate disease-associated transverse myelitis and does not necessarily exclude the presence of myelitis.[1][3]
When NMOSD or MOGAD is suspected, the relevant disease-specific diagnostic criteria should be applied in addition to characterizing the myelitis syndrome.[6][7]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 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. PMID: 12236201.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Peckham M, Hutchins TA, Amrhein TJ, et al.; Expert Panel on Neurological Imaging, American College of Radiology. 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. PMID: 42340276. Full guideline.
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 Jarius S, Aktas O, Ayzenberg I, et al.; Neuromyelitis Optica Study Group (NEMOS). Update on the diagnosis and treatment of neuromyelits 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. PMID: 37022481. Full text.
- ↑ Durand-Dubief F, Shor N, Audoin B, et al.; NOMADMUS Study Group. MRI management of NMOSD and MOGAD: Proposals from the French Expert Group NOMADMUS. Journal of Neuroradiology. 2025;52(1):101235. doi:10.1016/j.neurad.2024.101235. PMID: 39626832.
- ↑ 5.0 5.1 Sechi E, Krecke KN, Pittock SJ, et al. Frequency and characteristics of MRI-negative myelitis associated with MOG autoantibodies. Multiple Sclerosis. 2021;27(2):303-308. doi:10.1177/1352458520907900. PMID: 32103708. Full text.
- ↑ 6.0 6.1 Wingerchuk DM, Banwell B, Bennett JL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology. 2015;85(2):177-189. doi:10.1212/WNL.0000000000001729. PMID: 26092914.
- ↑ 7.0 7.1 Banwell B, Bennett JL, Marignier R, et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. The Lancet Neurology. 2023;22(3):268-282. doi:10.1016/S1474-4422(22)00431-8. PMID: 36706773.
- ↑ Barreras P, Fitzgerald KC, Mealy MA, et al. Clinical biomarkers differentiate myelitis from vascular and other causes of myelopathy. Neurology. 2018;90(1):e12-e21. doi:10.1212/WNL.0000000000004765. PMID: 29196574. Full text.