Transverse myelitis is segmental inflammatory demyelination of the spinal cord. Classified as multiple sclerosis (MS), neuromyelitis optica (NMO/Devic), post-infectious autoimmune reaction, or idiopathic. MRI characteristically shows hyperintense intramedullary lesion on sagittal T2/STIR sequences. Lesion length provides diagnostic clue by etiology: longitudinally extensive transverse myelitis (LETM) spanning >2 vertebral segments suggests NMO, while <2 segments is consistent with MS. Cord swelling (increased AP diameter) and gadolinium enhancement are seen in the acute phase. On axial sections, MS shows dorsolateral peripheral white matter involvement, while NMO shows central gray matter involvement ('pencil-thin' lesion). DWI may show restricted diffusion in the acute phase. Cord atrophy develops in the chronic phase. AQP4-IgG and MOG-IgG antibodies support serological diagnosis. Early high-dose corticosteroid therapy improves neurological recovery.
Age Range
10-60
Peak Age
35
Gender
Equal
Prevalence
Uncommon
The pathophysiology of transverse myelitis varies by underlying etiology. In MS, perivenous T-lymphocyte infiltration and macrophage-mediated demyelination targets central nervous system white matter — plaques form in dorsolateral peripheral white matter of the spinal cord. These plaques destroy myelin sheaths while axons are partially preserved, allowing remission. In NMO, AQP4 (aquaporin-4) antibodies target water channels on astrocyte foot processes — complement activation causes astrocyte damage, secondary oligodendrocyte loss, and extensive demyelination. Since AQP4 channels are most concentrated in central gray matter (especially periependymal regions), NMO lesions are centrally located and longitudinally extensive. In post-infectious myelitis, molecular mimicry causes viral/bacterial antigens to cross-react with nervous system antigens — this widespread inflammatory response is usually monophasic. The T2 hyperintensity seen on MRI reflects proton density changes produced by the combination of inflammatory edema (increased extracellular water) and demyelination (myelin loss — increased free water). Gadolinium enhancement indicates disrupted blood-brain barrier — active inflammation damages capillary endothelial tight junctions, allowing contrast to leak into interstitial space.
Sagittal T2 hyperintense cord lesion spanning >2 (usually ≥3) vertebral segments. The most characteristic MRI finding of NMO/NMOSD. Spinal cord lesions in MS are typically shorter than 1-2 segments. AQP4-IgG testing is strongly recommended when LETM is present.
Well-defined or slightly irregular hyperintense lesion within the spinal cord on sagittal T2. In MS, typically 1-2 vertebral segments in length with peripheral dorsolateral location. In NMO, extending over 3 or more vertebral segments (LETM) with central gray matter predominance. Signal may be homogeneous or patchy. Contrast with surrounding normal cord is prominent in the acute phase.
Report Sentence
Hyperintense intramedullary lesion spanning [X] vertebral segments at the level of [level] on sagittal T2/STIR, consistent with acute transverse myelitis.
In acute transverse myelitis, cord anteroposterior diameter is increased at the lesion site. Focal enlargement of normal fusiform cord contour is seen on sagittal images. On axial, cord diameter is increased compared to adjacent normal segments. Swelling is due to inflammatory edema and cellular infiltration. In the chronic phase, swelling gives way to atrophy.
Report Sentence
Spinal cord swelling at the lesion level (increased AP diameter) supports an active inflammatory process.
Patchy, heterogeneous enhancement is seen in the lesion area on post-gadolinium T1. Enhancement may be irregular and segmental. Homogeneous ring enhancement is not expected (ring enhancement suggests tumor). Enhancement indicates active inflammation — disappears in remission. Non-enhancing lesion suggests chronic or inactive phase.
Report Sentence
Patchy enhancement in the lesion area on post-contrast series supports active inflammatory myelitis.
NMO-specific central gray matter involvement on axial T2: H-shaped or 'pencil-thin' hyperintense lesion in the cord center. In MS, focal plaque is seen in dorsolateral peripheral white matter (smaller than half the cord cross-section). This axial distribution pattern is critical for etiological differentiation. Distribution may be variable in idiopathic myelitis.
Report Sentence
Gray matter-predominant hyperintense lesion in the cord center on axial T2, demonstrating distribution pattern consistent with NMO/NMOSD.
Mild to moderate restricted diffusion may be seen in the lesion area on DWI in the acute phase. ADC values are mildly decreased. This finding reflects the cytotoxic edema component. Marked DWI restriction suggests infarction rather than myelitis — careful differentiation is needed. Diffusion restriction disappears in subacute/chronic phase.
Report Sentence
Mild restricted diffusion in the lesion area on DWI reflects the cytotoxic edema component of the acute inflammatory process.
In the chronic phase, atrophy develops in the previously swollen cord segment — diameter decreases, cord becomes thin. Residual T2 hyperintensity (gliosis/cavitation) may persist in the lesion area. Focal T1 hypointensity (tissue loss) may be seen. Degree of atrophy correlates with permanence of neurological deficit.
Report Sentence
Cord atrophy and residual T2 hyperintensity at the site of prior myelitis, suggesting chronic demyelinating sequela.
Criteria
Spinal cord lesion <2 vertebral segments. Dorsolateral peripheral white matter involvement on axial. Accompanying periventricular/juxtacortical lesions on brain MRI. Oligoclonal bands positive.
Distinct Features
Relapsing-remitting course. Cord lesion is short, may be asymmetric. Brain MRI lesions strengthen diagnosis. McDonald criteria apply.
Criteria
Lesion ≥3 vertebral segments (LETM). Central gray matter predominant involvement. AQP4-IgG seropositive. Optic neuritis may accompany.
Distinct Features
Severe attacks, incomplete remission. Responds to plasmapheresis. MS treatments (interferon) may worsen NMO. Rituximab/azathioprine for attack prophylaxis.
Criteria
Development after viral infection (CMV, EBV, HSV) or vaccination. Monophasic course. AQP4-IgG and MOG-IgG negative. Brain MRI usually normal.
Distinct Features
Usually single attack, recurrence rare. Responds well to steroid treatment. Prognosis better than MS/NMO. Confirmable with infectious agent serology.
Distinguishing Feature
Spinal astrocytoma shows heterogeneous enhancement with focal mass effect and eccentric position. Myelitis is diffuse and centrally located with patchy enhancement. Astrocytoma shows progressive growth while myelitis shrinks with treatment. Astrocytoma shows irregular cord expansion, myelitis shows fusiform swelling.
Distinguishing Feature
Ependymoma is centrally located but forms a focal, better-defined mass. Polar cysts and hemosiderin cap sign are characteristic. In myelitis, borders are ill-defined, mass effect is minimal, and hemosiderin is not expected. Ependymoma enhances intensely and homogeneously while myelitis enhances patchily.
Distinguishing Feature
Serpentine flow voids on cord surface (dilated perimedullary veins) are pathognomonic for SDAVF — no flow voids in myelitis. SDAVF causes progressive myelopathy with slow course. Myelitis usually has acute/subacute onset. SDAVF is confirmed by myelography or MR angiography.
Distinguishing Feature
Spinal tuberculosis (Pott disease) involves vertebral body with paravertebral cold abscess formation — cord compression is extrinsic. In myelitis, pathology is intrinsic (intramedullary). Disc destruction, vertebral collapse, and paraspinal collection are distinguishing findings in TB. Bone/disc involvement is not expected in myelitis.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
specialist-referralTransverse myelitis requires urgent neurological evaluation. First-line treatment begins with high-dose IV methylprednisolone (1 g/day, 3-5 days). Plasmapheresis (PLEX) is applied for steroid-refractory cases or NMO suspicion. AQP4-IgG and MOG-IgG testing is mandatory for etiological classification. Brain MRI should be screened for MS lesions. In NMO diagnosis, MS treatments (interferon-beta, fingolimod) are contraindicated and may worsen the disease — this distinction is vital. Attack prophylaxis: interferon/natalizumab for MS, rituximab/azathioprine for NMO. Reversibility of neurological deficits depends on early treatment — initiating treatment within the first 7 days is critical for prognosis.
Transverse myelitis requires urgent neurological evaluation. High-dose IV methylprednisolone (3-5 days) is first-line treatment. Plasmapheresis should be considered with NMO suspicion. AQP4-IgG and MOG-IgG antibodies are important for diagnosis. Underlying etiology (MS, NMO, infection, SLE, sarcoidosis) should be investigated.