Transverse myelitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Spinal-cord inflammation interrupts descending motor, ascending sensory and autonomic pathways. Patients may describe a tight truncal band, ascending paraesthesia, limb heaviness, electric-shock sensations, constipation, urinary hesitancy or retention and sexual dysfunction. Upper-cervical disease can weaken respiratory muscles. Examination should seek a reproducible sensory level, upper-motor-neurone signs below the lesion and the pattern of sacral or segmental involvement, while remembering that reflexes may be reduced during early spinal shock.

The label becomes useful only after localisation and aetiological work. Gadolinium enhancement and cord swelling support activity but may be absent. Brain lesions, optic neuritis, antibody status, systemic features and CSF oligoclonal bands influence whether the episode is MS, AQP4-NMOSD, MOGAD or another inflammatory disorder. Infectious myelitis, B12 or copper deficiency, lupus, Sjogren syndrome, sarcoidosis and paraneoplastic disease require context-led tests.

Treatment is simultaneous rather than sequential: secure the cord from compression, collect time-sensitive samples, control inflammation, preserve ventilation and bladder drainage, and begin rehabilitation. Maintenance immunotherapy is not automatic after every idiopathic monophasic event. It depends on the cause and relapse probability and should be decided by a neuroinflammatory specialist after results and follow-up imaging are reviewed.

Key points

Transverse myelitis describes an inflammatory spinal-cord syndrome, not a final aetiological diagnosis; it may be idiopathic, post-infectious or part of MS, NMOSD, MOGAD, systemic autoimmunity, infection or malignancy.
Typical deficits evolve over hours to days and combine bilateral motor, sensory and autonomic dysfunction attributable to a spinal level, although asymmetry is common early.
Urgent MRI of the whole spine with contrast is required to exclude compression, epidural infection, tumour, vascular malformation and other structural emergencies before immunotherapy is assumed appropriate.
A deficit maximal within minutes suggests spinal-cord infarction; a progressive course beyond several weeks raises a compressive, neoplastic, dural arteriovenous fistula, metabolic or degenerative alternative.
Lesions spanning three or more vertebral segments suggest NMOSD, MOGAD, sarcoidosis or other systemic inflammation more than typical MS, but length is a clue rather than a diagnosis.
MRI brain and serum AQP4-IgG and MOG-IgG help predict recurrence and determine whether long-term disease-specific treatment is needed.
High-dose intravenous methylprednisolone is common first-line attack therapy after infection and compression are considered; severe steroid-incomplete disease should prompt early plasma-exchange discussion.
Bladder overdistension, constipation, venous thromboembolism, pressure injury, neuropathic pain, spasticity and respiratory decline require active treatment from admission.
Neurological recovery can continue for months, so coordinated physiotherapy, occupational therapy, rehabilitation medicine, continence care and psychological support are core treatment.
Do not diagnose relapse from symptoms alone when infection, fever, pain, fatigue or an established cord scar could be causing pseudo-worsening.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Idiopathic or post-infectious inflammation

Some acute inflammatory cord syndromes follow infection or have no identified cause after structural, vascular and systemic alternatives are assessed.

Multiple sclerosis

A shorter partial cord lesion with characteristic brain plaques and cerebrospinal-fluid findings may represent an MS attack.

NMOSD and MOG-associated disease

Longitudinally extensive, severe or recurrent myelitis raises AQP4 or MOG autoimmunity and changes relapse-prevention decisions substantially.

Systemic, infectious and malignant disease

Sarcoid, connective-tissue disease, infection, paraneoplastic immunity and infiltration can inflame the cord with broader clinical clues.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Spinal immune activation
Immune cells, antibodies or infection disrupt the blood–cord barrier and inflame a focal or longitudinal spinal segment.
2
Oedema and demyelination
Inflammation damages myelin and swells cord tissue, blocking motor, sensory and autonomic impulse transmission during attacks.
3
Tract and segmental dysfunction
Corticospinal, sensory, anterior-horn and sacral pathways fail according to lesion level, causing bilateral but often asymmetric deficits.
4
Axonal injury and recovery
Resolution of oedema permits early improvement, while axonal loss determines persistent weakness, pain and sphincter disability.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Evolving cord syndromeRed flag

Weakness and sensory symptoms progress over hours or days, with a band-like truncal boundary and new bladder, bowel or sexual dysfunction. Bilateral findings below one anatomical level are strongly localising.

High cervical dangerRed flag

Arm involvement, weak cough, breathlessness, reduced chest expansion or bulbar symptoms accompany a cervical lesion. Serial respiratory observations and critical-care input may be required before oxygen saturation falls.

Vascular onsetRed flag

A maximal deficit within minutes, often with acute back pain and disproportionate loss of pain and temperature, favours spinal-cord infarction over immune myelitis even if early MRI is unrevealing.

Demyelinating context

Previous optic neuritis, area-postrema symptoms, brainstem attacks, relapses or compatible cerebral lesions should trigger AQP4, MOG and MS-focused assessment rather than an idiopathic label.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Emergency MRI whole spine with gadoliniumFirst step
Why
Confirm intramedullary disease and immediately identify compression, abscess, haemorrhage, tumour or a vascular structural lesion.
Interpretation and limitations
Document axial location, length, swelling and enhancement. A normal early MRI does not completely exclude infarction or inflammation; neuroradiology review and repeat imaging may be needed if objective signs persist.
02
MRI brain and orbits
Why
Look for dissemination, optic-nerve disease and imaging patterns that support MS, NMOSD, MOGAD, ADEM or another cerebral process.
Interpretation and limitations
Interpret lesion morphology and distribution rather than simply counting white-matter spots. An incidental nonspecific scan should not convert a cord syndrome into MS.
03
CSF cells, protein, glucose, microbiology and oligoclonal bands
Why
Demonstrate inflammation, investigate infection and assess intrathecal immunoglobulin synthesis after imaging makes puncture safe.
Interpretation and limitations
Pleocytosis or raised protein supports inflammation but is nonspecific. Marked neutrophilia, very low glucose, organisms or malignant cells redirect treatment; paired serum is required for oligoclonal-band interpretation.
04
Serum AQP4-IgG and MOG-IgG
Why
Identify recurrent antibody-associated disorders whose prognosis and maintenance treatment differ from idiopathic transverse myelitis.
Interpretation and limitations
Use validated cell-based assays in a compatible phenotype, ideally before exchange. Low-positive MOG results and negative tests require expert interpretation rather than automatic diagnostic closure.
05
Cause-directed blood and infection screen
Why
Detect treatable nutritional, systemic autoimmune, infectious, vascular or malignant explanations selected from the history.
Interpretation and limitations
Typical tests may include full blood count, inflammatory markers, B12, folate, copper, HIV, syphilis, ANA/ENA and sarcoid assessment; avoid ordering every rare antibody without a clinical hypothesis.
06
Physiological and complication assessment
Why
Quantify immediate threats and establish rehabilitation baselines beyond the MRI abnormality.
Interpretation and limitations
Measure forced vital capacity for high lesions, bladder scan after voiding, renal function, skin integrity, venous-thromboembolism risk, swallowing where relevant and a structured motor/sensory disability score.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Spinal cord compression

Tumour, abscess, disc and haematoma require urgent contrast imaging because immune treatment without decompression can permit irreversible injury.

Spinal cord infarction

A deficit maximal within minutes and vascular or severe pain context favours ischaemia over inflammation evolving across hours or days.

Dural arteriovenous fistula

Progressive or stepwise myelopathy, flow voids and long cord oedema in an older adult suggest venous hypertensive disease.

Nutritional myelopathy

Symmetrical posterior-column and corticospinal signs with cobalamin, copper or vitamin-E deficiency usually evolve more gradually instead.

Additional chapter-specific clues

Compressive mimicRed flag

Severe local back pain, vertebral tenderness, fever, malignancy, immunosuppression, anticoagulation or recent procedure raises epidural abscess, malignant compression or haematoma and prioritises emergency imaging and surgical pathways.

Peripheral alternativeRed flag

Guillain-Barre syndrome can cause ascending weakness and areflexia but does not usually create a clear truncal sensory level or an intrinsic cord lesion; cauda-equina disease produces a different root and sphincter pattern.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First hoursProtect the cord and patientFirst stepAn acute or subacute bilateral sensorimotor syndrome with autonomic disturbance is identified.

1Perform ABCDE, document sacral and segmental neurology, check respiratory mechanics for cervical disease, scan the bladder and use the emergency spinal-compression pathway when red flags are present.
2Obtain urgent contrast MRI of the whole spine, involving spinal surgery, oncology or infection teams immediately if compression, abscess, haemorrhage or instability appears.
3After structural emergencies are excluded, acquire serum and appropriate CSF samples promptly and agree empiric antiviral or antimicrobial cover when infection remains plausible.
4Start pressure-area care, thromboprophylaxis when safe, catheterisation for significant retention and early rehabilitation assessment on the day of admission.

02Inflammatory attackEscalate deficit-led therapyEscalationMRI and examination support active inflammatory myelitis with no untreated contraindicating infection.

1Give intravenous methylprednisolone under the specialist protocol, commonly 1 g daily for three to five days in adults, and monitor metabolic, psychiatric, gastric and infectious complications.
2Reassess power, sensory level, gait, ventilation and sphincter function daily rather than relying on pain or paraesthesia alone to judge response.
3Discuss plasma exchange early for severe motor, respiratory or sphincter deficit or an inadequate steroid response; IV immunoglobulin may be considered in selected pathways when exchange is unsuitable.
4Treat neuropathic pain, spasms, constipation and bladder dysfunction without oversedation, and avoid allowing symptomatic medicines to obscure respiratory deterioration.

03After stabilisationDefine recurrence risk and rebuild functionThe acute deficit has plateaued and antibody, CSF and imaging results are becoming available.

1Integrate AQP4, MOG, brain MRI, oligoclonal bands, systemic tests and clinical history in a neuroinflammatory review, replacing the syndromic label with an aetiology where possible.
2Transfer to goal-based neurorehabilitation covering mobility, transfers, upper-limb use, continence, bowel routine, sexual health, fatigue, pain, mood, work and driving advice.
3Plan repeat clinical and imaging review and reserve maintenance immunotherapy for a defined relapsing disorder or a specialist-assessed high-risk phenotype.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Accelerates control of active inflammatory cord injury after urgent structural and infectious assessment.

Intravenous methylprednisolone

Specialist protocols commonly use 1 g once daily for three to five days in adults.

Monitor glucose, blood pressure, mental state, sleep, potassium and infection; consider gastric and bone protection according to duration and individual risk.

Removes circulating pathogenic mediators in severe steroid-refractory or antibody-associated myelitis.

Therapeutic plasma exchange

A typical rescue course comprises five to seven specialist exchanges, adjusted to response and local policy.

Central access, hypotension, hypocalcaemia, coagulopathy, sepsis and removal of concurrent medicines require planned apheresis monitoring.

Reduces burning, shooting or allodynic pain that can impede sleep, therapy and functional recovery.

Neuropathic-pain treatment

Choose and titrate one NICE-supported option slowly according to renal function, comorbidity and response.

Gabapentinoids, duloxetine and amitriptyline have distinct sedation, falls, anticholinergic, cardiovascular, renal and dependence considerations; avoid reflex polypharmacy.

May reduce painful spasms and improve care, sleep or gait when tone is functionally harmful.

Antispasticity treatment

Begin with physical measures; if needed, introduce low-dose baclofen and titrate under rehabilitation review.

Excess tone reduction can remove useful support for standing, while baclofen can cause weakness and sedation and must not be stopped abruptly after sustained use.

Relieves retention and prevents overdistension, renal injury and autonomic complications while bladder pathways recover.

Intermittent or indwelling urinary drainage

Use bladder-scan findings and continence or urology plans rather than a fixed drug-style regimen.

Use aseptic technique, review ongoing need, prevent traction and constipation, and distinguish catheter colonisation from symptomatic urinary infection.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Paralysis and respiratory failure

Severe cervical disease causes tetraparesis, weak cough and ventilatory failure, while lower lesions can remove independent walking.

Bladder, bowel and sexual dysfunction

Autonomic cord injury causes retention, incontinence, constipation, infection and sexual-health or relationship consequences after severe myelitis.

Pain, spasticity and contracture

Neuropathic pain and upper motor-neurone overactivity impair sleep, positioning, gait and skin care during incomplete recovery.

Immobility complications

Weakness causes thrombosis, pressure injury, osteoporosis, infection and deconditioning unless multidisciplinary rehabilitation begins alongside acute treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat a structured neurological examination, sensory-level map, gait or transfer assessment and respiratory measurements so subtle ascent or early recovery is visible.
Use bladder scanning, fluid balance, renal function and a documented bowel programme; painless retention and faecal loading can be missed in an insensate patient.
Inspect skin and equipment interfaces, reassess venous-thromboembolism risk and maintain passive range while weakness limits independent repositioning.
Monitor steroid or exchange complications with laboratory and bedside checks defined by the acute neurology and apheresis services.
At follow-up, track relapses, new optic or brainstem symptoms, pain, spasticity, falls, sexual health, mood, fatigue and participation rather than MRI appearance alone.
Give explicit emergency advice for rising weakness, breathlessness, a new sensory level, loss of bladder control, fever with back pain or acute pressure-area breakdown.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Reflexes can be absent

An acute intrinsic cord lesion may initially produce spinal shock with flaccidity and areflexia before the expected upper-motor-neurone pattern emerges.

Time course localises cause

Seconds to minutes suggests vascular injury, hours to days fits inflammation, and steady progression over weeks demands renewed structural, malignant or fistula assessment.

Length is contextual

A longitudinally extensive lesion is a powerful clue but neither proves AQP4 disease nor excludes MOGAD, sarcoidosis, infection or vascular mimics.

Bladder signs are objective

A post-void residual can establish autonomic cord dysfunction and prevent overdistension even when the patient reports only vague abdominal discomfort.

Recovery outlasts admission

Remyelination, resolution of spinal shock and rehabilitation gains may continue for many months, making early pessimistic prognostication unreliable.

Idiopathic is provisional

Some initially isolated attacks later declare MS, NMOSD or MOGAD, so planned clinical review and selective repeat testing are part of diagnosis.

11Common pitfallsFrequent interpretation and management errors.

01
Giving steroids for presumed transverse myelitis before excluding malignant compression, epidural abscess or spinal haematoma.
02
Using a normal early scan to dismiss objective cord signs without neuroradiology review or a plan to repeat imaging.
03
Calling every long lesion NMOSD and failing to obtain AQP4, MOG, systemic and infection evidence.
04
Overlooking respiratory decline in a high cervical lesion because oxygen saturation remains normal.
05
Leaving urinary retention, constipation, pressure risk and thromboprophylaxis until diagnostic tests are complete.
06
Promising a monophasic course before antibody status, brain imaging and longitudinal follow-up are available.