Skip to textbook content
Doctor’s PassportTextbook
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Neurology indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
Full textbook13 sectionsOpen only what you need
Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Transverse myelitis

Neurology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
!
Time-critical presentation

Any evolving bilateral weakness, objective sensory level, new urinary retention, saddle symptoms or respiratory compromise requires emergency neurological assessment and urgent spinal imaging; presumed inflammation must never delay exclusion of compressive cord or cauda-equina pathology.

Overview

Approach acute spinal-cord inflammation as a time-critical syndrome: localise the lesion, exclude compression and vascular disease, identify its cause and protect respiratory, bladder and mobility function.

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.

Aetiology

01

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.

02

Multiple sclerosis

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

03

NMOSD and MOG-associated disease

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

04

Systemic, infectious and malignant disease

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

Pathophysiology

  1. 1
    Spinal immune activation

    Immune cells, antibodies or infection disrupt the blood–cord barrier and inflame a focal or longitudinal spinal segment.

  2. 2
    Oedema and demyelination

    Inflammation damages myelin and swells cord tissue, blocking motor, sensory and autonomic impulse transmission during attacks.

  3. 3
    Tract and segmental dysfunction

    Corticospinal, sensory, anterior-horn and sacral pathways fail according to lesion level, causing bilateral but often asymmetric deficits.

  4. 4
    Axonal injury and recovery

    Resolution of oedema permits early improvement, while axonal loss determines persistent weakness, pain and sphincter disability.

Clinical features and red flags

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.

Investigations

  1. 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.
  2. 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.
  3. 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.
  4. 04
    Serum AQP4-IgG and MOG-IgG
    Why
    Identify recurrent antibody-associated disorders whose prognosis and maintenance treatment differ from idiopathic transverse myelitis.

Differential diagnosis

01

Spinal cord compression

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

02

Spinal cord infarction

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

03

Dural arteriovenous fistula

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

04

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.

Management

01First hoursProtect the cord and patientFirst stepAn acute or subacute bilateral sensorimotor syndrome with autonomic disturbance is identified.+
  1. 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.
  2. 2Obtain urgent contrast MRI of the whole spine, involving spinal surgery, oncology or infection teams immediately if compression, abscess, haemorrhage or instability appears.
  3. 3After structural emergencies are excluded, acquire serum and appropriate CSF samples promptly and agree empiric antiviral or antimicrobial cover when infection remains plausible.
  4. 4Start pressure-area care, thromboprophylaxis when safe, catheterisation for significant retention and early rehabilitation assessment on the day of admission.
02Inflammatory attackEscalate deficit-led therapy

Complications

01

Paralysis and respiratory failure

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

02

Bladder, bowel and sexual dysfunction

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

03

Pain, spasticity and contracture

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

04

Immobility complications

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

Monitoring and follow-up

  • 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.

Special situations

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.

Common pitfalls

  1. 01

    Giving steroids for presumed transverse myelitis before excluding malignant compression, epidural abscess or spinal haematoma.

  2. 02

    Using a normal early scan to dismiss objective cord signs without neuroradiology review or a plan to repeat imaging.

  3. 03

    Calling every long lesion NMOSD and failing to obtain AQP4, MOG, systemic and infection evidence.

  4. 04

    Overlooking respiratory decline in a high cervical lesion because oxygen saturation remains normal.

  5. 05

    Leaving urinary retention, constipation, pressure risk and thromboprophylaxis until diagnostic tests are complete.

  6. 06

    Promising a monophasic course before antibody status, brain imaging and longitudinal follow-up are available.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
NeurologyOriginal SBA

Cord syndrome with cancer history

A 62-year-old with metastatic prostate cancer develops thoracic back pain, progressive bilateral leg weakness, a T8 sensory level and urinary retention over twelve hours. What is the immediate investigation priority?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Neurology topics →
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG234 spinal metastases and metastatic cord compression
  • NICE NG220 multiple sclerosis diagnosis and management
  • Great Ormond Street Hospital acute transverse myelitis guidance
  • Association of British Neurologists clinical guidance collection

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
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.
    • 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.
    • Escalation
    MRI and examination support active inflammatory myelitis with no untreated contraindicating infection.
    +
    1. 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.
    2. 2Reassess power, sensory level, gait, ventilation and sphincter function daily rather than relying on pain or paraesthesia alone to judge response.
    3. 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.
    4. 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.+
    1. 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.
    2. 2Transfer to goal-based neurorehabilitation covering mobility, transfers, upper-limb use, continence, bowel routine, sexual health, fatigue, pain, mood, work and driving advice.
    3. 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.