Transverse myelitis: urgent MRI and IV steroids — the GP's role

Transverse myelitis (TM) is an acute or subacute inflammatory syndrome of the spinal cord producing bilateral motor weakness, a sensory level on the trunk, and bladder or bowel dysfunction at and below the affected level. It is uncommon — incidence approximately one to five cases per million per year in Australia — but its consequences are potentially catastrophic and time-sensitive. The general practice role is to recognise the clinical presentation, immediately exclude surgical emergencies (spinal cord compression must not be missed), and arrange same-day emergency transfer for MRI and neurology assessment.

The most important management principle is that speed matters. IV methylprednisolone started within 14 days of onset — and ideally within seven days — is associated with better visual and motor recovery in NMOSD and MOGAD per a 2020 review in Frontiers in Neurology. Spinal cord damage from delayed treatment is frequently irreversible.

A. Core clinical — the AU general practice framework

What transverse myelitis is: The Transverse Myelitis Consortium Working Group (2002) defined TM as a clinical syndrome of acute to subacute (hours to 21 days) spinal cord inflammation with bilateral motor, sensory, and autonomic dysfunction at and below the affected level. A sensory level — a band of altered sensation around the trunk — is the hallmark clinical sign.

The three aetiological categories that matter most to the GP:

1. Multiple sclerosis (MS): typically a short-segment spinal cord lesion (less than two vertebral segments on MRI), accompanied by multiple white-matter lesions in the brain, and oligoclonal bands in the cerebrospinal fluid. Affects approximately 25,000 Australians; incidence 5–8 per 100,000 per year per MS Australia. Female predominance ~3:1.

2. NMOSD (neuromyelitis optica spectrum disorder): defined by the 2015 Wingerchuk international consensus criteria. The cardinal MRI feature is a longitudinally extensive transverse myelitis (LETM) — a T2-hyperintense spinal cord lesion spanning three or more vertebral segments. AQP4-IgG (aquaporin-4 antibody) is positive in approximately 80% of NMOSD cases and is the key diagnostic test; it must be sent as a cell-based assay (not ELISA). NMOSD carries a severe relapse profile and always requires maintenance immunosuppression. Prevalence approximately 1–5 per 100,000; female-to-male ratio ~9:1 in AQP4-positive disease.

3. MOGAD (myelin oligodendrocyte glycoprotein antibody disease): defined by the 2023 Banwell international consensus diagnostic criteria. MOG-IgG is the diagnostic antibody (cell-based assay essential — do not use ELISA). LETM is common in MOGAD as well, but unlike NMOSD approximately 50% of MOGAD cases are monophasic and never relapse. Recovery is generally better than in NMOSD. Estimated prevalence 1.3–2.5 per 100,000.

Presenting features to recognise:

• Bilateral lower limb weakness, heaviness, or paralysis — developing over hours to days
• Sensory level — a distinct band of altered sensation, tingling, or numbness around the chest or abdomen
• Urinary retention (acute retention is a high-yield clinical sign — the patient cannot pass urine despite a full bladder)
• Urinary or faecal incontinence
• Back pain at the level of the lesion
• Recent viral illness one to four weeks prior (post-infectious TM)
• Concurrent or preceding visual disturbance (optic neuritis — red flag for NMOSD or MOGAD)

What to do in the room:

• Check vital signs; bladder palpation and if retention is present, catheterise immediately
• Neurological examination — motor power (pyramidal weakness below the level), deep tendon reflexes (may be brisk or in early spinal shock flaccid and absent), Babinski sign, sensory level on the trunk, perianal sensation and anal tone, postural BP
• Call neurology and arrange urgent transfer to emergency department for whole-spine MRI + brain MRI with gadolinium; do not wait for MRI to be available locally — transfer to a facility that can perform it within hours

B. What MRI and the laboratory show — the LETM discriminator

MRI is the critical investigation. The length of the T2-hyperintense cord lesion on MRI is the single most discriminating imaging feature:

• LETM (≥3 vertebral segments) — strongly suggests NMOSD or MOGAD; call ophthalmology to exclude concurrent optic neuritis
• Short-segment lesion (under 2 vertebral segments) with multiple T2 brain lesions and oligoclonal bands — favours MS

This discriminator is important but not absolute — some MOGAD and NMOSD cases have short-segment lesions, and some MS cases have longer lesions. Serological results and the full clinical picture always take precedence.

CSF analysis (after MRI has excluded mass lesion and confirmed it is safe to lumbar puncture):

• Lymphocytic pleocytosis in TM; neutrophilic in bacterial myelitis; no cells in vascular cord infarction
• Oligoclonal bands: positive in approximately 85% of MS, less commonly in NMOSD/MOGAD
• HSV, VZV, enterovirus, EBV PCR; VDRL/TPHA (syphilis); bacterial culture

Serology:

• AQP4-IgG — cell-based assay; sent to specialist laboratory
• MOG-IgG — cell-based assay; do not use ELISA
• HIV (with informed consent)
• Vitamin B12, folate, vitamin D
• ANA, ENA, anti-dsDNA, ANCA, complement — connective tissue disease
• Serum angiotensin-converting enzyme — sarcoidosis
• Paraneoplastic panel (anti-Hu, CRMP5) if malignancy is suspected

eTG Demyelinating disease provides specific guidance on the investigation sequence.

C. Acute treatment and maintenance — the treatment ladder

Acute attack — in hospital, neurologist-led:

Step 1: IV methylprednisolone 1 g daily for three to five days. This is the standard first-line treatment across MS, NMOSD, and MOGAD per eTG and Wingerchuk 2015. Starting treatment within 14 days of onset (ideally within seven days) is associated with better motor and visual recovery. Some neurologists add a two-week oral prednisolone taper; others do not.

Step 2: Plasma exchange (PLEX) — five to seven sessions on alternate days — if there is no meaningful response after five days of IVMP. This is particularly effective for AQP4-positive NMOSD and severe MOGAD, where the Frontiers in Neurology 2020 review documents substantially improved visual and motor outcomes. IVIG is an alternative if PLEX is unavailable or the patient declines central venous access.

Maintenance immunosuppression — aetiology-dependent:

For NMOSD, maintenance is always required after the first attack per the 2023 NEMOS recommendations. Untreated AQP4-positive NMOSD has relapse rates of 60% within a year and causes severe permanent disability with each relapse. PBS-listed options include:

• Rituximab — most-used first-line agent in Australia; off-label Authority Required for NMOSD
• Eculizumab (Soliris) — PBS Authority Required for AQP4+ NMOSD
• Satralizumab (Enspryng) — IL-6 receptor blocker; PBS Authority listing under specific criteria
• Inebilizumab (Uplizna) — anti-CD19; PBS Authority listing under specific criteria

For MOGAD, management is more selective per Banwell 2023. Treatment after a second attack is standard. After a first attack, treatment is considered for severe presentations or when MOG-IgG remains persistently positive at six months (associated with higher relapse risk). Options include rituximab, monthly IVIG, mycophenolate, or azathioprine.

For MS, refer to the treating neurologist for disease-modifying therapy selection — the MS pathway involves PBS-listed first-line agents (interferon-beta, glatiramer acetate) and high-efficacy agents (ocrelizumab, natalizumab, cladribine) depending on disease activity.

D. Australian operations — MBS, PBS, NDIS

MBS items:

• Items 23 / 36 / 44 — GP consultations for assessment, monitoring, and shared-care review
• MRI spine: items 63179 / 63183 / 63185 — GP-requested MRI rebatable for selected spinal cord indications (verify current clinical indicator requirements post-2024 reforms); some NMOSD/MOGAD/MS reviews require neurology referral for rebatable imaging
• MRI brain: items 63007 / 63010
• Items 965 / 967 — GPCCMP preparation and review (post-1-July-2025 single-plan framework) — chronic neurological disability qualifies
• Items 2715 / 2717 — Mental Health Care Plan — depression, anxiety, and adjustment to disability are common in TM survivors
• Item 715 — Aboriginal and Torres Strait Islander Health Assessment

PBS items:

• Methylprednisolone IV — hospital-only supply
• Rituximab — PBS Authority Required (various rheumatology and oncology indications; off-label Authority application for NMOSD on a case-by-case basis)
• Eculizumab, satralizumab, inebilizumab — PBS Authority Required under specific NMOSD criteria
• Symptomatic medications — baclofen, tizanidine (spasticity); gabapentin, pregabalin (neuropathic pain — SafeScript monitoring required); oxybutynin (bladder urgency) — all PBS General Schedule or Streamlined
• Physiotherapy under GPCCMP — allied health item 10970, up to five sessions per calendar year

NDIS: many TM survivors aged under 65 qualify for NDIS under acquired neurological disability — bladder and bowel management, mobility equipment, physiotherapy and occupational therapy, psychosocial support. For those aged 65 or over, My Aged Care provides equivalent home-support pathways.

E. Special populations

Aboriginal and Torres Strait Islander Australians: are underrepresented in the MS registry, with equivocal incidence data for MS relative to the general population. Access to specialist neurology and to disease-modifying therapy is substantially limited in remote and very remote areas. Coordination with Aboriginal Community Controlled Health Organisations and neurological telehealth services (RACP-supported outreach programs) is important for timely diagnosis and maintenance therapy access.

Women with NMOSD and pregnancy: AQP4-positive NMOSD carries elevated relapse risk in the postpartum period. Pre-conception counselling with a neurologist and obstetrician with experience in autoimmune neurological disease is essential. Rituximab requires careful timing relative to conception (half-life and B-cell recovery); eculizumab has limited pregnancy safety data.

Post-infectious and post-vaccination TM: Post-infectious TM follows viral illness (Mycoplasma, EBV, VZV, COVID-19) by one to four weeks. Post-vaccination TM is extremely rare; vaccine benefits continue to far outweigh this risk. Both are managed with IV methylprednisolone; maintenance immunosuppression is not usually required unless serological testing reveals underlying NMOSD or MOGAD.

Older adults: Spinal cord compression from vertebral metastasis or epidural abscess rises substantially in prevalence with age. In an older adult presenting with subacute myelopathy, malignancy must be actively excluded before assuming an inflammatory cause.

Children and adolescents: Acute disseminated encephalomyelitis (ADEM) is more common in children than adults and involves encephalopathy with multifocal CNS involvement; it is distinguished from TM by the brain MRI and clinical features. Paediatric NMOSD and MOGAD require specialist paediatric neurology management.

When to escalate

Call emergency services (000) or arrange Cat-1 transfer immediately for:

• Bilateral lower limb weakness or paraplegia developing over hours
• Sensory level on the trunk with bladder or bowel dysfunction
• Suspected spinal cord compression (back pain + weakness + bowel/bladder — surgical emergency)
• Cauda equina syndrome (saddle anaesthesia + bilateral leg weakness + urinary retention)
• Any acute myelopathy with systemic sepsis

Arrange urgent neurology review within one to two days for:

• Subacute myelopathy over days to weeks with progressive course but without acute deterioration
• Known MS or NMOSD patient with new neurological symptoms (potential relapse)

For stable patients in shared care with their neurologist:

• New sensory symptoms consistent with a minor relapse — neurology within one week
• Annual MRI brain and spine monitoring for the first two years, then as directed by neurology

What this article is and is not

This article provides educational information about transverse myelitis, NMOSD, and MOGAD based on current guidelines including eTG Demyelinating disease, Wingerchuk 2015 NMOSD criteria, Banwell 2023 MOGAD criteria, and NEMOS 2023 recommendations. It does not constitute personal medical advice and is not a substitute for assessment by a qualified healthcare professional.

Acute myelopathy is a neurological emergency. If you or someone you know develops bilateral leg weakness, a sensory level, or sudden urinary retention, call 000 or go directly to an emergency department. Dr Hoe Bing Lo is an AHPRA-registered general practitioner (MED0001212640, FACRRM) practising in Australia. This article has not yet undergone specialist AHPRA review and is flagged accordingly.

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Sources cited

1. Therapeutic Guidelines (eTG) — Demyelinating disease
2. Wingerchuk et al. — International consensus diagnostic criteria for NMOSD. Neurology 2015
3. Trebst et al. — NEMOS revised NMOSD recommendations 2023. J Neurology
4. Banwell et al. — MOGAD International Consensus Diagnostic Criteria. Lancet Neurology 2023
5. Frontiers Neurology — Rapid IV methylprednisolone in NMOSD 2020
6. Transverse Myelitis Consortium Working Group. Neurology 2002
7. MS Australia
8. HealthDirect — Transverse myelitis
9. NDIS — acquired neurological disability supports