Transverse Myelitis
Transverse myelitis (TM) is an acute inflammatory disorder of the spinal cord characterized by bilateral motor, sensory, and autonomic dysfunction below the level of the lesion. [1,2] It may occur as an isolated, post-infectious condition (idiopathic TM) or as the first presentation of multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD). [1,3]
Key Facts
| Fact | Detail |
|---|---|
| Definition | Acute inflammatory demyelination affecting the full width of the spinal cord |
| Incidence | 1-8 per million per year |
| Age distribution | Bimodal: 10-19 years and 30-39 years |
| First priority | Exclude compressive myelopathy (emergency MRI) |
| Classic triad | Motor weakness + sensory level + bladder dysfunction |
| Onset | Symptoms progress over hours to days (peak 4 hours to 21 days) |
| Key investigation | MRI spine with contrast + MRI brain + LP |
| Treatment | IV methylprednisolone 1g daily for 3-5 days |
| Prognosis | Partial TM has better prognosis than complete TM |
| Association with MS | 10-20% of partial TM will develop MS |
Clinical Pearls
Pearl 1: THE FIRST STEP IS ALWAYS TO EXCLUDE CORD COMPRESSION. Compressive myelopathy from disc, tumour, abscess, or haematoma requires emergency surgical decompression. Get an urgent MRI spine before attributing symptoms to TM.
Pearl 2: Partial TM (asymmetric, mild, affecting less than 2/3 of cord width) is associated with MS and has a better prognosis. Complete TM (symmetric, severe, full-width involvement) is more often idiopathic or associated with NMOSD and has worse prognosis.
Pearl 3: Always request MRI Brain in addition to MRI Spine. If brain lesions are present, the likelihood of developing MS is significantly higher (up to 90% at 14 years with 2+ brain lesions).
Pearl 4: Longitudinally extensive transverse myelitis (LETM - lesion spanning 3 or more vertebral segments) is characteristic of NMOSD and should prompt testing for AQP4-IgG antibodies.
Pearl 5: Bladder dysfunction occurs in over 90% of patients. Catheterization is often required in the acute phase. Urodynamic assessment may be needed for long-term management.
Incidence and Prevalence
| Population | Rate |
|---|---|
| Overall incidence | 1-8 per million per year |
| Paediatric incidence | 1-2 per million per year |
| All-cause acute myelopathy | Up to 25 per million per year |
Demographics
| Factor | Association |
|---|---|
| Age | Bimodal distribution: peak 10-19 years and 30-39 years |
| Sex | No clear sex predominance in idiopathic TM; female predominance in MS/NMOSD-associated |
| Race | NMOSD more common in non-Caucasian populations |
| Seasonality | Post-infectious cases may cluster after viral epidemics |
Aetiological Breakdown
| Aetiology | Proportion | Notes |
|---|---|---|
| Idiopathic (post-infectious) | 30-50% | Diagnosis of exclusion |
| Multiple sclerosis-associated | 20-30% | Especially partial TM |
| NMOSD-associated | 10-20% | Longitudinally extensive TM (LETM) |
| Post-infectious (identified agent) | 10-30% | EBV, CMV, VZV, Mycoplasma, COVID-19 |
| Systemic autoimmune disease | 5-10% | SLE, Sjögren's, sarcoidosis |
| Post-vaccination | Rare | Temporal association |
Stepwise Mechanism
Step 1: Triggering Event
- Preceding viral infection in 30-60% of cases (commonly respiratory or gastrointestinal)
- Common triggers: EBV, CMV, VZV, HSV, Mycoplasma, influenza, COVID-19
- Vaccination may rarely trigger (temporal association, not causation established)
- In MS/NMOSD: autoimmune process without clear trigger
Step 2: Immune Activation
- Molecular mimicry: cross-reactivity between pathogen antigens and myelin/axonal antigens
- In NMOSD: AQP4-IgG antibodies target aquaporin-4 on astrocyte foot processes
- In MS: T-cell mediated attack on myelin
- Blood-brain barrier breakdown allows immune cell infiltration
Step 3: Inflammatory Demyelination
- Inflammatory infiltrate (lymphocytes, macrophages) enters spinal cord
- Myelin sheath destruction (demyelination)
- Oedema and swelling of affected cord segments
- "Transverse" pattern: inflammation spans full width of cord
Step 4: Neurological Dysfunction
- Disruption of ascending sensory tracts → sensory level
- Disruption of descending motor tracts → weakness/paralysis
- Disruption of autonomic pathways → bladder/bowel dysfunction
- Acute phase: spinal shock with flaccid paralysis and areflexia
Step 5: Resolution or Progression
- Most patients (partial TM): partial or complete recovery over weeks to months
- Some patients (complete TM, NMOSD): permanent disability
- In MS: may be first relapse with subsequent relapses at different CNS sites
- In NMOSD: relapses may occur without adequate immunosuppression
Classification
| Type | Features | Association |
|---|---|---|
| Partial TM | Asymmetric, mild/moderate weakness, less than 2/3 cord width, 1-2 segment lesion | MS (high risk), better prognosis |
| Complete TM | Symmetric, severe paralysis, full-width involvement | NMOSD, idiopathic, poorer prognosis |
| Short-segment TM | Less than 3 vertebral segments | MS |
| Longitudinally extensive TM (LETM) | 3 or more vertebral segments | NMOSD (classic) |
NMOSD Pathophysiology
| Step | Detail |
|---|---|
| Antibody production | AQP4-IgG (anti-aquaporin-4) antibodies produced |
| Targeting | Antibodies bind astrocyte foot processes at blood-brain interface |
| Complement activation | Complement-mediated astrocyte injury |
| Secondary demyelination | Oligodendrocyte damage and demyelination follow |
| Necrosis | More severe tissue destruction than MS; higher disability |
Classic Triad
| Feature | Description |
|---|---|
| Motor | Weakness or paralysis below lesion level |
| Sensory | Sensory level with altered sensation below lesion |
| Autonomic | Bladder dysfunction (retention or incontinence), bowel dysfunction |
Symptom Frequency
| Symptom | Frequency |
|---|---|
| Weakness (legs > arms) | 90-100% |
| Sensory disturbance | 80-95% |
| Bladder dysfunction | 90-95% |
| Back/spinal pain | 50-70% |
| Band-like sensation around trunk | 50-60% |
| Bowel dysfunction | 50-70% |
| Sexual dysfunction | 50-70% |
| Lhermitte's sign | 20-40% |
Onset and Progression
| Phase | Timeframe | Features |
|---|---|---|
| Prodrome | Days before | Back pain, fever, malaise (in post-infectious) |
| Onset | Hours to days | Symptoms develop rapidly |
| Nadir | 4 hours to 21 days | Peak deficit reached |
| Recovery | Weeks to months | Variable; most improvement in first 3-6 months |
Symptoms by Spinal Level
| Level | Motor Findings | Sensory Level | Other Features |
|---|---|---|---|
| Cervical (C1-C4) | Quadriparesis, respiratory compromise | Neck/shoulders | Life-threatening; may need ventilation |
| Cervical (C5-C8) | Upper and lower limb weakness | Arms and below | Hand weakness, Horner syndrome possible |
| Thoracic | Paraparesis | Trunk with clear sensory level | Most common level |
| Lumbar/Conus | Leg weakness, flaccid | Legs, perineum | Lower motor neuron signs, saddle anaesthesia |
Red Flags
| Red Flag | Concern | Action |
|---|---|---|
| Asymmetric weakness | Compression, focal lesion | Urgent MRI |
| Fever + back pain + weakness | Spinal epidural abscess | Emergency MRI + surgery |
| Sudden onset severe pain | Spinal infarction, haemorrhage | Emergency MRI |
| High cervical symptoms | Respiratory compromise | Monitor respiratory function |
| Previous visual symptoms | MS or NMOSD | Brain MRI, optic nerve imaging |
| LETM pattern | NMOSD | Test AQP4-IgG, consider PLEX |
Structured Examination
General Inspection
- Respiratory distress (high cervical lesion)
- Posture, muscle wasting (if subacute)
- Catheter in situ (indicates urinary retention)
Motor Examination
| Finding | Upper Motor Neuron (Acute) | Upper Motor Neuron (Established) |
|---|---|---|
| Tone | Initially flaccid (spinal shock) | Spastic (develops over weeks) |
| Power | Weakness below lesion level | Weakness persists |
| Reflexes | Initially absent | Brisk, hyperreflexia |
| Plantars | Initially flexor | Upgoing (extensor) |
| Clonus | Absent initially | Present later |
Sensory Examination
| Modality | Finding |
|---|---|
| Pain/temperature | Reduced or absent below sensory level |
| Light touch | Can be preserved (posterior column sparing) or reduced |
| Proprioception | May be normal or impaired (posterior column involvement) |
| Sensory level | Well-defined horizontal level on trunk |
Finding the Sensory Level
- Start from sacral region and test ascending
- Identify level where sensation changes
- Document dermatome level (e.g., T6 sensory level)
Autonomic
- Bladder: palpate for distended bladder; check post-void residual
- Bowel: ask about constipation
- Cardiovascular: orthostatic hypotension in high lesions
Spinal Level Signs
| Level | Specific Signs |
|---|---|
| C5-C6 | Absent biceps reflex, sensory level at shoulders |
| C7-C8 | Absent triceps reflex, hand weakness |
| T4 | Sensory level at nipples |
| T10 | Sensory level at umbilicus |
| L1 | Sensory level at groin |
| S2-S5 | Saddle anaesthesia, absent bulbocavernosus reflex |
First-Line Investigations
| Investigation | Purpose | Expected Findings in TM |
|---|---|---|
| MRI Spine (whole) + contrast | Exclude compression, visualize inflammation | T2 hyperintense lesion spanning 2/3+ of cord width; may enhance |
| MRI Brain | Assess for MS/NMOSD brain lesions | May be normal or show demyelinating lesions |
| Lumbar puncture (after MRI) | CSF analysis | Lymphocytic pleocytosis, raised protein, +/- oligoclonal bands |
MRI Features
| Feature | Transverse Myelitis | Cord Compression |
|---|---|---|
| T2 signal | Hyperintense (bright) centrally | Hyperintense but with external compression visible |
| Cord swelling | Present in acute phase | May be compressed or displaced |
| Contrast enhancement | May enhance (active inflammation) | Variable |
| Extent | Short-segment (MS) or LETM (NMOSD) | Focal at level of compression |
| External cause | None | Disc, tumour, abscess, haematoma visible |
Short-Segment vs LETM
| Feature | Short-Segment TM | LETM |
|---|---|---|
| Length | Less than 3 vertebral segments | 3 or more vertebral segments |
| Association | MS, other | NMOSD, idiopathic, systemic disease |
| Location | Often dorsal/lateral | Often central |
| Prognosis | Generally better | Often worse |
Lumbar Puncture Findings
| Parameter | Typical Finding |
|---|---|
| Opening pressure | Normal |
| Cells | Lymphocytic pleocytosis (5-200 cells/mm³) |
| Protein | Mildly elevated (0.5-1.5 g/L) |
| Glucose | Normal |
| Oligoclonal bands | May be present (especially if MS) |
| Cytology | Normal (excludes malignancy) |
Additional Investigations
| Investigation | Indication | Purpose |
|---|---|---|
| AQP4-IgG (anti-aquaporin-4) | LETM, optic neuritis history | Diagnose NMOSD |
| MOG-IgG | Paediatric, recurrent TM | MOG-antibody disease |
| Visual evoked potentials | Suspected MS/NMOSD | Previous subclinical optic neuritis |
| Serum ACE, Chest CT | Suspected sarcoidosis | Systemic disease workup |
| ANA, ENA, dsDNA | Suspected SLE/connective tissue disease | Autoimmune workup |
| Viral serology | Post-infectious workup | Identify infectious trigger |
| HIV test | Risk factors | HIV-associated myelopathy |
| Vitamin B12, copper | Subacute combined degeneration | Exclude metabolic causes |
Management Algorithm
ACUTE MYELOPATHY PRESENTATION
(Weakness + Sensory Level + Bladder Dysfunction)
↓
┌─────────────────────────────────────────────────────┐
│ STEP 1: EXCLUDE COMPRESSION │
│ EMERGENCY MRI WHOLE SPINE + CONTRAST │
│ → If compression: EMERGENCY NEUROSURGERY │
│ → If no compression: proceed to TM workup │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ STEP 2: CONFIRM TRANSVERSE MYELITIS │
│ - MRI shows intramedullary T2 hyperintensity │
│ - ± Cord swelling │
│ - ± Contrast enhancement │
│ - No evidence of external compression │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ STEP 3: MRI BRAIN + LUMBAR PUNCTURE │
│ MRI Brain: Look for MS/NMOSD lesions │
│ LP: Cell count, protein, glucose, OCBs, cytology │
│ Bloods: AQP4-IgG, MOG-IgG (if LETM) │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ STEP 4: ACUTE TREATMENT │
│ IV Methylprednisolone 1g daily for 3-5 days │
│ │
│ If no response OR severe/LETM: │
│ → Plasma exchange (PLEX) 5-7 sessions │
│ → IVIG if PLEX unavailable │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ STEP 5: SUPPORTIVE CARE │
│ - DVT prophylaxis (LMWH) │
│ - Bladder catheterization if retention │
│ - Bowel care │
│ - Pressure area care │
│ - Early physiotherapy │
│ - Pain management │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ STEP 6: DETERMINE AETIOLOGY │
├─────────────────────────────────────────────────────┤
│ MS (brain lesions, OCB+, short-segment) │
│ → Disease-modifying therapy │
├─────────────────────────────────────────────────────┤
│ NMOSD (AQP4+, LETM, optic neuritis history) │
│ → Long-term immunosuppression (rituximab, │
│ eculizumab, inebilizumab) │
├─────────────────────────────────────────────────────┤
│ Idiopathic │
│ → Monitor for relapse; no maintenance treatment │
└─────────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────────┐
│ REHABILITATION │
│ - Inpatient neurorehabilitation │
│ - Physiotherapy │
│ - Occupational therapy │
│ - Long-term bladder management │
│ - Psychological support │
└─────────────────────────────────────────────────────┘
Acute Pharmacological Treatment
| Treatment | Dose | Duration | Notes |
|---|---|---|---|
| IV Methylprednisolone | 1g daily | 3-5 days | First-line; start early |
| Plasma exchange (PLEX) | 5-7 sessions | Alternate days | If no response to steroids OR severe/LETM |
| IVIG | 0.4 g/kg/day | 5 days | Alternative if PLEX unavailable |
| Oral prednisolone taper | Optional | 2-4 weeks | May follow IV steroids |
Supportive Care
| Intervention | Details |
|---|---|
| DVT prophylaxis | Enoxaparin 40mg daily + compression stockings |
| Urinary catheter | If post-void residual more than 100mL |
| Bowel management | Stool softeners, regular toileting |
| Pressure care | Regular repositioning, pressure mattress |
| Pain management | Neuropathic agents (gabapentin, pregabalin) |
| Early mobilization | Physiotherapy within 24-48 hours |
Long-Term Disease-Modifying Therapy
| Diagnosis | Treatment Options |
|---|---|
| MS (CIS/RRMS) | Interferon-β, glatiramer, dimethyl fumarate, ocrelizumab, natalizumab (depending on disease severity) |
| NMOSD (AQP4+) | Rituximab, eculizumab, inebilizumab, satralizumab (approved therapies) |
| MOG-antibody disease | Consider long-term immunosuppression if relapsing |
| Idiopathic TM | No maintenance therapy; monitor for relapse |
Acute Complications
| Complication | Incidence | Management |
|---|---|---|
| Urinary retention | More than 90% | Catheterization |
| Respiratory failure (cervical TM) | 10-20% of cervical cases | ICU, ventilatory support |
| DVT/PE | 10-20% | Prophylaxis essential |
| Pressure ulcers | Common if immobile | Pressure care |
| Autonomic dysreflexia (high lesions) | Variable | Monitor BP, identify/treat triggers |
| Pain (neuropathic) | 50-80% | Gabapentinoids, tricyclics |
| Spasticity | Develops over weeks | Baclofen, physiotherapy |
Long-Term Complications
| Complication | Notes |
|---|---|
| Chronic neuropathic pain | Common; requires ongoing management |
| Spasticity | May worsen over time |
| Chronic urinary dysfunction | May need long-term catheterization |
| Sexual dysfunction | Common; counselling and management |
| Depression/anxiety | Psychological support important |
| Fatigue | Characteristic of demyelinating disease |
| Incomplete motor recovery | Variable; depends on severity |
Relapse Risk
| Diagnosis | Relapse Risk |
|---|---|
| MS | High (recurrent relapses expected) |
| NMOSD | High without treatment (50-60% relapse in 1 year) |
| Idiopathic TM | Low (10-20% may eventually convert to MS) |
| MOG-antibody disease | Variable; may be monophasic or relapsing |
Natural History
| Severity | Outcome |
|---|---|
| Partial TM | 70-90% have good recovery |
| Complete TM | Only 30-50% have good recovery |
| LETM (NMOSD-type) | Higher disability; poorer recovery |
Recovery Timeline
| Phase | Timeframe | Recovery |
|---|---|---|
| Acute | First 2 weeks | Spinal shock, nadir of deficits |
| Early recovery | 2-8 weeks | Most rapid improvement |
| Continued recovery | 3-6 months | Ongoing improvement possible |
| Plateau | 6-12 months | Maximum recovery usually achieved |
Prognostic Factors
| Factor | Better Prognosis | Worse Prognosis |
|---|---|---|
| Severity | Partial TM | Complete TM |
| Lesion extent | Short-segment | LETM (3+ segments) |
| Onset speed | Slower (days) | Rapid (hours) |
| Early treatment | Yes | Delayed treatment |
| Aetiology | Post-infectious, MS | NMOSD |
| MRI T1 | Normal | Low signal (necrosis) |
Long-Term Outcomes
| Outcome | Approximate Rate |
|---|---|
| Full recovery | 30-40% |
| Partial recovery (ambulatory) | 30-40% |
| Severe residual disability | 20-30% |
| Death | 1-5% (mainly cervical/respiratory) |
Major Guidelines
| Guideline | Year | Key Recommendations |
|---|---|---|
| Transverse Myelitis Consortium Working Group | 2002 | Diagnostic criteria for TM (still widely used) |
| IPND Criteria for NMOSD | 2015 | Diagnostic criteria for NMOSD with/without AQP4-IgG |
| ABN Guidelines (UK) | 2022 | Management of acute myelopathy including TM |
Diagnostic Criteria (TMCWG 2002)
| Criterion | Requirement |
|---|---|
| Inclusion 1 | Bilateral sensory, motor, or autonomic dysfunction attributable to spinal cord |
| Inclusion 2 | Clear sensory level |
| Inclusion 3 | No evidence of cord compression on MRI |
| Inclusion 4 | Inflammation demonstrated (CSF pleocytosis, elevated IgG index, or gadolinium enhancement on MRI) |
| Inclusion 5 | Progression to nadir within 4 hours to 21 days |
| Exclusion | Previous irradiation, cord infarction, MS, sarcoidosis, infection, connective tissue disease (unless specific diagnosis made) |
Key Studies
| Study | Year | N | Key Findings | PMID |
|---|---|---|---|---|
| Scott et al. (Natural history) | 1998 | 91 | 1/3 good recovery, 1/3 fair, 1/3 poor; rapid onset predicts poor outcome | 9579704 |
| Wingerchuk et al. (NMOSD criteria) | 2015 | Consensus | IPND diagnostic criteria for NMOSD | 25972096 |
| Trebst et al. (TMCWG criteria) | 2002 | Consensus | Proposed diagnostic criteria for TM | 11988605 |
| Greenberg et al. (Plasma exchange) | 1999 | 22 | PLEX effective in steroid-refractory CNS demyelination | 9930028 |
| Weinshenker et al. (NMO-IgG) | 2006 | 102 | AQP4-IgG highly specific for NMOSD | 16636238 |
Evidence Levels
| Intervention | Evidence Level |
|---|---|
| IV methylprednisolone for acute TM | Moderate (standard practice, limited RCT data) |
| Plasma exchange for refractory cases | Moderate (observational data, class II) |
| Disease-modifying therapy for MS | High (multiple RCTs) |
| Immunosuppression for NMOSD | High (RCTs for rituximab, eculizumab, etc.) |
Simple Explanation
What is transverse myelitis? Transverse myelitis is a condition where part of your spinal cord becomes inflamed and swollen. The spinal cord is the bundle of nerves that runs down your back and carries messages between your brain and your body. When it becomes inflamed, these messages are disrupted.
What causes it? In many cases, it happens after a viral infection - the immune system becomes confused and attacks the spinal cord by mistake. In some people, it can be the first sign of another condition like multiple sclerosis (MS) or a condition called neuromyelitis optica (NMO). Sometimes we don't find a cause at all.
What are the symptoms?
- Weakness in your legs (and sometimes arms)
- Numbness or tingling, often with a "level" on your body below which sensation is changed
- Problems with bladder and bowel control
- Back pain
- Tight "band-like" feeling around your chest or abdomen
What tests will I need?
- MRI scan of your spine (and brain): This shows the inflammation
- Lumbar puncture (spinal tap): A small sample of fluid from around your spinal cord to look for inflammation
- Blood tests: To look for specific antibodies and rule out other causes
How is it treated?
- Steroids: High-dose steroid injections through a drip for 3-5 days to reduce inflammation
- Plasma exchange: If steroids don't work well enough, we may do a treatment that filters your blood
- Supportive care: We'll help manage bladder problems, prevent blood clots, and start physiotherapy
- Rehabilitation: You'll work with physiotherapists to regain strength and function
What is the outcome? Recovery varies a lot. About a third of people recover well, a third have some lasting symptoms, and a third have more significant disability. Recovery usually happens over weeks to months. Some symptoms may be permanent.
-
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: 11988605
-
West TW, Hess C, Cree BA. Acute transverse myelitis: demyelinating, inflammatory, and infectious myelopathies. Semin Neurol. 2012;32(2):97-113. doi:10.1055/s-0032-1322586. PMID: 22961186
-
Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2011;77(24):2128-2134. doi:10.1212/WNL.0b013e31823dc535. PMID: 22156988
-
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
-
Weinshenker BG, Wingerchuk DM, Vukusic S, et al. Neuromyelitis optica IgG predicts relapse after longitudinally extensive transverse myelitis. Ann Neurol. 2006;59(3):566-569. doi:10.1002/ana.20770. PMID: 16636238
-
Pittock SJ, Lucchinetti CF. Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin-4 channelopathies: a decade later. Ann N Y Acad Sci. 2016;1366(1):20-39. doi:10.1111/nyas.13177. PMID: 27575699
-
Greenberg BM, Thomas KP, Krishnan C, Kaplin AI, Calabresi PA, Kerr DA. Idiopathic transverse myelitis: corticosteroids, plasma exchange, or cyclophosphamide. Neurology. 2007;68(19):1614-1617. doi:10.1212/01.wnl.0000260970.63493.c8. PMID: 17485651
-
Llufriu S, Castillo J, Blanco Y, et al. Plasma exchange for acute attacks of CNS demyelination: Predictors of improvement at 6 months. Neurology. 2009;73(12):949-953. doi:10.1212/WNL.0b013e3181b87965. PMID: 19652141
-
Pittock SJ, Zekeridou A, Weinshenker BG. Hope for patients with neuromyelitis optica spectrum disorders - from mechanisms to trials. Nat Rev Neurol. 2021;17(12):759-773. doi:10.1038/s41582-021-00568-8. PMID: 34671137
-
Jacobs LD, Beck RW, Simon JH, et al. Intramuscular interferon beta-1a therapy initiated during a first demyelinating event in multiple sclerosis. N Engl J Med. 2000;343(13):898-904. doi:10.1056/NEJM200009283431301. PMID: 11006365
-
Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG; Therapeutics and Technology Assessment Subcommittee of American Academy of Neurology. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis. Neurology. 2011;77(24):2128-2134. PMID: 22156988
-
Beh SC, Greenberg BM, Frohman T, Frohman EM. Transverse myelitis. Neurol Clin. 2013;31(1):79-138. doi:10.1016/j.ncl.2012.09.008. PMID: 23186897
Common Exam Questions
| Question Type | Example |
|---|---|
| MCQ | A 35-year-old woman presents with bilateral leg weakness, sensory level at T6, and urinary retention. MRI shows T2 hyperintensity spanning C5-T2. What is the most important next investigation? |
| SAQ | Describe the clinical features of transverse myelitis and outline the acute management. |
| OSCE | Examine this patient's lower limbs. Demonstrate how to identify a sensory level. |
| Viva | Discuss how you would differentiate between transverse myelitis and cord compression. |
High-Yield Viva Points
| Topic | Key Points |
|---|---|
| First priority | Exclude cord compression with emergency MRI |
| Classic triad | Motor weakness + sensory level + bladder dysfunction |
| Partial vs complete TM | Partial: asymmetric, mild, MS-associated; Complete: symmetric, severe, NMOSD |
| LETM definition | 3 or more vertebral segments on MRI |
| NMOSD antibody | AQP4-IgG (anti-aquaporin-4) |
| Acute treatment | IV methylprednisolone 1g daily for 3-5 days |
| Second-line | Plasma exchange (PLEX) if steroid-refractory |
| Prognosis | 1/3 good, 1/3 fair, 1/3 poor; partial TM better than complete |
Common Mistakes
| Mistake | Correct Approach |
|---|---|
| Not excluding compression | ALWAYS get MRI before diagnosing TM |
| Forgetting MRI brain | Must assess for MS/NMOSD brain lesions |
| Missing LETM significance | LETM strongly suggests NMOSD; test AQP4-IgG |
| Delaying steroids | Start IV methylprednisolone early |
| Not doing LP | CSF analysis essential for diagnosis |
| Forgetting DVT prophylaxis | All immobile patients need LMWH |
Examination Cheat Sheet
| Parameter | Key Information |
|---|---|
| Definition | Inflammation across full width of spinal cord |
| Presentation | Motor + sensory level + bladder dysfunction |
| First investigation | Emergency MRI spine (exclude compression) |
| CSF | Lymphocytic pleocytosis, raised protein |
| Short-segment TM | Less than 3 segments; MS-associated |
| LETM | 3+ segments; NMOSD-associated |
| NMOSD antibody | AQP4-IgG |
| First-line treatment | IV methylprednisolone 1g daily x 3-5 days |
| Second-line | Plasma exchange (PLEX) |
| Prognosis | Partial TM: 70-90% good recovery; Complete TM: 30-50% |