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Transverse Myelitis in Hyderabad: Sudden Spinal Cord Inflammation That Demands Urgent MRI, Cause Identification, and Immediate Treatment — Because the Underlying Cause Determines the Next 20 Years
Urgent spine MRI, full aetiological workup, and same-day IV methylprednisolone for confirmed inflammatory myelitis at KIMS Neuroscience, Secunderabad, Hyderabad.
Acute inflammation of the spinal cord — spanning its full width at one or more levels — producing rapid-onset limb weakness, sensory loss below the affected level, and bladder/bowel dysfunction
Generally occurring independently, often as a complication of infection; it may also exist as part of a continuum of other neuro-inflammatory disorders including MS, NMO spectrum disorder, and ADEM
Peak deficit can occur anytime between 4 hours and 21 days after onset — can go from mild leg tingling to paraplegia within a day
At peak deficit, 50% of patients are completely paraplegic, with virtually all having a degree of bladder/bowel dysfunction
Is this isolated (idiopathic) transverse myelitis — or the first sign of MS, NMO, ADEM, lupus, sarcoidosis, or TB? The answer determines whether this is a single event or a chronic relapsing disease requiring long-term treatment
Vitamin B12 deficiency may predispose patients to inflammatory LETM including NMO syndromes — extremely relevant in vegetarian-diet Indian population; TB myelitis must also be excluded in all Indian cases
Approximately 33% of patients recover completely; the remainder have varying degrees of persistent disability — outcome strongly correlated with severity at nadir and speed of treatment
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About This Condition
When the Spinal Cord Suddenly Stops Working
A 31-year-old woman in Secunderabad wakes up feeling heaviness in both legs. By midday she cannot walk without support. By evening she has not passed urine since morning and has a band-like tightening sensation around her abdomen — as though a tight belt is being cinched around her lower chest. Her legs have lost feeling below the groin.
She comes to KIMS Emergency. Spine MRI performed within two hours of arrival shows a bright signal on T2-weighted imaging spanning four vertebral levels of the thoracic cord — the spinal cord is inflamed across its full width at multiple levels. This is transverse myelitis — and at KIMS, it triggers an immediate treatment and investigation pathway.
The treatment question is answered in hours: high-dose IV methylprednisolone is started that night. But the more consequential question — the one that determines her management for the rest of her life — takes days to answer: why did this happen?
Longitudinally extensive transverse myelitis is a heterogeneous disorder with varied clinical features, aetiologies, and outcomes. Even LETM patients who present with optic neuritis do not necessarily have NMO. The presence of NMO antibody predicts the increased risk of recurrence or conversion to NMO.
If she has NMO — she needs lifelong immunosuppression, and the MS medications that might otherwise be considered would be harmful. If she has MS — she needs disease-modifying therapy, but a different kind. If this is post-infectious myelitis — it may be a single event, never recurring. If she has lupus or another connective tissue disease — her myelitis is a manifestation of a systemic condition requiring systemic treatment. If she has TB myelitis — she needs six months of antituberculosis therapy.
At KIMS Neuroscience, the full cause-identification workup begins simultaneously with acute treatment — because these are not sequential questions.
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Speak directly with our transverse myelitis specialist team. No referral required. Monday to Saturday.
040-44885000Emergency line: 040-46324365What Transverse Myelitis Is — The Spinal Cord Attack Explained
Inflammation of the spinal cord disrupts motor, sensory, and autonomic signal transmission — and the level of the cord affected determines the pattern of disability.
The spinal cord is the primary communication cable between the brain and the body. Motor signals travel down from the brain to the muscles through the corticospinal tracts. Sensory signals travel up from the skin, joints, and organs to the brain through the spinothalamic tracts and dorsal columns. Autonomic signals controlling the bladder, bowel, and blood pressure also run through the cord.
In transverse myelitis, inflammation attacks the spinal cord — affecting its full width (hence “transverse”) at one or more vertebral levels. The inflammation disrupts all three types of signal transmission: motor (weakness and paralysis), sensory (numbness and loss of position sense), and autonomic (bladder retention or incontinence, bowel dysfunction, blood pressure instability).
The level of the cord affected determines the pattern of disability. A thoracic cord lesion at T4 produces weakness and numbness from the nipple line downward, with bladder and bowel dysfunction. A cervical cord lesion produces weakness in all four limbs. Knowing the neurological level from clinical examination and correlating it with the MRI lesion level is the first diagnostic step at KIMS.
Short-segment lesions
A transverse myelitis lesion spanning fewer than three vertebral levels — short-segment — is more likely to be caused by MS. These lesions are typically peripheral in the cord and often cervical, with concurrent brain MRI changes.
Longitudinally extensive (LETM)
A lesion spanning three or more vertebral levels — LETM — is the specific pattern most strongly associated with NMO spectrum disorder (NMOSD). This distinction on spine MRI is immediately visible to the KIMS radiologist and directly informs the differential diagnosis and investigation priority.
The Causes — Why Identifying the Aetiology Is Non-Negotiable
Transverse myelitis is not a final diagnosis — it is a clinical and radiological syndrome that can be produced by many different underlying conditions. Treating the syndrome without identifying the cause risks missing a recurrent, life-altering disease.
In a prospective study from Northwest India of 32 LETM patients, NMO spectrum disorder was the most common diagnosis affecting 14 patients, followed by 5 patients of idiopathic myelitis, 4 patients of para-infectious myelitis, 3 with MS, 3 with ADEM, and 1 each of MOGAD, sarcoidosis, and connective tissue disorder. The KIMS team investigates each of these in every transverse myelitis presentation.
NMO spectrum disorder (NMOSD)
The most common cause of LETM in India. All NMOSD patients in the Indian cohort were AQP4-IgG positive. AQP4-IgG testing is performed on the day of admission at KIMS — because if positive, it immediately mandates: avoiding MS-specific drugs, starting plasmapheresis early for severe attacks, and planning long-term rituximab or other NMOSD-specific prevention.
Multiple Sclerosis
Produces shorter cord lesions — typically one vertebral level, peripheral in the cord, often cervical. Brain MRI showing periventricular white matter lesions supports an MS first presentation.
ADEM
Post-infectious myelitis in the context of a recent viral illness — particularly in children. Brain MRI often shows additional white matter lesions.
MOGAD
MOG-IgG-positive myelitis — often with conus (lower cord) involvement. Tested concurrently with AQP4-IgG at KIMS.
Post-infectious (idiopathic) myelitis
Varicella myelitis was the most common infectious cause in the Indian prospective LETM cohort. Other triggers relevant in India include Mycoplasma pneumoniae, CMV, EBV, HSV, enteroviruses, and — increasingly — COVID-19 associated myelitis.
Tuberculous myelitis
TB myelitis was identified in 4 patients in a North-West India LETM cohort — a cause essentially absent from Western LETM literature but directly relevant in India's high-TB burden environment. TB can produce cord compression (Pott's spine — vertebral TB with cord compression), intramedullary tuberculoma, or immune-mediated post-TB myelitis. GeneXpert MTB, AFB staining, and MRI of the full spine are performed in all Indian transverse myelitis workups at KIMS.
Connective tissue disease — Lupus, Sjögren's, Mixed CTD
Systemic lupus erythematosus (SLE) is a significant cause of longitudinally extensive myelitis in young Indian women — where lupus is more common than in Western populations, affecting women of reproductive age disproportionately. ANA, anti-dsDNA, complement levels, and anti-phospholipid antibodies are tested in every transverse myelitis workup at KIMS.
Neurosarcoidosis
Spinal cord granulomatous infiltration — producing a long cord lesion with enhancement on MRI. Serum ACE, chest X-ray, and HRCT chest are included in the KIMS TM workup.
Vitamin B12 deficiency — subacute combined degeneration
Vitamin B12 deficiency may predispose patients to inflammatory LETM including NMO syndromes. Vegetarian and vegan diets — extremely common across Hyderabad and Telangana — are the primary risk factor for B12 deficiency in India. B12 deficiency can produce dorsal column myelopathy (loss of position and vibration sense, gait unsteadiness) that overlaps clinically and radiologically with inflammatory myelitis. Serum B12 and methylmalonic acid are tested at KIMS in every TM presentation.
Vascular myelopathy — spinal cord infarct
Not inflammatory, but can mimic transverse myelitis clinically — sudden cord dysfunction with a rapid nadir. The key distinguishing feature is the time to nadir: vascular myelopathy reaches maximum deficit within minutes to hours; inflammatory myelitis typically progresses over hours to days. MRI DWI sequences at KIMS can identify restricted diffusion indicating infarction.
Symptoms — The Clinical Picture of Transverse Myelitis
The three hallmarks of transverse myelitis are weakness, sensory loss, and bladder dysfunction — appearing together, below a specific spinal cord level, over hours to days.
Motor weakness
Leg weakness that may progress to complete paralysis. In cervical cord lesions, arm weakness is also present. The weakness is characteristically bilateral — both legs or all four limbs — distinguishing it from a stroke, which typically affects one side.
Sensory level
A horizontal line on the body below which sensation is reduced or absent. A sensory level at the nipple line (T4) indicates a thoracic cord lesion. A sensory level at the umbilicus (T10) indicates a mid-thoracic lesion. The patient often describes a tight band-like feeling at the level of the lesion — the "MS hug" or TM girdle sensation — which is highly characteristic of cord inflammation.
Bladder and bowel dysfunction
Inability to pass urine (urinary retention) despite a full bladder is one of the most consistent and distressing early symptoms of transverse myelitis. The patient may go 12–24 hours without voiding without noticing — because the urgency signal is also impaired. Urinary retention requiring catheterisation is common at KIMS admission for acute TM. Constipation and faecal urgency are also frequent.
Lhermitte's sign
An electric shock sensation down the back and into the legs when bending the neck forward — produced by a cervical cord lesion. Named after the French neurologist, it is pathognomonic of cervical cord involvement and is one of the most reliable symptom indicators of cord demyelination.
Pain
Back or neck pain at the level of the lesion — often the first symptom, preceding the weakness by hours to days. A young adult in Hyderabad presenting to their GP with acute-onset mid-back pain and leg heaviness after a recent viral illness must be urgently assessed for transverse myelitis, not prescribed analgesics and sent home.
Autonomic symptoms
Blood pressure instability, abnormal sweating, sexual dysfunction, and temperature dysregulation — from cord autonomic pathway involvement. These are not always volunteered by patients and must be specifically asked about.
Diagnosis at KIMS
The India-Specific Diagnostic Challenges
Transverse myelitis in India presents diagnostic and treatment questions that are different from Western practice — and KIMS addresses each as standard.
Delayed referral
Delayed diagnosis and delayed initiation of steroid therapy was associated with poor outcome in a North India paediatric TM cohort. Across Hyderabad and Telangana, transverse myelitis patients frequently present first to a GP or district hospital — where the differential diagnosis of acute-onset leg weakness may include musculoskeletal disease, nerve compression, or viral myalgia — and reach specialist neurology care after 2–4 days. Every day of cord inflammation without treatment deposits permanent damage.
The B12 mimicry problem
Subacute combined degeneration from B12 deficiency is common in vegetarian Indians and can produce MRI cord signal change in the dorsal columns. The clinical picture — progressive gait unsteadiness, numb feet, absent ankle jerks — can overlap with early transverse myelitis. At KIMS, serum B12 is tested on day 1 and B12 replacement is started concurrently with steroid treatment in confirmed deficiency — both conditions are treated simultaneously rather than sequentially.
The TB exclusion imperative
Tuberculous spondylitis (Pott's disease) can produce cord compression from vertebral body collapse and paravertebral abscess — mimicking inflammatory myelitis clinically but requiring surgical decompression and antituberculosis therapy, not steroids alone. Intramedullary tuberculoma produces an enhancing cord lesion identical to inflammatory myelitis on MRI. At KIMS, sagittal MRI of the full spine with attention to vertebral body integrity, disc space involvement, and paraspinal soft tissue is routine in TM assessment — to detect Pott's disease before steroids are given in isolation.
The Lupus connection
SLE-associated transverse myelitis is more common in young Indian women than in Western populations. A young woman with a first episode of LETM in Hyderabad must have ANA, anti-dsDNA, C3, C4, and anti-phospholipid antibody testing as standard — not as an afterthought. Lupus myelitis often requires hydroxychloroquine and systemic immunosuppression in addition to acute steroid treatment, and the underlying lupus determines the overall treatment plan.
Diagnosis at KIMS — The Simultaneous Workup
At KIMS, every transverse myelitis presentation triggers a simultaneous acute treatment and investigation protocol — the cause-identification workup runs alongside acute steroid therapy, because these are not sequential questions.
Day 1 — Acute treatment & investigation
Full spine MRI with gadolinium contrast (thoracic and cervical, full sagittal survey) and brain MRI. IV methylprednisolone started. Urinary catheter placed if retention confirmed. Blood drawn for: AQP4-IgG, MOG-IgG, ANA, anti-dsDNA, ANCA, anti-phospholipid antibodies, serum B12, methylmalonic acid, ACE, serum calcium, and HIV serology. Lumbar puncture for CSF analysis: protein, cells, glucose, oligoclonal bands, GeneXpert MTB, AFB, culture, cytology.
Day 2–3 — Extended workup
Chest X-ray and HRCT chest — for sarcoidosis and TB. Ophthalmological assessment for uveitis. Nerve conduction studies if peripheral nerve involvement suspected. FDG-PET if sarcoidosis is in the differential. Echocardiogram if lupus or antiphospholipid syndrome identified.
The LETM vs short-segment decision
Short-segment (< 3 vertebral levels), peripheral in cord, concurrent brain MRI lesions → MS workup priority (oligoclonal bands, McDonald criteria assessment). Long-segment (≥ 3 vertebral levels), central in cord → AQP4-IgG and NMO workup priority. Spinal MRI showed central pattern of involvement in NMOSD and eccentric pattern in MS — central involvement in NMOSD and eccentric/peripheral involvement in MS is a reliable MRI distinguishing feature in Indian LETM cohorts.
Treatment
Treatment — Acute, Cause-Specific, and Supportive
Acute treatment is started in hours, regardless of cause — because cord damage occurring during the diagnostic delay cannot be recovered. Long-term treatment is then tailored to the underlying aetiology identified by the simultaneous workup.
Acute treatment — regardless of cause
High-dose IV methylprednisolone (1g daily for 3–5 days) is the standard first-line treatment for all inflammatory transverse myelitis. It reduces inflammation, limits cord damage, and speeds recovery. At KIMS, it is started within hours of a confirmed inflammatory cord lesion on MRI — before the full cause-identification workup is complete — because the cord damage occurring during the delay cannot be recovered.
Plasmapheresis — for severe or steroid-refractory attacks
In NMOSD-associated myelitis with severe deficit (paraplegia, respiratory involvement), plasmapheresis is used as early second-line therapy — or as concurrent first-line therapy for the most severe presentations. Available at KIMS with established protocols.
IVIG — for post-infectious and ADEM-associated myelitis
For para-infectious myelitis and MOGAD-associated myelitis where steroid response is incomplete, IVIG is added at KIMS.
Long-term therapy is determined by the underlying cause
NMO-confirmed: Rituximab or newer biologics — see NMO page
MS-confirmed: Disease-modifying therapy — see MS page
Lupus myelitis: Hydroxychloroquine + cyclophosphamide or mycophenolate mofetil + continued prednisolone
Sarcoidosis myelitis: Long-term prednisolone + steroid-sparing agent
TB myelitis/Pott's disease: Full antituberculosis regimen + surgical decompression where indicated
B12 deficiency: High-dose IM vitamin B12 replacement — hydroxocobalamin or cyanocobalamin injections
Idiopathic isolated myelitis: Acute steroids; monitor for relapse indicating underlying disease
Bladder management
Urinary catheterisation in the acute phase. Bladder training programme during recovery — intermittent self-catheterisation education and pharmacological bladder management. Long-term urology follow-up for persistent bladder dysfunction. This is among the most disabling and most undermanaged TM complications in Indian practice.
Rehabilitation at KIMS
Physiotherapy from day 1 of admission — passive range of motion, positioning. Progressive weight-bearing and gait retraining as strength returns. Occupational therapy for upper limb function. Spasticity management — baclofen, tizanidine, physiotherapy. Neuropathic pain management — pregabalin, amitriptyline.
Prognosis
Severe weakness at onset, spinal shock, respiratory muscle weakness, mechanical ventilation, greater mean time to diagnosis, and delayed initiation of steroid therapy were all associated with bad outcome in a North India paediatric TM cohort. Nearly half the children in that cohort remained dependent at follow-up.
In the Indian adult LETM prospective study, 87.5% of patients had good clinical recovery at 6 months despite presenting with relapses and severe disease — demonstrating that even severe TM responds well to treatment when adequately managed.
The three most important predictors of good outcome at KIMS
Early treatment within 24–48 hours of cord symptom onset is the strongest predictor of good recovery
Severity at nadir matters — complete paraplegia at nadir recovers less completely than partial weakness
Cause identification shapes long-term outcome — NMO-associated myelitis with lifelong prevention has better outcomes than untreated recurrent NMO attacks
Severe weakness at onset, spinal shock, respiratory muscle weakness, and mechanical ventilation predict worse paediatric outcomes in North India cohorts
Despite severe presentations, 87.5% of adult Indian LETM patients had good clinical recovery at 6 months when adequately managed
Related Conditions
Transverse Myelitis belongs to the family of demyelinating and inflammatory disorders of the central nervous system:
FAQs
Frequently Asked Questions
Sudden leg weakness, a belt-like tightening around the chest, and inability to pass urine. This is the cord. This needs a spine MRI within hours — not days.
At KIMS Neuroscience, Secunderabad, Hyderabad, every transverse myelitis presentation is assessed with urgent spine and brain MRI, full aetiological workup — AQP4-IgG, MOG-IgG, ANA, B12, TB exclusion — and IV methylprednisolone started the same day for confirmed inflammatory myelitis. The cause-identification workup runs simultaneously with acute treatment, because the underlying cause determines the next 20 years of management. NMO prevention, MS disease modification, lupus treatment, TB therapy — all require a different approach. Getting it right at the first episode is everything.
International enquiries: info@kimsneurosciences.com