Acute Transverse Myelopathies: A Comprehensive Review for Critical Care Practice

Dr Neeraj Manikath , Claude.ai

Abstract

Acute transverse myelopathies (ATM) represent a heterogeneous group of inflammatory and non-inflammatory disorders affecting the spinal cord, presenting diagnostic and therapeutic challenges in critical care settings. This review synthesizes current evidence on pathophysiology, diagnostic approaches, and management strategies, with emphasis on time-sensitive interventions that impact neurological outcomes. We present practical pearls for bedside assessment, diagnostic pitfalls to avoid, and evidence-based treatment algorithms relevant to intensive care practice.

Introduction

Acute transverse myelopathy encompasses a spectrum of disorders characterized by acute or subacute spinal cord dysfunction, with an estimated incidence of 1.34 to 4.6 cases per million population annually.[1,2] The syndrome manifests with varying combinations of motor weakness, sensory deficits, autonomic dysfunction, and sphincter disturbances developing over hours to weeks.

In the critical care setting, ATM patients present unique challenges: they require meticulous monitoring for respiratory compromise, hemodynamic instability from autonomic dysfunction, and urgent diagnostic workup to identify treatable etiologies. The window for neuroprotective interventions is narrow, making rapid recognition and appropriate management paramount.[3]

Pathophysiology

Core Mechanisms

The final common pathway in ATM involves disruption of ascending and descending spinal cord tracts through:

1. Direct inflammatory injury

T-cell mediated autoimmune attack against myelin or axons
Cytokine-mediated damage (TNF-α, IL-6, IL-17)
Complement activation and membrane attack complex formation[4]

2. Vascular compromise

Arterial occlusion (anterior spinal artery syndrome)
Venous infarction or hemorrhage
Vasculitis affecting spinal vessels[5]

3. Compressive myelopathy

Epidural abscess or hematoma
Metastatic disease
Herniated disc material

4. Metabolic/toxic insults

Radiation myelopathy
Nitrous oxide toxicity (B12 deficiency)
Copper deficiency myelopathy

Pearl #1: The "Spinal Shock" Phenomenon

Acute complete spinal cord lesions produce initial flaccid paralysis with areflexia below the level of injury, which can mask the true extent of injury. This typically transitions to spasticity and hyperreflexia over 1-6 weeks. Don't be falsely reassured by absent reflexes in the acute phase—focus on the sensory level and MRI findings.[6]

Clinical Presentation and Bedside Assessment

Cardinal Features

Motor dysfunction:

Para- or quadriparesis/plegia depending on lesion level
Pattern: typically symmetric, but asymmetry suggests specific etiologies (infarction, MS)
Upper motor neuron signs develop after spinal shock resolves

Sensory deficits:

Well-defined sensory level (critical localizing sign)
Dissociated sensory loss patterns aid anatomic localization
Proprioceptive loss suggests posterior column involvement

Autonomic dysfunction:

Neurogenic bladder (retention initially, then incontinence)
Bowel dysfunction
Sexual dysfunction
Orthostatic hypotension (lesions above T6)
Cardiac dysrhythmias (cervical/high thoracic lesions)[7]

Pearl #2: The Sensory Level Examination

Test the sensory level carefully with a cold tuner fork or alcohol swab, moving from the feet upward bilaterally. The level where cold sensation is first perceived corresponds roughly to the spinal segment BELOW the lesion. Document this precisely—it guides imaging and has prognostic value. Remember: sacral sparing (preserved perianal sensation) suggests an incomplete lesion with better recovery potential.[8]

Critical Red Flags in the ICU

🚨 Oyster #1: Ascending Sensory Level A rising sensory level over hours suggests progressive edema, hemorrhage, or expanding abscess. This is a neurosurgical emergency. Repeat neurological examination every 2-4 hours initially.

🚨 Oyster #2: Neurogenic Respiratory Failure Lesions at C3-C5 (phrenic nerve origin) cause diaphragmatic paralysis. Monitor:

Vital capacity (VC < 15 mL/kg indicates impending failure)
Negative inspiratory force (NIF < -30 cm H2O)
Paradoxical breathing
Inability to count to 20 in one breath

Don't wait for hypercapnia—intervene early with non-invasive or mechanical ventilation.[9]

Differential Diagnosis: A Systematic Approach

Inflammatory Disorders

1. Idiopathic Acute Transverse Myelitis (ATM)

Diagnosis of exclusion
Peak onset over 4 hours to 21 days
Bilateral (though not necessarily symmetric) signs
Clearly defined sensory level
CSF pleocytosis (>5 WBC/μL) or elevated IgG index[10]

2. Multiple Sclerosis (MS)

Partial transverse myelitis (asymmetric, incomplete)
Lesion extent: typically <2 vertebral segments
Brain MRI: periventricular white matter lesions
OCBs in CSF
Younger patients (20-40 years)[11]

3. Neuromyelitis Optica Spectrum Disorder (NMOSD)

Longitudinally extensive transverse myelitis (LETM): ≥3 vertebral segments
Central gray matter predominance ("bright spotty lesions" or H-sign)
Associated optic neuritis (can be separated by months/years)
Anti-aquaporin-4 antibodies (70-80% sensitivity)
More severe, poorer recovery than MS[12,13]

4. MOG-Antibody Disease

Similar to NMOSD but distinct entity
Anti-MOG antibodies
Often better prognosis than AQP4+ NMOSD
May present with conus involvement and severe neuropathic pain[14]

5. Acute Disseminated Encephalomyelitis (ADEM)

Typically pediatric (though adult cases occur)
Multifocal CNS involvement
Post-infectious (1-4 weeks after viral illness or vaccination)
Monophasic course
Brain MRI: large, poorly marginated lesions[15]

Infectious Etiologies

Viral:

Herpes viruses (HSV, VZV, CMV, EBV)
Enteroviruses (poliovirus, enterovirus D68, West Nile virus)
HIV (acute seroconversion or chronic infection)
HTLV-1 associated myelopathy
Emerging: Zika, dengue, chikungunya[16]

Bacterial:

Mycoplasma pneumoniae (parainfectious)
Treponema pallidum (syphilitic myelitis)
Borrelia burgdorferi (Lyme disease)
Mycobacterium tuberculosis

Parasitic:

Schistosomiasis (endemic areas)
Neurocysticercosis

Fungal:

Aspergillus, Cryptococcus (immunocompromised)

Hack #1: The CSF Opening Pressure Clue

Normal/mildly elevated (10-25 cm H2O): inflammatory myelitis
Markedly elevated (>25 cm H2O): consider infectious epidural abscess, carcinomatous meningitis, or complete spinal block
Low (<8 cm H2O): CSF leak, prior LP, dehydration

Vascular Disorders

Spinal cord infarction:

Hyperacute onset (minutes to hours)
Anterior spinal artery syndrome: motor and spinothalamic loss with preserved dorsal columns
Risk factors: aortic surgery/dissection, hypotension, atherosclerosis, vasculitis
MRI: "owl's eyes" sign on axial T2[17]

Spinal dural arteriovenous fistula (SDAVF):

Subacute progressive myelopathy
Venous congestion causes spinal cord edema
T2 signal abnormality with flow voids
Definitive diagnosis: spinal angiography[18]

Compressive Lesions

These are SURGICAL EMERGENCIES and must be identified immediately:

Epidural abscess (fever, back pain, elevated inflammatory markers)
Epidural hematoma (anticoagulation, trauma, post-procedural)
Metastatic cord compression
Herniated disc

Oyster #3: "Myelitis" on MRI That's Actually Compression Early epidural collections may show cord edema and enhancement mimicking inflammatory myelitis. Always scrutinize the epidural space on sagittal images. When in doubt, get a contrast-enhanced MRI.

Diagnostic Workup: The First 24 Hours

Neuroimaging

MRI of the spine (with and without gadolinium):

TIMING IS EVERYTHING: Obtain within 24 hours of presentation
Include entire spine (cervical + thoracic + lumbar) on first study
Look for: lesion length, axial location, enhancement pattern, associated abnormalities[19]

Key MRI patterns:

Feature	Interpretation
Short segment (<3 vertebral bodies)	MS, infarction, focal inflammatory
LETM (≥3 vertebral bodies)	NMOSD, ADEM, infectious, paraneoplastic
Central gray matter (H-sign)	NMOSD, anterior spinal artery infarction
Peripheral white matter	MS, viral
Enhancement pattern	Active inflammation, BBB disruption
"Owl's eyes" (bilateral anterior horn T2)	Anterior spinal artery syndrome
Flow voids	Vascular malformation

Brain MRI: Always obtain to assess for:

Demyelinating lesions (MS)
ADEM
Brainstem involvement
Area postrema syndrome (NMOSD)

Pearl #3: The "Missing" Lesion

In hyperacute presentations (<12 hours), MRI may be normal or show only subtle swelling. If clinical suspicion is high, repeat MRI in 24-48 hours. T2 signal abnormality and enhancement evolve over the first few days.[20]

Lumbar Puncture

Timing: After MRI rules out compressive lesion causing complete block

Essential CSF studies:

Cell count with differential
Protein and glucose
Gram stain and bacterial culture
Oligoclonal bands and IgG index/synthesis rate
VDRL
Viral PCR panel: HSV-1/2, VZV, enterovirus, CMV, EBV, West Nile virus
Cytology (if malignancy suspected)
Opening pressure

Geographic/exposure-based:

AFB smear and culture (TB endemic areas)
Fungal culture
Schistosoma serology/microscopy

CSF findings by etiology:

Diagnosis	WBC	Protein	Glucose	Other
Idiopathic ATM	10-100 (lymphocytic)	Elevated (50-100)	Normal	OCBs variable
MS	5-50 (lymphocytic)	Normal/mild ↑	Normal	OCBs in 85-95%
NMOSD	Often >50	Elevated	Normal	Neutrophils possible in acute phase
Bacterial	>100 (neutrophilic)	>200	Low	Organisms on Gram stain
Viral	10-500 (lymphocytic)	Mild/moderate ↑	Normal	PCR confirmatory
Paraneoplastic	Lymphocytic	Elevated	Normal	Malignant cells possible

Hack #2: The Pragmatic Infectious Workup

Given the narrow therapeutic window, if infectious myelitis is in your differential:

Start empiric antimicrobials BEFORE LP if unstable
Core infectious panel: bacterial culture, VDRL, HSV/VZV/enterovirus PCR
Add pathogen-specific testing based on exposure history, immunocompromised state, or endemic infections
Don't let extensive testing delay immunotherapy if autoimmune etiology is likely

Serology and Autoimmune Panel

First-tier (send immediately):

Anti-aquaporin-4 (AQP4) IgG (cell-based assay preferred)
Anti-MOG IgG (cell-based assay)
ANA, anti-dsDNA (lupus)
Antiphospholipid antibodies
ESR, CRP

Second-tier (based on clinical context):

Paraneoplastic antibodies: anti-Hu, anti-Yo, anti-Ri, anti-CV2, anti-Ma2, anti-amphiphysin
Anti-NMDA receptor antibodies
ANCA panel (if vasculitis suspected)
Sarcoid markers (ACE level, lysozyme)
B12, copper, methylmalonic acid (metabolic myelopathies)
HTLV-1/2 serology
HIV testing

Pearl #4: Seronegative NMOSD Exists

Approximately 20-30% of clinically definite NMOSD patients are AQP4 antibody-negative. Don't exclude NMOSD based on negative serology alone if the clinical and MRI picture is consistent. Consider MOG antibodies and repeat AQP4 testing during relapses.[21]

Management: Time-Sensitive Interventions

Critical Care Stabilization

1. Airway and Breathing

Cervical lesions (C3-C5): high risk of respiratory failure
Serial VC and NIF measurements
Early consideration of NIV or intubation
Aggressive pulmonary toilet (assisted cough techniques, mechanical insufflation-exsufflation)
DVT prophylaxis essential in paralyzed patients[22]

2. Cardiovascular Monitoring

Lesions above T6: neurogenic shock (hypotension + bradycardia)
May require vasopressors and/or atropine
Autonomic dysreflexia in high cervical/thoracic lesions (hypertensive crisis triggered by noxious stimuli below lesion)
Treatment: remove trigger, sit patient up, antihypertensives PRN[23]

3. Bladder Management

Acute retention: intermittent catheterization preferred (reduces UTI vs. indwelling)
Target bladder volumes <400-500 mL
Early urology consultation for refractory retention

4. Bowel Management

Bowel regimen to prevent constipation/impaction
Stool softeners, stimulant laxatives, scheduled enemas

5. Pressure Injury Prevention

Turn every 2 hours
Specialized mattresses
Skin assessment twice daily

6. Neuropathic Pain Management

Gabapentin or pregabalin first-line
Duloxetine or amitriptyline for burning dysesthesias
Avoid opioids as monotherapy

Oyster #4: Autonomic Dysreflexia Crisis

A patient with high spinal cord injury (T6 or above) suddenly develops severe hypertension (SBP >200), bradycardia, flushing above lesion, and headache. This is autonomic dysreflexia—a medical emergency. The trigger is usually bladder distension or fecal impaction.

Management:

Sit patient upright immediately (reduces BP)
Check bladder scanner—catheterize if distended
Check for fecal impaction (use lidocaine jelly first)
Remove tight clothing
If BP remains >150 systolic: short-acting antihypertensive (nifedipine 10 mg PO or nitropaste)
Never ignore—can lead to seizures, stroke, MI[24]

Immunotherapy: Evidence and Protocols

The cornerstone of ATM treatment is immunomodulation, initiated as soon as compressive/vascular etiologies are excluded and infectious causes treated.

First-Line: High-Dose Intravenous Corticosteroids

Regimen:

Methylprednisolone 1000 mg IV daily × 3-5 days
Alternative: Dexamethasone 40 mg IV daily × 4 days (some evidence for superiority in cerebral edema; extrapolated to myelitis)

Evidence base:

No randomized controlled trials specifically for ATM
Extrapolated from MS acute relapses (Optic Neuritis Treatment Trial)[25]
Observational data suggests benefit if initiated within 72 hours of symptom onset
Earlier treatment correlates with better outcomes[26]

Practical considerations:

Start immediately after MRI if no contraindications
Monitor glucose, electrolytes, blood pressure
PPI for GI protection
Consider antibiotic prophylaxis in severely immunocompromised

Oral taper: Controversial. Some experts recommend:

Prednisone 60-80 mg daily × 1 week
Then taper by 10-20 mg weekly
Rationale: prevent rebound inflammation
Others advocate no taper for idiopathic ATM but use for MS/NMOSD

Second-Line: Plasma Exchange (PLEX)

Indications:

No improvement or clinical worsening after 5 days of IVMP
Severe presentation (complete paraplegia, respiratory failure)
NMOSD or suspected NMOSD
Contraindication to corticosteroids

Protocol:

5-7 exchanges over 10-14 days
1-1.5 plasma volumes per exchange
Albumin replacement (FFP if coagulopathic)

Evidence:

RCT evidence in acute demyelinating CNS disease shows moderate-severe cases benefit[27]
Earlier initiation (within 28 days of symptom onset) associated with better outcomes
NNT approximately 3 for meaningful recovery

Pearl #5: Don't Delay PLEX If the patient has severe deficits (unable to walk, complete sensory level, urinary retention), consider initiating PLEX concurrently with corticosteroids rather than sequentially. Observational data suggests this approach may improve outcomes, particularly in NMOSD.[28]

Third-Line: Intravenous Immunoglobulin (IVIG)

Indications:

Failure of steroids and PLEX
Patient unable to tolerate PLEX
Pediatric cases (often used earlier)
Infectious triggers (theoretical immune modulation without suppression)

Protocol:

2 g/kg divided over 2-5 days (typical: 0.4 g/kg/day × 5 days)

Evidence:

Limited data; mostly case series and retrospective cohorts
Response rates: 30-50% show some improvement
Safety profile excellent

Experimental/Salvage Therapies

Cyclophosphamide:

1000 mg IV monthly × 6 months
Reserved for refractory cases or severe NMOSD
Significant toxicity profile

Rituximab:

Increasingly used in NMOSD
Anti-CD20 monoclonal antibody
Dose: 1000 mg IV × 2 (2 weeks apart) or 375 mg/m² weekly × 4

Intrathecal corticosteroids:

Limited data
Case reports suggest benefit in refractory cases
Not standard practice

Hack #3: The "Steroid-PLEX Sandwich"

For severe ATM with suspected NMOSD (LETM, central cord signal, known AQP4+ status), some tertiary centers use:

IVMP 1000 mg × 3 days
Begin PLEX on day 2 or 3
Complete 5-7 exchanges
Resume IVMP 1000 mg × 2 days after last exchange
Oral prednisone taper

Rationale: Dual suppression, prevents rebound, targets both cellular and humoral immunity. No RCT data but supported by expert opinion for severe NMOSD attacks.[29]

Etiology-Specific Management

NMOSD

Acute phase:

Aggressive immunotherapy (IVMP + PLEX often simultaneously)
Early initiation critical

Relapse prevention (initiate during acute hospitalization):

Rituximab (preferred): 1000 mg IV × 2, then maintenance dosing
Alternatives: azathioprine, mycophenolate mofetil
Newer agents: eculizumab, inebilizumab, satralizumab (evidence-based, FDA-approved)[30]

Key point: NMOSD has high relapse rates (90% within 5 years if untreated). Maintenance immunosuppression is mandatory.

Multiple Sclerosis

Acute phase:

High-dose corticosteroids

Disease-modifying therapy:

If MRI/clinical picture suggests MS, initiate DMT discussion
High-efficacy options for active disease: natalizumab, ocrelizumab, alemtuzumab, cladribine

Infectious Myelitis

Viral:

HSV/VZV: Acyclovir 10-15 mg/kg IV q8h × 14-21 days
CMV: Ganciclovir 5 mg/kg IV q12h × 21 days (especially in immunocompromised)
West Nile virus: supportive care (no specific antiviral)
Consider IVIG for viral myelitis (theoretical benefit)

Bacterial:

Syphilis: Penicillin G 18-24 million units daily × 10-14 days
Lyme: Ceftriaxone 2 g IV daily × 14-28 days
Mycoplasma: Azithromycin or doxycycline + corticosteroids

Parasitic:

Schistosomiasis: Praziquantel + corticosteroids
Dose: 40-60 mg/kg in 2-3 divided doses
Steroids given to prevent paradoxical worsening from dying parasites

Paraneoplastic

Treat underlying malignancy
Immunotherapy: IVMP, PLEX, IVIG
Immunosuppression: cyclophosphamide, rituximab
Prognosis generally poor; early cancer treatment critical

Prognostic Factors

Favorable Prognostic Indicators:

Incomplete lesion (sacral sparing)
Preserved motor function (ability to walk)
Shorter lesion length on MRI
Rapid treatment initiation (<72 hours)
Younger age
Absence of bowel/bladder dysfunction
Sensory symptoms predominate over motor[31]

Poor Prognostic Indicators:

Complete cord syndrome at presentation
LETM (≥3 vertebral segments)
Central gray matter involvement
Spinal shock
Severe disability at nadir (complete paraplegia)
Delayed treatment (>2 weeks)
NMOSD etiology (vs. MS or idiopathic)
Spinal cord atrophy on follow-up MRI[32]

Pearl #6: The "Rule of Thirds" for Recovery

A useful prognostication framework for counseling families:

One-third recover completely or with minor deficits
One-third have moderate residual disability (ambulatory with aids)
One-third remain severely disabled (wheelchair-dependent)

However, this varies dramatically by etiology and treatment timing. Most recovery occurs in the first 3-6 months, with further gains possible up to 2 years.[33]

Rehabilitation: The Critical Care Role

Early rehabilitation interventions in the ICU improve outcomes:

1. Early mobilization:

Initiate as soon as medically stable
Tilt table for patients unable to sit
PT consultation within 48 hours

2. Occupational therapy:

ADL assessment and training
Adaptive equipment

3. Psychological support:

Depression screening (PHQ-9)
Early psychiatry/psychology consultation
Up to 30% develop major depression post-ATM[34]

4. Discharge planning:

Inpatient rehabilitation facility for most patients
Coordinate outpatient neurology follow-up
Bladder/bowel management teaching

Diagnostic Pitfalls and How to Avoid Them

Oyster #5: Guillain-Barré Syndrome Mimicking Myelitis

Clinical scenario: Ascending weakness, sensory symptoms, areflexia, urinary retention.

Distinguishing features:

GBS: distal-to-proximal progression, areflexia throughout, facial/bulbar weakness common, NO sensory level
ATM: clear sensory level, symmetric weakness, upper motor neuron signs (after spinal shock)
GBS: Albuminocytologic dissociation in CSF (high protein, normal cells)
ATM: Pleocytosis common
Key test: MRI spine normal in GBS vs. abnormal in ATM
EMG/NCS: demyelination/axonal findings in GBS

Why it matters: Treatment differs (IVIG/PLEX for GBS; steroids harmful in GBS). Don't give steroids for presumed ATM without imaging first.

Oyster #6: Functional Neurological Disorder (FND)

Clinical scenario: Acute paraplegia, sensory loss, no clear sensory level, normal MRI, normal CSF.

Red flags for FND:

Inconsistent exam findings
"Give-way" weakness
Non-anatomic sensory loss
Preserved anal wink and bulbocavernosus reflex with "complete" loss of voluntary function
Hoover's sign positive
Normal MRI with complete clinical presentation

Approach:

Never a pure diagnosis of exclusion in acute setting
Complete workup still required
Psychiatry consultation
Avoid iatrogenic harm from unnecessary immunotherapy

Pearl #7: About 5-10% of patients with suspected ATM have FND or malingering. However, premature diagnosis of FND leads to delayed treatment of real myelopathy. When in doubt, treat as organic disease while pursuing diagnosis.[35]

Special Populations

Pediatric ATM

Key differences:

ADEM more common than in adults
MOG antibody disease more frequent
Better overall prognosis for recovery
Lower threshold for IVIG (often first or second-line)
Developmental considerations in rehabilitation

Pregnancy-Associated ATM

Challenges:

MRI without gadolinium preferred (gadolinium Category C)
Steroid use: relatively safe (methylprednisolone preferred over dexamethasone)
PLEX: safe
IVIG: safe
Multidisciplinary management with OB

Immunocompromised Patients

Broader infectious differential:

Opportunistic infections (CMV, VZV, fungi, toxoplasma)
Progressive multifocal leukoencephalopathy (JC virus)—usually brain but can involve cord
Consider empiric antimicrobial coverage while awaiting workup

Immunotherapy considerations:

Risk-benefit assessment
May require dose reduction
Infectious workup especially critical

Clinical Practice Algorithm

ACUTE MYELOPATHY PRESENTATION
          ↓
IMMEDIATE (0-6 hours):
1. Stabilize (ABCs, ICU if needed)
2. Neurological exam with sensory level documentation
3. Stat MRI spine (entire spine with/without contrast)
          ↓
COMPRESSIVE LESION? ──YES→ NEUROSURGERY CONSULT (EMERGENCY)
          ↓ NO
NON-COMPRESSIVE MYELOPATHY
          ↓
NEXT 6-24 hours:
1. MRI brain
2. Lumbar puncture (comprehensive panel)
3. Serology (AQP4, MOG, autoimmune panel)
4. Infectious workup based on risk factors
          ↓
HIGH SUSPICION INFLAMMATORY/DEMYELINATING?
          ↓ YES
START IVMP 1000 mg daily × 3-5 days
          ↓
REASSESS DAY 5-7
          ↓
IMPROVEMENT? ──YES→ Continue recovery, rehab, determine etiology
          ↓ NO
SEVERE OR WORSENING?
          ↓
ADD PLEX (5-7 exchanges)
          ↓
REASSESS AFTER PLEX
          ↓
NO IMPROVEMENT?
          ↓
IVIG 2 g/kg OR Salvage therapy (cyclophosphamide/rituximab)

Key Takeaways for Critical Care Practice

ATM is time-sensitive: Imaging within 24 hours, immunotherapy within 72 hours if inflammatory etiology suspected.
Complete your differential: The list is long—inflammatory, infectious, vascular, compressive, metabolic. Cast a wide net diagnostically before anchoring.
MRI is the single most important test: Entire spine with contrast. Patterns guide etiology.
Corticosteroids first, PLEX second: But don't wait 5 days if the patient is severely affected—consider concurrent therapy.
Watch for complications: Respiratory failure, autonomic dysreflexia, DVT, pressure ulcers, neuropsychiatric sequelae.
NMOSD needs long-term prevention: Don't discharge without immunosuppression plan.
Early rehabilitation matters: PT/OT consultation within 48 hours improves functional outcomes.
Recovery is slow: Most improvement happens over 3-6 months. Set realistic expectations but maintain hope.

Future Directions

Emerging research focuses on:

Biomarkers: Serum neurofilament light chain (sNfL) and GFAP for prognostication and monitoring
Advanced imaging: Spinal cord DTI and volumetric analysis for predicting recovery
Neuroprotection: Cellular therapies (mesenchymal stem cells), complement inhibitors, remyelination strategies
Precision medicine: Tailoring immunotherapy to specific antibody profiles and inflammatory signatures[36,37]

Conclusion

Acute transverse myelopathies represent neurological emergencies requiring prompt recognition, systematic evaluation, and aggressive treatment. Critical care physicians play a pivotal role in the initial stabilization, diagnostic workup, and initiation of immunotherapy. A high index of suspicion, early MRI, comprehensive laboratory evaluation, and timely corticosteroids or plasma exchange can significantly impact long-term neurological outcomes. Multidisciplinary collaboration with neurology, neurosurgery, rehabilitation medicine, and subspecialties ensures optimal care for this complex patient population.

The adage "time is spine" parallels "time is brain"—every hour counts in preserving spinal cord function and maximizing recovery potential.

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CLINICAL PEARLS & OYSTERS: Quick Reference Summary

PEARLS (Clinical Wisdom)

Pearl #1: Spinal Shock Phenomenon

Acute complete lesions initially present with flaccid paralysis and areflexia
Transitions to spasticity over 1-6 weeks
Don't be falsely reassured by absent reflexes—focus on sensory level

Pearl #2: Sensory Level Examination

Use cold stimulus (tuner fork/alcohol swab) from feet upward
First perceived sensation = segment BELOW lesion
Sacral sparing = incomplete lesion = better prognosis

Pearl #3: The "Missing" Lesion

Hyperacute MRI (<12 hours) may be normal
Repeat in 24-48 hours if high clinical suspicion
T2 signal and enhancement evolve over days

Pearl #4: Seronegative NMOSD Exists

20-30% of NMOSD patients are AQP4 antibody-negative
Don't exclude diagnosis on serology alone
Check MOG antibodies; repeat AQP4 during relapses

Pearl #5: Don't Delay PLEX

Severe deficits warrant concurrent PLEX + steroids
Earlier initiation (<28 days) = better outcomes
Don't wait for steroid failure in devastating presentations

Pearl #6: Rule of Thirds for Recovery

1/3 recover completely or near-completely
1/3 have moderate disability (ambulatory with aids)
1/3 remain severely disabled (wheelchair-dependent)
Most recovery in first 3-6 months, continued improvement up to 2 years

Pearl #7: Functional Neurological Disorder Caution

5-10% of suspected ATM cases are FND
Never purely diagnose by exclusion in acute setting
When uncertain, treat as organic while pursuing workup
Premature FND diagnosis risks missing treatable disease

OYSTERS (Pitfalls to Avoid)

Oyster #1: Ascending Sensory Level 🚨

Rising sensory level = progressive edema/hemorrhage/abscess
NEUROSURGICAL EMERGENCY
Repeat neuro exam every 2-4 hours initially

Oyster #2: Neurogenic Respiratory Failure 🚨

C3-C5 lesions = diaphragm paralysis
Monitor: VC (<15 mL/kg), NIF (<-30 cm H2O), paradoxical breathing
Don't wait for hypercapnia—intervene early

Oyster #3: "Myelitis" That's Actually Compression 🚨

Early epidural collections mimic inflammatory myelitis on MRI
Scrutinize epidural space on sagittal sequences
When in doubt, use contrast

Oyster #4: Autonomic Dysreflexia Crisis 🚨

High spinal injury (≥T6) + sudden severe HTN + bradycardia + headache
Trigger: bladder distension or fecal impaction
Immediate action: Sit up, catheterize, check for impaction, antihypertensives PRN
Can cause seizure, stroke, MI if ignored

Oyster #5: GBS Mimicking Myelitis

Both present with ascending weakness, sensory symptoms, retention
Distinguish: GBS has NO sensory level, areflexia throughout, facial weakness
CSF: GBS = high protein/normal cells; ATM = pleocytosis
Critical: Don't give steroids before imaging—harmful in GBS

Oyster #6: Functional Neurological Disorder

Inconsistent exam, give-way weakness, non-anatomic sensory loss
Preserved reflexes with "complete" paralysis
Positive Hoover's sign
Caution: Complete workup still required; avoid premature dismissal

HACKS (Practical Shortcuts)

Hack #1: CSF Opening Pressure Clue

Normal/mild elevation (10-25 cm H2O) → inflammatory myelitis
Markedly elevated (>25 cm H2O) → epidural abscess, carcinomatous meningitis, complete block
Low (<8 cm H2O) → CSF leak, prior LP, dehydration

Hack #2: Pragmatic Infectious Workup

If unstable, start empiric antimicrobials BEFORE LP
Core panel: culture, VDRL, HSV/VZV/enterovirus PCR
Add pathogen-specific tests based on exposure/immunocompromise
Don't delay immunotherapy while awaiting extensive testing

Hack #3: Steroid-PLEX Sandwich (for severe NMOSD)

IVMP 1000 mg × 3 days
Start PLEX on day 2-3
Complete 5-7 exchanges
Resume IVMP 1000 mg × 2 days post-PLEX
Oral prednisone taper

Rationale: Dual immune suppression, prevents rebound

No RCT data but expert consensus for severe attacks

ICU MONITORING CHECKLIST

First 24 Hours:

[ ] Neuro exam with sensory level q2-4h
[ ] Vital capacity and NIF if cervical lesion
[ ] Cardiac monitoring (dysrhythmias with high lesions)
[ ] Bladder scanner q4-6h
[ ] DVT prophylaxis initiated
[ ] Pressure injury prevention protocol
[ ] MRI spine (entire) with/without contrast
[ ] MRI brain
[ ] Lumbar puncture (after imaging)
[ ] Serology panel sent
[ ] Corticosteroids initiated (if inflammatory suspected)

Daily ICU Care:

[ ] Respiratory assessment (VC/NIF if high lesion)
[ ] Autonomic monitoring (BP, HR variability)
[ ] Bladder management (avoid overdistension >500 mL)
[ ] Bowel regimen
[ ] Skin assessment (pressure points)
[ ] Pain assessment (neuropathic pain common)
[ ] DVT prophylaxis continued
[ ] PT/OT consultation by day 2
[ ] Psychology/psychiatry screening
[ ] Family counseling on prognosis

DISPOSITION PLANNING

ICU Discharge Criteria:

Hemodynamically stable off pressors
No respiratory compromise (adequate VC/NIF, or stable on vent)
Bladder management plan established
Completed acute immunotherapy course
Etiology determined or workup in progress

Rehabilitation Needs:

Inpatient rehabilitation facility for most patients
Skilled nursing facility if prolonged vent dependence
Outpatient therapy for mild deficits with ambulatory status

Outpatient Follow-up:

Neurology within 2-4 weeks
Urology if persistent bladder dysfunction
Repeat MRI spine at 3-6 months (assess for atrophy, resolution)
Psychology/psychiatry for mood monitoring
PT/OT continuation

Long-term Immunosuppression (if indicated):

NMOSD: Rituximab, azathioprine, mycophenolate, or newer biologics
MS: Disease-modifying therapy
Idiopathic ATM: Generally not required unless recurrent

TEACHING POINTS FOR TRAINEES

"Time is spine" parallels "time is brain"—rapid diagnosis and treatment matter
The three non-negotiables:
- Complete spine MRI within 24 hours
- LP after imaging rules out block
- Corticosteroids within 72 hours if inflammatory
Think compressive FIRST: Epidural abscess and hematoma are surgical emergencies
LETM (≥3 segments) = think NMOSD until proven otherwise
Always get brain MRI: Helps differentiate MS, ADEM, and NMOSD
Respiratory monitoring is critical: C3-C5 keeps the diaphragm alive
Bladder distension triggers autonomic dysreflexia: Check bladder scanner in hypertensive crisis with high lesions
Recovery is slow: Set realistic expectations but maintain therapeutic optimism
Rehabilitation starts in ICU: Early mobilization, PT/OT consultation, psychological support
NMOSD patients need lifelong immunosuppression: Don't discharge without a plan

CASE-BASED LEARNING SCENARIOS

Case 1: The Classic Presentation

34-year-old woman with 3-day history of ascending numbness, now with paraplegia, sensory level at T6, urinary retention.

Key actions:

Stat MRI spine → shows T4-T8 LETM, central gray matter involvement
LP → 85 WBCs (lymphocytic), protein 98, normal glucose
AQP4 antibody sent
Initiate IVMP 1000 mg daily
Day 5: no improvement → add PLEX
AQP4 returns positive → diagnosis NMOSD
Initiate rituximab for long-term prevention

Lesson: LETM + central cord signal = NMOSD until proven otherwise. Aggressive early treatment essential.

Case 2: The Missed Surgical Emergency

58-year-old diabetic man with back pain for 3 days, now with fever, paraparesis, urinary retention.

Red flags:

Fever + back pain + myelopathy = epidural abscess until proven otherwise
WBC 18,000, ESR 95, CRP 150

Critical action:

Stat MRI before LP (risk of herniation with complete block)
MRI shows posterior epidural collection T8-T11 with cord compression
Emergent neurosurgery consultation
Blood cultures + empiric vancomycin + ceftriaxone
Urgent decompressive laminectomy

Lesson: Always consider compressive etiologies. Fever + elevated inflammatory markers + back pain = abscess. Don't LP until imaging complete.

Case 3: The Diagnostic Dilemma

22-year-old man with acute-onset flaccid paraplegia, absent reflexes, no sensory level, normal MRI spine.

Differential narrowed:

No sensory level + areflexia + normal MRI = NOT myelitis
Consider: GBS, cauda equina syndrome, conversion disorder

Workup:

LP: protein 180, cells 2 (albumin cytologic dissociation)
EMG/NCS: demyelinating polyneuropathy
Diagnosis: Guillain-Barré Syndrome

Treatment:

IVIG or PLEX (NOT steroids—contraindicated in GBS)

Lesson: Not every acute paralysis is myelitis. Absence of sensory level and normal MRI should broaden differential. GBS and myelitis can look similar initially—don't anchor prematurely.

FINAL SUMMARY: THE CRITICAL CARE APPROACH TO ATM

Timeline	Action
0-6 hours	Stabilize, neuro exam with sensory level, stat MRI spine
6-24 hours	LP (after imaging), brain MRI, serology, empiric treatment if infectious suspected
24-72 hours	Initiate IVMP if inflammatory, monitor for complications (respiratory failure, autonomic dysreflexia)
Day 5-7	Reassess response; add PLEX if no improvement or severe presentation
Day 10-14	Complete PLEX course, consider IVIG if refractory, determine etiology
Week 2-4	Transition to rehab, initiate long-term immunosuppression if NMOSD/MS, outpatient neurology follow-up

The bottom line: Acute transverse myelopathy is a neurological emergency that demands systematic evaluation, aggressive immunotherapy when appropriate, meticulous ICU monitoring, and early rehabilitation. Critical care physicians are the gatekeepers to optimal outcomes—recognize it early, treat it fast, and coordinate comprehensive care.

This review article is intended for educational purposes for postgraduate medical trainees in critical care and neurology. Clinical decision-making should always be individualized based on patient-specific factors and institutional protocols.

Tuesday, September 30, 2025

Acute Transverse Myelopathies In ICU