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Approach to Deteriorating Lower Limb Weakness Post 3 Days of Fever

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Step 1: Localize the Lesion First (UMN vs LMN)

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Step 2: Build the Differential Diagnosis

A. Post-infectious / Para-infectious - MOST LIKELY

• Ascending flaccid paralysis, areflexia, minimal sensory loss
• Legs more affected than arms early
• Follows infection by 1-3 weeks (GI or respiratory)
• Key precipitants: Campylobacter jejuni (most common), CMV, EBV, influenza, SARS-CoV-2, Zika virus
• "Rubbery legs" is often the first description by patients
• Absence of fever at onset is a supportive diagnostic criterion - if fever is ongoing, consider other diagnoses but do not exclude GBS
• Subtypes: AIDP (most common in West), AMAN (common in Asia/children), AMSAN, Miller-Fisher (ophthalmoplegia + ataxia + areflexia)

"Fever and constitutional symptoms are absent at the onset, and, if present, cast doubt on the diagnosis" - Harrison's Principles of Internal Medicine 22E, p. 3663

• Paraplegia/paraparesis + sensory level + sphincter dysfunction = classic triad
• Follows viral infection in ~30% of cases (postinfectious myelitis)
• UMN signs: hyperreflexia, spasticity, Babinski positive
• Thoracic cord involved in 60-70% of cases
• Associated with NMOSD (anti-AQP4 antibodies), SLE, Sjogren's, antiphospholipid syndrome
• Back pain may be present

• Predominantly affects children
• Prodrome of fever + respiratory symptoms, then neurologic onset within 10 days
• Caused by enteroviruses, especially EV-D68, EV-A71, Coxsackievirus A7
• Biennial outbreaks in the US since 2014
• Flaccid limb weakness, may have brainstem involvement (rhombencephalitis)

• Anterior horn cell disease: pure motor, asymmetric, flaccid, no sensory loss
• Fever during paralytic phase distinguishes it from GBS
• Wild-type poliovirus, West Nile virus, Japanese encephalitis virus

B. Other Causes to Consider

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Step 3: History - Key Points to Ask

• Duration and progression of weakness (hours vs days; ascending vs descending)
• Nature of preceding illness - diarrheal/GI illness (Campylobacter), respiratory (EV-D68, influenza), rash (Zika, dengue), sore throat (EBV)
• Exact interval from fever onset to weakness (GBS: typically 1-3 weeks post-infection; AFM: within 10 days)
• Associated symptoms:
  • Tingling/numbness in feet (GBS)
  • Back/neck pain (transverse myelitis, epidural abscess)
  • Bladder/bowel dysfunction (spinal cord)
  • Shortness of breath, swallowing difficulty (GBS bulbar involvement - red flag)
  • Diplopia, facial weakness (GBS cranial nerve; Miller-Fisher)
• Vaccination history (polio, rabies)
• Travel history (endemic areas for polio, dengue, West Nile)
• Dietary/toxin exposure (canned food - botulism, tick attachment)
• Immunocompromise (HIV - CMV polyradiculitis)

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Step 4: Examination Priorities

1. Vital signs - respiratory rate and O2 sat (GBS can cause respiratory failure); BP fluctuations (autonomic dysfunction)
2. Bulk and tone of lower limbs
3. Power - MRC grading, symmetry, proximal vs distal pattern
4. Reflexes - deep tendon reflexes (absent = GBS/AFM/polio; brisk = myelitis)
5. Plantar response
6. Sensory examination - look for sensory level (myelitis), glove-stocking loss (GBS), or pure motor deficit (AMAN, polio)
7. Cranial nerves - bifacial weakness, ophthalmoplegia (GBS variants)
8. Autonomic - heart rate variability, BP, sweating
9. Spine - tenderness, percussion (epidural abscess)
10. Bedside spirometry - FVC <20 mL/kg or <1L = intubation threshold in GBS

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Step 5: Investigations

Urgent / First-line

Targeted / Second-line

CSF Interpretation in Context

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Step 6: Red Flags Requiring Immediate Action

• Declining FVC or O2 saturation - GBS respiratory failure is a leading cause of death; intubate early
• Rapidly ascending weakness reaching arms within hours
• Bulbar involvement (dysphagia, dysarthria, inability to clear secretions)
• Autonomic instability (wide BP swings, bradycardia/tachycardia) - cardiac monitoring mandatory
• Fever + back pain + rapid neurological deterioration - rule out spinal epidural abscess EMERGENTLY (neurosurgical emergency)

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Step 7: Management

GBS

• IVIG 0.4 g/kg/day x 5 days OR Plasmapheresis (PLEX) x 5 exchanges - equally effective; combination offers no added benefit
• No role for corticosteroids in GBS
• ICU monitoring for respiratory and autonomic complications
• DVT prophylaxis, physiotherapy, pain management (neuropathic pain is common)
• Monitoring: "20/30/40 rule" - intubate if FVC <20 mL/kg, MIP <30 cmH2O, or MEP <40 cmH2O

Transverse Myelitis

• IV methylprednisolone 1 g/day x 3-5 days is the first-line treatment
• Urgent MRI to exclude compression before LP and steroids
• If NMOSD suspected: aggressive immunosuppression (rituximab, azathioprine)
• Plasma exchange for steroid-refractory cases

Acute Flaccid Myelitis / Polio

• No specific antiviral therapy exists
• Supportive care, monitor for respiratory failure
• Physiotherapy and rehabilitation

Spinal Epidural Abscess (if confirmed)

• Emergency neurosurgical decompression + antibiotics

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Summary Algorithm

Post-fever lower limb weakness (deteriorating)
              |
    +---------+-----------+
    |                     |
  LMN signs            UMN signs
(flaccid, areflexia)  (spastic, hyperreflexia,
    |                  Babinski, sensory level)
    |                     |
    |              --> MRI Spine STAT
    |                  Transverse Myelitis?
    |                  Epidural Abscess?
    |
    +-----> ASCENDING? --> GBS most likely
    |           CSF (albuminocytological dissociation)
    |           NCS/EMG
    |           IVIG / Plasmapheresis
    |
    +-----> ASYMMETRIC + FEVER during paralysis
                --> Polio / AFM
                    CSF pleocytosis
                    Enterovirus PCR

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• Harrison's Principles of Internal Medicine 22E, GBS chapter, p. 3661-3665
• Bradley and Daroff's Neurology in Clinical Practice, GBS (Box 106.10, p. 2663-2666)
• ROSEN's Emergency Medicine, Transverse Myelitis, p. 1508
• Goldman-Cecil Medicine, Acute Flaccid Myelitis chapter, p. 3631