What is the most likely diagnosis and recommended acute management for a 30‑year‑old male who, ten days after an upper‑respiratory infection, presents with rapidly progressive symmetric proximal lower‑limb weakness, absent deep‑tendon reflexes, increased tone in the lower limbs, bilateral extensor plantar responses, left‑sided facial deviation, right facial nerve palsy with incomplete eye closure, dysphagia, and no sensory loss, bowel or bladder involvement?

Acute Transverse Myelitis with Overlapping Guillain-Barré Features

Most Likely Diagnosis

This patient has acute transverse myelitis, not Guillain-Barré syndrome, despite the post-infectious timing and ascending weakness. The combination of bilateral extensor plantar responses and increased lower-limb tone are red-flag signs that localize pathology to the corticospinal tracts of the spinal cord, brainstem, or bilateral cerebral hemispheres—indicating upper motor neuron (UMN) involvement rather than the peripheral nerve pathology of GBS. 1

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Critical Diagnostic Red Flags

The presence of extensor plantar responses (Babinski sign) with increased tone definitively points to UMN pathology and rules against classic GBS. 1

• Extensor plantar responses localize the lesion to the corticospinal tracts, indicating central rather than peripheral nervous system pathology. 1
• Increased tone (spasticity) in the legs signifies UMN dysfunction; in very acute spinal cord lesions, an initial flaccid "spinal shock" phase may rapidly evolve to spasticity within hours to days. 1
• The absent reflexes in this case likely represent the early "spinal shock" phase of acute myelopathy, which will evolve to hyperreflexia as the acute phase resolves. 1
• Post-infectious transverse myelitis frequently follows an upper respiratory tract infection, making the recent URTI a relevant temporal association. 1

Additional features that support myelitis over GBS:

• Acute transverse myelitis can present with rapidly progressive bilateral leg weakness and may lack an obvious sensory level early in the course. 1
• Bladder and bowel dysfunction can be absent in the first 24–48 hours of transverse myelitis. 1
• The bilateral facial nerve involvement and dysphagia indicate brainstem pathology, which can occur in extensive myelitis extending rostrally or in concurrent brainstem encephalitis. 1

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Immediate Diagnostic Workup (Do Not Delay)

1. Urgent Spine and Brain Imaging (FIRST PRIORITY)

Obtain MRI of the entire spine with and without gadolinium contrast immediately to exclude compressive lesions (epidural abscess, hematoma, tumor) and to identify intramedullary signal changes compatible with transverse myelitis. 1

• MRI must be performed before lumbar puncture when spinal cord pathology is suspected, because lumbar puncture can exacerbate herniation in the presence of mass effect. 1
• Epidural abscess, hematoma, or intradural tumor can produce acute bilateral leg weakness with UMN signs; lack of back pain does not rule out compressive spinal pathology. 1
• Given the bilateral facial palsy and dysphagia, also obtain MRI of the brain with contrast to evaluate for brainstem involvement (e.g., Bickerstaff brainstem encephalitis, neuromyelitis optica, or other inflammatory/demyelinating processes). 2

2. Immediate Neurology Consultation

An immediate neurology consult is mandatory for any patient with suspected acute myelopathy or an atypical presentation of GBS. 1

3. Cerebrospinal Fluid Analysis (After Imaging)

Perform lumbar puncture only after MRI excludes mass effect or compressive lesion. 1

• CSF showing albuminocytologic dissociation (elevated protein with normal cell count) supports GBS, whereas pleocytosis (elevated white-cell count) favors inflammatory or infectious myelitis. 1
• Marked pleocytosis (>50 cells/µL) strongly suggests an alternative diagnosis such as infectious or inflammatory myelitis; mild pleocytosis (10–50 cells/µL) can be seen in GBS. 1
• CSF should also be analyzed for cell count and differential, cytology for malignant cells, glucose, and viral/bacterial cultures. 3

4. Electrodiagnostic Studies

Nerve conduction studies and EMG should be performed to look for peripheral nerve abnormalities (reduced velocities, amplitudes, temporal dispersion, conduction block). 1

• Normal electrophysiologic findings within the first week of symptom onset do not exclude GBS. 1
• The "sural-sparing pattern" (normal sural sensory action potential with abnormal median/ulnar responses) is characteristic of GBS and helps differentiate it from other neuropathies. 1
• If nerve conduction studies are normal and MRI confirms myelitis, this definitively excludes GBS. 1

5. Additional Laboratory Tests

• Complete blood count, glucose, electrolytes, kidney function, liver enzymes to exclude metabolic or electrolyte dysfunction as causes of weakness. 3
• Serum creatine kinase (CK) is sensitive though nonspecific; elevation suggests muscle involvement. 3
• Serum antiganglioside antibody panel (including anti-GQ1b) to evaluate for Miller Fisher syndrome or other GBS variants, though this should not delay treatment. 3
• Aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies to evaluate for neuromyelitis optica spectrum disorder or MOG-associated disease. 2

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Immediate Management

If MRI Confirms Acute Transverse Myelitis

Initiate high-dose intravenous methylprednisolone (1 g/day for 3–5 days) as first-line therapy; this regimen improves outcomes in inflammatory myelitis. 1

• Early treatment with high-dose corticosteroids is associated with better functional outcomes. 1
• For compressive lesions identified on MRI, obtain urgent neurosurgical consultation for possible decompression. 1

If Imaging Excludes Myelopathy and GBS is Confirmed

Intravenous immunoglobulin (IVIg) 0.4 g/kg/day for 5 days (total 2 g/kg) is recommended for patients unable to walk unaided within 2–4 weeks of onset. 1

• Plasma exchange (200–250 mL/kg over 4–5 sessions) is an equally effective alternative to IVIg. 1
• Corticosteroids alone are not recommended for idiopathic GBS, as they have not demonstrated benefit. 1

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Critical Respiratory and Autonomic Monitoring

Assess respiratory function as the highest priority; approximately 20% of GBS patients and 30% of myelitis patients develop respiratory failure requiring mechanical ventilation. 4, 5

• Measure vital capacity, negative inspiratory force (NIF), and maximum inspiratory/expiratory pressures at presentation and serially. 3
• Apply the "20/30/40 rule": patient is at risk of respiratory failure if vital capacity <20 ml/kg, maximum inspiratory pressure <30 cmH₂O, or maximum expiratory pressure <40 cmH₂O. 3
• Single breath count ≤19 predicts need for mechanical ventilation. 3
• Admit to an inpatient unit capable of rapid ICU transfer for any patient with severe weakness limiting self-care, dysphagia, facial or respiratory muscle weakness, or rapidly progressive symptoms. 3

Continuously monitor for dysautonomia:

• Perform electrocardiography and continuously monitor heart rate and blood pressure for arrhythmias and blood pressure instability. 3
• Monitor for pupillary dysfunction and bowel/bladder dysfunction. 3
• Cardiovascular complications contribute to a 3–10% mortality rate even with optimal care. 4

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Prognosis

If Acute Transverse Myelitis

• Outcome depends on the severity and longitudinal extent of spinal cord involvement; some patients achieve full recovery, while others sustain permanent disability. 1
• Early treatment with high-dose corticosteroids is associated with better functional outcomes. 1

If Guillain-Barré Syndrome (After Exclusion of Myelopathy)

• Approximately 80% of patients regain independent walking by 6 months, with continued recovery possible up to 3 years or longer. 1
• Mortality ranges from 3% to 10%, primarily due to respiratory or cardiovascular complications. 1
• Advanced age and severe disease at onset are risk factors for poor outcome. 3

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Common Pitfalls to Avoid

Do not diagnose GBS in the presence of extensor plantar responses and increased tone—these are UMN signs that indicate spinal cord or brainstem pathology. 1

• The diagnostic criteria for GBS explicitly list extensor plantar responses and hyperreflexia/clonus as features that cast doubt on the diagnosis. 2
• Absent reflexes in acute myelopathy represent "spinal shock" and will evolve to hyperreflexia; the presence of extensor plantars reveals the underlying UMN pathology. 1

Do not perform lumbar puncture before MRI when myelopathy is suspected—this can cause herniation if a mass lesion is present. 1

Do not delay corticosteroid therapy for confirmed myelitis while awaiting additional test results—early treatment improves outcomes. 1

Do not dismiss the diagnosis of myelitis based on absent sensory level or absent bladder/bowel dysfunction in the first 24–48 hours—these features may emerge later. 1