What is the immediate management for sudden onset quadriparesis with MRI findings of cervical T2 hyperintensities and cord expansion?

Immediate Management of Sudden Onset Quadriparesis with Cervical T2 Hyperintensities and Cord Expansion

Obtain urgent MRI of the entire spine with and without IV contrast immediately to identify the underlying etiology (compressive vs. inflammatory vs. ischemic vs. infectious), as this will fundamentally determine treatment and prognosis. 1

Initial Stabilization and Assessment

• Perform emergent neurological examination documenting motor strength in all extremities using standardized scales (Bromage scale for motor function), sensory level, reflexes, and sphincter tone to establish baseline deficits 2
• Assess for spinal shock with hemodynamic monitoring, as patients may develop autonomic instability requiring vasopressor support 1
• Maintain spinal precautions until mechanical instability is excluded, particularly if trauma history exists 1
• Check for respiratory compromise as cervical cord lesions can affect diaphragmatic function; prepare for potential intubation if lesion extends to C3-C5 levels 1

Critical Imaging Protocol

MRI with gadolinium contrast is mandatory to differentiate between:

• Compressive lesions (epidural hematoma, disc herniation, tumor) requiring urgent surgical decompression 1
• Inflammatory/demyelinating conditions (transverse myelitis, multiple sclerosis, neuromyelitis optica) showing enhancement patterns 1
• Ischemic myelopathy (anterior spinal artery syndrome) typically without early enhancement 1
• Infectious etiologies (epidural abscess, viral myelitis) showing characteristic enhancement 1

Include diffusion-weighted imaging (DWI) in the MRI protocol, as it detects spinal cord ischemia earlier than conventional T2-weighted sequences 1

Time-Critical Decision Points

If Compressive Pathology Identified (Epidural Hematoma, Disc, Tumor):

Proceed to emergency surgical decompression within 8-12 hours of symptom onset, as delays beyond this window result in irreversible neurological damage 2

• Reverse anticoagulation immediately if patient is on anticoagulants before surgical intervention 2
• Involve neurosurgery emergently for operative planning 2
• Do not delay imaging or surgery for any reason if clinical features suggest compression 2

If Inflammatory/Demyelinating Pattern (Enhancement, Long-Segment T2 Hyperintensity):

Initiate high-dose IV methylprednisolone 1000 mg daily for 3-5 days for presumed transverse myelitis or demyelinating disease 3

• Start treatment empirically while awaiting definitive diagnosis if enhancement pattern suggests inflammation 3
• Obtain CSF analysis with cell count, protein, glucose, oligoclonal bands, and specific antibodies (aquaporin-4 for neuromyelitis optica) 1
• Consider plasma exchange if no response to steroids within 5-7 days 3

If Infectious Etiology Suspected (Fever, CSF Pleocytosis, Enhancement):

Start IV aciclovir 500 mg/m² every 8 hours within 6 hours if viral myelitis possible, while awaiting CSF results 4

• Obtain blood cultures and inflammatory markers (ESR, CRP, procalcitonin) urgently 1
• Perform lumbar puncture unless contraindicated by mass effect, checking opening pressure, cell count with differential, protein, glucose, Gram stain, cultures, and viral PCR 1
• Add broad-spectrum antibiotics if epidural abscess suspected based on imaging 1

If Ischemic Pattern (Anterior Cord Syndrome, No Enhancement):

Supportive care is primary, as no proven acute intervention exists for spinal cord infarction 1

• Optimize spinal cord perfusion by maintaining mean arterial pressure >85 mmHg 1
• Investigate vascular risk factors including aortic pathology, cardiac embolic sources, and hypercoagulable states 1
• Consider MR angiography to evaluate spinal vasculature if vascular malformation suspected 1

Common Pitfalls to Avoid

Do not assume degenerative changes on MRI explain acute quadriparesis, as spondylotic changes are common in asymptomatic patients and correlate poorly with acute neurological deficits 5

Do not wait for contrast-enhanced MRI if surgical compression is obvious on non-contrast sequences—proceed directly to decompression 1, 2

Do not dismiss the diagnosis if initial MRI appears normal—repeat imaging in 24-48 hours if clinical suspicion remains high, as early ischemic or inflammatory changes may not be immediately visible 1

Recognize that multilevel T2 hyperintensity (≥2 segments) predicts poor surgical outcome if degenerative myelopathy, but this should not delay decompression in acute compressive scenarios 1

Prognostic Imaging Features

While managing the acute presentation, note that certain MRI findings predict outcomes:

• "Snake eyes" appearance (bilateral T2 hyperintensity in anterior horns) indicates poor prognosis 1
• T1 hypointensity combined with T2 hyperintensity at the same level suggests worse outcomes than T2 changes alone 1
• Cord expansion with T2 hyperintensity in acute setting may represent edema (potentially reversible) versus infarction/necrosis (irreversible) 6
• Resolution of T2 hyperintensity on follow-up imaging correlates with better neurological recovery 1

Multidisciplinary Coordination

Activate a coordinated team involving neurosurgery, neurology, and critical care immediately upon presentation 2

Transfer to a center with neurosurgical capabilities if not available at presenting facility, as time to decompression is critical 1, 2