A 68-year-old patient with a 3‑day history of bilateral leg weakness, brisk deep‑tendon reflexes, urinary retention, inability to walk, and a sensory level at the T10 dermatome—what is the most likely diagnosis?

Diagnosis: Spinal Cord Compression

The most likely diagnosis is D. Cord compression. This 68-year-old patient presents with the classic triad of acute spinal cord pathology: bilateral leg weakness with upper motor neuron signs (brisk reflexes), a sensory level at T10, and urinary retention—all pointing to a compressive myelopathy requiring urgent neurosurgical evaluation 1.

Critical Distinguishing Features

Why Cord Compression is Most Likely

• Upper motor neuron signs are the key: Brisk (hyperactive) reflexes in both legs indicate the lesion is above the lower motor neurons, localizing pathology to the spinal cord itself rather than peripheral nerves or nerve roots 1
• Sensory level at T10: A clear dermatomal sensory level is pathognomonic for spinal cord pathology and directly localizes the lesion to the T10 vertebral level 1
• Acute presentation with urinary retention: The combination of bilateral motor deficits, sensory level, and bladder dysfunction developing over 3 days represents a surgical emergency requiring immediate MRI to exclude compression 1
• Age and acuity favor compression: At 68 years old, malignancy (metastatic disease), epidural abscess, or degenerative disease with acute cord compression are statistically most likely 1

Why NOT the Other Options

B. Guillain-Barré Syndrome (GBS) is excluded by:

• GBS presents with areflexia or hyporeflexia, not brisk reflexes—this is a cardinal feature distinguishing peripheral nerve disease from spinal cord pathology 2, 1
• GBS causes ascending weakness starting distally in legs, not a sensory level 2
• GBS does not cause urinary retention at onset; bladder dysfunction occurs late if at all and is part of dysautonomia, not early spinal shock 2, 1
• The "sural sparing pattern" on nerve conduction studies is typical for GBS, but this patient's upper motor neuron signs make electrodiagnostic testing unnecessary 2

A. Transverse Myelitis is less likely because:

• While transverse myelitis can present with similar features (bilateral weakness, sensory level, urinary retention), it typically progresses to maximal severity over 4 hours to 21 days with a subacute course 3, 4
• Transverse myelitis is a diagnosis of exclusion—you must first rule out cord compression with urgent MRI 3, 5
• The 3-day history is compatible with both, but at 68 years old, compressive etiologies (malignancy, abscess) are far more common than inflammatory myelitis 3
• Post-infectious or parainfectious inflammation is the most common cause of transverse myelitis, but this requires excluding structural lesions first 5

C. Cauda Equina Syndrome is excluded by:

• Cauda equina affects nerve roots below L1-L2, causing lower motor neuron signs (areflexia, flaccid weakness), not brisk reflexes 1
• The sensory level at T10 is too high for cauda equina, which causes saddle anesthesia and lower lumbar/sacral dermatomal loss 1
• Cauda equina does not produce a clear sensory level; it causes patchy, asymmetric sensory loss in lumbosacral distributions 1

Immediate Management Algorithm

Step 1: Urgent MRI Spine (Within Hours)

• Order MRI of entire spine (cervical, thoracic, lumbar) without and with contrast immediately to identify cord compression, epidural abscess, tumor, or other structural lesions 1
• Do not delay imaging for any reason—this is a neurosurgical emergency 1
• If MRI shows compression, consult neurosurgery emergently for decompression 1

Step 2: Supportive Care While Awaiting Imaging

• Bladder management: Place Foley catheter for urinary retention 6
• Prevent complications: DVT prophylaxis, pressure ulcer prevention, bowel regimen 2
• Pain management: Address any radicular or neuropathic pain with gabapentinoids if needed 2

Step 3: If MRI Excludes Compression

• Consider transverse myelitis as next most likely diagnosis 3, 4
• Perform lumbar puncture for CSF analysis (cell count, protein, glucose, oligoclonal bands) to evaluate for inflammation 1, 3
• Check inflammatory markers, autoimmune panel (ANA, anti-aquaporin-4 antibodies for neuromyelitis optica), infectious workup 3, 4
• Initiate high-dose IV methylprednisolone (1 gram daily for 3-5 days) if transverse myelitis is confirmed and compression excluded 3, 5
• Consider plasmapheresis if no response to steroids 6, 7

Critical Pitfalls to Avoid

• Never assume GBS based on bilateral weakness alone—always check reflexes carefully. Brisk reflexes exclude GBS and point to spinal cord pathology 2, 1
• Do not delay MRI to obtain CSF or other tests—spinal cord compression requires surgical decompression within hours to prevent permanent paralysis 1
• Do not start steroids before imaging—if an epidural abscess is present, steroids can worsen infection and delay diagnosis 1
• Recognize spinal shock: Early acute spinal cord injury may transiently present with areflexia before reflexes become hyperactive, but the sensory level and urinary retention still localize to cord pathology 1