Spinal Cord Compression (Compression of Spinal Cord)
The most likely diagnosis is A - Compression of Spinal Cord. The combination of lower limb weakness, a defined T10 sensory level, urinary retention, and subacute progression over 3 days is pathognomonic for spinal cord pathology requiring emergency imaging and neurosurgical evaluation 1.
Clinical Reasoning
Why Spinal Cord Compression is Most Likely
A defined sensory level at T10 is the critical diagnostic feature that localizes pathology to the spinal cord itself, not peripheral nerves or nerve roots 1.
The acute onset over 3 days with bilateral lower limb weakness and urinary retention indicates an evolving myelopathy requiring emergency intervention 1.
The combination of motor, sensory, and autonomic dysfunction at a specific spinal level is pathognomonic for spinal cord pathology 1.
Urinary retention is a classic presenting feature of spinal cord compression, representing disruption of sacral spinal cord segments S2-S4 which control bladder function 2, 3.
Why Other Diagnoses Are Less Likely
Guillain-Barré Syndrome (Option B) is unlikely because:
GBS typically presents with ascending weakness starting distally in the legs, progressing upward over days to weeks 4.
GBS causes areflexia due to peripheral nerve involvement, whereas spinal cord compression typically causes hyperreflexia (though early spinal shock may cause temporary areflexia) 4.
GBS does not produce a defined sensory level like T10; it causes a stocking-glove sensory pattern 4.
The site of lesion in GBS is peripheral nerves and nerve roots (polyradiculoneuropathy), not the spinal cord 4.
Transverse Myelitis (Option C) is possible but less likely because:
Transverse myelitis typically follows a viral infection or immune-mediated process 1.
The absence of infectious prodrome makes structural compression more likely in this acute presentation 1.
While transverse myelitis can present similarly, it is a diagnosis of exclusion after ruling out compressive lesions 1.
Cauda Equina Syndrome (Option D) is incorrect because:
Cauda equina syndrome affects lumbosacral nerve roots below L1-L2, causing lower motor neuron signs with areflexia 1, 4.
A T10 sensory level is too high for cauda equina syndrome, which would produce saddle anesthesia and lower lumbar/sacral dermatomal patterns 1, 4.
The site of lesion in cauda equina is lumbosacral nerve roots, not the thoracic spinal cord 4.
Immediate Management Algorithm
Step 1: Emergency MRI
Obtain MRI of the entire spine without and with contrast immediately to differentiate between compressive lesions and non-compressive myelopathy 1, 4.
Do not delay imaging - spinal cord compression requires urgent surgical decompression within hours to prevent permanent neurological deficit 1.
Step 2: Urgent Neurosurgical Consultation
Contact neurosurgery immediately upon clinical suspicion, as timing of decompression is critical for neurological recovery 1.
Early surgical decompression within 24 hours is associated with better functional outcomes in compressive myelopathy 1.
Step 3: Bladder Management
Initiate intermittent catheterization for urinary retention 2.
Avoid indwelling catheters when possible to reduce infection risk 2.
Critical Pitfalls to Avoid
Do not assume lumbar pathology based solely on lower limb symptoms - cervical and thoracic cord compression can present with isolated lower extremity findings 5, 6.
Do not wait for additional testing before obtaining MRI if spinal cord compression is suspected clinically 4.
Do not misinterpret early areflexia as evidence against spinal cord injury - spinal shock can cause temporary areflexia before reflexes become hyperactive 4.
Do not focus only on the sensory level - image the entire spine, as cervical lesions can present with lower limb symptoms only 5, 6.