A 62-year-old man presents with progressive spastic gait, weakness and atrophy of the hands, and a positive Hoffman sign. On sagittal T2-weighted MRI of the cervical spine, the structure marked **A** (cervical spinal cord) shows intermediate signal intensity within hyperintense CSF, with focal T2-hyperintense signal within the cord at the C5-C6 level. Which of the following best explains the clinical presentation and imaging finding?

Explanation

## Why option 1 is correct Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults over 55 years. The clinical triad of **upper motor neuron signs in lower limbs** (spastic gait, hyperreflexia), **lower motor neuron signs in upper limbs** (atrophy, weakness, positive Hoffman sign), and progressive course is pathognomonic for CSM. The T2-hyperintense signal within the cervical cord (**A**) represents myelomalacia—irreversible neuronal loss and demyelination from chronic compression by osteophytes, disc bulging, and hypertrophic ligamentum flavum. This finding mandates urgent surgical decompression (ACDF, laminectomy, or laminoplasty) to prevent further irreversible changes, though established myelomalacia does not reliably reverse post-operatively. The intermediate signal of the normal cord within hyperintense CSF is the expected baseline appearance on T2-weighted imaging (Gray's Anatomy 42e Ch 23; Harrison 21e Ch 446). ## Why each distractor is wrong - **Option 2 (MS)**: While MS can affect the cervical cord, plaques are typically dorsolateral, **<2 vertebral bodies in length**, and occupy **<50% of cord cross-sectional area**. MS is treated with interferon-beta, fingolimod, or natalizumab—agents that **worsen NMOSD**. The clinical picture of lower motor neuron signs in the upper limbs with spastic gait in a 62-year-old is far more consistent with degenerative CSM than demyelinating disease. - **Option 3 (NMOSD)**: NMOSD presents with **longitudinally extensive transverse myelitis** (≥3 vertebral bodies), often involving >50% of cord cross-sectional area, and is aquaporin-4 antibody positive in 80%. While the T2-hyperintense cord signal could superficially resemble NMOSD, the clinical presentation (Hoffman sign, lower motor neuron hand atrophy in an older patient) and the degenerative imaging context (vertebral body C5, disc C5-C6) point to spondylotic compression, not autoimmune demyelination. Critically, NMOSD requires different treatment (rituximab, eculizumab, satralizumab) and interferon-beta would be contraindicated. - **Option 4 (Syringomyelia)**: Syringomyelia presents as a fluid-filled cavity (syrinx) within the cord, often secondary to tethering, trauma, or spinal cord infarction. While T2-hyperintensity can be seen, syringomyelia does not typically produce the mixed upper and lower motor neuron signs in this distribution, nor is it the most common cause of cord dysfunction in this age group. Management is conservative unless there is progressive neurological decline. **High-Yield:** T2-hyperintense signal within the cervical cord on MRI = myelomalacia (irreversible) in CSM; **early surgical decompression is indicated for symptomatic CSM before cord signal changes become irreversible**. Distinguish MS (dorsolateral, <2 bodies, <50% area) from NMOSD (longitudinally extensive, ≥3 bodies, >50% area, AQP4+) because interferon-beta/natalizumab worsen NMOSD. [cite: Gray's Anatomy 42e Ch 23; Harrison 21e Ch 446]