A 58-year-old man with a 6-month history of progressive gait disturbance and clumsy hands presents to the orthopedic clinic. On examination, he has a wide-based spastic gait, hyperreflexia, positive Hoffman sign, and Lhermitte sign on neck flexion. MRI of the cervical spine shows the findings marked **A** in the diagram: disc herniation with cord compression and focal intramedullary T2 hyperintensity at the C6 level. Which of the following pathophysiological mechanisms BEST explains the neurological deficit in this patient?
A. Compression of the posterior longitudinal ligament causing isolated posterior column dysfunction
B. Demyelination of the dorsal root ganglia leading to sensory ataxia and proprioceptive loss
C. Mechanical compression of the cord combined with microvascular ischemia of the anterior spinal artery territory, causing demyelination of lateral corticospinal tracts and posterior columns
D. Inflammatory edema of the spinal cord from disc material irritation without mechanical compression
Explanation
Why option 1 is correct
The clinical anchor directly states that cervical spondylotic myelopathy (CSM) from disc herniation is caused by mechanical compression and microvascular ischemia of the cervical spinal cord. The ischemia specifically affects the anterior spinal artery territory, producing demyelination of the lateral corticospinal tracts (explaining the spastic gait and hyperreflexia) and posterior columns (explaining the proprioceptive loss and Lhermitte sign). The T2 hyperintensity (myelomalacia) at the compressive level is the hallmark imaging finding that confirms this pathophysiology. This combination of static mechanical compression with dynamic ischemic injury is the defining mechanism of CSM per AOSpine Guidelines 2017.
Why each distractor is wrong
Option 2: Dorsal root ganglion compression is not the primary pathophysiology of cervical spondylotic myelopathy from disc herniation. The cord itself is compressed, not the ganglia, and the neurological pattern (spasticity, hyperreflexia, Hoffman sign) reflects upper motor neuron signs from corticospinal tract involvement, not isolated sensory ganglion pathology.
Option 3: The posterior longitudinal ligament contributes to compression but is not the sole or primary mechanism. Moreover, isolated posterior column compression would not explain the prominent spasticity, hyperreflexia, and positive Hoffman sign, which require lateral corticospinal tract involvement. The anchor emphasizes COMBINED compression and ischemia affecting both tracts.
Option 4: Inflammatory edema alone without mechanical compression does not account for the imaging findings of disc herniation with cord compression and T2 hyperintensity myelomalacia. While inflammation may contribute, the primary driver is mechanical compression superimposed on ischemia, not inflammation in isolation.
High-YieldNEET PG
T2 hyperintensity (myelomalacia) at the compression site is an ominous sign predicting limited recovery and mandates urgent surgical decompression; it reflects irreversible demyelination from combined mechanical compression and anterior spinal artery ischemia.
AOSpine Guidelines for Degenerative Cervical Myelopathy 2017
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