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RA Cervical Spine Emergency — SCE Rheumatology MCQ

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HardRheumatology EmergenciesRA Cervical Spine EmergencySCE Rheumatology

A 48-year-old woman with longstanding rheumatoid arthritis and known atlantoaxial instability develops increasing upper-neck pain, right-sided partial ptosis, miosis and facial anhidrosis. Examination also shows brisk lower-limb reflexes and bilateral extensor plantar responses. There is no vertigo, nystagmus, dysphagia or crossed sensory loss. MRI demonstrates asymmetric right posterolateral compression of the upper cervical cord by C1–C2 instability and retro-odontoid pannus. What is the most likely mechanism of her Horner syndrome?

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Correct answer: A — Interruption of descending right hypothalamospinal sympathetic fibres by upper cervical cord compression

The correct answer is A. Ocular sympathetic first-order fibres descend ipsilaterally from the hypothalamus through the brainstem and upper cervical cord before terminating at C8–T2. Asymmetric cord compression from rheumatoid C1–C2 instability and retro-odontoid pannus can therefore interrupt these fibres, producing ipsilateral Horner syndrome. The bilateral pyramidal signs independently support cervical myelopathy. Vertebral artery compromise could cause a lateral medullary infarction, but associated vestibular, bulbar, cerebellar or crossed sensory signs would be expected. Cluster headache causes severe orbital or temporal attacks rather than progressive neck pain with myelopathy. A cavernous sinus lesion affects postganglionic fibres and would usually cause ocular motor abnormalities; facial anhidrosis is less likely because facial sudomotor fibres have already separated along the external carotid route.

Reference: Khan Z, Bollu PC. Horner Syndrome, Anatomy section. StatPearls, updated 2026. https://pubmed.ncbi.nlm.nih.gov/29763176/