Delayed presentation of severe cervical myelopathy two years post-motorcycle accident: a case report

Myelopathy, defined as spinal cord dysfunction, can arise from a variety of aetiologies, with degenerative cervical myelopathy (DCM) being the most common.¹ DCM is a progressive neurodegenerative disorder caused by spinal cord compression resulting from degenerative or congenital factors. The global adult prevalence of DCM is 2.3%, rising to 5% in individuals over 40 years of age.² Māori and Pacific peoples in New Zealand are thought to be at elevated risk of developing DCM due to narrower cervical canal dimensions.³

The clinical progression of DCM is highly variable, characterised by stepwise neurological decline followed by periods of quiescence.⁴ Given this unpredictability, early recognition of DCM-related signs and symptoms is critical to prevent irreversible neurological impairment.^1,4,5 We report a case of DCM diagnosed 2 years post-motorcycle accident, with a 1-year history of progressively worsening symptoms.

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Case report

A 43-year-old Māori male presented to a secondary care orthopaedic spine centre with a 2-year history of persistent neck pain and bilateral C6 radicular arm pain. Over the past year, these symptoms had worsened, and the patient developed fine motor skill impairment, upper limb weakness, balance impairment and urinary incontinence, significantly affecting his ability to work and ambulate.

His medical history revealed a motorcycle accident 2 years prior, which resulted in a traumatic brain injury and skull and rib fractures. No cervical cord injury was diagnosed at that time. One-year post-accident, an MRI was arranged by a neurosurgeon for bilateral radicular arm pain, revealing multi-level neuroforaminal narrowing and mild C4/5 spinal cord compression (Figure 2a). Surgery was not indicated at the time due to a lack of clinical DCM features, and epidural steroid injections were administered for radicular pain, providing only temporary relief.

Upon examination at the orthopaedic spine centre 1 year later, examination revealed a wide and unsteady gait, positive Romberg’s sign, global hyperreflexia, bilateral Hoffman’s and inverted supinator signs. Upper limb weakness was generalised but most marked for wrist extension, flexion, and finger abduction bilaterally. Repeat MRI (Figure 2b) demonstrated progressive C4/5 cord compression with myelomalacia and multi-level neuroforaminal compression. His modified Japanese Orthopaedic Association score was 11/18, indicating severe DCM, necessitating surgical decompression. The patient was scheduled for a C4/5 anterior cervical discectomy and fusion at the time of writing this report.

Discussion

DCM is a progressive condition that, if not diagnosed early, can lead to chronic disability,⁵ unemployment and diminished quality of life.⁶ Surgical decompression, indicated for moderate, severe or progressive cases, aims primarily to halt further deterioration rather than reverse existing deficits.⁷ Early recognition and timely referral for evaluation are crucial to prevent irreversible impairment.^1,4,5

Key DCM symptoms include hand numbness, paraesthesia, dexterity loss, clumsiness and balance disturbances,⁸ with diagnostic signs such as hyperreflexia and positive Babinski, Hoffman, clonus and inverted supinator reflexes.⁹ Cervical spine MRI is necessary to correlate clinical findings with MRI evidence of cord compression.^1,7

In this case, despite the absence of initial DCM features, symptoms worsened over the year, emphasising the importance of serial symptom monitoring and patient education when spinal cord compression is suspected or identified.⁷ Educating patients on symptoms necessitating urgent surgical reassessment facilitates timely intervention.⁷ Understanding of DCM among New Zealand primary care clinicians is reportedly low.¹⁰ Improving knowledge within primary care clinicians, in collaboration with surgical specialists, would facilitate patient education and monitoring, while maintaining a low referral threshold for surgical evaluation.

Conclusion

This case emphasises the importance of ongoing monitoring and patient education in individuals with suspected DCM or asymptomatic spinal cord compression. Early recognition of DCM should prompt referral for diagnostic and surgical evaluation. Future research should aim to develop clinical criteria to aid the timely recognition of DCM in primary care and community settings.