Case report

Spinal cord injury without radiological abnormality (SCIWORA) is well recognised in paediatric trauma.¹ The laxity and flexibility of the cervical spine in children, allows for excessive movement without bony injury and can result in cord damage without radiological abnormality. This is rare in the adult population.¹ We present a case of adult SCIWORA to highlight the importance of thorough neurological examination and early diagnosis of cord injury in trauma.

A 61 year old man fell 15 feet off a ladder, hitting his head on a brick wall. He was not rendered unconscious and was helped up to his feet by his family. The ambulance crew found him walking around in no apparent distress, but complaining of some neck pain. He was immobilised with a collar, head blocks and tape, and was transported on a spinal board to the accident and emergency department.

On arrival, he was found to be fully conscious with no evidence of significant head injury. He had a pulse of 60, his blood pressure was 150/80. He complained of pain in his neck, tingling in his arms and was unable to extend his left elbow.

He was tender over the mid-cervical spine. Initial neurological examination revealed bilateral reduction in sensation to light touch over the C6–C8 distribution and reduced power in wrist flexion bilaterally. In the lower limbs there was symmetrical reduction in sensation extending up to the T12 level. Power at the left ankle and left hallux was reduced in both flexion and extension. The tone was normal in all four limbs.

Radiographs of the cervical, thoracic and lumbar spines showed degenerative changes but no soft tissue swelling, loss of alignment or fractures (fig 1).

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Figure 1

Plain cervical spine radiographs.

Subsequent computed tomography of the cervical spine demonstrated a fracture of an osteophyte on the anteroinferior border of C3, and a small osteophytic fragment from the posterior superior aspect of C5, which had entered the spinal canal (fig 2).

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Figure 2

Computed tomography demonstrating an osteophyte fracture with fragment lying in the spinal canal at the C5 level.

After discussion with the orthopaedic consultant, the patient was given methylprednisolone and was nursed at 45 degrees in a hard collar.

Magnetic resonance imaging was performed on the following day. It demonstrated a well defined area of increased signal intensity on T2 weighting and FLAIR sequences within the cord at the level of C5. T1 weighting showed no increase in the signal pattern. These findings were considered to be consistent with localised contusion and oedema of the spinal cord at the C5 level (fig 3).

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Figure 3

Magnetic resonance imaging demonstrating spinal cord contusion at the C5 level.

Forty eight hours after admission, neurological examination revealed spasticity in the left lower limb and reduced tone in both upper limbs. Reflexes were present and brisk in both lower limbs. Power was reduced in both upper limbs with the loss being greatest in the left upper limb and in the left lower limb.

Joint position sense was reduced in both upper limbs but normal in the lower limbs. Sensation to pin prick was reduced on the left in the distribution of C6 to S4. Table 1 summarises the neurological findings.

A diagnosis of central and left anterior spinal cord syndrome at C6 level was made. A neurosurgical opinion was sought; flexion/extension views were requested. These revealed no instability of the cervical spine. Conservative treatment was advised. The patient's neurological signs did not improve.

Discussion

SCIWORA in paediatric trauma is well documented and hence clinical suspicions of spinal cord injury are not allayed by normal views of the cervical spine on plain radiographs. This case of adult SCIWORA demonstrates the importance of relying on clinical skills to identify spinal cord injury even in the non-paediatric population. Normal plain radiographs of the adult cervical spine do not exclude neurological damage in the presence of an abnormal neurological examination.

Early diagnosis of spinal cord injury is important to optimise outcome. Administration of a bolus dose of methylprednisolone (30 mg/kg) within three hours of injury followed by a methylprednisolone infusion of 5.4 mg/kg per hour for 24 hours or administration of a bolus dose of methylprednisolone within eight hours of injury followed by an infusion for 48 hours results in a significantly better neurological outcome.² In this case of adult SCIWORA methylprednisolone was administered based on the clinical findings and results of computed tomography performed on the day of admission, before definitive radiological imaging by magnetic resonance imaging.