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Is it an inflammatory myelopathy?
  1. Tarig Abkur1,2,
  2. Mark Silva1
  1. 1 Department of Neurology, Gloucestershire Royal Hospital, Gloucester, UK
  2. 2 Department of Neurology, Southmead Hospital, Bristol, UK
  1. Correspondence to Dr Tarig Abkur, Department of Neurology, Gloucestershire Royal Hospital, Gloucester, UK; tarig.abkur1{at}

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A 65-year-old right-handed retired male firefighter presented following a fall. He had a 3-month history of scrotal paraesthesia that had insidiously evolved to bilateral leg weakness. Following hospital admission, he developed acute urinary retention requiring catheterisation.

He had a history of ulcerative colitis, which was well controlled with mesalazine. He was an ex-smoker and did not drink alcohol.

Cranial nerve and upper limb examinations were unremarkable. On lower limb examination, tone was normal. He had mild (Medical Research Council grade 4/5) bilateral and symmetrical weakness involving hip and knee flexion, and ankle dorsiflexion. There was a sensory level to T7. Joint position was impaired in the lower limbs, and vibration sense was absent below the xiphisternum. Knee and ankle jerks were absent, and plantar responses were mute.

Question 1. What is the most likely site of the lesion?

Although there were no obvious upper motor neurone signs, three clinical signs on lower limb neurological examination suggested localisation to the spinal cord. Firstly, the presence of a sensory level at T7 implied involvement of the thoracic cord. Secondly, the pyramidal pattern of weakness (flexors preferentially affected more than extensors in the lower limbs) suggested corticospinal tract dysfunction, and finally, the acute sphincter dysfunction in the context of lower limb weakness pointed to involvement of the lower cord. It is important to keep in mind that peripheral lesions affecting the cauda equina may also present with a sphincter disturbance, but this would not explain the sensory level.

Cord pathologies can present without upper motor neurone signs particularly in the acute phase (spinal shock). However, this patient’s symptoms had started 3 months before admission. Conus medullaris lesions often have a mixture of upper and lower motor neurone signs with early sphincter dysfunction. Nevertheless, if this patient has a lesion involving the conus medullaris it would have to extend upwards to T7 to explain the …

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  • Contributors TA drafted the article and reviewed the literature. MS acted as a senior author and reviewed the manuscript for important intellectual content.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Provenance and peer review. Not commissioned. Externally peer reviewed by Holger Allroggen, Coventry, UK.

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