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Spinal vascular disease: a neglected cause of myelopathy
  1. Robin S Howard
  1. Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Correspondence to Dr Robin S Howard, Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK; robinhoward{at}nhs.net

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Recent reviews of both spinal cord infarction and spinal dural arteriovenous malformations have highlighted the importance of vascular disease as a cause of acute or chronic myelopathy.1–3 Spinal cord stroke is generally encountered following aortic surgery, aortic dissection or after periods of prolonged hypotension associated with advanced vascular disease. Fibrocartilage embolism is a rare but important cause of spinal cord infarction, particularly in young people where the consequences can be devastating. Retrograde embolisation of fragments of the nucleus pulposus from the vertebral vasculature to the radiculomedullary arteries is provoked by physical exertion, trauma and Valsalva manoeuvre, and may account for 5% of spinal cord infarction.4

Spinal cord infarction generally affects the anterior spinal territory and causes a sudden flaccid paralysis associated with areflexia, loss of sensation to pain and temperature, and autonomic deficits (atonic bowel/bladder, paralytic ileus and loss of sphincter tone). There is often acute back pain at the onset, usually at the level of the lesion.5 Dorsal column function is generally well preserved although there is considerable variability. Other acute presentations of cord infarction include respiratory failure, posterior spinal artery territory infarction causing loss of proprioception, complete transverse cord infarction with loss of all motor, sensory and autonomic modalities below the lesion, Brown-Séquard syndrome and central cord involvement. Following spinal surgery, urgent spinal imaging is essential to exclude compressive epidural haematoma.

New spinal cord infarction diagnostic criteria emphasise three major components: first, the rapid development of severe deficits within 12 hours; second, MR imaging excluding compression; and third, cerebrospinal fluid (CSF) showing no inflammatory changes. The MR imaging is normal in about a third of patients, but characteristic abnormalities may include T2 hyperintensity ‘owl eyes’, pencil-like …

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