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Intracranial dural fistula as a cause of diffuse MRI enhancement of the cervical spinal cord
  1. FADY G JOSEPH,
  2. PIA AMSLER,
  3. C M WILES
  1. Department of Neurology, University Hospital of Wales, Cardiff
  2. Department of Neuroradiology
  1. Dr F G Joseph Fadyjoseph{at}netscapeonline.co.uk
  1. S F S HALPIN
  1. Department of Neurology, University Hospital of Wales, Cardiff
  2. Department of Neuroradiology
  1. Dr F G Joseph Fadyjoseph{at}netscapeonline.co.uk

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We read the recent short report by Boussonet al 1 on spinal MR findings in a patient with progressive myelopathy and intracranial dural arteriovenous fistula with great interest.

MRI of lower brain and spinal cord.

We recently had a 42 year old man admitted as an emergency with a 3 week history of stepwise altered sensation in both lower limbs ascending to the torso which progressed to weakness involving his legs and hands. Two years before this he had an episode of severe backache associated with a tight band of pain around the waist and significant bilateral leg weakness. Resolution ocurred only after 4 months, when he was able to walk normally. On the current admission examination showed a spastic tetraparesis; there was minimally increased tone in the upper limbs, mild weakness of the small muscles of both hands, and marked pyramidal weakness of the legs with extensor plantar responses. He was unable to support his weight and was in urinary retention. He had a sensory level at T5 although dorsal column function was preserved.

Brain and spinal cord MRI showed increased signal in the medulla extending into the upper cervical cord down to C4 (figure). Slightly prominent vessels were seen overlying the right cerebellar hemisphere and a varix was visible close to the torcula. There was no enhancement in the cord or medulla and no abnormal flow voids in the spinal veins. The changes were thought to represent a spinal cord infarct and in view of the “stuttering” course in his history we proceeded to cerebral angiography. This showed an arteriovenous fistula supplied by the left middle and posterior meningeal artery and both occipital arteries. Venous drainage was into prominent varices lying just to the left of the midline and in front of the transverse sinus and then on the transverse sinus itself.

After an unsuccessful attempt at embolisation via the arterial route, the fistula was occluded by packing the varix with Guglieni detachable coils.

He made an uneventful recovery; after 2 months of intensive neurorehabilitation he recovered full function in his upper limbs and now has sufficient power in his legs to be able to walk with the aid of crutches.

This case emphasises that an intracranial arteriovenous fistula should be included in the differential diagnosis of increased signal on MRI of the cervical cord, even when dilated veins are not, as in this case, very apparent. Prodromal symptoms can occur and a careful history in a patient with ascending paraparesis and tetraparesis is essential. Endovasculaar occlusion at these fistulae can lead to useful inprovement in neurological function.

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