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Recanalisation of spinal dural arteriovenous fistula after successful embolisation
  1. D BIRCHALL,
  2. D G HUGHES
  1. Department of Diagnostic Radiology, Hope Hospital, Stott Lane, Manchester M6 8HD, UK
  2. Department of Neurosurgery
  1. Dr D G Hughes dhughes{at}fsl.ho-man.ac.uk
  1. C G H WEST
  1. Department of Diagnostic Radiology, Hope Hospital, Stott Lane, Manchester M6 8HD, UK
  2. Department of Neurosurgery
  1. Dr D G Hughes dhughes{at}fsl.ho-man.ac.uk

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A 55 year old man presented with a 3 month history of progressive sensorimotor paraparesis. Examination showed a spastic paraparesis with grade III weakness and a sensory level at T11.

Sagittal gadolinium enhanced T1 weighted images showed multiple areas of enhancement within the spinal canal posterior to the lower thoracic spinal cord (arrow, figure A), and 3D phase contrast magnetic resonance angiography obtained in the coronal plane confirmed dilatation of the coronal venous plexus. Selective angiography of the right seventh intercostal artery showed a spinal dural arteriovenous fistula (AVF) arising from a spinal ramus branch (small arrow) and draining into a hypertrophied coronal venous plexus (large arrows, figure B). Transcatheter embolisation using 30% N-butyl-cyanoacrylate achieved complete occlusion of the lesion (figure C), and the patient initially made a clinical improvement.

The patient's paraparesis recurred within 6 months, at which stage surgery showed recanalisation of the AVF (white arrow, figure D). The ghost of a collateral collapsed coronal plexus was noticed (black arrow, figure D), a remnant from the previous embolisation. The draining medullary vein from the AVF was identified and transected, and the patient made a good postoperative recovery with gradual improvement in his neurological status.

Sneha-India and the International Council for Research into the Fetal Origins of Adult Disease

First World Congress

Fetal Origins of Adult Disease

Sponsored by the British Medical Journal

2-4 February 2001, Mumbai, India

Poor fetal growth is associated with an increased risk of adult cardiovascular disease and diabetes, which has led to the hypothesis that these disorders originate through undernutrition in utero. Evidence also links fetal growth with later osteoporosis, neurological and psychiatric disease, hormone related cancers, and atopy. This conference will bring together, for the first time, clinicians, epidemiologists, and basic scientists working in this field.

Topics include:

Cardiovascular disease, diabetes, cancer, osteoporosis, asthma, aging, mental health, maternal nutrition, control of fetal growth, placenta, hormonal programming, immune function, neural programming, strategies for preventing disease.

Plenary speakers include:

Claude Lenfant (USA), Nick Hales (UK), Christopher Martyne (UK), Chittaranjan Yajnik (India), Michael Meaney (Canada), Jeffrey Robinson (Australia), Jane Harding (New Zealand), Kent Thornburg (USA), John Challis (Canada), Alan Jackson (UK), Keith Godfrey (UK), Patrick Bateson (UK), Peter Gluckman (New Zealand).

Scientific committee chairman: David Barker, Southampton, UK

Organising committee chairman: Anand Pandit, Pune, India

Further details from: Ms Alifiya S Motiwala

tel: 00 91 22 651 6439 / 645 6763

fax: 00 91 22 651 6438

email: mrcssc{at}vsnl.com

Alternatively, fill in the ‘Yes, I am interested’ reply slip on our website:

www.sneha-india.org

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