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THE enigma of foot lameness in the horse has puzzled veterinary surgeons since the dawn of the profession. Navicular disease emerged as a recognised disease back in the mid-19th century, but understanding of the precise pathophysiology has proved elusive. There have been many false dawns. The description of the thrombosis theory as a unifying explanation for lameness and ‘navicular changes’ as seen on radiographs was one such example (Colles 1982). Another was the discovery that intra-articular analgesia of the coffin (distal interphalangeal) joint abolished lameness in a large proportion of horses with foot lameness (Dyson 1991). Surely, this was the problem – it was osteoarthritis of the coffin joint all along. However, first, a poor response to medication was documented (Dyson 1991). This was followed by clinical evidence that horses with lameness localised to the navicular bursa by local analgesia also responded in approximately 90 per cent of cases to intra-articular analgesia of the coffin joint (Dyson and Kidd 1993). Then there was the discovery that intra-articular analgesia of the coffin joint consistently resulted in analgesia of the heel of the foot, and further, if a large volume of local anaesthetic was used, this would result in analgesia of the whole of the sole (Schumacher and others 2006). Finally, experimental evidence confirmed unequivocally that amphotericin-induced synovitis of the navicular bursa could be alleviated by intra-articular analgesia of the coffin joint (Pleasant and others 1997).
In 1998, Wright and others described core lesions of the deep digital flexor tendon, and fibrillation of …
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