Hopping-type forelimb lameness when ridden
Most forelimb lameness is readily apparent when a horse is trotted in hand or on the lunge. Occasionally lameness is only apparent ridden, for example associated with proximal suspensory desmitis. However there is a category of forelimb lameness which is only apparent ridden and is characterised by a hopping-type gait, as if the horse wants to break to canter. Such lameness is usually much more obvious on one rein than the other, and may be sensitive to the diagonal on which the rider sits. The lameness may deteriorate with repeated exercise and affected horses may become increasingly reluctant to work due to pain. These cases are frustrating to investigate. Generally there is no response to any local analgesic technique up to and including the shoulder. Radiographic examination of the neck and cranial thoracic vertebrae, shoulder, elbow, cranial ribs and sternum reveals no detectable abnormality. Scintigraphic and ultrasonographic examinations are negative. Such horses do not respond to rest, physiotherapy, chiropractic treatment, acupuncture or non-steroidal anti-inflammatory drugs.
An 11 year old Irish draft cross Thoroughbred gelding Novice event horse, which had been in the owner’s possession for six years, showed a progressive deterioration in its performance during the five months prior to presentation.
There was slight enlargement of the cranial aspect of the left brachium compared with the right, but no pain on palpation or manipulation of the limb. The horse sometimes stood with the left forelimb slightly caudal to the right forelimb, especially immediately after work. When examined moving in hand at trot on a hard surface in a straight line, the horse had a stiff, stilted hindlimb gait. On the lunge on a soft surface the horse showed limited hindlimb impulsion and was inclined to become disunited in canter. On a firm surface on the lunge the horse shortened its forelimb stride length and was unbalanced, tending to look to the outside of the circle, taking intermittent marginally lame steps (grade 1/8) on the left forelimb on the left rein.
When ridden there was a stiff hindlimb gait and limited hindlimb impulsion and engagement, with right hindlimb lameness predominating (grade 3/8). The horse was on the forehand in trot and canter, and took intermittent hopping steps on the left forelimb, as if it was about to break into canter, especially on the left rein.
Left front palmar digital nerve blocks improved the horse’s balance on the lunge on a firm surface. Left front palmar (at the base of the proximal sesamoid bones) nerve blocks abolished the lameness on the lunge, but there was no change in the hopping-type lameness when ridden.
Right hind plantar (at the junction of the proximal ¾ and distal ¼ of the metatarsus) and plantar metatarsal nerve blocks did not influence the right hindlimb lameness. The hindlimb gait in both trot and canter was substantially improved after bilateral perineural analgesia of the deep branch of the lateral plantar nerve, and further improved by infiltration of local anaesthetic solution around the left and right sacroiliac joints. The hopping-type left forelimb lameness when ridden became more consistent and severe.
Palmar metacarpal (subcarpal) nerve blocks, median and ulnar nerve blocks, and intra-articular analgesia of the elbow and shoulder joints did not alter the hopping-type left forelimb lameness.
Radiographic examination revealed a thin, broad, curvilinear mineralised radiopacity, convex cranially, cranial to biceps brachii (Fig.1). Ultrasonographic examination revealed a thin, curvilinear echogenic line, consistent with bone, cranial to the intertubercular bursa, caudal to the braciocephalicus muscle, creating some acoustic shadowing over the central portion of the intertubercular bursa and the tendon and muscle of biceps brachii. No abnormality of the tendon or muscle of biceps brachii, the intertubercular bursa or the brachiocephalicus muscle was detected. This bone plate (Fig. 2) is typical of heterotopic ossification in man, and was believed likely to be the cause of the hopping-type forelimb lameness.
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