A rider may feel a change in their horse’s performance during ridden exercise, but when assessed moving in hand, the horse is not detectably lame. Some people then use the term ‘bridle lameness’, with the assumption that the gait irregularity is in some way caused by the rider and is not related to the horse’s discomfort. It is certainly true that an excessively large rider who does not ride in synchrony with a horse can induce gait asymmetry, which, over time, may become a permanent lameness. However, it is also true that a primary pain-related lameness may only be apparent when ridden or manifest as a change in performance. For example, a horse may have difficulties in left shoulder-in, or in canter flying changes, or simply it may become more difficult to turn in one direction compared with previously.
I am going to describe two case scenarios which I believe highlight the importance of ridden exercise as part of a lameness investigation.
An Intermediate event horse started to show a left forelimb lameness which varied in severity. According to the rider, the lameness was consistently apparent on the left rein when the horse was ridden. When examined by a veterinarian, a low-grade left forelimb lameness was seen in hand. Nerve blocks were performed, and lameness was improved but not abolished when the carpal region was desensitised. Nothing obvious was found to explain the cause of lameness when this area was examined using radiography (x-rays), ultrasonography or magnetic resonance imaging. The horse had a six months period of rest and rehabilitation, but as soon as ridden work was resumed, the left forelimb lameness recurred.
Routine palpation revealed a marked pain response in the caudal neck region on the left side. No lameness was detectable in hand. On the lunge, the horse showed variable left forelimb lameness on the left rein associated with spontaneous changes in head and neck position. If the horse stretched its’ head and neck down, no lameness was apparent, but when the head and neck were in a neutral position, the horse showed left forelimb lameness. When ridden to a contact, left forelimb lameness was consistently apparent; in the walk, the horse took markedly shorter steps with the left forelimb compared with the right forelimb. The horse was more uncomfortable in 10m diameter circles in rising trot compared with trotting around the periphery of the arena, tilting the head with the nose to one side. The horse had a very irregular rhythm in the left shoulder-in and was resistant. However, if ridden on a long rein, the horse stretched down the head and neck, and the lameness immediately improved dramatically. This combination of clinical features raised a high suspicion of primary neck pain as the cause of lameness when ridden.
Desensitising the foot using nerve blocks ironically resulted in the development of left forelimb lameness in hand, which was also associated with the horse’s head and neck constantly being tipped to one side. Although desensitisation of the carpal region did produce a mild improvement in the lameness seen in hand, the horse kept shaking its head, and there was absolutely no change to the horse’s ridden performance or the lameness. We have previously observed that forelimb lameness associated with nerve root compression is often only apparent when ridden, or is substantially worse when ridden compared with in hand, and is altered by head and neck position. It was concluded that the left forelimb lameness seen when the horse was ridden was highly likely due to cervical nerve root compression.
A Novice event horse had progressively deteriorated in its flat work, becoming increasingly difficult, although had continued to jump impressively well. This had culminated in a top-ranking international rider being bucked off during a dressage test. It was suggested that the horse may have a brain tumour, so the head had been scanned with negative results. Further investigation included a whole-body bone scan, the results of which were equivocal. Gastroscopy revealed severe gastric ulceration, and the horse received five complete courses of treatment combined with appropriate management changes (for example, turn out for 22 hours daily). The horse was assessed moving in hand both subjectively and objectively using ‘The lameness locator’, and a low-grade lameness was identified. Some nerve blocks were performed with no apparent improvement in the low-grade lameness. The hindlimb suspensory ligaments were scanned and were deemed to be normal.
The owner was at her wit’s end. She correctly assumed that the recurrent gastric ulceration must be the result of a stressor which had not been identified. The horse was evaluated ridden by a second professional rider, who had taken over the ride several months previously. The horse was difficult, resistant, bucking and kicking out, rearing, spinning, and when it did go forwards, had an unsteady head carriage, a ‘stiff’ back and took short forelimb and hindlimb steps. The horse could only be assessed in trot because it would not canter.
Sequential nerve blocks were performed, and the horse was reassessed ridden. After desensitisation of the front feet, the hindlimb suspensory ligaments and infiltration of local anaesthetic solution around the sacroiliac joints, the horse’s performance was transformed. The horse took much longer steps both in front and behind, was much more forward going, showed no resistances, and did not buck, rear, spin or kick out. The horse went forwards willingly in both trot and canter. The rider said that the horse had never previously been so compliant; he had never previously felt such range of motion of the lumbar region (swing behind the saddle); he had never previously felt that he could communicate with the horse via the reins because the horse had been ‘wooden in the mouth’, but now the horse was responsive.
The final diagnosis was bilateral front foot pain; bilateral hindlimb proximal suspensory desmopathy, and lumbosacroiliac joint region pain.
These two very different examples show the value of ridden exercise as part of an investigation of lameness or poor performance. Seeing a horse ridden does add in some variables that may complicate the situation, such as saddle fit that does not fit correctly (for example, tight tree points) and rider ability, balance and straightness. However, despite this, I believe that ridden exercise is a vitally important part of lameness investigation (unless a horse is too lame to be ridden) or poor performance assessment. The clinical problems experienced by a rider need to be understood in order to reach an accurate diagnosis, on the basis of which a treatment and management strategy can be devised.
Copyright Sue Dyson, 2023
Sue Palmer, aka The Horse Physio, is an award-winning ACPAT and RAMP registered Chartered Physiotherapist, an Intelligent Horsemanship Recommended Trainerand holds an MSc. Formerly a competitive rider and BHSAI, she works full-time treating horses. Sue shares her passion for ethical and harmonious horsemanship through multiple courses, books, and articles. Sign up at www.thehorsephysio.co.uk to be the first to hear about new releases.
Available as an in-person, hands-on course with or without your own horse. Contact Sue for dates, venues and availability.
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Other online courses coming soon include:
Confidence from the ground: Exercises for the horse owner
Finding the sore spot: Exercises for the horse owner
Pole work: Exercises for the horse owner
Warm-up: Exercises for the horse owner
Stretching: Exercises for the horse owner
Easing stiffness: Exercises for the horse owner
“Harmonious Horsemanship: How to use the Ridden Horse Ethogram to Optimise Potential, Partnership, and Performance” (due for release summer of 2023)
Coming soon: 100 Handy Hints On Horsemanship (with illustrations by Sarah Brown)
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