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© James Rooney, D.V.M. Gradual loss of function of the suspensory ligament of the hindleg of the horse has been recognized for many years. In earlier times it was most often seen in older horses, particularly older, multiparous mares. The sinking of the hind fetlocks became more apparent late in pregnancy. It often, but not always, seemed to disappear – return to normal – after parturition. In recent years such loss of function has been seen in younger performance horses, particularly the Paso Fino and particularly the Peruvian Paso Fino. While egg bar shoes seem to help some of these horses, the condition appears to be essentially irreparable. By loss of function I mean loss of strength of the suspensory, loss of the ability to maintain the fetlock joint in its usual, normal position. It should be noted that the suspensory ligaments, both fore and hind, are really highly modified muscles, the mm. interossei. While they are largely composed of tendinous tissue, there is muscle present, Figure 1. 
Figure 1: Schematic frontal view of suspensory showing the location of the muscular tissue. It is also noted that there are histological features of the tendinous tissue which are somewhat different from that seen in other tendons. The nuclei of the tenocytes have the characteristics of chondroid cells . While that suggests an adaptation to frequent and/or continuous movement, the significance of these differences remains to be determined. Old Mare To my knowledge there has been no serious study of the suspensory ligaments of older mares. I regret that I did not get around to that while still active in the postmortem room. Perhaps some younger pathologist will undertake the task. Since many of these older mares “recover” normal fetlock angulation after parturition, there may not be obvious structural, anatomical changes in all cases. Tendons and ligaments lose strength to varying degrees with age and in vitro tests of suspensory strength in affected and normal older mares would be of interest. What is apparent is that the weight of the foal in utero, is directly related to the sinking of the hind fetlocks late in gestation. That will be of importance later in our discussion. Younger Horses I know that damaged suspensories from Paso Fino horses have been examined pathologically. Unfortunately, threats of legal action apparently caused a prominent university (which should have done better) to stop publication of the results. There are, also, specimens of damaged suspensories in fixative in various people’s hands, but I have been unable to obtain any for examination. What I suggest for pathogenesis, therefore, cannot address all the possibilities which thorough pathological study might raise. Pathogenesis Pathogenesis is the study of the development of a disease process. Often, and certainly in the case of suspensory dysfunction, we do not have complete information and, so, cannot completely develop the natural history of the disease process. What we can do is take the information we have and try to construct a reasonable and coherent history as far as possible. Once that is done, the gaps which have to be filled will be more readily apparent. As already mentioned old mares show evidence of at least temporary suspensory dysfunction during the latter stages of gestation. This may be related immediately to the increasing weight of the fetus, shifting the center of mass of the horse toward the hind quarters, Fig. 2, and thereby increasing the static loading of the hindlegs. An equally efficient way to increase the static loading of the hindlegs is to move the feet forward beneath the body, Figure 3.
The shifting of the hind feet under the body is one of the principal features of the process of collection. As discussed in some detail in Rooney 1998 (The Lame Horse) collection is the normal response of the horse to a scary situation. Collection renders the animal alert: head and neck raised, feet under the body and ready to perceive, analyze and react immediately by flight to a dangerous situation. As riders know, collection is a reflex chain process which can be elicited and maintained by the appropriate use of the reins and leg aids. Collection is induced in this way because the horse is more alert and ready to move in a coordinated, graceful manner. If a horse, performing as required, works in the collected manner, the hindlegs are carrying more weight (load) than if not collected. If the work period is prolonged, obviously the horse is carrying that additional weight on the hindlegs for a considerable period of time. Such rather prolonged periods of collected work seem to be characteristic for the Paso Fino horse, for example. In an unforced situation such as free in field or paddock the horse only collects itself when a suddenly interesting or threatening situation occurs. The collected condition is maintained only briefly and not for the prolonged periods enforced by trainer/riders. If, in addition, the rider sits back in the saddle, in back of the line of action of the center of mass of the horse, additional load is added to the hindlegs.. This style of riding is adopted, I presume, in order to reduce the load on the forelegs thereby allowing flashier, higher-going movement of the forelegs. This strategy seems to be one employed by saddle horse riders as well, particularly, with three-gaited saddle horses. Why The Suspensory? A reasonable question is why the suspensory is affected and not the superficial or deep flexor tendons. The answer is a bit complicated, particularly if you are not too familiar with anatomy. With increasing loading of the leg, the fetlock dorsiflexes, and tension increases in all three tendons. The fetlock dorsiflexion, however, is accompanied by coffin joint plantar flexion, and that flexion decreases the tension in the deep flexor tendon. The superficial and deep flexor tendons – but not the suspensory – are tied together through the metatarsus (from hock to fetlock) by heavy deep fascia. As the load on the leg increases, then, the suspensory undergoes greater strain (becomes tenser). The tension in the superficial flexor and deep flexors increases also because of fetlock dorsiflexion. The tension in the deep flexor is decreased by coffin plantar flexion, however, and since the deep and superficial flexors are tied together by deep fascia, neither experiences the amount of tensile increase experienced by the independent suspensory. In other words the increasing tension in the superficial and deep flexor tendons caused by fetlock dorsiflexion is countered in part by the decreasing tension caused by coffin plantar flexion. Heredity Is what I have said all there is to it? Is it all environment – the way the horse is ridden and worked? The straight-out answer is that the answer is not known. The greater frequency of the problem in the Peruvian Paso Fino suggests, but certainly does not prove, that there is an hereditary component. Experience indicates that most abnormal conditions in all animals are not a function of environment alone but of the variable interaction of environment and heredity. The genetic part could be as follows. The Paso Fino works collected. If one selects for breeding the most successful animals, they will be the ones who either collect “best” or who are already, built (by conformation; e.g., heredity) in a more collected fashion: that is, the short-coupled individual with a strongly sloping croup and a tendency to sickle hocks. The story here is not unlike that for swayback in American Saddlebreds which I shall address in another piece. Pedigree information on horses affected and not affected with suspensory dysfunction certainly exists. Such data could be placed in the hands of a geneticist for careful analysis. (I hasten to note that I am not a geneticist and not qualified to undertake such an analysis.) Posterior tibial tendon dysfunction is a condition in the human which may be analogous to suspensory dysfunction in the horse. Unfortunately, the cause of that condition in man is not known either. Bottom Line It would be nice to offer an easy solution for suspensory dysfunction in the young horse. Obviously, with the information presently available that is not possible. I do not intend to preach on this subject (or any other, for that matter!), but the solution – easy or otherwise – is in the hands of horse owners and their breed organizations. What has been done here is to show the role mechanics can or might play in the pathogenesis of the condition. There is obviously more to be learned. Mosier et al. Pathoanatomy and Etiology of Posterior Tibial Tendon Dysfunction. Clinical Orthopaedics and Related Research. 365:12-22. 1999. Return to the Hoof Anatomy & Physiological Function Articles listing page. Return to the Farriery Articles listing page.
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