An additional question is how tendons of different stiffness could be accommodated within the limb if the material properties of tendon are relatively consistent? A tendon that has to withstand the same force but only have half the stiffness must be the same thickness and twice the length. To accommodate this added length within a segment, the muscle fibres would need to be shorter (no major effect feasible in gastrocnemius as muscle fibres are a very small fraction of segment length) or the segment be longer. Alternatively, such a change could be achieved by changing MTU moment arm or EMA, although that would result in a higher tendon force and therefore require a higher tendon CSA and therefore a longer tendon. One could imagine a system where either tendon or GRF moment arm (i.e. EMA) changes through stance in a manner that is advantageous for tendon mechanics and energy storage, effectively a cam, but this does not seem to be common, at least in the literature to date, though the horse biceps has some of these features.
[PATCHED] Glass Horse Distal Limb
One example of a specialized MTU design of this type is that of the biceps brachii in the horse, which is responsible for protraction of the forelimb during locomotion [48]. In summary, as the horse moves over the foot through stance, the moment arm of the GRF at the shoulder gradually rises stretching the biceps muscle, which has a substantial internal tendon and is highly pennate in structure. Through most of stance, the GRF exerts an extensor moment on the carpus holding the leg in extension and balancing the flexor moment of the stretched digital flexor tendons. In late stance, the balance of forces at the carpus means that this joint starts to flex at which point there is nothing to prevent the digital flexor tendons from flexing the carpus and digits folding the leg. The leg is then free to be swung forward by elastic shortening of the biceps flexing the elbow and extending the shoulder. The observed kinematics of leg swing (accelerations and joint angles) can be accounted for by this largely passive system. We propose that the role of the muscle fibres within the spring is to modulate storage and return of elastic energy by changing the force length properties of the biceps MTU [44]. Examples of why this would be useful include when the foot breaks away from the surface earlier or later affecting energy stored in tendons at catapult release, changes in foot weight owing to dirt or a horseshoe and if a horse needs to lift its feet higher to jump an obstacle.
They will then have a gait that looks something like this and the characteristic of the gait is the circumduction of the foot. The fact that the foot is making a circle like that is what makes this gait so characteristic. If the condition is mild the hand may not be flexed up like that and the only manifestation might just be a little circumduction and the hand may not be swinging normally the way the other hand swing. That is called the hemiplegic gait. It's important to understand why they do what they do when you cut the pyramidal tract. On the left side you have abnormalities of tone that manifests on the right side. So you develop flexion hypertonia in the upper limb and extensor hypertonia in the lower limb and that accounts for the leg being like that and the hand being like this. In addition, they develop much more distal weakness than proximity weakness. Their shoulder is strong and the fingers are very weak.
The patient stands with unilateral weakness on the affected side, arm flexed, adducted and internally rotated. Leg on same side is in extension with plantar flexion of the foot and toes. When walking, the patient will hold his or her arm to one side and drags his or her affected leg in a semicircle (circumduction) due to weakness of distal muscles (foot drop) and extensor hypertonia in lower limb. This is most commonly seen in stroke. With mild hemiparesis, loss of normal arm swing and slight circumduction may be the only abnormalities.
Thoroughbred racehorses are subject to non-traumatic distal limb bone fractures that occur during racing and exercise. Susceptibility to fracture may be due to underlying disturbances in bone metabolism which have a genetic cause. Fracture risk has been shown to be heritable in several species but this study is the first genetic analysis of fracture risk in the horse.
Bone fractures with non-traumatic origin occur in Thoroughbred racehorses, with the majority of fractures occurring in the distal limbs; bones subject to high impact and load during exercise and racing. Fracture is the main reason for euthanasia of horses on the racecourse [10], with an average of 60 horses per year suffering a fatal distal limb fracture during racing in the UK (both flat and National Hunt jump racing) [11]. The prevalence of all fatal and non-fatal fractures occurring during training is between 10-20% [12, 13]. Studies of the pathology of equine fracture indicate evidence of stress-related damage to the bone prior to fracture, which may be related to metabolic disturbances in bone re-modelling [14, 15].
This study demonstrates for the first time that DSLD, a disease process previously thought to be limited to the suspensory ligaments of the distal limbs of affected horses, is in fact a systemic disorder involving tissues and organs with significant connective tissue component. Abnormal accumulation of proteoglycans between collagen and elastic fibers rather than specific collagen fibril abnormalities is the most prominent histological feature of DSLD. Because of this observation and because of the involvement of many other tendons and ligaments beside the suspensory ligament, and of non-ligamentous tissue we, therefore, propose that equine systemic proteoglycan accumulation or ESPA rather than DSLD is a more appropriate name for this condition.
Though DSLD has been believed to be a disorder confined to the suspensory ligaments (SLs) of the distal limbs of horses, the mechanism of this disease remains largely unknown. The objectives of this study were to 1) identify whether tissues other than SLs are affected by DSLD and 2) characterize the pathology present in such tissues. This study was initiated because pilot findings from our laboratory suggested that the abnormalities in the collagenous tissue of affected horses are not confined to the SLs distal limbs, but may be manifested systemically, in virtually all collagen containing tissues. In this preliminary work abnormal accumulations of yet to be identified proteoglycans appeared to be present not only in the SL, but also in the superficial and deep digital flexor tendons (SDFT and DDFT, respectively), patellar and nuchal ligaments, aorta, coronary arteries and sclerae of DSLD-affected horses.
Historically, the pathology associated with the clinical syndrome DSLD has been thought to be limited to the suspensory ligaments of the distal limb of horses. The findings of this study suggest that DSLD is in fact a systemic disorder involving many tissues and organs with a significant connective tissue component. Tissues with histological lesions in addition to the suspensory ligament documented in this study include deep and superficial digital flexor tendons, patellar ligaments, aorta, coronary arteries, nuchal ligaments, and ocular sclerae. In light of these observations, a more appropriate term for this disease process may be equine systemic proteoglycan accumulation (ESPA).
Articular stress fracture arising from the distal end of the third metacarpal bone (MC3) is a common serious injury in Thoroughbred racehorses. Currently, there is no method for predicting fracture risk clinically. We describe an ex-vivo biomechanical model in which we measured subchondral crack micromotion under compressive loading that modeled high speed running. Using this model, we determined the relationship between subchondral crack dimensions measured using computed tomography (CT) and crack micromotion. Thoracic limbs from 40 Thoroughbred racehorses that had sustained a catastrophic injury were studied. Limbs were radiographed and examined using CT. Parasagittal subchondral fatigue crack dimensions were measured on CT images using image analysis software. MC3 bones with fatigue cracks were tested using five cycles of compressive loading at -7,500N (38 condyles, 18 horses). Crack motion was recorded using an extensometer. Mechanical testing was validated using bones with 3 mm and 5 mm deep parasagittal subchondral slots that modeled naturally occurring fatigue cracks. After testing, subchondral crack density was determined histologically. Creation of parasagittal subchondral slots induced significant micromotion during loading (p
Functional adaptation is readily detectable by 4 months of race training [19]. Contact stresses on the palmar or plantar regions of the distal end of the MC3/MT3 bones from the proximal sesamoid bones are more than twice the stresses imposed on the dorsal region at the canter; this is a result of more load being shifted to the suspensory apparatus during increased fetlock joint extension [20]. As training increases, adaptation in the subchondral plate leads to sclerosis of the trabecular bone in the palmar/plantar aspect of the condyles, endochondral ossification of the joint surface, and advancement of the tidemark to the articular surface [11], [14]. These changes are associated with site-specific microdamage accumulation in calcified cartilage and the underlying subchondral bone of the parasagittal condylar grooves [11], [12], [14]. Microcrack initiation occurs in the calcified cartilage layer [14] and stimulates a targeted remodeling response that results in the formation of resorption spaces containing activated osteoclasts in the damaged bone [14]. This reparative response is associated with an increase in bone porosity, and may make horses more vulnerable to stress fracture if athletic activity is ongoing [14]. Accumulation and coalescence of these microcracks leads to development of macroscopic crack arrays in the subchondral bone of the condylar grooves [11], [12], [14]. Crack propagation through porous bone compromises the overlying cortical shell at the distal end of the MC3/MT3 bone [15], [21]. Once the cortical shell of the distal end of the MC3/MT3 bone is mechanically compromised, crack propagation proximally along trabecular planes can easily develop, thereby rendering the horse at high risk of developing condylar stress fracture [15], [21]. 2ff7e9595c
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