Mechanical and Neurological Lameness in the Forelimbs and Hindlimbs

Chapter 48Mechanical and Neurological Lameness in the Forelimbs and Hindlimbs



Sue J. Dyson, Mike W. Ross*




General Considerations


Mechanical lameness reflects altered biomechanical forces affecting limb function. The biomechanics of limb function depend on normal functioning of peripheral nerves, muscles, tendons, and ligaments. Appropriate muscle contraction and relaxation are important factors in limb biomechanics. A muscle that cannot contract with sufficient force or a muscle that cannot relax and stretch can result in an altered gait. Mechanical lamenesses are typically most obvious at the walk and often become less evident or disappear at the trot. Gait alterations may not be evident at the canter, although a horse with a mechanical lameness may not be capable of generating a smooth canter and may appear to be hopping or “off” behind at the canter. Mechanical lamenesses include altered gaits caused by decreased and increased joint flexion.


The importance of proper functioning of the neuromuscular system for a normal hindlimb gait is exemplified by horses with chronic motor neuron disease and myopathy from equine polysaccharide storage myopathy (EPSSM). Both of these neuromuscular disorders can be associated with a fibrotic myopathy-type or stringhalt-type of gait. Horses with EPSSM may develop prolonged or intermittent upward fixation of the patella. Underlying myopathy was found in some but not all horses with shivers (shiverers).1,2 Neuropathy is known to be a cause of stringhalt3,4 and was found in horses with fibrotic myopathy.5 Trauma to peripheral nerves may also cause a mechanical lameness. The possible role of altered proprioceptive input to the affected limb is intriguing and is discussed under appropriate headings.


Equine protozoal myelitis or myeloencephalitis (EPM) with involvement of motor neurons causing selective denervation may also cause mechanical lameness. In horses with EPM, lameness cannot be abolished using diagnostic analgesia. Horses with lameness from EPM should, however, also exhibit proprioceptive deficits and ataxia and usually exhibit muscle atrophy. Lameness in horses with EPM may be caused by pain arising from atrophied muscles, nerve root pain, or pain originating from peripheral nerves. EPM is unlikely to cause an obvious mechanical lameness without accompanying ataxia. It is difficult to accept that EPM could cause selective damage to motor neurons sufficient to cause a mechanical lameness without also causing concurrent spinal cord white matter damage and ataxia, but it does do so occasionally, and neurological deficits may be subtle early in the disease. Careful neurological evaluation by a clinician with expertise in equine neurological evaluation is an important part of examining a horse with mechanical lameness because distinguishing between gait abnormality caused by mechanical lameness and gait abnormality caused by neurological disease may be difficult.


Electromyography and muscle biopsy may aid in determining the cause of mechanical or neurologically mediated lameness. Concentric needle electromyography of denervated muscle often reveals abnormal spontaneous activity such as positive sharp waves, fibrillations, and myotonic bursts. Abnormal spontaneous activity may also be present in muscles of horses with myopathy, but these findings are generally mild and may be absent. Biopsy of the semimembranosus or semitendinosus muscle is useful for evaluating evidence of denervation atrophy and EPSSM. However, if denervation of a single muscle or part of a muscle causes the gait alteration, sampling error may result in a false-negative result.


Mechanical lameness does not always cause pain, and horses usually do not respond to nonsteroidal antiinflammatory drug therapy. Methocarbamol therapy is indicated only when muscle cramping from central nervous system disease is suspected. Phenytoin therapy has proved to be useful in some horses with mechanical lameness, particularly those with stringhalt.


Mechanical lameness in the horse is the result of abnormal structure or function of the musculoskeletal system or, more commonly, of the neuromuscular system. Possibly a variety of underlying problems can result in the same type of mechanical lameness. Limb dysfunction may also be caused by an imbalance of flexor and extensor muscle activity as a result of a primary neurological cause.



Anatomical Considerations


A number of unique anatomical features in the equine hindlimb contribute to mechanical lameness. The configuration of the patellar ligaments in the stifle joint allows locking of the stifle into an extended position (see page 94). The stay apparatus minimizes the muscular effort required for a horse to stand for long periods. The reciprocal apparatus links the actions of the stifle and hock, primarily through the fibularis (peroneus) tertius and superficial digital flexor tendons, such that an abnormal action in either joint affects the action of both.


Innervation patterns to the muscles of the hindlimbs may also contribute to mechanical lameness. The semitendinosus muscle, for example, receives innervation from two different nerves: the caudal gluteal and sciatic nerves. Often more than one muscular branch innervates long muscles such as the semitendinosus and possibly the semimembranosus. Damage to one nerve or to a muscular branch can result in partial denervation of a large muscle, with resultant altered biomechanical forces leading to abnormal limb action.



Upward Fixation of the Patella (Locking Stifle) and Delayed Release of the Patella



Clinical Characteristics


Horses and ponies with upward fixation of the patella are episodically unable to flex the stifle or the hock and drag the extended limb behind them on the toe (see Figures 5-18 and 48-1)image. The condition occurs most commonly after a period of standing still and tends to decrease with continued exercise. An intermittent form of patellar fixation, called delayed release of the patella, also occurs, in which the patella appears to catch briefly, sometimes followed by exaggerated flexion of the stifle and hock. Low-grade intermittent upward fixation or delayed release of the patella is relatively common, but it is often difficult to detect and is not necessarily observed daily. Affected horses have a slightly jerky movement of the patella that may be most apparent during deceleration from trot to walk and when the horse is working in deep footing, especially on turns. Affected horses may appear to be in some discomfort, may be resistant to work especially in deep footing, and can become irritable. Both upward fixation of the patella and delayed release may occur unilaterally or bilaterally. Fifty-five of 78 horses (70.5%) with upward fixation of the patella were affected unilaterally and 23 (29.5%) bilaterally.6


image

Fig. 48-1 Diagrammatic representation of the common mechanical hindlimb gait abnormalities. A, In horses with upward fixation of the patella, the hindlimb is periodically held in rigid extension. The fetlock joint is flexed, and the horse walks on the toe. Horses with intermittent upward fixation can have a gait similar to shivers (see D). B, Horses with fibrotic myopathy show slapping of the affected hindlimb downward just before the end of the cranial phase of every walk stride. Hock flexion is near normal, but fibrous tissue in the caudal thigh region limits the cranial phase of the stride. C, Horses with stringhalt exaggerate flexion of the hock with the hindlimb in a normal (adducted) position. This gait occurs at every walk stride. Excessive hock flexion causes some horses to hit the ventral abdomen with the dorsum of the hindlimb. D, Horses with shivers often have abnormal tail head elevation and hold the affected hindlimb in a flexed and raised position away from the midline (abducted). This abnormal gait occurs sporadically, not at every walk step, which helps to distinguish it from stringhalt.


Warmbloods, Thoroughbreds, Standardbreds, and some pony breeds (e.g., Shetland and Miniature ponies) may be predisposed to upward fixation of the patella.6 The episodic nature of intermittent upward fixation of the patella adds to the difficulty of detecting an affected horse. Careful observation while moving the horse over from side to side, turning in small circles, or walking down an incline can be particularly useful. Clinical signs of upward fixation of the patella or delayed release of the patella are most commonly seen in young horses, especially those kept stabled, and signs may diminish or disappear if the horse becomes fitter and stronger. However, clinical signs may recur if the horse is confined to box rest for an unrelated reason. Persistent upward fixation of the patella has also been described in a foal.7



Cause


Upward fixation of the patella has been attributed to abnormal laxity and to increased tenseness of patellar ligaments. Decreased force of muscle contraction of the thigh muscles (quadriceps and biceps femoris) that move the patella out of the locked position may also cause upward fixation of the patella. This may be the explanation for upward fixation of the patella occurring in unfit horses, those in poor condition, or those with underlying myopathy, causing weak or stiff muscles. Horses and ponies with overly straight hindlimbs may be prone to upward fixation of the patella because such conformation can result in overextension of the stifle joint, leading to patellar locking.6,7 Sixteen of 78 horses (20.5%) with upward fixation of the patella had straight hindlimb conformation.6 Foot conformation may also play a role. Thirty-one of 78 horses (39.7%) had long toes and/or a higher inside wall of the hind foot of the affected limb(s).6 Permanent upward fixation of the patella occurs rarely secondary to luxation or subluxation of the ipsilateral coxofemoral joint (see Chapters 50 and 126).



Biomechanical Basis


Upward fixation of the patella is caused by failure of the medial patellar ligament to unhook from the medial ridge of the femoral trochlea, causing the stifle to lock in extension. Abnormalities of the fibrocartilage at the medial aspect of the patella also possibly make the joint prone to locking. Once the stifle is locked in extension, the hock is also fixed in extension through the action of the reciprocal apparatus. The biomechanical basis for stifle hyperflexion after the brief period of patellar catching in intermittent upward fixation of the patella (or delayed release of the patella) is not entirely clear and may be from increased force of contraction of the biceps and quadriceps muscles during the transient locking phase. Clearly, therapy for this disorder should be directed at correcting the underlying cause. Unfortunately, for many horses an exact cause is never determined.



Medical Therapy


Exercise is an important part of therapy for horses with upward fixation of the patella. Conditioning exercise, including work on hills, may result in complete resolution of the problem in some horses. Uphill work may be more beneficial than downhill exercise. Horses that respond to conditioning exercise indicate that muscle dysfunction can play an important role in the development of upward fixation of the patella. Corrective trimming and shoeing is also important; the toe should be shortened to facilitate breakover, and mediolateral imbalance should be corrected. It has been suggested that rounding the medial aspect of the foot to promote medial breakover may be beneficial together with elevation of the lateral heel using a wedge-heel shoe.6 Thirty-three of 64 (51.6%) horses with upward fixation of the patella had a successful outcome following corrective trimming and shoeing, dietary management to promote better condition, and exercise, and a further 13 (20.3%) improved.6


If underlying myopathy such as EPSSM is the cause, diet change to one that is high in fat and low in starches and sugars9 and continued exercise conditioning may be beneficial. The most effective diets are those that provide at least 20% to 25% of total daily energy from fat and less than 20% of total daily energy from starches and sugars.


Another medical therapy is administration of estrogenic compounds. The rationale is presumably that estrogens can cause tendon and ligament relaxation. Whether horses with upward fixation of the patella have overly tense patellar ligaments and whether estrogen has any effect on patellar ligaments and tendons are unclear. Estrogen effects on muscle cell metabolism and muscle tone are possible. Anecdotal evidence suggests that some horses may benefit from this type of therapy. Intramuscular injection of 1 mg of estradiol cypionate per 45 kg of body weight (i.e., 11 mg/500 kg) once weekly for 3 to 5 weeks has been recommended.


Injection of iodine-containing counterirritants into and around the medial and middle patellar ligaments has also been advocated.10 It has been proposed that maturation of a fibrous and inflammatory response may result in stiffening of the ligaments and thus relieve upward fixation of the patella.11 Injection of a 2% solution of iodine in oil or of ethanolamine oleate has been advocated. Injection of 1 to 1.25 mL of these compounds into numerous sites in and around the distal aspect of the medial and middle patellar ligaments is recommended. However, in an experimental study in normal horses, injection into the medial and middle patellar ligaments with iodine in almond oil provoked more fibroplasia and infiltration of inflammatory cells than ethanolamine.11



Surgical Therapy


Medial patellar desmotomy may be necessary, although this should be considered only in horses with upward fixation of the patella that is unresponsive to conditioning exercise or medical therapy, or for horses that are persistently locked for several days. Because the transected ligament eventually heals with a fibrous union, the main benefit of surgery may be temporarily to alter the action of the stifle joint such that the horse is capable of conditioning exercise. Development of fragmentation of the apex of the patella (sometimes referred to as patellar chondromalacia) and associated lameness may occur after medial patellar desmotomy, although rest for 3 months postoperatively may reduce the risk (see Figure 46-4) (Figure 48-2).12 Treatment of fragmentation of the apex of the patella is by arthroscopic debridement (see Chapter 46). Middle patellar desmitis is also a potential untoward sequela.6,13

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Jun 4, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Mechanical and Neurological Lameness in the Forelimbs and Hindlimbs

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