Mechanical and Neurological Lameness in the Forelimbs and Hindlimbs

Chapter 48Mechanical and Neurological Lameness in the Forelimbs and Hindlimbs

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.

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

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

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

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

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