Equine Lameness for the Layman. G. Robert Grisel, DVM
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LH limb. Unless chronic and severe, it would be unlikely for a forelimb lameness to precipitate compensatory lameness in a hind limb.
Associated lameness, though secondary, does not generate complicated asymmetry and, therefore, does not need to be designated until the veterinary diagnostic phase of examination. Causes of associated gait deficits generally reside in the same locality as the primary source of lameness. Their presence further alters the horse’s gait and may affect both the degree and nature of abnormal movement within a specific anatomic region. Variations in the amount of local inflammation and/or modifications in motion or weight bearing can precipitate associated problems within the affected limb.
Examples of associated lameness might include the following:
Greater trochanteric bursitis (also known as “whorlbone”) is commonly associated with distal tarsitis (or lower hock pain). The greater trochanteric bursa is a small synovial sac that lubricates the middle gluteal muscle tendon as it courses over the greater trochanter of the femur just outside of the hip joint. Inflammation within the greater trochanteric bursa often occurs as a result of chronic excessive pelvic limb adduction (i.e. pulling the limb underneath the center of the body) during movement (VL 7a). This motion results in increased strain of the middle gluteal muscle and its associated tendon. Excessive limb adduction is, in turn, a gait characteristic classically associated with distal tarsitis. Therefore, greater trochanteric bursitis is a common consequence of chronic hock pain.
VL 7a Scan/Click to view video. www.getsound.com/tutorials/7a
Lameness within the carpus (or “knee”) will often induce inflammation of the brachiocephalics muscle, which forms an attachment between the horse’s neck and upper limb (humerus). In an attempt to avoid or reduce carpal flexion, some animals will overuse the brachiocephalicus muscle in order to achieve ample forelimb protraction during movement (VL 7b). This action, in turn, can result in associated inflammation (termed myositis) and pain.
VL 7b Scan/Click to view video. www.getsound.com/tutorials/7b
In some cases of chronic (long-term) navicular inflammation, horses will develop associated inflammation of the coffin joint, a portion of which resides just in front of (or dorsal to) the navicular bone (fig. 7.2). In this instance, many professionals implicate the close proximity of the two structures as the reason for the associated lameness: inflammation in the navicular region may “diffuse” into the nearby coffin joint.
7.2 Relative Locations of the Navicular Bone and Coffin Joint
Inflammation originating in the navicular region can indirectly “diffuse” into the coffin joint (highlighted in pink) and vice versa.
Sources of associated and compensatory lameness are genuine in that they precipitate their own gait deficits. Both may persist even after the primary source(s) of lameness are successfully treated.
Referred lameness, on the other hand, is not authentic; it is merely a visible extension of a problem existing somewhere else in the horse. This form of secondary lameness can be expressed in a variety of ways, depending on the location and nature of the primary issue. Areas of the body displaying referred asymmetry do not require direct diagnostic or therapeutic attention since corresponding gait deficits will disappear upon resolution of the primary inciter. Expected manifestations of referred lameness are discussed in chapter 10 (p. 46).
The adept observer not only acknowledges the presence of both primary and secondary components of lameness, but accurately distinguishes between the two. Always considering the potential for physiologic relationships between two or more coexisting gait deficits better prepares us for this task.
8 Painful versus Non-Painful Lameness
To most of us, a lame horse is a horse in pain. While this is true in the majority of cases, gait abnormalities can also be generated by issues that don’t hurt. The adept observer has the ability to recognize both forms.
As you might imagine, pain-mediated lameness is easier to diagnose for the average veterinarian. Hands-on manipulation of the body and limbs (such as palpation and flexion testing) can be used to increase discomfort associated with specific anatomic regions, thereby helping the practitioners aim their diagnostic efforts. Local anesthesia (perineural and synovial blocks) can be used to confirm or deny suspicions with regard to potential sources of pain. The animal’s response to empirical treatment in the form of local anti-inflammatory or arthrotherapy can also help to implicate various structures as the point of origin.
Non pain-mediated issues, by contrast, cannot be accentuated through manipulation nor be “blocked out” during lameness examination. They are often invisible upon diagnostic imaging and refractory to medical therapy. Many non-painful issues, therefore, can only be diagnosed via their display of characteristic gait deficits. This is where meticulous visual analysis becomes a critical part of the workup.
Non-painful issues comprise those that are biomechanical (usually restrictive) and neurologic in origin. Biomechanical lameness usually results from abnormal interaction between soft tissue and bone. Since tendons, ligaments, and muscles attach to bone (directly and indirectly, respectively), they are most often implicated as sources for biomechanical lameness. Intermittent upward fixation of the patella (IUPF) and fibrotic myopathy of the hamstring musculature are two well-described biomechanical problems that occur in horses. Each are further characterized in chapters 16 and 19 (respectively) because, like most biomechanical issues, their corresponding gait deficits are distinctive (pp. 91 and 127).
Horses can also exhibit non-painful lameness in response to neurologic disease. Neurologic lameness often arises as a consequence of compromised motor innervation (in which nerves are supplying inadequate input to the muscles that move the body and limbs) and/or decreased proprioception (in which reduced sensory output from the limbs affects spatial awareness). Neurologic lameness can be weight-bearing and/or non weight-bearing in nature (see chapter 9—p. 43), depending on the nerves and structures affected. Circumduction is a gait deficit most evident at the walk and often attributed to neurologic disease (VL 8a).
VL 8a Scan/Click to view video. www.getsound.com/tutorials/8a
Non-painful issues usually produce non weight-bearing lameness. This is easily demonstrated via the application of a splinted brace to one of your knees. The splint, when properly positioned, should not be uncomfortable nor prevent you from bearing a normal amount of weight on the limb during full extension. Yet it will effectively prohibit flexion of your limb, thereby resulting in a visibly obvious gait deficit as you try to ambulate.
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