Traditional investigations into the etiopathogenesis of canine cranial cruciate ligament (CCL) disease have focused primarily on the biological and mechanical insults to the CCL as a passive stabilizing structure of the stifle. However, with recent collaboration between veterinarians and physical therapists, an increased focus on the role of muscle activity and aberrant motor control mechanisms associated with anterior cruciate ligament (ACL) injuries and rehabilitation in people has been transferred and applied to dogs with CCL disease. Motor control mechanisms in both intact and cruciate-deficient human knees may have direct translation to canine patients, because the sensory and motor components are similar, despite moderate anatomic and biomechanical differences. Components of motor control, such as muscle recruitment and the coordination and amplitudes of activation are strongly influenced by afferent proprioceptive signaling from peri- and intra-articular structures, including the cruciate ligaments. In people, alterations in the timing or amplitude of muscle contractions contribute to uncoordinated movement, which can play a critical role in ACL injury, joint instability and the progression of osteoarthritis (OA). A better understanding of motor control mechanisms as they relate to canine CCL disease is vitally important in identifying modifiable risk factors and applying preventative measures, for development of improved surgical and rehabilitative treatment strategies. The purpose of this review article is to analyze the influence of altered motor control, specifically pelvic limb muscle activation, in dogs with CCL disease as evidenced by mechanisms of ACL injury and rehabilitation in people.

Objective: Identify relevant electromyography (EMG), kinematic, and kinetic changes resulting from monopolar radiofrequency energy (MRFE)-induced cranial cruciate ligament (CCL) injury and eventual rupture in dogs. Study design: Experimental, repeated measures. Animals: Five purpose-bred female dogs free of orthopedic and neurologic disease. Methods: Surface EMG, joint kinematics, and ground reaction forces were assessed at a trot in the pelvic limbs at baseline, at 2 and 4 weeks after unilateral MRFE-induced CCL injury, and at 4, 8, and 16 weeks after CCL rupture (CCLR). Results: After MRFE-induced injury, average hip joint range of motion (ROM) during stance decreased within the untreated pelvic limb. After CCLR, stifle flexion angles decreased within the treated limb at 8 weeks and within the untreated pelvic limb at all time points, whereas average tarsal joint ROM decreased in the treated limb and increased in the untreated limb. Peak vertical ground reaction force and impulse decreased within the treated limb. Qualitative alterations of many EMG values were noted after MRFE-induced injury and CCLR, although significant differences between limbs or from baseline values were not detected. Conclusion: Monopolar radiofrequency energy-induced injury altered contralateral hip kinematics, suggesting early regional compensatory gait alterations. After CCLR, additional compensatory gait patterns occurred in both pelvic limbs. Clinical impact: The qualitative analysis of trial-averaged EMG data in this small population supports a relationship between neuromuscular function and induced CCL injury leading to rupture.

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