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Kinetic, kinematic and electromyographic analysis of cranial cruciate ligament rupture using a monopolar radiofrequency energy model




Adrian, Caroline Patricia, author
Haussler, Kevin Keith, advisor
Kawcak, Christopher E., advisor
Riegger-Krugh, Cheryl, committee member
Reiser, Raoul F., II, committee member
Palmer, Ross H., committee member
McIlwraith, C. Wayne, committee member
Taylor, Robert A. (Robert Augustus), 1946-, committee member

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Canine cranial cruciate ligament rupture (CCLR) is a common cause of pain and lameness in dogs that leads to abnormal pelvic limb biomechanics and ultimately to the development of stifle osteoarthritis (OA). Traditional research into the causes of CCLR has focused on instability secondary to failure of the passive structures within the joint. The purpose of this project was to recognize the role of dynamic components as possible contributors to CCL disease, such as neuromuscular dysfunction of muscles (dynamic stabilizers) surrounding the stifle joint. The present studies were performed to characterize alterations in muscle activity in the limb with CCLR and intact contralateral pelvic limbs, as well as measure biomechanical, clinical and physiologic parameters in all four limbs in dogs with subacute, acute and chronic CCLR (within the same dog during the study). Monopolar radiofrequency energy (MRFE) provided a unique model of CCL injury in which to assess subclinical timeframes. Electromyographic (EMG) parameters, collected simultaneously with ground reaction forces and kinematics, were assessed bilaterally within the vastus lateralis, biceps femoris and gastrocnemius muscles at 6 timepoints post MRFE-induced CCL injury and subsequent rupture. The treated limb denotes the pelvic limb that received MRFE surgery and subsequently ruptured the CCL. The untreated limb refers to the contralateral, non-surgical pelvic limb. Kinematic compensations showed an increase in stifle flexion in the untreated limb compared to the treated limb at all time points post CCLR. Kinetic variables were altered in the treated pelvic limb compared to the untreated limbs post CCLR. No compensatory changes in kinetic or kinematic variables were found in the thoracic limbs at any point post CCL injury or rupture. This study provided a qualitative description of muscle activity post CCL injury and subsequent rupture. No significant differences were found in muscle onset, activation duration or percentage of peak amplitude normalized to baseline between the treated and untreated pelvic limbs at all time points. Clinical and physiologic outcome parameters were collected concurrently throughout the duration of the study to evaluate their association with CCL injury and rupture. Joint effusion was the only outcome parameter associated with subclinical CCL injury. However, the majority of these parameters, such as pain, lameness, range of motion, cranial drawer test and radiography, were associated with subsequent rupture of the CCL. In conclusion, kinematic variables, specifically femorotibial flexion angles, were decreased in the contralateral pelvic limb post CCLR, with minimal changes in subclinical time points at 2 and 4 weeks post MRFE-induced CCL injury. Future studies with larger samples sizes are needed to confirm EMG activity in stabilizing muscles of the stifle to further investigate the role of neuromuscular control in stifle stability. Several outcome parameters such as thigh circumference, pain, lameness, range of motion, cranial drawer test and radiography, and have been shown to be useful in identifying the presence of CCLR, but not subclinical CCL disease.


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cranial cruciate ligament
monopolar radiofrequency energy


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