Abstract
Introduction and Aims: The effects of injury to the posterior cruciate ligament (PCL) and posterior-lateral corner (PLC) on physical function are not as well documented compared to the more common injury to the anterior cruciate ligament. This study aimed at improving our understanding of PCL/PLC injury through gait analysis and electromyographic (EMG) testing.
Method: We studied 19 patients, average age 30 years (20–55) with clinically and radiologically confirmed PCL/PLC deficiency in isolation. Ninety percent of patients complained of instability when performing the activities of daily living and all complained of pain. All patients were assessed using the Lysholm and Gillquist functional knee score as well as gait analysis, including Kinematics, Kinetics and EMG of the quadriceps, hamstrings and gastrocnemius muscles. Findings were compared to our normal database. The mean Lysholm score was 51/100 (24–90). Those with a Lysholm greater than 50 were designated as ‘copers’.
Results: There were 12 ‘non-copers’ and seven ‘copers’. Fifty percent of patients demonstrated a varus thrust through stance. Forty-two percent of patients demonstrated hyperextension of the knee through stance. Sixty-three percent of patients demonstrated premature and prolonged hamstring activity. Thirty-seven percent of patients had premature activity of the gastrocnemius muscle in stance. Fifty-seven percent of the ‘copers’ demonstrated premature and prolonged hamstring activity through the gait cycle compared to forty-five percent of ‘non-copers’ (non-significant p=0.25 Fishers Exact Test). Fifty-five of ‘non-copers’ demonstrated premature activity of the gastrocnemius muscle in stance compared to none of the ‘copers’ (significant p=0.025 Fishers Exact Test).
Conclusion: The observed varus thrust may be responsible for the development of medial and patellofemoral compartment osteoarthritis, a recognised problem in PCL deficient knees. Hyperextension that occurs dynamically during gait could explain failure of PCL/PLC reconstruction over time. The observed abnormal hamstrings activity is unlikely to be a compensatory mechanism.
These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.
None of the authors is receiving any financial benefit or support from any source.
