PROPRIORECEPTIVE DEFICIT FOLLOWING ACL IN JURY - AFFERENT SIGNAL DEFICIT OR COMPENSATORY MECHANISM

It was suggested that the ACL has not mechanical functions but also ac ts as proprioceptive organ. In cruciate deficient knees pathological p atterns of muscle control were found. These findings could be caused b y a disturbed afferent signal from the disrupted ACL or by secondary c hanges in muscle innervation, which shall protect the instable knee ag ainst subluxation. 33 patients with unilateral operative ACL repair (2 1 cases with primary suture, 12 cases with autogenous ligamentum-patel lae-reconstruction; average post op 36.5 yr) were examined clinically and with the KT 1000 arthrometer (MEDMETRIC Inc.). Patients history wa s evaluated by using the LYSHOLM score. During a cycling task the elec tromyographic activity was monitored from the thigh muscles (M. vastus lat. and med., lat. and med. hamstrings). In comparison to the ACL de ficient patients, we tested 25 healthy subjects of same age and activi ty level. In the ACL group the following differences to the normals we re found: the M. vastus Int. showed a significantly delayed onset, ear lier end and shorter duration. M. vastus med. had the same pattern; th e delayed begin of activity and the shorter duration were statisticall y significant. M. biceps femoris showed a significant later onset and shorter duration. So did the medial hamstrings; the differences, howev er, were not statistically significant. There was no significant diffe rence between operated and healthy leg in the ACL group. By comparing the primary sutures and the ligamentum-patellae-reconstructions no sig nificant differences were found. The instable patients (KT 1000 > 3 mm ) of the ACL group showed more distinct differences in the EMG pattern than the patients with stable knee joints. The bilateral occurrence o f the changed EMG patterns in the ACL group and the more distinct chan ges in unstable knees suggest that this phenomenon is not only caused by a deficit of afferent signals from the disrupted ACL. It seems to b e a secondary acquired mechanism to compensate anterior instability of the knee.