LAUSR

increase in passive torque from 10° to 20° of dorsiflexion measured before isometric contractions. Tendon thickness was measured by digital calipers. Plantarflexor EMG was recorded during strength and functional tests. ANOVA and Wilcoxon tests were used to assess weakness and function. RESULTS: Marked weakness was evident on the involved side at 20° plantar flexion (deficit 26±18%; P<0.01) with no weakness at 20° dorsiflexion (deficit 6±17%; P=0.39). Compared to the noninvolved side, dorsiflexion range of motion was decreased 6±8° and tendon thickness was 7±3 mm greater (P<0.001) on the involved side. Passive joint stiffness was similar between the involved and noninvolved sides. Only 3 of 18 patients could perform a decline heel rise on the involved side versus 18 of 18 on the noninvolved side (P=0.01). There was no difference in EMG amplitude between the involved and noninvolved sides during all tests. CONCLUSION: Normalized passive joint stiffness and reduced dorsiflexion ROM were likely due to a stronger, protected repair. EMG data confirmed that end-range weakness was not due to neural inhibition. Weakness with the plantar flexors in a shortened position may be due to inefficient transmission of contractile forces through the thickened tendon when the muscles are in a shortened position.