The high incidence of internal-rotation problems in children with cerebral palsy justifies consideration of the abnormal muscle function and consequent structural changes in bone and joint which contribute to internal-rotation gait. The structural changes can be determined by clinical examination in combination with roentgenography. The abnormal gait movements and the abnormal timing of muscle contraction can be studied accurately only with special equipment.
Seven children were selected for special electromyographic study as well as the more routine clinical evaluation. Simultaneous electromyograms and motion-picture recording of gait made it possible to record the timing of contraction of the muscles.
The electromyographic finding of greatest significance appeared to be abnormal activity of the hamstrings; their contraction occurred simultaneously with the abnormal internal-rotation movements at the hip. Electromyograms of the adductors showed varied and inconclusive correlation with the abnormal internal-rotation movements. In many instances the calf muscles were overactive, with swing-phase contraction. The iliopsoas contracted consistently in early swing phase and did not appear to be associated with abnormal internal rotation.
On the basis of clinical factors as well as the electromyographic information, surgical procedures were decided on and carried out. Postoperative follow-up included electromyograms of the transferred muscles. When internal rotation was accompanied by crouch, operative treatment consisted in transfer of the insertion of the medial hamstrings to the lateral aspect of the femur; in some instances the gracilis tendon was included. The patients treated by derotation osteotomy are not included in this report.
The result of surgical treatment was rated as excellent, good, fair, and poor. The only poor result was obtained in the bilateral transfer of the semitendinosus, semimembranosus, and gracilis to the lateral distal aspect of the femur in a twelve-year-old patient with spastic quadriplegia and considerable ataxia (Case 5).