The remaining eight children demonstrated improvement in functional strength by video assessment. There was no change in muscle mass noted in the five children studied with MRI scans. Statistically significant changes were noted in foot length, but not width or foot progression angle. Discussion Mountains of papers and books have been written on the clubfoot. There is still no consensus on the pathologic anatomy or choice of treatment in regard to the central muscle imbalance as a factor in persistent deformity following treatment for clubfoot thesis of this work.
Little evidence is available in the current literature.
Although studies of skeletal muscle in clubfoot have consistently shown structural abnormalities, the validity of such studies has been questioned on the basis that the affected limbs had been previously immobilized, and the changes found might be secondary to immobilization rather than a primary muscle abnormality. Technical error should be reduced to a minimum in experienced hands, yet the ratio of unsatisfactory results remains constant. Our thesis that muscle imbalance is responsible is supported by the finding that no child with an intoeing gait had normal peroneal strength, and no child with a normal gait had deficient peroneal strength. We postulate that, in the newborn with clubfoot, the peroneal muscle-tendon units are overstretched as a result of the equinovarus posture of the foot. Quantitative pretreatment assessment of peroneal strength in the newborn is obviously impossible.