The foot drop component of cavovarus foot deformity in patients with Charcot-Marie-Tooth disease is commonly treated by tendon transfer to provide substitute foot dorsiflexion or by tenodesis to prevent the foot from dropping. Our goals were to use three-dimensional foot analysis to evaluate the outcome of tibialis posterior tendon transfer to the dorsum of the foot and to investigate whether the transfer works as an active substitution or as a tenodesis.Methods:
We prospectively studied fourteen patients with Charcot-Marie-Tooth disease and cavovarus foot deformity in whom twenty-three feet were treated with tibialis posterior tendon transfer to correct the foot drop component as part of a foot deformity correction procedure. Five patients underwent unilateral treatment and nine underwent bilateral treatment; only one foot was analyzed in each of the latter patients. Standardized clinical examinations and three-dimensional gait analysis with a special foot model (Heidelberg Foot Measurement Method) were performed before and at a mean of 28.8 months after surgery.Results:
The three-dimensional gait analysis revealed significant increases in tibiotalar and foot-tibia dorsiflexion during the swing phase after surgery. These increases were accompanied by a significant reduction in maximum plantar flexion at the stance-swing transition but without a reduction in active range of motion. Passive ankle dorsiflexion measured in knee flexion and extension increased significantly without any relevant decrease in passive plantar flexion. The AOFAS (American Orthopaedic Foot & Ankle Society) score improved significantly.Conclusions:
Tibialis posterior tendon transfer was effective at correcting the foot drop component of cavovarus foot deformity in patients with Charcot-Marie-Tooth disease, with the transfer apparently working as an active substitution. Although passive plantar flexion was not limited after surgery, active plantar flexion at push-off was significantly reduced and it is unknown whether this reduction was the result of a tenodesis effect or calf muscle weakness.Level of Evidence:
Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.