In this study, the joint motion of the index finger induced by each extrinsic muscle was examined using a marker-based motion capture system together with a tendon force monitoring sensor. The protocol used in this study, i.e., gradual pulling of the musculotendinous junction of the index finger extrinsic muscles, simulated the contracting muscle, allowing us to quantify the resulting motion trajectories at the phalangeal joints.
The results of this study show that the individual extrinsic muscles generated motion at multiple index finger phalangeal joints. Whereas the FDP generated motion at all the phalangeal joints, the FDS, as expected, did not generate motion at the DIP joint. The EIP and EDC generated similar phalangeal joint motion. Using biomechanical model, Kamper et al. found that the combined actuation of FDP and FDS generated ranges of motion of 43, 75, and 63 degrees at the MCP, PIP, and DIP joints, respectively . Becker and Thakor obtained range of motion data from 15 human subjects: 70.8, 103.8, and 61.2 degrees for the MCP, PIP, and DIP joints, respectively . However, the motion data in the current study are not directly comparable with the motion data involving activation of multiple muscles.
To a great extent, the anatomical arrangement of the tendons explains observed joint motion. The extrinsic flexors originate in the forearm, cross over multiple joints, and insert into either the middle or the distal phalanx. The FDP spans the MCP, PIP, and DIP joints, inserting at the base of distal phalanx, and the FDS spans the MCP and PIP joint, inserting at the middle phalanx. Therefore, the FDP generated motion at the MCP, PIP and DIP joints, while the FDS generated motion at the MCP and PIP joints. The extensor tendons pass over the MCP joint and trifurcate into medial, central, and lateral slips at the PIP joint. The central slip inserts into the base of middle phalanx, while the medial and lateral slips pass on either side of the PIP joint, inserting into the distal phalanx . The extensors mainly generate motion at the MCP and PIP joints as observed in this study. The encircling series of fibers (sagittal band) that are connected to the extensors enhance the MCP joint motion . The migration of the medial and the lateral slips toward each other generate DIP joint extension. The tighter the proximal pull on the extensors, the more closely the slips migrate towards each other producing additional extension of the DIP joint . The force applied in this study (i.e., 10% of the maximum force) might not have relocated the slips enough, producing relatively small extension motion (<5 degrees) at the DIP joint. It is also known that DIP extension is mainly achieved by the activation of the intrinsic muscles through the extensor mechanisms [16, 22].
The motion generated at the phalangeal joints showed strong interjoint coordination. The EDC and EIP tendons generated simultaneous, linearly coupled motion at the MCP and PIP joints. Although the FDP tendon also generated simultaneous, linearly coupled motion at the PIP and DIP joints, the FDP and FDS tendons generated a distinct inter-joint coordination pattern at the MCP and PIP joints. Within the 0–3% force range, the motion generated at the PIP joint (34.1 ± 17.1 degrees by FDP; 39.3 ± 12.3 degrees by FDS) was almost three times the motion generated at the MCP joints (10.7 ± 7.9 degrees by FDP; 13.2 ± 4.1 degrees by FDS). The motion generated (within 0–3% force range) at the PIP joint was approximately 80% of its total range of motion. However, the motion generated at the MCP joint was approximately 50% of its total range of motion. The loading of flexors between 3–10% generated comparable ranges of motion at the MCP (8.9 ± 4.8 degrees by FDP; 11.6 ± 2.5 degrees by FDS) and PIP (7.7 ± 3.5 degrees by FDP; 8.6 ± 3.3 degrees by FDS) joints. Thus, in the 0–3% force range, the PIP joint flexion leads the MCP joint flexion. The joint impedance could be a possible reason for this observation. The passive joint characteristics such as the number of muscles crossing the joint could govern its impedance. The MCP joint has more muscles crossing it than the PIP joint, providing higher impedance and thus less motion at the MCP joint. The joint impedance increases as it flexes. After a certain level of flexion, the impedance of the PIP joint becomes equivalent to the MCP joint causing similar motion at both joints. In the current study this point of matched impedance was observed after the 3% force.
Based on the motion data determined in this study, it is possible to speculate some role of the intrinsic muscles in phalangeal joint motion. We comprehend three possible movement manifestations of the intrinsic muscles. First, the intrinsic muscles assist in the flexion of the MCP joint. An extrinsic flexor with a 10% force generated almost full flexion at the PIP joint, but only a sub maximal joint flexion at the MCP joint. Kamper et al.  stated that the activation of the intrinsic muscles may be necessary to produce MCP flexion beyond 60 degrees. Darling et al.  observed activation in the intrinsic muscles during finger flexion, especially during fast flexion movements. Hence, activation of intrinsic muscles is necessary to generate extreme and fast flexion at the MCP joint. Second, the intrinsic muscles facilitate the finger movements that require simultaneous flexion and extension at the MCP and IP joints, respectively. Darling et al. observed simultaneous movements of the finger joints during various daily living grasp and release tasks . The pulling of extrinsic muscles generated either concurrent flexion or extension at the MCP and the IP joints, i.e. the joints were rotated in one direction only. Landsmeer and Long stated that lumbricals and interosseous were involve in the motion generating MCP flexion with simultaneous extension of the IP joints . Kamper et al. speculated that intrinsic muscles may assist MCP flexion indirectly by increasing the resistance to the IP flexion . Thus, flexing MCP joints, while retaining the IP joints at relatively extended positions, may require contribution from the intrinsic muscle. Third, the intrinsic muscles are responsible for the abduction-adduction of the MCP joint. Though abduction-adduction motion was not quantified in this study, during the data collection negligible abduction-adduction motion was observed at the MCP joint due to the actuation of the individual extrinsic muscles. It follows that the abduction-adduction motion available to the MCP is generated by the intrinsic muscles. The intrinsic muscles are oriented on the radial and ulnar side of the MCP joint, which facilitates both abduction and adduction of the MCP joint. Future studies delineating the motion contribution of the intrinsic muscles would be useful in drawing concrete conclusions about their role in phalangeal joint motion. However, such studies will be faced with the challenges of not disturbing the local anatomy and retaining the intact kinematics.
We acknowledge several limitations of this study. First, the mechanical properties of the cadaveric tissues may be different from live tissues. The relationship between the muscle force and joint movements is dependent upon the mechanical characteristics of the joint. The intrinsic muscles, articular cartilage, ligaments, joint capsule, synovial fluid, and opposing bone surface are determinants of the mechanical characteristics of a joint. Moreover, the cadaveric specimens were mostly obtained from the elderly subjects, whose stiffness might be higher than those of young subjects. These discrepancies could affect the joint characteristics (e.g., impedance), limiting the generalization of our results to live hands and a diverse age population. Future studies evaluating changes (in vivo vs. in vitro) in the joint characteristics could be useful in extending the results of this study to live hands. In vivo studies using electrical stimulation could also be performed to validate the kinematic role of the individual extrinsic muscles. Second, the tendons were loaded to only 10% of their maximum force potentials. This loading force was judged reasonable because phalangeal motion requires sub-maximal activation of the muscles, and the purpose of this study was to examine the motion (not the strength) generated by the individual tendons. Nevertheless, most of the joint motion trajectories tended to level off at the higher end of the force application. Third, a moderate level of variability was observed in the starting joint positions, which could be due to the subjective preconditioning procedure and the accidental tension prior to muscle loading. The latter scenario is more probable because the starting joint position was found to be shifted in the direction of the movement, i.e., having a more flexed starting position for the flexors and more extended starting position for the extensors. This experimental artifact might have decreased the ranges of motion by 3–5 degrees. Finally, to standardize hand and wrist mounting positions, the phalangeal joints of the middle, ring, and little fingers were locked into full extension, which might have restricted the flexion mobility of the finger motion, especially at the MCP joint.
Despite of these limitations, the results of this study provide novel insights into the functional manifestation of the index finger joints by individual extrinsic muscles.
The knowledge of the kinematic role of individual muscles could be used for designing neuromuscular electrical simulation protocols , reconstructive surgeries , and planning of diagnosis and treatment modalities of the finger joint problems.