Presumed muscle adaptation induced by longstanding spasticity is regarded as the major contributor to the passive movement limitation

The flexor carpi ulnaris muscle is held largely responsible for the limited range of LY2109761 motion and the contracture around the wrist. Therefore, this muscle is frequently subject of surgical treatment of the spastic arm. In patients with CP, development of lower extremity muscles has been reported to be compromised, causing shortness and/or an increased passive muscle stiffness. The mechanisms by which spasticity of the FCU results in a limited passive movement around the wrist and elbow are unknown. Several pathophysiological mechanisms may underlie the altered spastic FCU development. Due to the spasticity and the related reduced ability of CP patients to extend the wrist, FCU is largely maintained in a shortened position. Based on effects found for immobilization of experimental animal muscle in a shortened position, both impeded growth of myofibre diameter and diminished addition of serial sarcomeres within myofibres have been presumed in spastic muscle. However, to our knowledge, quantitative data regarding spasticity related differences in serial sarcomere number are insufficient and hard to obtain, as this requires isolation of myofibres along their full length. For pennate muscle, such as FCU, myofibre diameter is also a major determinant of both muscle slack and optimum length. As such, changes in myofibre cross-sectional size could result in a shift in the muscle operating length range in vivo, and affect the wrist range of motion. Regarding the cross-sectional size of spastic myofibres, both atrophy and hypertrophy of slow, as well as fast myofibre types, have been reported in muscles from different limbs without a clear relation to the degree of limitation of joint movement. In addition, some studies reported similar cross-sectional areas of spastic and control myofibres comparing several muscles from different limbs. From the above we can conclude that alleged muscle stiffness is not unequivocally related to myofibre cross-sectional size and muscle shortness in CP. Other factors that may affect muscle stiffness are a change in the intrinsic, mechanical properties of the myofibres, the intramuscular connective tissue, or altered myofascial loads of the epimuscular myofascial connections of the spastic muscle with extramuscular connective tissues, synergists and/or antagonist muscles. Single myofibre segments obtained from different spastic muscles of the forearm have been reported to be stiffer than those of control muscle. However, fascicle segments of spastic muscles have been reported to be more compliant than similar segments in control muscle, suggesting spasticity related deterioration of intramuscular connective tissue. Furthermore, the analysis of the amount of connective tissue in human muscle tissue obtained from muscles in the leg and arm has shown diverse results. Above-mentioned variability in results may exist because comparisons were made between biopsies obtained from different muscles within one limb, muscles of different limbs or from biopsies taken from different locations within a muscle. The purpose of this study was to test the hypothesis that the limited range of wrist motion is caused.

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