Note that the tertiary perimysia, that arethickened in spastic FCU, do not envelop fascicles or groups of fascicles from their origin to insertion, but rather enter and cross the muscle transversely at certain levels. By selection, tertiary perimysia were absent in the fascicle segments used for mechanical measurements. Enhanced thickness and presumably stiffness of such tertiary perimysium will more likely affect muscle function via its extramuscular connections by myofascial force transmission, rather than affect the stiffness of an isolated FCU. In other words its connections are crucial for enhanced stiffness. Thickening and presumed stiffening of the tertiary perimysium as XAV939 apparent in a majority of our CP subjects, suggests that, in spastic muscle, these structures are loaded relatively more than in controls. Such increased loading occurs by enhanced force transmission from the muscular stroma to structures other than the muscle’s origin or insertion tendons. Epimuscular force transmission may occur from the intramuscular stroma onto the epimysium of synergistic muscles or extramuscular neurovascular tracts, as well as onto other structures such as septa, general fascia, interosseal membrane and periost. Epimuscular loads exerted on a muscle can have distal or proximal directions. In CP patients, the presence of enhanced distal loads on FCU seems evident from the observations that after distal FCU tenotomy the muscle is kept at length and that subsequently extending the wrist stretches both passive and active FCU muscle. These distal loads applied to FCU are exerted via extramuscular connective tissue structures. Branches of the neurovascular tracts that are embedded in these structures generally enter the muscle from proximal directions. If neurovascular tracts are thicker, such loading will chiefly yield in proximal epimuscular loads on FCU. Myofascial force transmission via such tracts has also been shown to be effective in rodents. If the extramuscular connective tissue is stiffer in spastic patients, extending the wrist will cause simultaneous proximally and distally directed epimuscular loads to be exerted on FCU. A very special effect of oppositely directed myofascial loads on FCU is that force can be transmitted locally through the muscle without being exerted at its origin and insertion. Because of this condition, it is feasible that a very small fraction of the sarcomeres arranged in series within FCU myofibres is kept at high length, whereas simultaneously the remainder of the sarcomeres within those fibres are at low lengths. Note that in spastic patients, it is conceivable that such specific local conditions have sizable effects on joints involved without being very apparent in muscular morphology. The following conclusions are drawn. No significant differences between control and spastic muscle were found regarding slope of the passive length-tension curves of myofibre segments, crosssection or myofibre type proportions. The altered connective tissue composition of FCU, secondary to spasticity, is manifest exclusively by thickening of its tertiary perimysium in a majority of our CP subjects.