Epimuscular myofascial force transmission between antagonistic and synergistic muscles can explain movement limitation in spastic paresis

Abstract

Details and concepts of intramuscular, extramuscular and intermuscular myofascial force transmission are reviewed. Some new experimental data are added regarding myofascial force transmission between antagonistic muscles across the interosseal membrane of the lower hind limb of the rat. Combined with other result presented in this issue, it can be concluded that myofascial force transmission occurs between all muscles within a limb segment. This means that force generated within sarcomeres of an antagonistic muscle may be exerted at the tendon of target muscle or its synergists.

Some, in vivo, but initial indications for intersegmental myofascial force transmission are discussed. The concept of myofascial force transmission as an additional load on the muscle proved to be fruitful in the analysis of its muscular effects. In spastic paresis and for healthy muscles distal myofascial loads are often encountered, but cannot fully explain the movement limitations in spastic paresis. Therefore, the concept of simultaneous and opposing myofascial loads is analyzed and used to formulate a hypothesis for explaining the movement limitation: Myofascially transmitted antagonistic force is borne by the spastic muscle, but subsequently transmitted again to distal tendons of synergistic muscles.

Introduction

Researchers as well as clinicians have grappled to explain the limitations in movement capability and the particular resulting joint positions (e.g. equinus of the ankle and a flexed position of the wrist) of patients suffering from spastic paresis.

This state of affairs may be irritating for scientists, but clinicians are affected more seriously: They are presented with patients suffering from the affliction and have to make decisions regarding treatment, despite the lack of detailed understanding of the mechanisms of the movement impairments. To be able to do that adequately they have developed a system of practical knowledge and concepts in which they can consider interventions to improve the patients’ condition. This knowledge has its definite value and contains elements that are not easily obtained by researchers, but usually lacks validation by detailed confrontation with experiential results. For a more detailed discussion see Smeulders and Kreulen (2007, Fig. 4, p. 650).

The other symposium articles presented in the present issue of this Journal, as well as the present work represent an attempt to try to limit the gap between the two types of disciplines as much as possible, and bridge it if possible.

The prime defect of spastic paresis is one of impeded neural control, thought to lead to exaggerated reflex activity in the affected muscle leading to enhanced resistance to lengthening, particularly if the lengthening of the muscle is executed rapidly. As a consequence the joint is held in a flexed position. This means that the target muscle and its synergistic muscles or muscle groups are kept at relatively low lengths for extended periods of time.

The question is raised time and again if we should consider a muscle that has been under spastic neural control for a long time a muscle with physiological muscle properties not principally different from healthy muscles, but fully adapted to the altered conditions imposed by the spastic neural control, or alternatively should be considered as having pathological characteristics itself.

Almost without exception in the clinical, as well as the scientific approach, of spastic paresis, muscles are considered as independent mechanical actuators, and as a consequence the movement limitation and characteristic joint posture is ascribed either to the acute effects of enhanced activity during stretching from low lengths or to limitations imposed by enhanced extramuscular connective tissue structures on the joint in the case of extended exposure to a particular joint position.

If one considers the acute effects after imposing spastic motor control of muscle (i.e. in a state of no muscle pathology), it is hard to understand why one active and shortened muscle should be able to maintain the specific and deviant joint position. A short muscle is likely to be active at the ascending limb of its length force curve and is likely to be able to exert only relatively small forces. As a naïve consideration, one could think that simply voluntarily increasing excitation of the antagonistic muscles, which are at higher lengths, should yield a net moment for ample movement away from the characteristic joint posture. Only severe limitations on excitation of the antagonistic muscle could prevent such action (It should, however, be noted that recent work reports indications of at least some limitation in antagonistic excitation in spastic paresis (Rose and McGill, 2005)). In addition, if the situation in spastic paresis would be very simple, the effect of botulin toxin, which inhibits neuromuscular signal transmission, should have acute effects on the movement limitations, as soon as it binds to its receptors at the postsynaptic sarcolemma. Clinically, it is clear that this is not the case.

Considering the recent work on epimuscular myofascial force transmission (Huijing, 1999a, Huijing, 1999b, Huijing, 2002a, Huijing, 2003, Huijing and Baan, 2003, Huijing and Jaspers, 2005, Yucesoy et al., 2003a, Yucesoy et al., 2003b), it is clear that muscles should not be considered as being mechanically independent. A prime purpose of this review is to analyze the principles of movement limitations of muscle under spastic control as a function of myofascial force transmission.