Department of Rehabilitation Medicine, Emory University, Atlanta, GA, USA
The generation of controlled and precise contractile forces in our skeletal muscles is what fundamentally allows us to maintain posture, manipulate objects, and interact with our environment (Ghez, 1991). In this context, what we generally term "weakness" is often a major reason for loss of control in the genesis of a muscular contraction. Muscle weakness can occur from lesions at various levels of the nervous system that impact the output of either the upper motor neuron (UMN) or lower motor neuron (LMN). Disorders of LMNs refer to lesions that occur in the cells of the ventral gray column (or "horn") of the spinal cord or brain stem or in their axons (Waxman, 2003) and are discussed in more detail in Chapter 40 of Volume II, "Neuromuscular Rehabilitation: Diseases of Motor Neuron, Peripheral Nerve and Neuromuscular Junction". UMN lesions, occurring as a result of damage to the cerebral hemispheres or lateral white columns of the spinal cord (Waxman, 2003), are typically caused by strokes, traumatic brain injuries, infections, or tumors. Muscle weakness is considered one of the major causes of disability in patients with UMN lesion (Sahrmann and Norton, 1977; Gowland et al., 1992; Fellows et al., 1994). In light of this fact and considering that the primary symptom of cerebral injury is manifested in impairments of strength and motor control, the concept of weakness can be viewed in the context of stroke and traumatic brain injury.
Accordingly, the purpose of this chapter is to identify and describe weakness of the upper extremity (UE) through exploration of impairment in movements following cerebral injury. The present perspective of weakness is presented with respect to strength and the consequent relationship of strength to function. Weakness involves many factors and is discussed by addressing features of UMN, secondary muscular adaptations, and finally age related changes in the motor system. The extent to which weakness is a factor in determining a prognosis of motor recovery is explored, followed by aspects of therapeutic intervention. In concluding, limitations in our current knowledge about UE weakness are identified and suggestions for future study are provided.
Ng and Shepherd (2000) define strength as "the capacity of a muscle or group of muscles to produce the force necessary for initiating, maintaining, and controlling movement". Weakness, defined as the diminution of strength, would therefore reflect the reduced capacity of muscles to produce the necessary tension during conditions of voluntary loading of the musculoskeletal system (Smidt and Rogers, 1982; Bourbonnais and Vanden Noven, 1989). The measurement of strength is often recorded as the maximal amount of force exerted in a single attempt.
Factors contributing to inadequate strength as a basis for weakness
Several major determinants of strength include: recruitment, cross-sectional area, fiber type, length-force and force-velocity relationship, and kinesiol-ogy (Frontera et al., 2001b).
A coordinated, properly sequenced recruitment of motor units is an important precursor to the development of strength. The force generated by a normal muscle contraction depends on the number and type of motor units recruited, and the characteristics of that motor unit discharge. Tension is increased when either the number or rate of active motor units is increased.
The size of a muscle cross-sectional area is proportional to force generation and is related to the number and size of muscle fibers (Maughan et al., 1983). The length-force relationship of a muscle corresponds structurally with the number of cross-bridges, which are determined by the overlap of actin and myosin. Maximum force occurs with muscle length that offers maximum overlap between actin and myosin. Taking into account that muscle length is limited by the anatomy of joint motions, maximum force of a muscle is typically found to occur during the middle of the joint range of motion (ROM) (Frontera et al., 2001b).
Velocity and type of muscle contraction can also affect force generation, with the greatest force developing with a rapid eccentric contraction, compared to a slow concentric contraction. Moreover, torque generation is affected by the origin/insertion of a muscle relative to the axis of rotation about a joint. Insertions closer to the center of rotation produce a great arc of movement, but a lower maximal force. A greater force but smaller arc is generated when the insertion of the muscle is farther from the joint center.
Other functional constituents of the neuromus-cular system relevant to strength include local muscular endurance (the ability to resist muscular fatigue) and muscular power (force applied multiplied by the velocity of movement) (Deschenes and Kraemer, 2002). Limitations in endurance often interfere with completion of functional activities. For example, individuals with stroke may have enough strength to initiate gripping forces, but cannot maintain adequate force to continue to hold an object during transport. As many common movements take place in less than 0.2 ms, the ability to produce force quickly is also vital in daily activities. Consequently, muscular power, a function of speed and strength, should be another perspective to consider in evaluation of the impairment of weakness.
In summary, weakness can result from inadequate strength caused by limitations in force production. In addition, the resultant weakness is affected by architectural characteristics of muscle and how the generation of muscle torque changes over time (endurance) because of the task-specific demands upon the speed of movement (power).
18.3 The weakness-disability connection
Weakness is recognized as a major impairment causing disability (Gowland et al., 1992; Canning et al., 1999; Ng and Shepherd, 2000) and thus a primary obstacle to stroke recovery. The magnitude of joint torque generated in the hemiplegic UE may be impaired by as much as 53% compared to the nondominant arm of healthy individuals (McCrea et al., 2003). Strength is also impaired in the arm ipsilat-eral to the lesion (Colebatch and Gandevia, 1989; Andrews and Bohannon, 2000; Jung et al., 2002) by as much as 15% (McCrea et al., 2003).
To date, findings from studies of the hemiplegic UE suggest a moderate to strong correlation existing between muscle weakness and impaired motor function in patients after stroke (Ng and Shepherd, 2000). Torques measured during hand grip have been correlated with some hand function tests among patients in the acute and sub-acute post-stroke stages (Sunderland et al., 1989). In addition, isometric strength of elbow flexors strongly correlates with functional hand to mouth movements (Bohannon et al., 1991). Completion of the hand to mouth maneuver (simulating eating) relates positively to actual elbow flexor muscle strength (Spearman correlation = 0.829) and inversely to elbow flexion active ROM deficits (—0.853). Indeed, Bohannon et al. noted that patients with less than 3.0 kg of elbow flexion force cannot fully bring their hands to their mouths. Weakness in muscle contraction and the degree of co-contraction in paretic wrist flexors and extensors also correlate significantly with upper limb motor impairment and physical disability measures (Chae et al., 2002b). Muscle strength as reflected by electromyographic (EMG) activity correlates positively with UE scores on the Fugl-Meyer motor assessment (FMA) and the arm motor ability test (AMAT), while the presence of co-contraction of the antagonist muscles (as represented by the ratio of agonist to antagonist EMG activity) is inversely related to these outcome measures.
However, as Ng and Shepherd caution, correlations from these cross-sectional studies only indicate a level of association, not an actual causal relationship. Data from Alberts and colleagues (2004) indicate that absolute strength is not a predictor of dexterity in the UE, and that the ability to control grip forces has a greater impact on UE function than maximal strength. Indeed, patients who have sustained strokes are able to show improved control of force and torque generation in a functional activity, such as turning a key (Fig. 18.1), after repetitive task training without necessarily demonstrating large changes in UE strength. Accordingly, more research is required to explore the mechanisms by which an increase in strength may cause an increase in function as a basis for providing better justification in the treatment of UE weakness.
Figure 18.2, adapted from Ng and Shepherd (2000), outlines mechanisms contributing to impairment of muscle weakness. It is chosen as a model to discuss UE weakness to illustrate the multi-factorial aspects
of this impairment. These mechanisms may be classified into three primary categories:
1 features of UMN;
2 features of secondary muscular adaptation due to altered patterns of use (immobility and inactivity);
3 features associated with age-related changes in motor system.
Features of the UMN include:
1 lack of excitation arising in descending pathways,
2 direct changes in the agonist motor units,
3 active restraints of agonist motor activation,
4 passive restraints of agonist activation.
Features resulting from secondary muscular adaptation include:
1 length associated changes of muscle fibers and connective tissues in shortened position;
2 specific disuse weakness (atrophy of muscle fibers and impairments in motor unit activation).
Additionally, features associated with the aging process are possible contributing factors to weakness of a limb. Collectively these changes result in deficiencies in generating force and sustaining force output. Recognition of the many factors contributing to weakness allows the clinician to identify areas of movement impairment that may be amendable
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