The primary basis of the functional approach to musculoskeletal pain syndromes is the interdependence of all structures from both the central nervous and musculoskeletal systems in the production and control of motion. Movement of noncontractile and contractile elements is produced and controlled by muscle activity. Ultimately, it is the central nervous system in response to various stimuli that controls the activity of muscles and, consequently, the pattern of motion in an individual’s musculoskeletal system. The muscular system lies at a functional crossroad because it is influenced by stimuli from both the central nervous system and the musculoskeletal system. Dysfunction in any component of these systems is ultimately reflected in the muscular system in the form of altered muscle tone, muscle contraction, muscle balance, coordination, and performance. Therefore, a strictly localized lesion does not exist. Muscle imbalance is a systemic change in the quality of muscle dysfunction that results in altered joint mechanics, leading to pain, dysfunction, and eventually degeneration. Muscle imbalance is the altered relationship and balance between muscles that are prone to inhibition or weakness and those that are prone to tightness or shortness. Moderately tight muscles are usually stronger than normal. However, in the presence of pronounced tightness, some decrease of muscle strength occurs. This weakness is called “tightness weakness,”¹ to express the closed association between muscle weakness and altered viscoelasticity of the muscle. Therefore, when diagnosing muscle weakness, careful differential diagnosis has to be made. The treatment of tightness weakness is not in strengthening, which would increase tightness and possibly result in a more pronounced weakness, but in stretching, oriented toward influencing the viscoelastic property of the muscle, that is, the noncontractile but retractile connective tissue. Stretching of tight muscles also results in improved strength of inhibited antagonistic muscles, probably mediated via the Sherrington’s law of reciprocal innervation.

The etiology and terminology of muscle tone is full of controversies, partly because various authors’ definition of muscle tone differs. Therefore, a detailed differential diagnosis has to be made among others because each condition requires a different type of treatment.² Unfortunately, a precise and adequate analysis is often neglected. An imprecise diagnosis results in disappointing therapeutic results. Unfortunately, the detailed physiology of muscle tone is unknown, and muscle tone changes caused by altered or impaired function have not been studied sufficiently in the laboratory or in the clinic.

In principle, it is necessary to differentiate whether the main changes occur in the connective tissue of the muscle (viscoelastic properties) or in overactivation of the contractile components of the muscle (contractile properties). According to Mense and Simons, “Muscle tension depends physiologically on 2 factors: the basic viscoelastic properties of the soft tissues associated with the muscle, and/or the degree of activation the contractile apparatus of the muscle.”³ In the former, we speak about muscle tightness, stiffness, loss of flexibility, or extensibility (length), and in the latter, it is a real increase of muscle contractile activity such as in spasmodic torticollis or trismus. In principle, with respect to viscoelastic changes, the muscle gets shorter at rest (decreased extensibility) either because of shortening of contractile muscle fibers or because of retraction of the connective tissue within the muscle and the adjacent fascia. With respect to contractile changes, the increased muscle tone may involve the majority of muscle fibers or only a limited number found as “taut bands” in trigger points.

Clinically, resting muscle tone presents a combination of both situations (contractile and viscoelastic properties), and it is the role of the clinician to establish an appropriate diagnosis.³ However, measuring muscle tone objectively presents a dilemma. Tests of viscoelasticity involve measurements of the velocity of motion, viscosity, thixotropy, and resonant frequency when load is gradually applied.³ Tests of contractile activity are simpler in that electromyogram can be used; however, this is not without inherent difficulties as in trigger points where only small loci in the muscle show increased electrical activity.³

A detailed differential diagnosis of muscle tone is necessary for the proper treatment approach, and this can be accomplished by a combination of inspection and palpation (see Table 11.1). Layer palpation of the skin, subcutaneous tissue, fascia, fat, and any other structure in the area concerned, although purely subjective, is a practical clinical tool and with much practice and experience, detecting the type of muscle tone present in the concerned area can be skillfully achieved. Inspection of posture, movement patterns, and gait also yields invaluable clinical information about the underlying source of increased muscle tension.

Muscle imbalance should be considered a systemic reaction of the striated muscles. It is therefore
a general reaction of the whole muscle system, and not just an isolated response of an individual muscle.⁴ This view is strongly supported by recent findings of neurodevelopmental kinesiology that shows developmental movement patterns corresponding to the muscle imbalance found in children when their motor system is fully myelinized (at the age of 6-7 years) or in adults.^5,6,7 The basis from a neurodevelopmental viewpoint is that neonatal and early infant posture is maintained by a “tonic” muscle system. Subsequent neurodevelopment of the upright posture occurs with the coactivation of a “phasic” muscle system with the “tonic” muscle system. Failure of this coactivation between the tonic and phasic muscle system results in a muscle imbalance and is clearly evident in children with cerebral palsy where the “tonic” muscle system prevails. In addition, the typical muscle responses seen in chronic low back pain patients are observed to be identical or very similar to those that are seen in some structural lesions of the central nervous system. For example, in spasticity seen in a cerebrovascular accident or cerebral palsy, muscles that develop spasticity or even spastic contractures are those that commonly respond by tightness in musculoskeletal conditions. It is proposed that these typical muscle responses observed in the hemiplegic posture may be an extreme expression of the imbalance between the muscular chains that exist to some extent under normal physiologic conditions. Thus, the tendency for some muscles to develop weakness or tightness does not occur randomly but rather in typical “muscle imbalance patterns.”⁸ Furthermore, the development of these patterns can be predicted clinically, and preventative measures should be taken because muscle imbalance does not remain limited to a certain part of the body, but gradually involves the whole striated muscular system.⁹ A thorough evaluation is necessary to introduce preventive measures because muscle imbalance usually precedes the appearance of pain syndromes.

Muscle imbalance develops mainly between predominantly “tonic” muscles, that is, muscles that are prone to develop tightness, and predominantly “phasic” muscles, that is, muscles that are prone to develop inhibition (see Table 11.2). Muscle imbalance involves muscles of the whole body; however, if the imbalance is more evident or starts to develop gradually and predictably in the pelvic region, we speak about the pelvic or distal crossed syndrome, and if it is more evident or starts in the shoulder girdle/neck region, we term it as a proximal or shoulder girdle crossed syndrome.¹⁰

The proximal (upper, shoulder neck) crossed syndrome is characterized by the development of tightness in the upper trapezius, levator scapulae, and pectoralis major, and, on the other hand, inhibition in the deep neck flexors and lower stabilizers of the scapula. Topographically, when the inhibited and tight muscles are connected, they form a cross (see Fig. 11.1). This pattern of muscle imbalance produces typical changes in posture and motion. In standing,
elevation and protraction of the shoulders are evident, as are also rotation and abduction of the scapula, a variable degree of winging, and a push-forward head position. This altered posture is likely to stress the cervicocranial and the cervicothoracic junctions. In addition, the stability of the shoulder blades is decreased, owing to the altered angle of the glenoid fossa, and, as a consequence, all movement patterns of the upper extremity are altered.

The distal (lower, hip pelvic) crossed syndrome is characterized by tightness of the hip flexors and spinal erectors and inhibition and weakness of the gluteal and abdominal muscles. As in the upper crossed syndrome, a line connecting the tight and inhibited muscles forms a cross (see Fig. 11.2). This imbalance results in an anterior tilt of the pelvis, increased flexion of the hips, and a compensatory hyperlordosis in the lumbar spine. This imbalance tends to overstress both hip joints and the lower back.

A combination of these two syndromes is expressed in a layer (stratification) syndrome (see Fig. 11.3). When a layer syndrome is observed in a patient, it is a sign of a poorer prognosis in terms of rehabilitation because of the fixed muscle imbalance patterns at the central nervous system level.

Examination of joints must precede evaluation of muscles to exclude any anatomic barrier. In clinical practice, it is advisable to begin muscle evaluation by analyzing erect standing posture and gait. This analysis requires experience and keen observational skill. In addition, it serves as a screening tool by providing quick and reliable information to direct the clinician the necessary tests that need to be performed in detail and those that can be omitted. The clinician is given an overall view of the patient’s muscle function through posture and gait analysis and is challenged to look comprehensively at the patient’s entire motor system and not to limit attention to the local level of the lesion. Evaluation of muscle imbalance in a patient with an acute pain syndrome, however, is unreliable and must be undertaken with precaution. A precise evaluation of tight muscles and movement patterns can be performed only if the patient is or is almost pain free. Its usefulness is greatest in the chronic phase or in patients with recurrent pain after the acute episode has subsided.