For more than 15 years, researchers have focused on classifying patients with low back and neck pain (Ford JJ, Hahne AJ. 2013; Foster NE, et al. 2011; McKenzie R. 1981; O’Sullivan P. 2005; Van Dillen L, et al. 2003; Weiner B. 2008b; Delitto A, et al. 1995; Fritz J, et al. 2007; Kamper SJ, et al. 2010). However, as physical therapists, we do not have a framework or an identity for the knowledge we have about the anatomical or physiological system of the body, as other health professions do (Jull G., Moore A. 2013). In this context, the American Physical Therapy Association adopted a guiding principle in June 2013 stating that “the identity of physical therapy is the movement system, which is the core of physical therapy education, practice, and research” (APTA 14–13; APTA 15–13; Sahrmann SA. 2014).

The human movement system 

(Sahrmann S. 2002, 2010)

The primary effectors of movement are the musculoskeletal, neurological, and cardiopulmonary systems. Movement will be affected by impairments in any effector system, such as muscle weakness, relative stiffness issues, changed activation patterns, and pain. The other systems serve as support systems for the effectors, although they are also impacted by movement and inactivity. The evaluation is intended to detect deficits in the contributing systems and diagnose the movement system. Treatment is centered on movement in all of its manifestations, from manipulation to mobilisation to well-designed exercise programmes and education in proper functional and fitness activity performance.

The kinesiopathologic model

(Sahrmann S. 2002, 2010)

Movement system impairment syndromes are thought to be caused by repeated movements and lengthy alignments of daily tasks, as these behaviours generate alterations in the effector systems that can be classified as impairments. According to this notion, a sequence of impairments develop, culminating in a primary impairment that eventually causes pathological alterations in tissues. The syndrome is made up of various impairments that, when combined, contribute to the primary impairment, the diagnosis. These connections are depicted in the kinesiopathological model.

The goal of the kinesiopathological model is to emphasise the basic scheme for the development of movement system dysfunction syndromes. The basic mechanism underpinning the alterations is that the ‘body takes the path of least resistance for movement’. Biomechanics serves as a bridge between effector systems and is crucial to the adaptations caused by repeated motions and sustained alignments in daily activities. Personal traits also play a major role in modifying the types of adaptations caused by activities. Repeated movements can be considered characteristic of motor performance at first, but with time and repetition, a more permanent type of motor learning takes place. Tissue adaptations cause deficits in movement, which are thought to be in a joint’s accessory motion. This impairment is caused by changes in the relative flexibility of the joint as well as the relative stiffness of the muscles and connective tissues surrounding the joint. The restricted movement generates tissue microtrauma, which progresses to macrotrauma. This chain of events has resulted in movement system impairment syndrome. The disorders can be broadly classified based on whether the predominant weakness is in force output or motor pattern coordination. Force production deficits necessitate strengthening exercises in addition to guaranteeing appropriate activation patterns, whereas motor pattern coordination impairments necessitate just activation pattern training.

Movement System Impairment Examination

The exam is intended to offer a diagnosis, the primary disability, and the contributing variables. The patient first performs the test motion in his or her natural or preferred manner (primary test), while the therapist observes the precision of the motion and takes note of the influence on symptoms. The therapist next educates the patient on how to rectify the movement (the secondary test) and observes the effect on symptoms. The examination places a strong emphasis on identifying the motions of the spine and extremities that produce pain and teaching the patient how to move in order to eliminate or minimize the symptoms. This adaptation is required not only for specific exercises but also for all basic functional activities.

One of the benefits of the test is that the patient learns which movements produce discomfort and how to reduce or eliminate the symptoms. Another benefit is that the test items that the patient fails to correctly do become the exercise. The condition, or diagnostic, is the movement direction(s) that most frequently cause symptoms. The exam also offers data on specific muscle performance, such as length, strength, stiffness, and activation patterns. As a result, the therapist gets important guidelines for constructing the neuromuscular workout program.

Treatment of Movement System Impairment

When a patient fails a test, the exam becomes an exercise in many ways. The identification of the incorrect movement direction also provides guidance for functional activity correction. As part of the assessment, the patient learns which movements create discomfort and how to remedy them. Functional activities, which are also a type of therapeutic exercise, must be corrected. Functional exercises encompass everything from rolling to sleeping position, transitioning from supine to sitting, sit-to-stand and reverse, walking, and stair climbing. The patient’s sitting position and chair types must be evaluated, as well as any fitness programs or sports in which he or she participates.

Movement System Impairment Research

To assess the validity of the classifications and examine parts of the kinesiopathologic model, clinical and laboratory-based studies of people with chronic low back pain who were not in an acute flare-up were conducted.

Therapists were reliable in detecting the influence of specific movement tests on symptoms and finding impaired movement. The accuracy of classification was between 70 and 80% (Henry SM, et al. 2013; Norton BJ, et al. 2004; Trudelle-Jackson E, et al. 2008). The finding that correction and prevention of spinal motion imposed by extremity movements during examination tests decreased or eliminated symptoms supported the premise that symptoms are related to lumbar spine movement during both direct spinal motion and movement of the extremities (Van Dillen LR, et al. 2001; Van Dillen LR, et al. 2003; Van Dillen LR, et al. 2009). Imposed spinal movement includes lumbar flexion-rotation during seated knee extension and lumbopelvic rotation during prone hip rotation (Van Dillen LR, et al. 2001; Van Dillen LR, et al. 2003; Van Dillen LR, et al. 2009). Validity was proven for extension, extension-rotation, and rotation based on the results of examination tests connected with direction-specific lumbar motions (Van Dillen LR et al. 2003). Mobility-capture experiments supported the fundamental hypothesis that patients with low back pain had a few degrees of spinal mobility that occurred too frequently. Knee flexion and hip rotation in the prone position were two tests used to measure spinal readiness to move. Participants with LBP displayed earlier and greater lumbopelvic rotation than back-healthy participants in both tests (Scholtes SA et al. 2009). The initiation of motion in participants with low back pain was only a few seconds earlier and less than 5 degrees higher than the commencement of motion in back-healthy participants, confirming the notion that such lumbar motion readiness is problematic (Scholtes SA et al. 2009). The lumbopelvic rotation during hip rotation in prone position was observed to trigger symptoms in 60% of males with LBP but only about 30% of women (Gombatto SP, et al. 2006; Hoffman SL, et al. 2011; Scholtes SA, Van Dillen LR, 2007; Hoffman SL, et al. 2011; Hoffman SL, et al. 2011; Hoffman SL, et al. 2011).

Lumbopelvic rotation also occurred earlier in men than in women (Gombatto SP, et al. 2006; Hoffman SL, et al. 2011; Scholtes SA, Van Dillen LR. 2007; Hoffman SL, et al. 2011; Scholtes SA, Van Dillen LR. 2007; Hoffman SL, et al. 2011). The hip lateral rotation test results also revealed discrepancies between two LBP classifications (Van Dillen LR et al. 2007). In the rotation syndrome, the same degree of hip lateral rotation of both the right and left lower extremities provoked the onset of lumboplevic rotation, whereas in the extension-rotation syndrome, the onset varied with hip lateral rotation of the right vs. left lower extremity. This finding lends support to the basic concept of relative flexibility: the lumbar spine moves too easily in a specific direction, and this behaviour differs according to classification. The test of trunk lateral bending revealed symmetrical onset of lumbopelvic rotation in the rotation syndrome and asymmetrical onset in the extension-rotation syndrome (Gombatto SP et al. 2008; Gombatto SP et al. 2013). Early lumbar motion quantification revealed symmetrical motion to the right and left in the rotation syndrome and asymmetrical motion in the extension-rotation syndrome.

Research investigations support the concept that early and regular repetition of modest degrees of lumbar motion in certain directions contributes to tissue microtrauma that progresses to macrotrauma. Support the concept that clinical examination findings can consistently and validly identify patients with LBP based on symptom-producing motions and the readiness of the spine to move in a specific direction. Furthermore, correcting or stopping the spinal motion can reduce or eradicate the symptoms; however, preventing the offending motion and lumbar stabilisation should be emphasised during functional tasks and exercises. According to one study, patients with LBP had a more difficult time limiting lumbopelvic rotation during hip lateral rotation than back-healthy participants (Scholtes SA et al. 2010; Scholtes SA et al. 2013). This finding implies that specific instruction and training are required to gain the best benefits from a stabilisation strategy.

Conclusion

The Movement System Impairment Syndrome approach arose from a thorough assessment and treatment of low back pain patients. A routine assessment revealed that spinal motions in specific directions frequently triggered symptoms. Symptoms were reduced or abolished when the movement was corrected or prevented during extremity motions.

A derived kinesiopathologic model proposes that the impaired, painful movements exist prior to the development of symptoms, implying that there are signs before symptoms and that the impairments (specifically altered activation patterns) are caused by musculoskeletal and nervous system adaptations. The inherent relative (directional) fexibility of the joint, as well as the relative stiffness of muscle and connective tissues, are key characteristics of the model. This becomes troublesome since the body moves along the path of least resistance. Syndrome classification is based on the willingness to move in a specific way.

Clinical and laboratory investigations have been conducted to evaluate the examination, the validity of the classifications, and the model’s elements. Future research will evaluate the efficacy of classification-specific treatment, the mechanisms that induce movement readiness, and the underlying diseased tissue alterations.

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