Osteopathic model of the development and prevention of occupational musculoskeletal disorders

Pathophysiology

The biomechanical–structural model views health from the perspective of the musculoskeletal system and its interconnected groups of bones, muscles, ligaments, tendons, and fascia. Disturbances of the musculoskeletal system result in spinal reflex disturbances and subsequent dysfunction of somatic and visceral structures which lead to morbidity [41].

Poor ergonomic design of the work environment leads to awkward movements and postures that place biomechanical stresses on joints, muscles, and tendons. Injury occurs when demands are placed upon tissues that are greater than the tissue’s structural or physiological capacity to meet the demands. The incidence of occupational injuries is related to physically demanding factors, including substantial physical exertion, lifting or carrying more than 10 lbs, using stairs and inclines, kneeling or crouching, and reaching [4]. These risk factors reflect ergonomic stresses resulting from prolonged or awkward postures, repetition without adequate recovery time, or the requirement to lift or move excessive loads. Some ergonomic stressors bring soft tissues into proximity of bone, leading to friction and inflammation, and others place undue strain on muscles and connective tissues [5], [7]. Baseline postural abnormalities and dysfunctional movement patterns likely predispose the worker to these effects.

When muscles are used in unsuitable ergonomic environments, additional motor units must be activated to maintain strength, which begins within the first minute of a contraction, particularly with a fatiguing effort [42]. Tonic muscles are more susceptible to motor unit recruitment than phasic muscles [42]. Abnormal shear stress develops between newly recruited motor-units and adjacent motor-units. Eventually, shear transmission leads to myocyte damage as the muscle continues working despite fatigue or somatic dysfunction [5]. This process impairs movement patterns and joint mechanics.

Dysfunctional movement patterns and altered joint mechanics increase the physical strain exerted on tendons and often place tendons against the abrading surface of adjacent bone [7]. Tendon straining results in fiber deformation [43]. The collagen fibers become more parallel as strain increases, slide adjacent to one another, and generate shear forces [43]. The tendon will recoil back to its original conformation when unloaded if the strain stays below 4%; strains of 4–8% result in microscopic failure, and strains of 8–10% result in macroscopic failure [43].

Microtrauma within tendons may also result from nonuniform stresses produced by changing motor unit activation patterns. Nonuniform stress creates regions of excessive loading in the substance of the tendon and excessive shear forces between adjacent fibrils. Accrued microinjuries result in steady deterioration in the quality of the tendon matrix [44]. Transformation of the tendon matrix from organized type I collagen fibrils to randomly organized, small diameter fibrils containing type I and type II collagen follows; these changes bring about tendinopathy [44]. Some workers have medical comorbidities, such as Ehlers–Danlos syndrome, diabetes, and rheumatoid arthritis, that make their tendons more vulnerable to this process [45].

Dysfunctional joint mechanics also increase the load exerted on some ligaments, and with the application of a constant load, fascia and ligaments lengthen, or creep, because of disrupted crosslinks within the collagen fiber matrix of fascia and ligaments [6], [41]. There is less capacity for creep to occur without significant damage in ligaments relative to other myofascial structure because of the relative rigidity necessary for ligamentous function. Therefore, ligamentous creep is associated with declining ligamentous tension, subsequent joint laxity, reduced stability, corrupted afferent signals, and increased injury risk. High frequency repetitive motion tasks produce a significant degree of creep requiring extended recovery periods. There is a risk of creep accumulating from one day to the next if recovery is incomplete, which leaves the worker predisposed to injury [6]. Workers with benign joint hypermobility syndrome, Marfan syndrome, and Ehlers–Danlos syndrome are especially vulnerable to this effect [7].

Interventions

To mitigate these processes, one must attempt to achieve the best possible interface between the worker and the work environment. Preplacement physical examinations are a primary prevention intervention meant to determine a new hire’s capacity to meet the demands of the job and to identify any disorders or medications that may place the employee at risk for injury [46]. Studies investigating preplacement examinations have been too heterogeneous for statistical pooling of results, and the quality of the evidence for all outcomes is very low [46]. However, a Cochrane review supports the use of job‐specific preplacement examinations [47].

Another primary prevention intervention is a workplace ergonomic program. Many employers use systematic ergonomic improvement processes to remove risk factors that could lead to musculoskeletal injuries with the goal of improving employee performance and productivity. However, except for office environments and computer workstations, evidence supporting the effectiveness of ergonomic interventions is inconclusive [15], [16], [26], [34], [48]. Ergonomic assessments are best used in conjunction with job-matching processes.

Education programs attempt to mitigate the risk of work-related back injuries by increasing the participant’s knowledge, thereby altering the individual’s behaviors to mitigate biomechanical risk. These programs typically cover anatomy, biomechanics, lifting, postural changes, and home exercises [48]. However, a systematic review [48] and metaanalysis [49] presented strong and consistent evidence that education alone does not seem to prevent back pain and comprehensive “back schools” are not effective in preventing neck and back pain.

Job-rotation programs are often recommended as a primary and secondary prevention measure to mitigate continuous exposure to risk factors for musculoskeletal disorders. In terms of risk control, job rotation is defined as a strategy for rotating workers between tasks with different physical demands to avoid overloading specific body parts [50]. Currently, only weak evidence supports job rotation as a strategy for the prevention and control of musculoskeletal disorders, and although it does not appear to reduce the exposure of physical risk factors, there are positive correlations between job rotation and higher job satisfaction [13], [50].

Strength training is gaining acceptance as a primary and secondary prevention intervention [22], [29], [32], [33], [37]. It appears that implementation of strength training at the workplace not only prevents deterioration of work ability among manual workers with chronic pain, but also bolsters mental resources and improves perceptions of work demands [38]. A 2016 systematic review [51] found strong evidence for using resistance training for the prevention of work related upper extremity injuries resulting from sedentary work. Physical therapists could work with supervisors to develop strength training programs that harden workers to their duties and maintain balance between tonic and phasic musculature.

Shoe inserts and lumbar supports have been used to align and support the musculoskeletal system to decrease demands placed upon tissues with the hope of preventing musculoskeletal pain and injuries. However, evidence from systematic reviews [49], [52] suggests that shoe insoles do not prevent low back pain. There is moderate evidence that lumbar supports are no more effective than no intervention or lifting training in preventing low back pain. There is conflicting evidence for lumbar supports being effective supplements to other preventive interventions [53]. Furthermore, National Institute of Occupational Safety and Health has asserted that there is insufficient evidence to support the use of lumbar supports as a primary prevention measure [54]. These findings are not unexpected as they do nothing to improve muscle strength, muscle endurance, or joint mechanics.

Osteopathic manipulative treatment (OMT) may be used for primary prevention by optimizing workers’ musculoskeletal system, secondary injury prevention as part of an early symptom intervention program, or tertiary prevention as a component of a comprehensive injury management program [41]. According to this model, the goals of the OMT techniques are to restore balanced posture and efficient function of musculoskeletal components. These goals may be accomplished using high-velocity, low-amplitude, muscle energy, counterstrain, myofascial release, ligamentous articular techniques, and functional techniques [41].

Any identified muscle imbalance syndromes should be managed to maintain functional homeostasis. The Janda approach to treatment of muscle imbalance follows a three-step process: (1) normalization of the peripheral structures using the techniques noted above, (2) restoration of balance between the tonic and phasic muscle systems, and (3) balance and coordination training [7].

Pathophysiology

The neurologic model considers how autonomic equilibrium, neural reflex activity, segment facilitation, afferent nerve signals, and nociception contribute to injury and disease. With the neurological model, the physician considers the function of the patient’s central and peripheral nervous system, including both the somatic and autonomic components [9]. The implications of this model are particularly significant for workers with preexisting proprioceptive deficits, peripheral sensitization, central sensitization, autonomic dysfunction, or fibromyalgia.

Musculoskeletal disorders occur when the demands of work exceed the strength or endurance of the worker. The disparity between demands and capacity produce abnormal tissue stresses, early fatigue, and muscular imbalances [7]. Consequently, one of the body’s inherent reflexes will eventually activate as a protective response known as the myotatic reflex, the inverse myotatic reflex, the withdrawal reflex, and the ligamento-muscular reflex [55]. The reflexes send information to the spinal cord where the signal is processed, and a response is generated. Except for the inverse myotatic reflex, the descending systems respond by facilitating both alpha- and gamma-efferent neurons to provoke a protective action [55]. Coactivation of alpha- and gamma-efferents helps to maximize the protective response by contracting the muscle and increasing its sensitivity to stretch [55]. These reflexes are normally fleeting; however, when they persist, they produce somatic dysfunction. Somatic dysfunction is impaired or altered function of skeletal, arthrodial, and myofascial structures, along with associated vascular, lymphatic, and neural elements. Somatic dysfunctions produce tissues texture changes, positional asymmetry, motion restriction, and tenderness, which are amendable to OMT [41].

There is normally a balance between reflex habituation and sensitization with repetitive stimulation; however, this balance is disrupted when inflammation is present. The normal dampening effects of habituation shift toward sensitization, which is a state of subthreshold excitation that requires less afferent stimulation to trigger a reflex response [55]. Sensitization is also known as spinal facilitation, and long-term sensitization begins if sensitization continues for several minutes. If the stimulus endures, spinal fixation will begin to develop. Nociceptive input for as little as 20–45 minutes may produce increased reflex sensitivity for three or more weeks [55]. Peripheral inflammation causes some spinal cord microglial cells to begin expressing proinflammatory cytokines including interleukin-1β and tumor necrosis factor-α, which facilitate excitatory pain circuits and impede inhibitory pain circuits [56]. This process produces hyperalgesia and allodynia. Referred pain and hyperalgesia may ultimately cross multiple spinal segments as the cytokines diffuse to neighboring spinal levels [57]. Once fixation is well established, interneurons die by a process that primarily affects the inhibitory interneurons, often replacing them with excitatory interneurons. These spinal reflex pathways may be left in state of permanent excitability, responding to all input in an exaggerated fashion, which increases the neuron drive to the associated somatic and visceral structures [55].

Not all muscles react in the same manner—tonic and phasic muscles work synergistically. Tonic muscles are the prime movers or agonists and are prone to hypertonicity and shortening [7]. Phasic muscles are the synergists that work with the agonist to produce movement or stabilization around a joint, and they may be secondary movers, stabilizers, or neutralizers [7]. The synergistic interactions of tonic and phasic muscles assure balanced movement patterns. Phasic muscles have a propensity for lengthening and becoming hypotonic. Due to high-frequency firing of gamma-efferent neurons, the small alpha-motoneurons of tonic muscles respond to stretch by discharging for much longer duration relative to the large alpha-motoneurons innervating phasic muscles [58]. This action suggests that a tonic muscle will respond more readily to stretch and become more hypertonic than its phasic synergist.

The relationship between muscle length and spindle firing rate is used by the central nervous system to gauge position [59], which requires the spindle fibers to remain passive with no fusimotor activity [60]. With somatic dysfunction, the fusimotor system is activated [55]. This activation impairs position sense, alters movement patterns and affects biomechanics [61], [62], [63], [64]. The impaired joint mechanics stress the area of the tendon commonly affected by tendinopathy [8].

The musculoskeletal system receives sympathetic innervation and receives no parasympathetic innervation. Muscle hypertonicity and nociception activate afferents and stimulate the sympathetic nervous system. This affects functional changes of the associated vascular structures and results in vasoconstriction with decreased oxygen and nutrient delivery, and subsequent tissue texture changes [55].

Interventions

Preshift stretching sessions are commonly used in workplaces for primary prevention of injuries by lengthening hypertonic muscle and reducing resting tone [39], [48], [65]. However, stretching may produce creep and tendon deformation, and reduce muscle force generation [43]. A previous systematic review [65] provided mixed findings but demonstrated some limited beneficial effect of stretching in preventing work-related musculoskeletal disorders for occupations not requiring heavy exertion. Therefore, stretching programs should be limited to occupations that are sedentary, such as office work and data entry [39]. This may be related to which muscles are being stretched relative to which muscles are being over- or underutilized. When phasic muscles are stretched, they lengthen and become more hypotonic, which results in further muscle imbalance, performance declination, and greater risk of injury [7]. However, tonic muscles become less hypertonic when stretched, restoring muscle balance [7].

OMT is directed at restoring normal muscle function and joint mobility to reduce the level of afferent input to the spinal cord and brain [66], and it is also used to restore autonomic balance [55]. The OMT techniques used for this domain of worker health include counterstrain, cranial osteopathic manipulative medicine, paraspinal inhibition, rib raising, and progressive inhibition of neurological structures [41].

Balanced ligamentous tension, balanced membranous tension, and craniosacral techniques can influence autonomic nervous system activity by increasing parasympathetic function and decreasing sympathetic activity, compared with sham therapy and control group [67]. The compression of the fourth ventricle (CV-4) technique has been shown to lower the tone of the sympathetic nervous system and enhance fluid exchange [68]. Rib raising is believed to temper sympathetic nervous system activity by activating the thoracic sympathetic chain ganglia adjacent to the costotransverse articulation [69], while counterstain has been shown to decrease the amplitude of the stretch reflex [70].

Pathophysiology

In industry, effective injury reduction programs should go beyond traditional methods of job-related ergonomic risk factors and address factors that appear to decrease capacity, including smoking, nutrition, and body weight. The metabolic–energy (nutritional) model addresses the need for homeostatic balance between the body’s energy reserves and the energy demands [9]. The goal of the metabolic–energy (nutritional) model is to optimize self-regulatory and self-healing mechanisms by promoting balanced energy expenditure and exchange, which augments cellular, tissue, and organ functions [9]. This is achieved through nutritional counseling, diet, and exercise advice [9], [41]. According to this model, any factor (e.g., advanced age, poor nutrition, smoking, and obesity) that limits a person’s physiologic reserves will increase their risk of injury, delayed recovery, impairment, and disability [9]. Certain medications such as anticholinergics, alpha-agonists, and anticonvulsants decrease one’s physiologic reserve by impairing fatigue resistance and coordination [71]. Preexisting physical deconditioning, muscular imbalance, physical impairment, pain, and medical comorbidities are also known to lower physiologic resources and leave workers susceptible to the effects of fatigue [72], [73], [74], [75].

Muscle fatigue leaves workers vulnerable to overuse and overexertion injury, as well as slips, trips, and falls [72], [73], [74], [75]. Reduced oxygen availability lessens the recruitment of fatigue-resistant type I (slow-twitch) muscle fibers. Consequently, more type II (fast-twitch) muscle fibers need to be activated under hypoxemic conditions to maintain a constant workload. Type II muscle fibers are associated with an increased rate of metabolite accumulation and fatigue development compared with type I muscle fibers [76], [77].

Phasic muscles have a greater proportion of type II fibers, which are high in glycolytic enzymes and myosin ATPase activity and depend on anaerobic metabolism [78]. Consequently, these muscles fatigue rapidly and respond to irritation by weakening; this weakening is a significant problem that produces muscular imbalance associated with abnormal joint mechanics and early fatigue [78]. Preexisting muscle imbalances increase a worker’s susceptibility to this effect. Phasic muscles must work harder to compensate for dysfunctional tonic muscle to maintain proper movement patterns [79]. As the phasic muscles fatigue, ability to compensate is lost and injury ensues.

Calcium accumulates with sustained muscle use and degrades cell membrane proteins by activation of protease calpain, which leads to calcium influx, leakage of lactate dehydrogenase, and cell death [5], [80]. Dead and damaged cells release endogenous proteins called damage-associated molecular patterns, which bind to the nucleotide binding domain and leucine-rich-repeat-containing receptors within monocytes, macrophages, and dendritic cells [81]. This process activates proinflammatory pathways that produce inflammatory mediators, and bradykinin, prostaglandin E2, and serotonin are liberated and sensitize group IV nociceptors [82], [83]. Nociceptor stimulation disrupts alpha- and gamma-efferent homeostasis further.

These inflammatory mediators act upon the vasculature and result in vasodilation and increased vascular permeability [84]. Excessive accumulation of interstitial fluid is deleterious to tissue function [84]. The formation of edema increases the diffusion distance of oxygen and nutrients, and it also limits the diffusion and clearance of toxic byproducts of cellular metabolism [84]. This leads to poor nutritional support and waste clearance for the innermost cells of the involved capillary bed, and the vitality of these cells rapidly declines [84]. This effect is accelerated by poor baseline nutritional status, and plasma proteins accumulate in the area and trigger chronic inflammation, fibrosis, and dysfunction if they remain stagnant [85]. Pain develops as prostaglandins and nitrogenous waste builds up. Group III and group IV nociceptors are stimulated, and gamma-efferent firing rate is increased [83]. Functional impairment and disability may result if the cycle of dysfunction continues uninterrupted.

Interventions

There are many significant cofactors for workplace injuries that cannot be accounted by through ergonomic factors or employee characteristics such as aging, medical history, and physical impairments. Preplacement physical ability testing (PAT) was first implemented during World War II to meet this shortfall [86]. These tests are intended to measure a new hire’s physical capacity and fatigue resistance. Occupational injuries decrease significantly when the results of a well-designed PAT are compared with the job requirements to identify limitations and to assign restrictions for the purpose of job matching [18]. A meta-analysis [87] of the three predictive validation studies of pre- and post-implementation of a physical ability test battery were performed at 175 locations in different industries including food distribution, soft drink distribution, and retail distribution. These studies covered a total of more than 21 million worker-hours pre- and post-implementation. The findings indicated that newly hired employees who passed a battery of strength and endurance tests based on ergonomic analysis had a 47% lower relative worker compensation injury rate (α<0.001) and 21% higher relative retention (α<0.05) [87].

More energy is required to work with an injury, and it is diverted away from healing to meet the demands of continued activity [9]. Work restrictions based on knowledge of the workers’ duties are an important component of secondary and tertiary prevention programs for work-related injuries and the maintenance of energy homeostasis. Risk, capacity, and tolerance must be considered to return a patient to work after injury [88]. Risk is the chance of incurred harm to the patient or public if specific work tasks are undertaken, and it is the reason for physician-imposed restrictions concerning what the injured worker should not do [88]. Capacity refers to measurable limits of strength, flexibility, and endurance; if needed, objective measurement of strength, flexibility, and endurance can be gathered with a functional capacity evaluation. A capacity deficit is a reason for physician-described limitations for the injured worker [88]. Tolerance is a psychological concept and not quantifiable; it describes what the employee is willing to do. Brief physician-imposed restrictions may be appropriate for acute injuries. However, long-term physician directed restrictions or limitations may lead to iatrogenic disability [88].

Nutritious foods supply the building blocks needed to recover from an injury. The 2015–2020 Dietary Guidelines for Americans [89] advise following a healthy eating pattern across one’s life span. These guidelines can help workers understand how they should eat to maximize the recovery process and focuses on eating a variety of foods, while limiting calories from added sugars and saturated fats and reducing sodium intake [89]. A healthy eating pattern includes a variety of vegetables from all the subgroups, including those that are dark green, red, or orange; legumes; and starchy tubers. Whole fruits and grains, fat-free or low-fat dairy (including milk, yogurt, cheese) and fortified soy beverages are recommended. The recommended protein sources are seafood, lean meats and poultry, eggs, legumes, nuts, seeds, and soy products. A healthy eating pattern limits saturated fats and trans fats, added sugars, and sodium.

The triage theory suggests that modest micronutrient deficiencies induce reallocation of nutrients to processes necessary for immediate survival at the expense of long-term health. Certain groups, such as patients who are obese, are susceptible to nutrient deficiencies that may impair healing and delay recovery and increase the risk of developing chronic medical conditions. Most vitamins are deficient in patients who are obese, particularly the fat-soluble vitamins, folic acid, vitamin B12, and vitamin C [90]. Gastric bypass surgery often leads to the malabsorption of nutrients and subsequent nutritional deficiencies. The most common deficiencies are vitamin B12, folate, zinc, iron, copper, calcium, and vitamin D [91]. Vegan diets are growing in popularity for many reasons. However, people following a vegan diet are at risk for deficiencies in vitamin B12, iron, calcium, vitamin D, omega-3 fatty acids, and protein [92]. Patients in these categories should have their micronutrient levels monitored annually and supplementation provided if indicated.

From 2014 to 2016, 15.5% of working adults in the United States were current tobacco smokers [93]. Smoking cessation interventions should be included in each level of injury prevention. Smoking appears to lower the threshold of fatigue, while reducing maximal aerobic capacity [94]. Furthermore, smoking reduces parasympathetic nerve activity and activates sympathetic cardiac control [94]. There is also evidence of adverse effects on intervertebral discs, muscles, tendons, cartilage, and ligaments [95]. Clinical and experimental studies have revealed that smoking-induced skeletal muscle damage is due to impaired muscle metabolism, increased inflammation and oxidative stress, overexpression of atrophy related genes and activation of various intracellular signaling pathways. Besides a reduction of the muscle mass and strength, smoking is also associated with a higher risk of muscle pain. There is a positive relationship between the daily mean number of cigarettes, the total number of cigarettes smoked in life, and the severity of rotator cuff tears. Smoking is also a strong risk factor for distal biceps tendon rupture; smokers have a 7.5 times greater risk of distal biceps tendon rupture compared with nonsmokers [96]. Occupational medicine physicians are encouraged to screen all injured workers for tobacco use, offer smoking cessation counseling, and provide pharmacotherapy when appropriate [97].

Pathophysiology

The respiratory–circulatory model considers the role played by the circulation of blood and lymph through the body to maintain extracellular and intracellular environments by delivering oxygen and nutrition, while removing metabolic waste [9], [41]. Cardiac disease, respiratory disease, peripheral vascular disease, venous insufficiency, and musculoskeletal dysfunction interfere with the respiratory–circulatory function, thereby increasing the potential for developing disease and delaying recovery from injury.

Cells need a relatively constant and favorable environment to produce the energy needed for normal function. Circulation is the cell’s connection to the rest of the body, delivering the required nutrients and removing metabolic waste products. Intramuscular pressures near activated motor units often exceed systemic blood pressure compressing small blood vessels, producing local hypoxia. Upon reperfusion, free radicals damage the skeletal muscle membrane and impair sarcoplasmic reticulum ion pump function [5]. Blood vessels also constrict in response to the increase in sympathetic tone, which aggravates local hypoxia. Exaggerated sympathetic outflow is harmful if it remains unchecked, and prolonged vasoconstriction leads to tissue ischemia and pain, further increasing the sympathetic tone and impairing recovery [55].

The extracellular matrix is an acellular three-dimensional macromolecular network composed of collagens, proteoglycans, glycosaminoglycans, elastin, fibronectin, laminins, and several other glycoproteins. This matrix organizes cells and provides them with environmental signals that direct site-specific cellular regulation [85]. Local inflammation leads to the formation of reactive oxygen and nitrogen species, and the release of hydrolytic enzymes. These substances destroy extracellular matrix proteins. This alters the compliance characteristics of extracellular matrix gel state such that interstitial pressure fails to increase as edema forms. Excessive accumulation of interstitial fluid is deleterious to tissue function as the diffusion and clearance of toxic byproducts of cellular metabolism is impeded [84]. The vitality of neighboring cells decline as they fail to get nutrition and waste accumulates; pain will be apparent as prostaglandins and nitrogenous waste builds up and local hypoxia develops [84].

Edema also creates undue fascial stress that causes the extracellular matrix to exert force upon fibroblasts [98]. Mechanotransduction induces changes within the fibroblast nucleus, altering gene expression [98]. Some fibroblasts differentiate into myofibroblasts, which have contractile properties and produce prestress within the fascia and fascial binding ensues [98]. Fascial binding disrupts the fluid channels of the interstitial space. Anchoring filaments, which attach to lymphatic endothelial cells to facilitate lymphatic filling, lose their mechanical integrity and more fluid accumulates [84]. If fascial distortions persist, fibrotic changes occur, and chronic motion restriction develops.

Interventions

Management is aimed at restoring normal mechanics of the thoracic spine and rib cage and improving movement of the transverse diaphragms. The OMT techniques used in this model are osteopathic cranial manipulative medicine, ligamentous articular strain, myofascial release, and lymphatic pump techniques [41]. Counterstrain may improve local circulation and result in improved delivery of nutrients, increased removal of metabolic waste, and reduced swelling [99]. These techniques are usually performed after treating any somatic dysfunctions of the spinal transition zones. Transition zones are areas susceptible to somatic dysfunction and biomechanical stress which lead to fascial binding and impaired diaphragmatic function. Dysfunction in these regions will result in alterations of the pressure gradients between the zones, adversely affecting the respiratory pumping mechanism, and the venous and lymphatic circulation [100].

Brief stretching of the fascia decreases transforming growth factor-β1 mediated fibrinogenesis and is a likely mechanism of action for myofascial release technique [101]. A systematic review by Ajimsha et al. [102] assessed the quality, results, and limitations of 19 RCTs. Myofascial release was demonstrated to be equal to or more effective than sham, conventional, and no treatment for various musculoskel etal and painful conditions. The authors concluded that myofascial release may be useful as either a sole therapy or as an adjunct therapy for a variety of musculoskeletal conditions, such as subacute low back pain, fibromyalgia, lateral epicondylitis, and plantar fasciitis [102].

Pathophysiology

The goal of the behavioral–psychosocial model is to improve the psychological and social elements of overall health [41]. This model recognizes that patient outcomes are strongly influenced by the patient’s perception of the environmental and psychological context of the primary complaint.

The psychological risk factors for injury and disability include dysfunctional aspects of thoughts, feelings, and behaviors that are barriers to achieving homeostasis. Social risk factors are exogenous stressors, such as lack of job control, low supervisor support, and complexity of the workers’ compensation system. These stressors are barriers to recovery for individuals that rely on passive coping strategies. Passive coping strategies, such as avoidance, suppression, rumination, and habitual motivation are associated with dysfunctional health behaviors and impaired recovery from injury [103], [104]. For example, passive coping strategies my lead to nonadherence to ergonomic measures, failing to exercise, continuing to smoking, and failing to follow dietary recommendations.

Fear-avoidance beliefs and behaviors, catastrophizing, distress, and pain behaviors appear to be closely associated development of disability. Catastrophization, anxiety, and negative emotions facilitate excitatory descending pain pathways and inhibit inhibitory descending pain pathways [105]. Psychological factors, especially distress, depressive mood, and somatization, increase one’s vulnerability for transition from acute to chronic low back pain [106]. The development of serious disability due to low back pain in a cohort of subjects with both structural and psychosocial risk factors was strongly predicted by baseline psychosocial variables, whereas structural variables on both MRI and discography testing at baseline had only weak association with back pain episodes and no association with disability or future medical care [107].

Central nervous system development and brain function later in life are adversely affected by exposure to adverse childhood experiences in a dose dependent manner, leaving those exposed with dysfunctional coping mechanisms and susceptibility to central sensitization [108]. Personality disorders are often the ultimate expression of these experiences; they complicate physician-patient interactions and employee-supervisor interactions. Borderline personality disorder is the most common personality disorder and is equally prevalent in men and women. People with borderline personality disorder use medical care more often than the general population. The causes are not yet clear, but genetic factors and adverse life events seem to interact to lead to the disorder. Borderline personality disorder is characterized by a pervasive pattern of instability of interpersonal relationships, poor self-image, and marked impulsivity beginning by early adulthood and present in a variety of contexts [109]. These workers are ill-equipped to handle stress and conflict. Proper modulation of the autonomic nervous system is vital to a functional stress response. The key component of this system appears to be the vagus nerve [110]. The Polyvagal Theory proposes that the evolution of the mammalian autonomic nervous system provides the neurophysiological substrates for adaptive behavioral strategies [111]. Evidence suggests that dysfunction of the parasympathetic component of the autonomic nervous system is a possible neurophysiological determinant of borderline personality disorder [108]. The exaggerated vagal withdrawal promotes mobilization behaviors which compromise social engagement. This leaves one prone to impulsiveness, hyperreactivity and emotional dysregulation, and each are a barrier to recovery from injuries.

Interventions

The assistance of a Workers’ Compensation liaison can help a patient navigate the complexities of the workers’ compensation system and facilitate approval for treatment modalities, imaging studies, and specialty referrals. This mitigates external stress and allows the worker to concentrate on recovering.

Periodic screening for depression, anxiety, and substance use disorders may be offered as a component of the company’s wellness program. A systematic metaanalysis [112] examined the effectiveness of workplace mental health interventions aimed at facilitating the recovery of employees diagnosed with depression or anxiety and found moderate evidence for two primary prevention interventions including enhancing employee control and promoting physical activity. Stronger evidence was found for cognitive behavioral therapy-based stress management. Little evidence was found for other secondary prevention interventions, such as counselling. Tertiary interventions with a specific focus on work, including exposure therapy and cognitive behavioral therapy (CBT)-based and problem-focused return-to-work programs, showed strong evidence for improving symptoms and a moderate evidence base for improving occupational outcomes [112].

Adding cognitive-behavioral interventions appears to lead to fewer health care visits, less work absenteeism, and less long-term disability for patients with work-related pain [14], [27], [28]. Cognitive behavioral training (CBTr) is rooted in cognitive behavioral theory, but it is not therapy. It is a didactic curriculum broken up into a series of progressive, purposefully ordered sessions, each one with a specific focus [14]. CBTr unfolds sequentially, guiding the participant through the process of retraining the brain and dissolving the emotionally dependent thinking, and it is meant to mitigate kinesiophobia and catastrophization, and foster problem-solving [14]. Success with CBTr is largely dependent on the active, cooperative participation of the worker.

The forebrain can influence the origin of the descending pathway located in brainstem nuclei via a mechanism termed cognitive emotional sensitization. Patients who are misinformed about pain will often consider their pain as threatening and demonstrate cognitive distortions such as catastrophic thinking and rumination. These patients tend to not comply with active treatments. A 2011 Institute of Medicine report on pain [113] recommended providing patients with pain education focusing on self-management and biological and psychological factors early in the patient’s course to prevent pain from becoming chronic. Pain physiology education helps to amend pain perceptions including catastrophizing and fear avoidance. Providing written pain education materials alone has not been shown to alter perceptions [114]. However, improvement was noted when the same written material is provided with two face-to-face educational sessions. Pain physiology education is indicated when the clinical picture is characterized by central sensitization and when maladaptive illness perceptions are present [114].

The use of a clinical decision tool, such as the Subgroups for Targeted Treatment-Musculoskeletal (STarT MSK) questionnaire to identify misconceptions regarding pain, fear avoidance, or catastrophizing may be advantageous [20]. The STarT MSK questionnaire assigns the patient to one of three stratified risk categories based on STarT MSK results. This stratified management approach improved care use and disability measures at 4- and 12-month follow-ups; measures of physical and emotional functioning, pain intensity, quality of life, days off work, and treatment satisfaction have been shown to be higher than those of the nonstratified current best practice control group [19], [20]. Low risk patients identified by the STarT-MSK tool should receive conservative care as determined by current clinical guidelines and OMT protocols for the given diagnoses. Moderate risk patients should receive guideline-directed care along with referral to physical therapy. High risk patients should receive care per guideline recommendations and are referred for psychologically augmented physical therapy if available. Limiting OMT techniques to gentle modalities such as Jones strain-counterstrain and myofascial release is recommended for this group. A referral for CBT can be considered to address any cognitive distortions if psychologically augmented physical therapy is not available.

The endocannabinoid system plays a functional role in nociception and each of the brain structures important for processing anxiety, fear, and stress [115]. Stress induces altered expression of two endocannabinoid molecules, anandamide (AEA), and 2-arachidonoyl glycerol (2-AG). Stress exposure reduces AEA levels and increases 2-AG levels. The decline of AEA levels contributes to the manifestations of the stress response and anxiety behavior, including activation of the hypothalamic–pituitary–adrenal axis [115]. Evidence suggests that OMT may ameliorate these effects by increasing levels of AEA [116], [117].

Furthermore, suboccipital decompression appears to decrease stress by increasing vagal tone. Rib raising decreases sympathetic tone by releasing the costotransverse articulations found underneath the sympathetic chain ganglion arising from T1 to L2 [118]. A single cranial OMT session appeared to restore sympathovagal balance after an acute mental stressor by dampening parasympathetic withdrawal and sympathetic tone [119].