CHAPTER 111 Deconditioning
INTRODUCTION
Most patients with an episode of low back pain will improve significantly in a relatively short period of time, while others with seemingly minor injuries and often times minimal imaging abnormalities go on to develop chronic low back pain and significant disability. It is believed that there is a reduced level of physical activity associated with their pain leading to a decreased level of fitness or deconditioning. In recent years there has been great interest in why some develop chronic pain and subsequent disability and deconditioning. There is also great interest in what is occurring from a physical as well as a psychological perspective. Deconditioning, or its related terms detraining and disuse, is a multifactorial process that occurs in multiple body systems and is often secondary to an inciting event. Medline lists more than 2.6 million articles published since 1996 related to deconditioning of the heart, vessels, cardiovascular set-points, bone, cognition, affect, and muscles. The common factor for the pathologic change to these varied systems revolves around exercise or, more precisely, a lack of exercise exacerbating pathology. Though deconditioning is a common search term, it is not an entity defined in Steadman’s Medical Dictionary. Moreover, existing literature has used the term in various related manners, depending upon whether the investigator is a physiologist, neurologist, physiatrist, or orthopedic surgeon. The favorite terms in the literature associated with deconditioning are: decreased exercise tolerance, decreased VO2 max, decreased ability of adaptation to functional demands, and general decreased performance in occupation and/or activities of daily living. With such an array of connotations and denotations, is it any wonder that the literature is conflicting at times?
Chronic low back pain is one of the most costly as well as the one of the most common diseases affecting industrialized societies today. While the incidence of lower back injuries has not changed over time, disability rates have increased sharply over the past 20 years.1 It has been estimated that a percentage as small as 20% of low back pain patients account for 90% of the costs.2 The enormous costs for the treatment including lost productivity and worker replacement has been estimated as high as US$837 billion3,4 secondary to chronic spinal disorders.
It has been proposed that with chronic pain there comes inactivity, disuse, and deconditioning. Kottke5 in 1966 stated, ‘The functional capacity of any organ is dependent within physiologic limits upon the intensity and frequency of its activity. Although rest may be protective for a damaged organ it results in progressive loss of functional capacity for normal organs.’ The decrease in function will be proportional to the duration, degree, and type of limitation of activity. Hasenbring et al.6 proposed physical disuse as a risk factor for chronicity in lumbar disc patients. Disuse or disuse syndrome and deconditioning are terms associated with this loss of functional capacity.
The disuse syndrome was first described by Bortz in 1984.7 He pointed out how our society had become progressively more sedentary, adhering to an anthropologic law called the Principle of Least Effort. This, stated simply, says when an organism has a task to perform it will seek that method of performance that demands the least effort. Focusing on the long-term adverse consequences of inactivity, he described the identifying characteristics of the syndrome as cardiovascular vulnerability, obesity, musculoskeletal fragility, depression, and premature aging. He did not consider the reasons for inactivity but observed that disuse is physically, mentally, and spiritually debilitating.
Mayer and Gatchel8 introduced the term ‘deconditioning syndrome’ in 1988. They felt deconditioning may be a response mediated physically by the injury as well as psychologically by a variety of secondary factors. Some of these include injury-imposed inactivity, neurologically mediated spinal reflexes, iatrogenic medication dependence, nutritional disturbance, and psychologically mediated responses to prior psychiatric distress, vocational adjustment problems, and/or limited social coping resources.9 As a result of inactivity, physical deconditioning represented by muscle inhibition/atrophy, decreased cardiovascular conditioning, decreased neuromuscular coordination, decreased ability to perform complicated repetitive tasks, and musculotendinous contractures ensues. They use the term ‘deconditioning syndrome’ to represent the cumulative disuse changes, physical and psychological, produced in the chronically disabled patient suffering from spinal and other chronic musculoskeletal disorders.
We will review the physical and psychological consequences of inactivity or disuse in patients with CLBP. Physical measurements have addressed muscle function or strength and endurance isometrically, isokinetically, and isotonically. Methods such as magnetic resonance imaging (MRI), computed tomography (CT) scanning, and electromyography have been utilized to measure changes in muscle composition and function. Cardiovascular capacity and motor control or coordination have also been measured in CLBP patients. Psychosocial issues or variables such as distress, depression, anxiety, and fear-avoidance beliefs and their relationship with CLBP will be reviewed.
DECONDITIONING: A HISTORICAL PERSPECTIVE
Original interest in a deconditioning syndrome was prompted primarily by two things. First, as part of the practice of medicine at one time, bed rest was often a prescribed treatment. However, physicians began to realize a multitude of adverse consequences secondary to this imposed immobility. Second, as the space program evolved, astronauts spent longer periods of time in a weightless environment, stimulating further interest on the affects of immobilization. Sixty years ago Dietrick et al.10 studied the effects of immobilization by placing four normal men in plaster casts from the umbilicus to the toes for 6 weeks and then followed them through a 4–6 week recovery period. They and other investigators observed a multitude of physiologic and metabolic changes. While our patients with CLBP certainly have not been immobilized to such a degree, a short review of that literature is enlightening.
During exercise, cardiac output, heart rate, and left ventricular function all increase. Even with moderate exercise cardiac output may triple, heart rate may double, and left ventricular effort may more than triple. Oxygen uptake with heavy exercise rises six times higher than that seen at rest. With inactivity, physical fitness decreases rapidly. Resting heart rate was reported to increase by 0.4 beats per minute during an immobilization period.11 Stroke volume decreased by as much as 30% during maximal exercise following a period of immobilization.11 The maximal oxygen uptake (VO2 max) is felt to be the most sensitive measure of physical fitness. A decrease in VO2 max of 21% after 30 days of bed rest was observed by Greenleaf.12 Pulmonary function as measured by total lung capacity, forced vital capacity, forced expiratory volume, alveolar–arterial oxygen tension difference, and membrane diffusing capacity remained unchanged or showed decreases only in proportion to decreases in cardiovascular output and maximal oxygen uptake.10,11 In these studies the immobilization was virtually absolute and cognitive, emotional, and social effects were observed as well as the physiologic and metabolic effects. With immobilization, skeletal muscle obviously undergoes atrophy as well as decreased strength, endurance, and coordination. Muller13 reported strength loss of approximately 3% per day for the first 7 days in the muscle of the upper extremity immobilized in a cast. Little further strength loss was observed with further immobilization. Bone marrow content is lost during immobilization, resulting in osteopenia or osteoporosis.14 This skeletal calcium loss is associated with increased urinary calcium excretion which begins to rise on the second or third day of immobilization.10,14 Decreased physical activity alone without actual confinement to bed may result in skeletal calcium loss.15 Gaber et al.16 have shown that patients with CLBP have an increased incidence of osteopenia and osteoporosis. Another metabolic consequence is a negative nitrogen balance with losses of 29–83 grams during 6–7 weeks of immobilization. This loss reflects the equivalent of 1.7 kilograms of muscle protoplasm.10
Before beginning our discussion of a deconditioning syndrome as it relates specifically to patients with CLBP, there are several terms should be defined. Verbunt et al.17 defined ‘disuse’ as performing at a reduced level of physical activity in daily life. They described ‘physical deconditioning’ as a decreased level of physical fitness with an emphasis on the physical consequences of inactivity for the human body, whereas Mayer and Gatchel8 included the psychological effects secondary to inactivity or disuse along with the physical consequences as part of their definition of the deconditioning syndrome. Verbunt chose to include the term ‘disuse syndrome’ in their discussion as well. The ‘disuse syndrome’ is defined as a result of long-term disuse, which is characterized by both physical and psychosocial effects of inactivity. Our discussion here will include a review of the literature on disuse or what is actually known about the level of physical activity in daily life of patients with CLBP. We have chosen to utilize the term deconditioning syndrome as defined by Mayer and Gatchel to represent the cumulative changes secondary to disuse, both physiological and psychological, produced in the patient suffering from CLBP. Thus, we can see how disuse leads to the deconditioning syndrome. The assumption is that we can show a significantly reduced level of physical activity resulting in deconditioning in patients with CLBP.
DISUSE
In 1946, Young18 described the effects of use and disuse on nerve and muscle. Introducing the term disuse into the medical literature, he described it as not using the musculoskeletal system during periods of immobility. Then Bortz in 1984 referred to the disuse syndrome and included many of the adverse consequences of inactivity in his definition beyond those affecting muscle and nerve. For purposes of this discussion we will define disuse as performing at a reduced level of physical activity.17 We are sure many of us hold the belief that our patients with CLBP are leading a very sedentary existence with an activity level significantly below that of the norm. But, in actuality, what is known about the activity level of these patients? In a group of patients with chronic pain (but not specifically low back pain) the Baecke Total Physical Activity Score was significantly higher in female than in male patients, a finding not observed in healthy controls.19 This study also revealed a statistically significant reduction in a physical work capacity index of 34% in males and only a 17% reduction in found in women, which hardly reached the significance level. The authors concluded that chronic pain may have a greater impact on activity level in male patients than in female patients, whereas Protas20 and Verbunt et al.21 found that physical activity in the daily life of patients with CLBP did not differ significantly from healthy age- and gender-matched controls. The physical activity in daily life expressed as whole-body acceleration measured with a triaxial accelerometer and as the ratio between average daily metabolic rate, measured by the doubly labeled water technique, and resting metabolic rate, measured by ventilated hood, was reported by Verbunt et al.21 Both techniques were used simultaneously for 14 days. They noted that the mean level of physical activity did not differ in CLBP patients when compared with healthy controls. Thus, they could not confirm the presence of disuse in this group of patients. Given that 77% of the patients in this study were employed despite their back problems, it is possible that the patients participating in this study were in relatively better physical condition than other patients with CLBP. Further measurements revealed no difference in percentage of body fat and body mass between patients and controls. They found it remarkable that although patients felt disabled because of their back pain as shown in their Rowland Disability Questionnaire scores, their level of physical activity as actually measured was not decreased in comparison with controls. They also noted there was no correlation between pain intensity and physical activity levels.
Several theories as to the reasons for the differing results with regards to the presence or absence of disuse have been offered. Work status may indeed have a significant impact on physical activity levels. On the one hand, in the study by Verbunt et al.21 77% of the CLBP subjects were working, whereas in Neilens and Plaghki’s studies19,22,23 only 20–34% of subjects had a paying job. Different methods for assessment of the degree of inactivity have also been employed. While Verbunt utilized physiologic measurements, others used self-reporting to assess physical activity levels. A discrepancy in reported functioning by patients and actual functioning has been reported.24,25 Physical activity levels as reported by patients with CLBP and as reported by their physical therapists revealed that the patients significantly underestimated their level of activity.25 It also has been shown that patients with CLBP have greater difficulty actually estimating their level of exertion during a performance test.24 From these studies, it would appear that self-reporting of activity levels in patients with CLBP is unreliable.
In summary, it is surprising that so few studies have been performed on the level of physical activities in daily life or disuse in patients with CLBP. The results have been equivocal and thus, despite what our beliefs may be about the activity level of these CLBP patients, the literature does not support the definitive presence of a reduced activity level. This lack of a decreased activity level particularly seems to be the case, at least in patients with CLBP, who continue to work. The study by Verbunt et al.21 is the most scientifically well designed of these and they were unable to confirm the presence of disuse in a group of CLBP patients. The work status and/or varying methods of reporting activity level may offer some explanation for the inconclusive results reported here.
DECONDITIONING IN CHRONIC LOW BACK PAIN
Cardiovascular capacity
Endurance or cardiovascular capacity in patients with CLBP has been measured utilizing various methods. The most widely accepted measure of cardiovascular fitness is maximal oxygen uptake (VO2 max). The various methods of measurement have included measurement of VO2 max as well as utilizing submaximal exercise testing. Interestingly, the results have not led to a definitive conclusion about the cardiovascular capacity of patients with CLBP. In measuring parameters such as predicted VO2 max utilizing a symptom-limited treadmill test or bicycle ergometer some studies have shown significantly lower levels of cardiovascular fitness in patients24,26–28 whereas Wittink et al.29 and several others have failed to demonstrate a significantly reduced level of aerobic fitness in patients with CLBP.30–32 A lower cardiovascular capacity was shown for men compared with controls but not for women in some studies.19,22,23
Wittink et al.29 tested a sample of 50 patients with CLBP with a mean duration of symptoms of 40 months. Oxygen consumption (VO2) was measured during a symptom-limited modified treadmill test. Prediction equations were employed to estimate VO2 max. The mean observed VO2 max values for men and women with CLBP were consistent with those found in earlier studies that tested normal subjects. Given these results, they concluded that rather than being a group of significantly deconditioned subjects, at least from an aerobic standpoint, this group of patients with CLBP represented a sample of moderately fit individuals. Furthermore, their data suggest that aerobic fitness levels are independent of diagnosis, duration of pain, pain intensity, work status, or smoking. Previously, Wittink et al.33 had subjects with CLBP perform three symptom-limited maximal exercise tests: a treadmill, an upper extremity ergometer, and a bicycle ergometer test. The treadmill test was found to be by far the best test for measuring aerobic fitness in these patients. Wittink et al.34 went on to show that there is no significant relation between aerobic fitness and pain intensity in patients with CLBP and that a lack of cardiovascular fitness therefore does not contribute to pain intensity in patients with CLBP. In a follow-up sample, patients reported significantly less pain before and after treadmill testing at the end of a functional restoration program compared with their pain intensity with testing before the program. Since their predicted VO2 max had not changed, the authors noted that there had been a decreased pain intensity independent of aerobic fitness levels.
Hurri et al.32 measured VO2 max in 245 subjects with CLBP, 81 who were treated as inpatients, 88 treated as outpatients, and 76 controls with a history of CLBP but who were still working. They performed bicycle ergometer tests four times over a 30-month period. The estimated VO2 max of their patients was not significantly different than reference values of healthy persons. Battie et al.30 noted that aerobic fitness did not affect the risk of back injury in a prospective study. He did observe that it might affect the response to the problem and subsequent recovery. Cady et al.,35 in his oft quoted study from 1979 on a group of firefighters, showed a graded and statistically significant protective effect for increasing levels of fitness and conditioning. A criticism of Cady’s study was that fitness level included both cardiovascular or endurance parameters as well as strength measures, making it impossible to isolate the benefits of these individually.
On the other hand, some investigators have shown what most of us would believe to be true, that indeed there is a significantly decreased level of cardiovascular fitness in CLBP patients. Brennan et al.26 used bicycle ergometry to determine a predicted VO2 max in 40 patients with herniated discs with an average duration of symptoms of 87 days. Comparing these results with those of a matched control group revealed a significantly reduced predicted VO2 max for the patients. Others,24,27 in addition to van der Velde and Meirau,28 have also shown diminished cardiovascular capacity in patients with CLBP. Their original experimental objective was to determine the effects of 6 weeks of exercise on aerobic capacity and on measures of pain and disability in patients with CLBP.28 Baseline measurements determined that the percentile rank of aerobic capacity for the patients with CLBP was statistically significantly lower than those measures for the controls. Patients who completed a 6-week program of aerobic, muscular endurance, and flexibility exercises showed a statistically significant improvement in the mean percentile rank for aerobic capacity. In addition, they showed significant decreases in pain and disability after completion of the exercise program.
We can see that despite what our preconceived ideas may be regarding a decreased aerobic capacity in patients with CLBP, the literature is inconclusive. Instead, it reveals that a decreased aerobic capacity may or may not actually be present in these individuals. Work status again has been offered as a possible reason why the results have varied so, the thought being that even in the presence of CLBP those individuals continuing to work are more likely to possess a fitness level equal to the norm. Unfortunately, information pertaining to work status is not available for all of the studies considered here. It is notable that in most studies where no difference in cardiovascular capacity was reported, most of the subjects being studied were still working. The cardiovascular capacity was better for CLBP patients who were working compared with those who were not in one study.36 In several studies19,22,23 male subjects had decreased cardiovascular capacity when compared with controls, whereas females did not. Speculation as to why this may be so centered on the idea that when men lose their job there is a greater degree of inactivity, whereas in the case of women they remain more active at home with tasks such as cooking, cleaning, and childcare. This keeps them at an activity level equivalent to that of healthy females.
Muscle changes: composition and performance
Skeletal muscle has incredible plasticity associated with it. It can adapt to almost any array of functional demands we place upon it. The level by which muscle function declines with inactivity depends upon the level of training before inactivity began and the duration of inactivity. In discussing muscle, it is important to understand the function of muscle subtypes. Type II (predominantly subtypes a and b) fibers are generally ‘fast twitch.’ They can track fast and are maximally powered by glycolysis, and therefore fatigue quickly. They are usually recruited late when the body needs to exert ‘maximal effort.’ Type I fibers are generally ‘slow twitch.’ They contrast slowly and are metabolically inexpensive, utilizing aerobic metabolism. In the acute period (14–30 days), fiber type is preserved even with activity reduction greater than 75% given the absence of an associated neuromuscular injury (i.e. foot drop such as from an L4 nerve root impingement).37,38 In the subacute period (30–90 days), large progressive shifts of type IIa fibers to type IIb fibers (both fast twitch fibers) occur at a rate of 5–19%.39 This shift can precede fatty replacement of muscle (apoptosis) in animal models. There is also a 15% decrease in the number as well as the size of type I (efficient slow twitch muscle fibers).40 In chronic detraining (90 days to 9 months), power lifters showed oxidative muscle (type I) fibers increased by 1.4 times,41 while type II fibers (fast twitch) decreased by 60% in axial muscles.42,43 It has been noted that the very young (less than 20 years old) may exhibit a certain immunity to fiber-type change in the face of detraining.44,45
A changed fiber cross-sectional area (atrophy) also occurs with deconditioning and detraining. In athletes both type I and type II fibers decreased in size by 9–23% in as little as 6 weeks of detraining.46 In a chronic period (7 months) there can be as much as 37% atrophy across all muscle fiber types.41 Mayer et al.47 noted in CT that CLBP patients (in both operative and nonoperative segments) had significantly decreased muscle bulk with evidence of fatty replacement of muscle. The authors further correlated this observational qualitative finding of atrophy with a quantitative finding of greater than 50% mean reduction in strength testing for the atrophied spinal muscle group compared to age- and gender-matched controls. Several other studies have shown smaller cross-sectional areas of the paraspinal muscles by CT or MRI scanning in subjects with CLBP.48–50 It remains debatable, but some papers have shown that larger muscles (postural muscles of the back and lower extremities) become atrophic at a faster rate than extremity muscles.
Few authors have actually correlated strength performance to atrophy, but generally strength is largely preserved during short periods of convalescence although eccentric strength decreases earlier than other aspects of neuromuscular performance (7–21 days). In the subacute period (4–12 weeks) there are declines in strength, measured by both force and power, of 7–15%.51,52
For chronic periods, decreases in power were 40–60% for trained muscles in the arms and legs, but less dramatic decreases of 15–37% were noted in the contralateral untrained arm.37,53 Muscle endurance times are also decreased with deconditioning. Decreased strength as well as decreased endurance for trunk/spinal musculature was seen in patients with chronic low back pain despite having similar physical activity levels as age- and gender-matched controls.49,54 Mayer et al.55 demonstrated significant strength deficits for both trunk flexors and extensors for a group of CLBP patients utilizing a Cybex prototype sagittal trunk strength tester. Using a dynamic isokinetic lifting device, Kishino et al.56 show significantly decreased isokinetic as well as isometric lifting capabilities for patients with CLBP. Houston et al.37 have noted a capillary density diminution in as few as 15 days after training cessation. However, other authors have noted that even after 90 days of detraining, capillarization remained largely unchanged with only minor decreases in VO2 max.57 Mujika and Padilla, who have analyzed much of the existing data, surmise that capillaries and muscles are preserved in trained athletes and may account for their greater speed to reach previous training levels than in sedentary individuals.58,59
Rapid and progressive reduction in mitochondrial oxidative enzymes creates a rapid decrease in the efficiency of muscle cells to manufacture APT.59 Further, ‘run-time exhaustion’ or subthreshold muscle failure is associated with decreased mitochondrial density and/or efficiency.60 Deconditioned, formerly trained individuals retain higher enzymatic and mitochondrial numbers than sedentary individuals and will reach peak performance levels faster when they resume activity.61
Motor control is also adversely affected in the presence of CLBP. Performing a standardized reach task, postural control in patients with CLBP was more affected in those with severe low back pain compared with moderate pain.62 Patients with CLBP showed a delayed-onset contraction of abdominal muscles during motion of the upper extremities.63,64 Patients with low back pain were shown to have decreased trunk motion patterns while performing a repetitive wheel rotation task.65 Haines66 showed immobility, as well as decreased coordination and balance. Several surface EMG studies have shown reduced recruitment patterns and lower maximum integrated electromyography in paraspinal muscles in CLBP patients.67,68 Moreover, studies of movement patterns have shown the delayed onset of contraction of the transversus abdominis indicating a deficit of motor control, hypothesized to result in inefficient muscular stabilization of the spine.69
Obesity
Several studies have addressed the issue of obesity in the presence of chronic pain and deconditioning, some specifically in a population of patients with CLBP. In an experimental study where subjects (not necessarily patients with CLBP) were placed at bed rest, it was shown that lean body mass decreases during 30 days of bed rest whereas body weight did not change.12 This finding suggests that the percentage of body fat will increase as the percentage of muscle mass decreases. During a period of reconditioning, this inverse relationship was confirmed.70 Furthermore, it has been shown that with increasing aerobic fitness there is a significant decrease in the percentage of body fat. Verbunt et al.21 showed that the percentage of body fat of CLBP patients did not differ from controls, which is in agreement with the findings of others.49 Toda et al.71 was able to show that in female patients with CLBP there was an increase in the percentage of body fat when compared to healthy age- and gender-matched controls but were unable to show this same difference in men. Given the study design, it is impossible to state that this information provides definitive scientific evidence that an increased body fat percentage is the result of deconditioning in CLBP. Obesity itself may actually contribute to the occurrence of back pain and was already present before back pain began.
Psychosocial changes
Why some patients develop CLBP and significant disability has become an evermore perplexing question. This small percentage of patients with oftentimes seemingly minor injuries and imaging studies comparable to others who recover as expected with little or no disability end up consuming a great majority of the dollars spent on treatment. The fear-avoidance model as an explanation of how and why some individuals with musculoskeletal disorders develop a chronic pain syndrome was first proposed by Lethem et al.72 in 1983. They described how fear of pain and avoidance of it result in the perpetuation of pain behaviors and experiences, even in the absence of demonstrable organic pathology. Fear-avoidance refers to the avoidance of movements or activities based on the fear of increased pain or re-injury. Thus, it is thought to play a role in the development of the deconditioning syndrome. Avoidance is a type of learned behavior which postpones or averts the presentation of an adverse event.
Vlaeyen et al.73–75 have proposed a fear-avoidance model with two opposing behavioral responses: confrontation and avoidance, and present possible pathways by which injured patients get caught in a downward spiral of increasing avoidance, disability, and pain. The model predicts several ways that pain-related fear can lead to disability:
It has been proposed that there is a subgroup of CLBP patients who have a tendency to cope with pain using endurance strategies as opposed to avoidance strategies.6 In this fear-avoidance model of chronic pain, patients appear to ignore their pain and ‘stick it out’ despite the pain. This ‘stick it out/grit their teeth’ behavior also results in complaints of persistent pain. These individuals are likely to report a physical activity level that fluctuates greatly over time as a reaction to their pain. They will tend to persevere or push on until increasing pain prevents it. This period of increased activity is then followed by a period of rest or reduced activity followed again by resumption of increased activity. This has been referred to as ‘all or nothing’ behavior, representing the so-called ‘overactivity/underactivity’ cycle seen in many chronic pain patients.78,79
What do we know about the effect of pain-related fear on physical performance? A significant correlation was found between pain-related fear and range of motion measured with a flexometer.80 Using a simple task such as lifting a 5.5 kg weight in the dominant arm and holding it until pain or physical discomfort made it impossible to continue, Vlaeyen et al.73 found a significant correlation between lifting time and results from the Tampa Scale for Kinesiophobia (TSK). The TSK was developed as a measure of fear of movement/(re-)injury.81 The term kinesiophobia refers to an excessive, irrational, and debilitating fear of physical movement and activity resulting from a feeling of vulnerability to painful injury or re-injury. Using the knee extension–flexion unit (KEF, Cybex 350 system) Crombez et al.82 found a significant association between performance level and pain-related fear, but no relationship between performance and pain intensity in a group of patients with CLBP. They had chosen the knee extension–flexion test specifically because patients believed it put minimal strain on their backs. In a follow-up study utilizing trunk extension–flexion and a weight lifting task, they showed that pain-related fear was the best predictor of behavioral performance.83 They felt the study also supported the idea that pain-related fear is more disabling than pain itself. These studies provide evidence that pain-related fear is associated with escape/avoidance of physical activities, resulting in poor behavioral performance.
Somewhat surprising then are the results of Wittink et al.84 who performed a maximal symptom-limited modified treadmill test in patients with CLBP. The Short Form − 36 mental health (MH) scale results were correlated with results from treadmill testing. The results showed that the reason to stop testing and time walked on the treadmill were determined by pain intensity increase and not by low mental health. Although patients with low mental health were more likely than patients with high mental health to stop testing because of pain, the results did not reach statistical significance.
How pain-related fear affects daily activities and the development of disability has been studied as well. Waddell et al.85 developed the Fear-Avoidance Beliefs Questionnaire (FABQ) in 1993. It was developed based on theories of fear and avoidance behavior and focused specifically on patients’ beliefs about how physical activity and work affected their low back pain. The FABQ is a self-report questionnaire of 16 items where each is answered on a seven-point Likert scale from strongly disagree to strongly agree. Answer analysis indicated a two-factor structure. Factor 1 (FABQ1) concerns fear-avoidance beliefs about the relationship between low back pain and work while Factor 2 (FABQ2) concerns fear-avoidance beliefs about physical activity in general. The two main findings of this study were: first, there was little direct relationship between pain and disability; and the second main finding is the strength of the relationship between fear-avoidance beliefs about work and both work loss and disability in activities of daily living. Waddell et al. concluded that ‘fear of pain and what we do about it is more disabling than the pain itself.’ In a study comparing people matched for pain intensity and duration, fear-avoidance beliefs were found to be an important factor discriminating people with considerable sick leave from those with no sick leave.86 Vlaeyen et al.74 have shown that fear of movement (re)injury is a better predictor of self-reported disability levels as measured with the Rowland Disability Questionnaire than either via medical findings or pain intensity levels. Disability was most strongly correlated with the more specific pain-related fear measures as compared to more general measures of anxiety.87 Verbunt et al.88 were able to show that a fear of injury correlated significantly with disability as measured with the Roland Disability Questionnaire. They found no statistically significant association between disability and aerobic fitness or fear of injury and aerobic fitness. Thus, while fear of injury correlated with disability, they were unable to demonstrate that fear of injury leads to physical deconditioning.
Prospective studies have attempted to address whether fear-avoidance beliefs are a precursor to chronic pain or a consequence of the pain. Work by Klenerman et al.89 supports the idea that pain-related fear is a precursor of disability. In a large prospective cohort study, Linton et al.90 observed that individuals who scored above the median score on a modified version of the FABQ had twice the risk of having an episode of pain during the following year. While not a prospective study, Fritz et al.91 showed that fear-avoidance beliefs were present in some patients with acute low back pain of less than 3 weeks’ duration. The presence of these beliefs did not explain a significant amount of the variability in the initialdisability levels; however, they were significant predictors of 4-week disability and work status. In a prospective study of 252 patients presenting with low back pain in an effort to isolate risk factors for the development of chronic pain the results did not support the fear-avoidance concept as such a risk factor.92 The information from these studies suggests that there is a subgroup of patients with fear-avoidance beliefs prior to an injury or who develops the beliefs shortly thereafter.
Other psychosocial variables such as distress, depression, and anxiety have been mentioned in the deconditioning syndrome and have been studied in the presence of CLBP. A systematic review of prospective cohort studies in low back pain to evaluate the evidence implicating psychological factors in the development of chronicity in low back pain was recently undertaken by Pincus et al.93 Only six studies met their acceptability criteria for methodology, psychological measurement, and statistical analysis. They concluded that it was not possible to differentiate between psychological distress, depressive symptoms, and depressive mood and therefore chose to use the term distress to represent a composite of these parameters. The most consistent finding was that distress is a significant predictor of unfavorable outcome, particularly in the primary care setting. They also concluded from their review that somatization as well as distress was confirmed as having a role in the progression to chronicity in low back pain. The supporting evidence was felt to be strong for the role of psychological distress/depression and moderate for the role of somatization. They felt the evidence for fear/anxiety is surprisingly scarce in that the single acceptable study that looked at fear-avoidance found it had no significant predictive power when analyzed together with other parameters.92 For a group of patients specifically diagnosed with acute radicular pain and a disc prolapse or protrusion, Hasenbring et al.6 looked at various psychological predictors, somatic predictors, and social predictors. Results of multivariate or regression analysis indicated that depressive mood and specific pain-coping strategies are high-risk factors for the development of persistent pain. Relevant coping strategies were extreme tendencies to cope with physical and mental efforts, avoiding behavior on the one hand, extreme tendency to stick it out or to bagatellize on the other, or the nature of communication of the pain experience to others. An example of a maladaptive coping strategy was the tendency toward nonverbal/motoric expressive behavior such as groaning, twisting their faces, or rubbing the painful areas during pain. The extent of disc displacement was the only significant predictor of persistent pain among somatic predictors. Sitting occupation and social status were shown to be high-risk factors of chronicity of pain among the social variables investigated.
Polatin et al.94 evaluated 200 patients with CLBP using a structured clinical interview. They reported a 45% point prevalence and a 64% lifetime prevalence of a major depressive episode. They further found that 55% of those who had concurrent major depressive disorder developed it before the onset of the low back pain but 45% became depressed after the onset of their pain.94 In a meta-analysis of studies of chronic pain and depression, 21 of 23 articles related the severity of pain to the degree of depression.95 The authors also concluded that the duration of pain was related to the development of depression in three of three studies of patients with diverse kinds of pain symptoms. They found that depression following the onset of pain was supported in 15 of 15 studies attempting to address this issue but that it preceded the onset of pain in 3 of 13 studies reviewed. Depressed subjects were found to have a reduced work capacity in one study.70
On the other hand, aerobically fit people were found to have reduced psychosocial stress responses in a review of 34 studies on the relationship between physical fitness and stress response.96 Self-reported stress was decreased and scores for subjective health and well-being were improved in 100 healthy police officers following their participation in an aerobic training program which resulted in improved physical fitness.97 Higher levels of physical activity were associated with a better mood, whereas inactive but fit subjects reported a poorer mood than inactive and unfit individuals.98 The authors concluded that the positive relationship between physical activity and mental mood was less mediated by improved fitness and more by participation in the performance of physical activity as a social event. A meta-analysis of the available literature in 1991 concluded that aerobic but not anaerobic exercise was associated with lower levels of anxiety.99
While treatment is beyond the scope of this chapter and will be covered elsewhere, a brief mention of treatment specifically related to fear-avoidance beliefs seems warranted here. These beliefs and fear of movement/(re-)injury in particular have been shown to be strong predictors of physical performance and pain disability. Given this association, research has begun to be carried out on the effects of treatment specifically aimed at fear-avoidance behaviors. In a small study of six patients Vlaeyen et al.100 showed that improvements in pain-related fear and pain catastrophizing occurred only during a period of exposure in vivo and not during graded activity. Decreases in pain-related fear also concurred with decreases in pain disability and pain vigilance, and an increase in physical activity levels. Further, all improvements remained at 1-year follow-up. Woby et al.101 found that reductions in fear-avoidance beliefs about work and physical activity, as well as increased perceptions of control over pain, were uniquely related to reductions in disability even after controlling for reductions in pain intensity, age, and sex. However, changes in the cognitive factors were not significantly associated with changes in pain intensity in a group of patients with CLBP. In a recent investigation, patients were treated with operant behavioral treatment plus cognitive coping skills treatment or operant behavioral treatment plus group discussion.102 Patients improved with respect to level of depression, pain behavior, and activity tolerance post-treatment and at 12-month follow-up. Treatment also resulted in a short- and long-term decrease in catastrophizing and enhancement of internal pain control. Klaber et al.103 treated patients in an exercise program of eight 1-hour sessions held twice per week designed to encourage movement of the back and strengthen and stretch all the main muscle groups in the body but not focusing on the back. The treatment program also included cognitive–behavioral principles. They compared patients treated with this program versus those allocated to ‘normal general practitioner care.’ High fear-avoiders fared significantly better in the exercise program with behavioral–cognitive principles than in usual general practice care at 6 weeks and 1 year. Those who were distressed or depressed were significantly better off at 6 weeks, but benefits were not maintained at 1 year. In a randomized clinical trial of patients with low back pain of less than 8 weeks’ duration, George et al.104 showed that patients who initially had elevated fear-avoidance beliefs appeared to have less disability following fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. However, patients with lower fear-avoidance beliefs appeared to have more disability from fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. The fear-avoidance treatment group also had a significant improvement in fear-avoidance beliefs. There are only a few investigations in this area and conclusions should be drawn cautiously. Given that, it appears as if there is a group of patients possessing fear-avoidance beliefs who may derive greater benefit from treatment programs which address these behaviors.
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