Putting the Biopsychosocial Model Into Practice

Putting the Biopsychosocial Model Into Practice

Craig Liebenson

Ryan Van Matre


Although pain is a normal human experience, the understanding of pain by the health care has changed in recent years. Current research suggests up to 25% of populations in developed countries experience chronic pain, or pain existing beyond normal tissue healing times of 3 to 6 months.1,2 The rates of chronic pain have been increasing. During the 1990s, one in seven patients reported chronic pain. Current studies show that rates have escalated to one in four individuals living with chronic pain.1,2 This is especially true with the prevalence of low back pain (LBP), because individuals with activity limited by pain generally assume structural factors are the sole cause of their pain and disability. This is not to suggest that structural factors don’t play a role, but the traditional medical model in the treatment of pain reinforces the focus on damaged or diseased tissues. Many health care systems have financial incentives in place where diagnosis drives the intervention, which, in turn, drives the defrayment of the health care provider (HCP).3 With rising pain and disability rates, increasing costs, and the recent surge of illicit drug use as an unintended consequence of prescription pain medication, those at the forefront of treating both acute and chronic pain are being called to task.4,5

This chapter offers a different clinical reasoning pathway for the treatment of dysfunction caused by pain and offers perspective on how acute pain can be better managed to avoid chronicity. Although this pathway in clinical practice may seem challenging to implement, it is important to both the patient and the clinician while adding value in the health care marketplace.

Numerous studies worldwide acknowledge nearly equal presence of pathologies in asymptomatic and symptomatic individuals.6,7,8 This fact, combined with the generally displeasing results of traditional care for LBP, has fueled the critical evaluation of the biomedical model.9,10,11 According to the International Association for the Study of Pain (IASP), pain is not simply the result of structural injury or pathology but is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage …”.1

This modern concept of pain challenges the traditional belief, commonly seen in orthopedics, where every disease can be explained by the underlying deviation from normal anatomy.12 Clinicians and patients assume the greater the tissue abnormality, the greater the pain and dysfunction. Pain science research suggests other mechanisms at work perpetuating the pain experience.

This is a problem as research shows clinicians are underprepared to treat this challenging population. Outdated models and poorly validated treatments have resulted in additional costs, overmedicalization, and frustration.13,14,15 Although the genesis of pain may be from physical sources, it is also heavily modulated in the dorsal horn, and by descending influences largely of psychological origins.16 Evaluation of both the source of pain and the psychophysical perception that lead one to fear and avoid activity should be addressed so reactivation can occur.17,18,19 This approach is supported by the World Health Organization’s revised guidelines on disability, where the goal of health care
is to enable patients to return to participation and independent functioning in their chosen activities.20

With increasing epidemiologic rates of chronic pain, a poor history on pathoanatomy emphasis, and the frustration of clinicians treating chronic pain patients, health professionals are called to take a more comprehensive understanding of the pain experience through the biopsychosocial (BPS) model.21,22 The BPS approach is one where the total patient, in both their physical being and how they process their pain, becomes our subject. Current pain science reveals pain as an “output” from the neuroimmune system that stirs the body to take action. Although the incoming nociception factors into the equation, an individual’s culture, past experience, environment, and expectation play important roles in the development of pain.12,23 What a patient thinks, feels, and believes about his or her condition will in turn impact his or her examination, treatment, and prognosis.19 Rather than focusing on structural causes and cures, this paradigm emphasizes on the goal of having the patient better understand pain neuroscience while maintaining or restoring function.24 Such an approach is of value, regardless of the pathoanatomic diagnosis. The BPS approach is not only the main subject of this chapter, but also of the entire book that follows. It serves as the basis of clinical rationale for all interventions with the notion that simply getting the patient to better understand the BPS model may be therapeutic in and of itself.23,25,26,27,28

The BPS Model

Pain has been interpreted since the time of Descartes as signaling tissue damage (Fig. 3.1). The biomedical model of finding the structural cause and then treating or “fixing” it to elicit a cure is on the basis of this outdated understanding of pain. It is now acknowledged that a structural cause for pain may not exist and a structural cure is not often successful. The Cartesian model leads one to assume if cure is not brought about, the problem must be psychogenic. The dualism inherent in the early Renaissance suggests pain is either in the mind or body, but not both! According to the new definition of pain by IASP, pain is associated with both a disagreeable physical sensation and an emotional experience.29,30 Thus, it is sensorial (nociceptive) and affective (emotional) and should not be defined dichotomously as either physical or psychological. It is well established that an individual’s cognitions, such as fear, anxiety, and pain catastrophization, are strongly correlated with pain and disability.12 Clinicians treating pain need to take into consideration the patient’s thoughts and beliefs about their pain condition and use prudence as what is said may positively or negatively influence those beliefs. The principle, “first, do no harm” takes on new meaning when using appropriate clinical language.

The BPS model views pain as involving ascending nociceptive input (danger messages) from the periphery (Cartesian model), descending modulation that inhibits or facilitates nociception (gate control theory of Melzack and Wall), and central processes with neurologic, affective, and cognitive dimensions (Figs. 3.2, 3.3, 3.4).16 Therefore, the perception of pain is heavily influenced by both nociception and one’s attitudes, beliefs, and social environment (Fig. 3.5). And to complicate matters more, this process of feedforward/feedback signal modulation is under constant autonomic adaptation.

Although most patients recover from pain episodes quickly, the recurrence rate and dissatisfaction with medical care are high. Additionally, the minority which develop persistent disabling pain account for the majority of costs.13

Figure 3.1 The Cartesian model of peripheral activation of pain pathways. From Descarte’s L’Homme (Paris 1644).

Figure 3.2 The gate control theory of pain. (A) Ascending pathways from small- and large-diameter fibers to the dorsal horn of the spinal cord and to higher centers. From Suchdev PK. Pathophysiology of pain. In: Warfield CA, Fausett JH, eds. Manual of Pain Management. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2002. (B) The excitatory (white circle) and inhibitory (black circle) links from the substantia gelatinosa (SG) to the transmission (T) cells, as well as descending inhibitory control from brainstem systems. The round knob at the end of the inhibitory link implies that its actions may be presynaptic, postsynaptic, or both. All connections are excitatory, except the inhibitory link from SG to T cell. From Bonica JJ, Loeser JD. History of pain concepts and therapies. In: Loeser JD, ed. Bonica’s Management of Pain. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. (Modified from Melzack R, Wall PD. The Challenge of Pain. New York, NY: Basic Books; 1983.)

Figure 3.3 Ascending nociceptive pathways. From Mense S, Simons DG. Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment. Baltimore, MD: Lippincott Williams & Wilkins; 2001.

Figure 3.4 Descending antinociceptive modulation. From Mense S, Simons DG. Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment. Baltimore, MD: Lippincott, Williams & Wilkins; 2001. (Redrawn from Basbarum AI, Fields HL. Endogenous pain control system: brainstem spinal pathways and endorphin circuitry. Ann Rev Neurosci. 1984;7:309-338.)

Figure 3.5 The biopsychosocial model. Reproduced with permission from Waddell G. The Back Pain Revolution. Edinburgh, Scotland: Churchill Livingstone; 1998.

In patients who fail to recover, the limitations of the biomedical approach are even more evident. In an attempt to find the structural cause of LBP, overly sensitive tests are ordered, with high false-positive rates. The patient either is told that nothing is wrong and is labeled “psychogenic” or is told about the pathology and is asked to take rest, take medicines, and to learn to live with pain. When patients can no longer tolerate the symptoms, they are informed that they should have injections and eventually surgery. The emphasis of dysfunctional anatomy fuels patient’s beliefs where something is injured and needs to be fixed. This belief becomes a powerful driver of the pain experience. Fear of pain develops in the individual because no one has addressed the patient’s thoughts and beliefs, which are often the largest predictor of recovery.12 The fear of pain becomes worse than the pain itself,31 because fear has shown to play a greater role in the debilitation of movement and recovery.32,33,34,35,36

Waddell11 in his Volvo award-winning paper stated, “Conventional medical treatment for low-back pain has failed, and the role of medicine in the present epidemic must be critically examined.” The low back epidemic is caused by a number of factors and the reasons for low back disability epidemic are presented in Table 3.1.

Table 3.1 Medical Reasons for the Low Back Disability Epidemic

A) Overemphasis on a structural diagnosis

B) Overprescription of bed rest

C) Overuse of surgery

Overemphasis on Bed Rest

Because of the failure to pinpoint specific pain generators in LBP, bed rest and analgesics have become routine treatment. The positive early course of most LBP episodes has given justification to this practice of symptomatic treatment. As it turns out, this seemingly benign prescription of prolonged bed rest has now been shown to be one of the most costly errors in musculoskeletal care. Allan and Waddell45 said, “Tragically, despite the best of intentions to relieve pain, our whole approach to backache has been associated with increasing low back disability. Despite a wide range of treatments, or perhaps because none of them provide a lasting cure, our whole strategy of management has been negative, on the basis of rest. We have actually prescribed low back disability!”

Deyo et al performed a controlled clinical trial by comparing 2 days of bed rest with 2 weeks and concluded that a shorter period of bed rest was as effective as a longer one.77 The negative effects associated with prolonged immobilization were not seen with brief bed rest. A more recent study confirmed Deyo’s work, which reported that 4 days of bed rest led to more sick leave than advice to continue normal activity.78

Danish guidelines concluded bed rest should only be taken for severe pain for 1 to 2 days.79 Van Tulder et al found no evidence in favor of bed rest for acute LBP.80 Vroomen et al demonstrated there was no evidence of effectiveness of bed rest for sciatica.81

Overuse of Surgery

The biomedical model seeks to find the anatomy or biomechanics at fault. This seems logical to both the clinician and patient for if the faulty biomechanics or pathoanatomy can be surgically corrected, it is expected the patient will recover from pain and disability.13,14,15 The overuse of surgery has been one of the most problematic interventions in back pain. Bigos and Battie75 said, “Surgery seems helpful for at most 2% of patients with back problems, and its inappropriate use can have a great impact on increasing the chance of chronic back pain disability.” As previously discussed, focus on the biomedical aspects alone leads to limited efficacy with decreasing pain and disability. In fact, focusing on such models may actually increase fear in patients leading to increased pain.82,83 From a value perspective, such reliance on the biomedical model with focus solely on treatment of tissues has shown limited efficacy in decreasing pain and disability and may increase abnormal illness behavior.13,14,15,84 Saal and Saal85 supervised care for a group of patients referred by neurologists for surgery. They attempted rehabilitation for these patients and made the following observations, “Surgery should be reserved for those patients for whom function cannot be satisfactorily improved by a physical rehabilitation program … Failure of passive non-operative treatment is not sufficient for the decision to operate.”

In 1970, Hakelius performed a study revealing most of the sciatica patients responded to conservative care.86 In 1992, Bush et al57 published that “86% of patients with clinical sciatica and radiologic evidence of nerve root entrapment were treated successfully by aggressive conservative management.”

Surgery indeed has a place as Danish guidelines recommend spinal surgery for disc herniation, cauda equina syndrome, spinal stenosis, and stabilizing back surgery so long as appropriate indications are present.79 Table 3.2 summarizes the Danish guidelines indications for spinal surgery.

Table 3.2 Surgical Indications for Disc Herniation According to Danish Guidelines

  • After 4-6 weeks of conservative care

  • When there is a positive correlation between clinical findings and imaging reports

  • Progressive weakness in the leg

  • Severe leg symptoms in spite of medication

From Cherkin DC, Deyo RA, Street JH, Barlow W. Predicting poor outcomes for back pain seen in primary care using patients’ own criteria. Spine. 1996;21:2900-2907.

A Cochrane Collaboration systematic analysis found considerable evidence on clinical effectiveness of discectomy for carefully selected patients with sciatica caused by lumbar disc prolapse that has not been resolved with conservative management.87,88 They found 65% to 90% of sciatica patients, whose symptoms lasted 6 to 24 months, had good to excellent outcomes. In contrast, only 36% of conservatively treated patients had good to excellent outcomes. Although often referenced to defend the aggressive recommendation for surgery, there is no consensus in the literature.84 A study of spinal stenosis patients found that there is no difference in surgical outcomes in patients who delay surgery by opting for a trial of conservative care.89 In 1983, Weber reported with properly selected patients there is no difference in outcome between
surgically and conservatively treated patients at 10 years.90 However, the study by Gogan and Fraser suggests the long-term results of surgery are superior to conservative care.91

Gibson et al87 concluded, “There is a serious lack of scientific evidence supporting surgical management for degenerative lumbar spondylosis.” They found no acceptable evidence for the efficacy of any form of decompression for degenerative lumbar spondylosis or spinal stenosis. Also, there is no acceptable evidence of the efficacy of any form of fusion for degenerative lumbar spondylosis, back pain, or “instability.”

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Apr 17, 2020 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Putting the Biopsychosocial Model Into Practice

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