Putting the Biopsychosocial Model Into Practice

Craig Liebenson

Ryan Van Matre

LEARNING OBJECTIVES

After reading this chapter, you should be able to:

Understand the limitations of a biomedical approach in managing chronic pain patients.
Understand what you say matters as a clinician with regard to patient outcomes.
Understand the importance of functional reactivation as a guiding principle in patient care.
Understand the importance of psychosocial factors such as fear-avoidance behavior in a patient when there is failure to achieve a satisfactory outcome.
Understand the “decision points” of care when implementing the biopsychosocial model into clinical practice.
Understand the sensitive nature of the nervous system: protective, plastic, and dynamic.
Understand that pain experience is always unique and influenced by environment, culture, experience, and attitude.
Understand how to offer neuroscience education from the patient’s perspective in order to have the patient reconceptualize their pain experience.

“Let fear then, be a kind of pain or disturbance resulting from imagination of impending danger, either destructive or painful.

–ARISTOTLE

Introduction

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.

True or False?

Pain occurs only when you are injured.
Pain is not possible when there are no nerve messages coming from the painful parts of the body part.
Chronic pain means that an injury hasn’t healed properly.
The worse the injury, the worse the pain.
The body tells the brain when it’s in pain.
Receptors on nerves work by opening gates in the wall of the nerve.
When there is an injury, there are special pain receptors that convey pain messages to the brain.
The brain sends messages down your spinal cord that can change messages going up your spinal cord.
The brain decides when you will experience pain.
When a message comes to the end of the nerve, the nerve sometimes releases a chemical.
Nerves adapt by increasing or decreasing their resting level of excitement.
Nerves can adapt by growing more receptors.
Nerves adapt by making gates stay open longer.
Nerves from the brain to the spinal cord never release the same chemicals as nerves coming from the body to the spinal cord.
It is possible to ignore pain.
When you are injured, the circumstances and environment you are in will not affect the amount of pain you experience, as long as the injury is exactly the same.
During an injury, special receptors convey danger messages to the spinal cord.
All other things being equal, an identical back injury in a factory worker who hates his job would probably hurt more than a soccer player during the championship game.
Pain is produced to allow you to take action.

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 a Structural Diagnosis

HCPs struggle in treating chronic pain patients.³⁷^,³⁸^,³⁹ It is common for doctors to overuse diagnostic imaging as part of the initial evaluation of an LBP patient. This is performed for two misguided reasons. One is to rule out the presence of serious diseases (i.e., tumors, infections), which may be missed by history and physical examination. Second is the belief that structural pathologies (e.g., herniated discs, arthritis), identified with imaging, are strongly correlated with symptoms.

This isn’t to suggest that by incorporating the BPS approach is to assume the role of psychiatric consultation. History and physical examination are still needed to establish rapport and exclude serious disease. It is common in today’s overloaded health care facilities to see clinicians spending less time physically examining the patient and spending more time documenting, expediting imaging, additional testing, and intervention. This is tragic because history and examination have shown to be 99% sensitive for identifying the “red flags” of serious disease.¹¹^,⁴⁰^,⁴¹^,⁴² The physical examination serves an equally powerful role in establishing trust in the clinician-patient encounter. Verghese et al has discussed not only this loss, but also the essential process to develop a caring, two-way patient-doctor relationship, which benefits not only patients and their families, but also the physician.⁴³^,⁴⁴ Once trust is established, the role of reassurance takes prominence in the clinical encounter. This pathway gives hope to the patient.

No “Red Flags” of Tumor, Infection, or Fracture Were Missed as a Result of Not Routinely Imaging Acute Patients

Long-term follow-up of 437 patients revealed no serious disorders were missed as a result of not performing routine imaging on acute patients.
A “red flag” checklist mostly from history alone was used.
1.4% of patients did have serious conditions, such as crush fracture, kidney carcinoma, and prostate carcinoma, but they were suspected on initial evaluation and referred for additional tests.

From McGuirk B, King W, Govind J, Lowry J, Bogduk N. Safety, efficacy and cost-effectiveness of evidence-based guidelines for the management of acute low back pain in primary care. Spine. 2001;26:2615-2622.

Patients who find themselves accelerated to imaging fail to understand the false-positive rates. The prevalence of clinically insignificant herniated discs or degenerative conditions is high, which makes these tests inappropriate as screening procedures (Fig. 3.6). The problem is many individuals who have pain unrelated to the structural findings will be mislabeled and potentially receive unnecessary treatments. They may think of themselves as “sick,” when in fact, most of these common changes are related more to age than to symptoms. The “experience” of the patient has also changed because future pain episodes may be directly attributed to the abnormal finding on the x-ray or magnetic resonance imaging (MRI), valid or not. Clinical experience reveals many patients carry their abnormal imaging revelations with them, which serve as a “scar” on their cognitive pain profile. The question should be asked, “Where did this emphasis on pathoanatomy come from?”

After the discovery by Mixter and Barr that compression of a nerve root by a herniated disc could cause sciatica, the belief in the pathoanatomical basis for back and leg pain has been a fundamental dogma.⁴⁵^,⁴⁶ Structural evidence of a lumbar disc herniation in a patient with appropriate symptoms is present more than 90% of the time.⁴⁷^,⁴⁸^,⁴⁹^,⁵⁰ Unfortunately, even when using advanced imaging techniques, such as myelography, computed tomography scans, or MRI, the same positive findings are also present in 28% to 50% of asymptomatic individuals.⁴⁷^,⁴⁸^,⁴⁹^,⁵⁰^,⁵¹ Similarly, in the neck, the false-positive rate for imaging has been reported to be as high as 75% in the asymptomatic population.⁵²^,⁵³ Thus, imaging tests have high sensitivity (few false-negatives) but low specificity (high false-positive rate) for identifying symptomatic disc problems.⁵⁴

Figure 3.6 False-positive rates for disc herniation with various imaging modalities. Imaging findings of disc abnormalities increase in frequency with age in patients without symptoms. (CT, computed tomography; DJD, degenerative join disease; MRI, magnetic resonance imaging.) From Bigos S, Müller G. Primary care approach to acute and chronic back problems: definitions and care. In: Loeser JD, ed. Bonica’s Management of Pain. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

Furthermore, the presence of structural pathology in an asymptomatic individual does not predict a greater likelihood of future problems.⁵⁵^,⁵⁶ Borenstein et al performed MRI on 67 asymptomatic people; 31% had abnormality of disc or spinal canal.⁵⁵ The MRI findings were not predictive of future LBP. Individuals with the longest duration of LBP were not those with the greatest anatomical abnormalities. Carragee et al studied discograms and reported that a painful disc injection did not predict LBP on follow-up at 4 years.⁵⁶ Although discograms have high sensitivity for identifying tears in asymptomatic patients, it was the psychometric profiles (what the patient believed of their condition) that were found to strongly predict future LBP and work loss.

Even when the diagnosis of disc herniation is relevant, such pathology has a tendency to resolve without surgical intervention. Bush et al⁵⁷ reported, “A high proportion of intervertebral disc herniations have the potential to resolve spontaneously. Even if patients have marked reduction of straight leg raising, positive neurologic signs, and a substantial intervertebral disc herniation (as opposed to a bulge), there is potential for making a natural recovery, not least due to resolution of the intervertebral disc herniation.” This group found similar results in the cervical spine, concluding that most cervical disc herniations regress with time without resorting to surgery.⁵⁸ Yukawa et al found in sciatica patients treated conservatively and followed up for 3 years that 57% had a reduction in the size of disc herniation and only 3% had an enlargement.⁵⁹

Other structural pathologies have been overstated as causes of back pain. There is little relationship between radiological signs of degeneration and clinical symptoms.⁶⁰^,⁶¹^,⁶²^,⁶³^,⁶⁴^,⁶⁵^,⁶⁶^,⁶⁷ Nachemson⁶⁸ said, “Even when strict radiographic criteria are adhered to, ‘disk degeneration’ is demonstrated with equal incidence in subjects with or without pain.” According to a recent review by Jarvik and Deyo, the prevalence of disc degeneration among asymptomatic individuals of middle age ranges from 46% to 93%.⁶⁹ They concluded that findings such as bulges, dehydration, and loss of disc height should not automatically be viewed as abnormalities because they are strongly related to age. However, there are certain exceptions, such as disc extrusions, moderate or severe canal stenosis, and nerve root compression, which are significantly correlated with symptoms.⁷⁰ Van Tulder in a systematic evaluation of the literature concluded that spondylosis, spondylolisthesis, spina bifida, transitional vertebrae, and Scheuermann disease are not associated with LBP.⁶⁷ Videman et al, in a study of cadaver specimens, found no correlation between structural pathology and a history of LBP.⁷¹^,⁷²^,⁷³ Segmental instability and isolated disc resorption are other diagnoses that again cannot be validated.⁶⁸

There is iatrogenic risk with ordering imaging as Kendrick et al reported that patients who received x-rays were more likely to report a longer duration and greater severity of pain, reduced functioning, and poorer health status than those who had not.⁷⁴ They concluded that “radiography encourages or reinforces the patient’s belief that they are unwell and may lead to greater reporting of pain and greater limitation of activities.” Most LBP patients do not have structural pathology, which can be clearly diagnosed as the cause of symptoms.⁷⁵ For this reason, most of these patients are classified as “nonspecific back pain.” According to Frymoyer,⁷⁶ “most commonly, diagnosis is speculative and unconfirmed by objective testing.” An interesting exception involves patients with chronic pain in whom, according to Bogduk, the pain generator can be identified the majority of the time with the use of a double anesthetic block technique.

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

Randomized Controlled Trial Demonstrates Limitations of Bed Rest Prescription

281 acute LBP subjects (<72 hours).
Compared 4 days of bed rest with continuation of normal activities (insofar as pain allowed).
At 7 days, 1 month, and 3 months, pain intensity, functional disability (Roland-Morris scale), and spinal mobility were similar for both groups.
Relapse rate was similar for both groups.
Increased days of sick leave in bed rest group.

From Rozenberg S, Delval C, Rezvani Y, et al. Bed rest or normal activity for patients with acute low back pain: a randomized controlled trial. Spine. 2002;27:1487-1493.

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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