Chronic Pain: A Call to Treat the Patient Beyond the Label

"What’s happening to me?"

The answer to this question is much less complicated for a person with acute or immediate postoperative pain that has a simple biomedical and mechanical mechanism.

This traditional biomedical diagnosis of these conditions can provide the individual with a clear explanation of "what’s wrong with me" by labeling specific structures and tissue lesions. Treatment can be directed toward the offending tissue or injury with relatively good results.

For many people with chronic pain, there is no specific, simple mechanical mechanism to associate a diagnostic condition with the problem.

Often, these people experience pain that is systemic in nature and not directly related to a specific structure or tissue injury. When it comes to dealing with people with chronic pain, attempts to provide a reasonable answer to the question "what’s wrong with me?" have proven to be a challenge.

Assigning these various diagnostic "labels" to conditions, such as fibromyalgia (FM), chronic fatigue syndrome (CFS), non-celiac gluten sensitivity, metabolic disorders, irritable bowel syndrome (IBS), and Chronic Lyme disease (CLD), for people with chronic pain can confuse the individual when trying to answer the question "what’s wrong with me?" .

The traditional use of "labeling" conditions may lead clinical practice to treat a condition as an isolated tissue problem may be part of the poor outcomes often encountered in the treatment of these conditions.

Several reports have shown an increase in the number of people diagnosed with these different conditions over time. This shows that more and more people are struggling to make sense of their chronic pain through these various diagnostic conditions.

For example, 20 years ago it was estimated that 6 million people in the United States suffered from FM, while updated prevalence studies place FM in the United States at around 10 million patients, with that prevalence being more than 2 times higher in women .

According to the Centers for Disease Control and Prevention, 300,000 new cases of CLD have been reported each year in the United States, increasing the total number of people affected by CLD. This increase in “labeling” people has a major impact on women’s health physical therapist (PT) based on the higher prevalence of chronic pain in women.

1. First, many of these conditions have been shown to have several overlapping signs and symptoms, and many people with FM may also have the CFS label attached to them, complicating the person’s search for answers, let alone treatment. .
    
2. Second, for many of these diagnostic conditions, there are no definitive medical tests and often the diagnosis is made through a process of elimination, which adds uncertainty for people and further complicates the diagnostic process.
    
3. Lastly, adding the word “syndrome”   or providing a non-descriptive label does not help people with their initial “what’s wrong with me” question but may actually create more uncertainty.

Accurate diagnosis of some medical conditions that have a specific mechanical source of disease or pathology is vital to applying the most appropriate treatment for these conditions. For patients suffering from chronic pain, the label for the condition may not add value to selecting appropriate treatment.

A proper examination is necessary to rule out important medical pathologies that could be the source of chronic pain. However, once ruled out, consideration of the patient’s condition from a biopsychosocial perspective is more appropriate than treatment toward a medical label of a condition.

According to clinical practice guidelines directed toward chronic pain conditions, patients should be educated about the nature of their illness, ensure that education is closely linked to evidence of the biological nature of their problem, and avoid "syndromes." and geography (i.e. lower back).

It is argued that a "syndrome" explanation may not only fail to provide a clear biological understanding of "what is wrong with me", but may also increase fear and avoidance, which in turn increases the experience of pain. Additionally, the guidelines require educational models to decrease unnecessary fear related to movement, leisure, and work activities.

One educational model that has shown some success in helping patients with a biological understanding of “what’s wrong with me” has been pain neuroscience education (PNE). PNE is an educational strategy that focuses on teaching patients more about the neurobiological and neurophysiological processes involved. in your experience with pain.

The current best evidence regarding musculoskeletal pain provides strong support for PNE to positively influence pain ratings, dysfunction, prevention of fear and pain catastrophizing , movement limitations, pain awareness, and healthcare utilization, including in patients with FM and CFS.

The goal of this clinical commentary is to review current pain theory and how 4 conditions common to women (FM, CFS, IBS, and CLD) can be explained through neurobiological and neurophysiological bases. The article details each of these links to conditions related to clinical presentation and biology. We also provide several suggestions for changes in physical therapy treatment to address these overlapping aspects of the conditions to allow for more comprehensive care for the individual.

An overview of the problem

The “big picture” neurobiological view of pain has been presented using the definition coined by Moseley: Pain is a multiple system activated by an individual’s pain-specific neuromatrix . The neuromatrix is ​​activated when the brain perceives a threat. To develop a clinical understanding of this definition, it is important to understand the neuromatrix, production, and threat.

Neuromatrix

It is now well established that, during a human pain experience, multiple areas of the brain are activated and these areas working together have become known as the pain neuromatrix. Several imaging studies have highlighted the most common brain areas in the pain neuromatrix. The most commonly activated areas are the anterior cingulate, primary sensory cortex, thalamus, anterior insula, prefrontal cortex, and posterior parietal cortices.

During a painful task, these increasingly active brain areas are thought to communicate with each other, essentially developing a “pain map.” None of the activated regions in the pain neuromatrix are solely related to pain processing, but have other necessary functions, such as roles in executive function, sensory localization, and emotional awareness.

During chronic pain states , these regions may be increasingly taxed by the tasks involved in pain processing and therefore suffer from their primary function. The neuromatrix-based theory of pain explains many problems commonly seen in patients with chronic pain, such as problems with concentration and attention, body temperature regulation, sleep disorders, and short-term memory problems.

Given the enormous complexity of neuronal activation, synaptic activity, neurotransmitters and modulators, the primary “pain map” can also be influenced by neighboring neuronal circuits. it is likely to influence the individual experience of pain.

The fact that a person’s "pain map" can be modulated by adjacent maps in relation to their knowledge, memories, past experiences, beliefs, etc., makes each person’s experience of pain individualized and personal .

Evolution

Various peripheral processes associated with tissue injury and disease states (i.e., chemical, thermal, and mechanical factors) stimulate nociceptors , and nociceptive information is sent to the brain for processing and interpretation. The brain interprets the information (neuromatic pain) sent by the tissues (nociception and other sensory signals) and pain is produced by the brain.

Pain is, therefore, an output , a decision, by the brain, based on the final result of the pain neuromatrix and its interaction with the various neighboring elements. Maps, influenced by various biological and psychosocial factors. However, pain is only a response to a threatening situation such as an injury.

Several biological systems are compromised during a pain experience. This may include the sympathetic nervous system, immune system, endocrine system, motor response, and changes in the gastrointestinal (GI) system (Figure 1).

In a stress response, these various biological systems are increased or suppressed to cope with the impending situation ("fight and flight"). The driving force behind these stress responses are powerful catecholamines such as epinephrine (adrenaline) and the hormone cortisol.

If we were to consider the idea that the biological sensitivity of FM, CFS, CTE, IBS, and non-celiac gluten sensitivity are the same, one must consider why certain biological systems are more affected than others. The precise mechanism is unknown, complex and probably multifactorial. Some authors have implicated genetic predispositions, biological "memory" of previous episodes of stress, and the "weak link" theory .

Another possible consideration may be the specialist the patient sees. When patients present to their primary health care provider with a constellation of signs and symptoms, they will likely be referred to a specialist who best fits the constellation of symptoms, whether a rheumatologist, endocrinologist, immunologist, etc. It is argued that each discipline, with its narrow focus on a particular system, can be a source of classification that depends on the system they explore. This assumption is consistent with current evidence investigating the immune system in FM, endocrine system in CFS and CLD, and the GI system in IBS.

Similarities in clinical presentation, diagnosis and treatment

The concept that the various conditions are biologically similar is not so far-fetched when one considers the overlap between the clinical signs and symptoms common to the various conditions.

When you look at the significant overlap of the most common symptoms, it is understandable why the medical community has such difficulty specifically diagnosing any of these conditions and why many chronic pain sufferers end up with multiple "labels."

It is interesting to note that many of the common symptoms can be found in hyperthyroidism and hypothyroidism, including fatigue, constipation, muscle weakness, muscle pain and tenderness, joint stiffness, depression, memory impairment, changes in appetite, nervousness, anxiety and irritability. and difficulty sleeping.

This does not imply that patients with FM or CFS suffer from hyper or hypothyroidism, but as seen in alterations in thyroid function, there are significant changes in cortisol and in the hypothalamic-pituitary-adrenal (HPA) axis, which is involved in thyroid function. In fact, some FM researchers have stated that "Hypothyroidism can mimic the symptoms of FM."

To further complicate the situation for people with chronic pain conditions, it is now well established that many of these conditions can only be truly diagnosed through a process of elimination.

With the absence of concrete, objective data (i.e., image analysis or blood tests), the diagnostic process is likely to add even more uncertainty and further contribute to the notion of a common characteristic of the various labels.

Although imaging is common with these conditions, there is little clinical utility due to false positive and negative results. The use of blood tests in the diagnostic process is also of little value due to potential biomarkers , such as cytokines, which have a short half-life. This makes the use of blood tests for clinical diagnosis very challenging due to questionable accuracy.

As we move beyond the commonality of symptoms and lack of diagnostic testing and into the current best treatment for FM, CFS, IBS, and CLD, the overlap becomes even more apparent. In line with the big picture, the current best treatment for FM, CFS, IBS, and CLD includes a combination of cognitive therapy, movement/exercise, and medications aimed at calming the central nervous system (i.e., antidepressants). and/or membrane stabilizers).

Similarities in underlying biology

If we view FM, CFS, IBS, and CLD from a “big picture” view in terms of current thoughts related to the underlying biology, a similar pattern emerges regarding the biological processes found with each condition.

Fibromyalgia

The original 18 American College of Rheumatology tender points were research criteria and had little or no value in the clinical diagnosis of FM. Over the years, FM research has changed from a rheumatological focus to inflammatory, muscular and now immune responses.

Several authors now emphasize the idea that the neuroimmuno-endocrine system is a driving force behind the presentation of FM. Similarly, individuals with FM are shown to have alterations in their HPA axis, which in turn alters cortisol production. The importance here is that cortisol regulates the immune system, specifically cytokine production.

Several of the FM studies show that with an altered HPA axis and subsequent increased cortisol, greater amounts of proinflammatory cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α are produced than with time lead to a pro-inflammatory state in individuals with FM. The immune system, through cytokine signaling, is thought to play a major role in FM.

To further complicate matters, the female hormone estrogen , when added to the pro-inflammatory shift already driven by cytokines, further exacerbates the pro-inflammatory state. This may partially explain why FM is 10 times more common in women than in men.

Chronic Fatigue Syndrome

Recently, 4 leading international experts in the field of CFS met to discuss their work associated with CFS. The final result? "Despite many years of research, the diagnosis of CFS remains one of exclusion and we do not know the cause of CFS." This honest admission, once again, highlights the complexity of chronic pain and the search for individual causes.

The HPA axis and cortisol come into play as a biological mechanism involved in individuals with CFS. The HPA axis controls the level of cortisol, which in turn controls vital parts of energy expenditure, including the circadian rhythm and stress responses. and energy metabolism.

Evidence points to chronic stress (i.e. chronic pain) leading to hypoactivity of the HPA axis, which in turn decreases cortisol levels.

Another biological area specific to CFS that is receiving additional attention is nitric oxide , which is being correlated with CFS-specific problems such as vasoconstriction, reduced endogenous opioid function, changes in neurotransmission, and inflammation. It is interesting to note that CFS nitric oxide science results are linked to inflammatory changes and relate to the immune system and cytokine function, so they end up in the same place.

Irritable bowel syndrome

IBS is very poorly understood regarding its etiology and diagnosis. To complicate it further, IBS is now being subclassified as IBS-C ( constipation dominant), IBS-D ( diarrhea dominant), IBS-M ( mixed ), and IBS-U ( no substrate ).

Several potential causes have been theorized, including alterations in intestinal bacterial colonization, small intestinal bacterial overgrowth, and dietary habits. Recently, attention has been directed to the immune system, especially mast cells.

Mast cells secrete histamine, serotonin and cytokines. It is postulated that this increase in cytokine release from mast cells, coupled with already altered system-wide cytokine production due to long-term stress and cortisol, results in increased central nervous system sensitization.

With increased sensitivity of the nervous system it can be easily understood how individuals develop sensitization to various foods and how distension of tissues in the GI system can produce pain (hyperalgesia and allodynia) and affect bowel movements. This connection between the GI system, the central nervous system and the HPA axis is often referred to as the "gut-brain axis" , once again representing the close relationship between the various systems.

Chronic Lyme disease

Of the 4 conditions, the least amount of information is available for CLD. Over the past 5 years, the Centers for Disease Control and Prevention has reported 300,000 new cases per year, far above the expected "real" cases of CLD, pointing to a mismatch in the diagnosis of CLD and the clinical presentation of CLD.

Several authors point out the difficulty in diagnosis and many authors claim that CLD overlaps and resembles CFS. With respect to the underlying biological mechanisms, CLD is once again linked to altered HPA axis, cortisol levels, and cytokine levels.

It should be noted that these different conditions may, in fact, be more similar than different.

Adding support to this argument are brain scan studies showing that patients with FM, CFS, CTE and IBS show activation in similar areas. Again, this is not surprising, as activation of pain neuromatrices is not tissue- or disease-specific.

Treat the patient, not the label

There are other diagnostic labels that could be included (central sensitization syndrome, non-celiac gluten sensitivity disorder, and metabolic syndrome) with others potentially coming your way. How does a therapist proceed to treat these conditions?

An easy place to start, clinically, is to see these labels for what they are: chronic pain conditions.

The brain does not process information in terms of tissues, diagnoses or conditions, but in terms of threat.

Doctors should treat the patient, not the "label." Therefore, it is recommended that when you encounter people with these conditions you remember:

• They hurt, probably for a long time.
• They are tired
• They have been let down by the medical community, including the physical therapist
• They have lost hope
• They need help

In addition to treating the patient, not the label, some key clinical elements must be considered.

1. First, these patients must be treated with dignity, respect and compassion.
    
2. Second, the therapist should not attempt to remove the label from the patient. In many cases, patients identify themselves with their label. It is recommended that doctors call it whatever the person wants to call it.

Having developed an understanding of these underlying biological problems, therapists can adopt treatments such as cognitive therapy (education), exercise and movement as important in the management of chronic pain. These treatments should be aimed at improving broader systemic functions of the immune system, neural function, and endocrine control, not correcting isolated mechanical deficits.

If pain occurs according to threat , it seems reasonable to argue that if we modify the threat, we alter a pain experience.

One intervention to achieve this would be patient education (i.e., PNE). By providing a better understanding of the biology of the pain experience, the patient gains an answer to the question: “What’s wrong with me?”

It is not linked to topography or a syndrome, but is in line with current best evidence guidelines. PNE has been shown to positively influence pain catastrophizing and fear prevention, specifically in FM and CFS.

Research shows that PNE delivery is best achieved through the use of metaphors, examples, and images. An example of a PNE metaphor that can be used to explain how chronic pain can be viewed as a state of chronic stress is a story about a lion entering a room. This metaphor for a highly stressful situation, the lion in the room, can be used to help the patient better understand some of the biological processes he is experiencing in her body.

In this metaphor, the various physical and psychosocial stressors are represented as a lion. That he lives with them daily. The therapist guides the patient to see the benefits of an immediate, adaptive “fight and flight” response that is normal for short periods.

In contrast, this adaptive response with a scenario where the lion remains in the room for months and years can be used to show the long-term maladaptive effect of stress on various biological systems, including fatigue, sleep disturbance, GI, bowel and bladder sensitivity, nerve sensitivity issues and muscle pain.

However, education alone is not the answer. Current evidence shows that education must be linked to action , especially movement. Evidence supports specific aerobic exercise for the various conditions discussed here.

Aside from the various cellular and direct biological effects (i.e. cellular nutrition, tissue oxygenation, etc.), aerobic exercise has very definite benefits for treating chronic pain. Aerobic exercise has been shown to involve various endogenous mechanisms through the release of endorphins and enkephalins , which can relieve pain.

Additionally, aerobic exercise has been shown to decrease nerve sensitization , which is important since FM, CFS, IBS. and CLD shows a clinical presentation of central sensitization. It doesn’t take much exercise to evoke positive changes.

For example, Hoffman et al have shown that 10 minutes of aerobic exercise at 50% of maximal oxygen consumption (VO2 max) produces a hypoalgesic effect . Fulcher and White have shown that with aerobic exercise at 3 minutes of walking, adding 1 to 2 minutes every other day with the goal of 30 minutes, 5 days a week, resulted in a positive change in pain and function in patients with CFS.

Aerobic exercise powerfully strengthens the immune system. Additional interventions complementary to PNE and a skillfully stimulated exercise program should include other behavioral strategies such as sleep hygiene, dietary consultation, relaxation and meditation, breathing exercises, and goal setting.