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Opioid Management Debate https://www.instituteforchronicpain.org Sun, 05 Feb 2023 13:55:45 +0000 Joomla! - Open Source Content Management en-gb What is Chronic Pain? https://www.instituteforchronicpain.org/providers-and-payers/opioid-management-debate/item/200-what-is-chronic-pain https://www.instituteforchronicpain.org/providers-and-payers/opioid-management-debate/item/200-what-is-chronic-pain What is Chronic Pain?

Patients and healthcare providers commonly think of pain as a symptom of an underlying injury or illness. Say, for example, you hurt your low back while lifting. Perhaps, you’ve injured a muscle or ligament, or perhaps it’s an injury to the spine, like a disc bulge or herniation. Either way, you now have pain and the pain is the symptom of the injury. The same might be true for any health condition that causes pain, particularly when it first starts.

Acute pain defined

We call this type of pain acute pain.  Acute pain has two characteristics. First, just as described, acute pain is a symptom of an underlying health condition. Second, its duration is

Patients and healthcare providers commonly think of pain as a symptom of an underlying injury or illness. Say, for example, you hurt your low back while lifting. Perhaps, you’ve injured a muscle or ligament, or perhaps it’s an injury to the spine, like a disc bulge or herniation. Either way, you now have pain and the pain is the symptom of the injury. The same might be true for any health condition that causes pain, particularly when it first starts.

Chronic pain is not long-lasting acute pain

Sometimes pain doesn’t go away. It can last for longer than six months. In fact, it can last for years. In these situations, there is a tendency among patients and some healthcare providers to continue to see the pain as a symptom of the underlying health condition that started it. They think of chronic pain as simply the long-lasting pain of an injury or illness that hasn’t yet healed.

This line of thinking leads to getting a lot of healthcare. Surgeries, injections, and other interventional procedures are common attempts to reduce pain by focusing on the underlying condition that started the pain. The typical chronic pain patient has had any number of such procedures and therapies.

These procedures and therapies aren’t very effective. At best, they tend to provide temporary reductions in pain. Studies of healthcare expenditures show that in the last twenty years the rates of pain-related surgeries, injections and narcotic pain medications are at an all time high. At the same time, applications for pain-related disability are also at an all time high.1 Obviously, these procedures and therapies don’t work so well.

The truth is, once pain is chronic, it’s pretty hard to stop, particularly if the focus of care is to try to fix the underlying injury or illness that started it all.

The reason is that chronic pain is something more than the pain of a health condition that hasn’t healed. The importance of this point is hard to underestimate.

Chronic pain defined

Chronic pain has two characteristics that are different from acute pain. First, chronic pain lasts longer than six months. Second, and most importantly, chronic pain is pain that occurs in addition to the pain of the original health condition. In fact, the original, underlying condition may or may not have healed. It doesn’t really matter. Chronic pain is pain that has become independent of the underlying injury or illness that started it all.

Once pain has become chronic, attempts to fix the underlying injury or illness that started it tend to fail to reduce pain. The mistake that patients and some healthcare providers make is to think that chronic pain is just a long-lasting version of acute pain. However, chronic pain is pain that has taken on a life of its own. Chronic pain is pain that is occurring over and above any pain that may or may not occur from the underlying injury or illness that started it. As such, attempts to cure the original health condition commonly miss the mark.

Cause of chronic pain

What then is the cause of chronic pain? To answer this question, we need to understand some facts about the nervous system.

Whatever its initial cause, pain is a function of the nervous system. Say you injure your low back. Nerves around the site of the injury detect it and sends signals that travel on a highway of nerves from the injury to the spinal cord and up to the brain. Once they get to the brain, the brain processes the signals and they register as pain in the low back. The whole highway, from the nerves in the low back to the brain, is the nervous system.

At the same time as the signals travel from the injury to the brain, the whole nervous system becomes reactive. Like a fire detector in a building sounding the alarm in response to fire, the nervous system sets off the alarm bells when in pain. Our muscles become tense. We guard and grimace. We cry and are emotionally alarmed. The nervous system controls all these reactions. We can think of it as the whole nervous system going into red alert.

This reactivity of the nervous system is all well and good when it comes to acute pain. It helps us to know that something is wrong. Becoming alarmed, we protect against further injury and seek help. Once the original injury or illness heals, everything about the nervous system usually comes back to normal.

In some people, however, the nervous system can stay in a persistent state of reactivity even upon healing of the original acute injury or illness. The whole nervous system becomes more and more reactive in a process called wind-up. This reactivity of the nervous system comes to maintain pain in a vicious cycle, over and above the pain of the original condition that started it all. The end state of this process is a highly reactive nervous system called central sensitization.

The hallmarks of central sensitization are increasingly widespread pain and increasingly intense pain. Suppose you have an injury to your neck and come to have chronic neck pain. In this process, central sensitization develops independdnelty of whether the initial injury heals.  Subsequently, you develop pain in your shoulders and upper back as well as tension headaches in adition to neck pain. The pain may become so intense that even touch can hurt.

Other problems occur as well with central sensitization. Since the nervous system also controls our emotional lives, a highly reactive nervous system leads to anxiety and irritability, poor sleep, fatigue, and eventually depression. These psychological problems are secondarily stressful. The stress adds to the reactivity of the nervous system, making the pain worse.

The upshot of it all is that chronic pain develops from acute pain but becomes an altogether different type of pain, which we call chronic pain, by way of central sensitization and is not the result of a long-lasting injury or illness.

Central sensitization can occur with all acute pain conditions. It can occur with spine-related acute injuries, whiplash injuries, tension headaches, migraine headaches, rheumatoid arthritis, osteoarthritis, and endometriosis. It can occur with injuries from a motor vehicle accident or following surgeries.

The importance of treating the nervous system in chronic pain

Chronic pain is thus categorically different from acute pain. It’s not just that it lasts longer. It’s that the whole nervous system is involved, maintaining the chronicity of the pain, over and above whatever pain that might continue, if any, from the original health condition that started it.

Earlier, we commented on the frequent failure of surgeries, injections, and other interventional procedures to permanently reduce pain. From here, we can see why. They are attempts to fix the injury or condition that started it all. The original condition, however, is typically not what’s responsible for maintaining pain on a chronic course. That is to say, the treatments fail because none of them address the most important cause of chronic pain – central sensitization.

The only treatment that fully addresses central sensitization is chronic pain rehabilitation.

References

1. Brook, M. I., Deyo, R. A., Mirza, S. K., Turner, J. A., Comstock, B. A., Hollingworth, W., & Sullivan S. D. (2008). Expenditures and health status among adults with back and neck problems. Journal of the American Medical Association, 299, 656-664.

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) What is Chronic Pain Thu, 20 Apr 2017 16:47:15 +0000
CBT and Central Sensitization https://www.instituteforchronicpain.org/blog/item/145-48cbt-and-central-sensitization https://www.instituteforchronicpain.org/blog/item/145-48cbt-and-central-sensitization

A study published this month in Pain produced what is likely some of the most important research findings this year for the field of chronic pain rehabilitation. The study demonstrated that basic CBT interventions can reduce central sensitization (Salomons, et al., 2014). Countless studies in the past have shown that CBT and CBT-based chronic pain rehabilitation programs are effective in reducing self-reported pain in chronic pain patients.

In these studies, we have had to infer that CBT reduces central sensitization: because CBT is effective at reducing chronic pain based on verbal self-report, and because central sensitization is a leading cause of chronic pain, we have inferred that CBT must reduce central sensitization. Now, we have a study that directly demonstrates it.

In their well-designed study, Salomons, et al., are the first to experimentally induce a form of central sensitization in a group of previously pain-free subjects, deliver a CBT intervention, and measure the reduction in central sensitization that results from the CBT intervention. As such, they are the first to demonstrate that CBT reduces central sensitization as measured in the laboratory and not simply rely on inferences based on self-reported pain levels.

The study design

The study consisted of 34 healthy women who did not have pain. Through a series of pain-provoking procedures, the researchers induced secondary hyperalgesia in these healthy women. Secondary hyperalgesia is a type of central sensitization. Central sensitization is largely considered a common, if not the most common, cause of chronic pain. In secondary hyperalgesia, the nerves in the general location of the pain become reactive in an increasingly wider area. As a consequence, it takes less and less stimuli to cause pain in this widening area around the site of the original pain.

Along side this series of pain-provoking procedures, the researchers provided half the group of healthy women with a few basic cognitive behavioral interventions for pain. The CBT intervention consisted of both providing the subjects with information about the sensory, cognitive, and affective aspects of pain and engaging them in cognitive restructuring in order to reduce the stress response that accompanies pain. Cognitive restructuring is an intervention that helps people to make sense of their pain differently, from understanding it as something that is alarming or frightening to understanding the pain as something that is more benign and not harmful or perhaps even beneficial. For the other half of women, they provided a psychotherapy focusing on becoming more assertive in interpersonal communication skills.

By comparing CBT for pain with a non-pain related psychotherapy, they attempted to determine the effectiveness of the CBT itself.

The provision of some form of psychotherapy to both groups is important because it controlled for the effectiveness of non-specific therapeutic factors of psychotherapy. Let me explain. To do so, we need to stray from our original topic a bit.

One of the most consistent findings in the last four decades of psychotherapy outcome research has been that a large percentage of what accounts for the effectiveness of psychotherapies are factors that are common to all psychotherapies. So, whether we are talking about cognitive behavioral therapy for pain or diabetes or depression, or psychodynamic therapy for dysfunctional relationship patterns, or family systems therapy for teenage behavior problems, they all tend to have some things in common, which contributes to what makes them effective. That is to say, despite having some obvious differences, they each share certain factors and these factors are in part what make them all effective.

These factors tend to be characteristics of the relationship between the provider and the patient. We tend to refer to these characteristics in general as the qualities of the ‘therapeutic relationship.’ For example, research consistently finds that, in whatever type of psychotherapy that one pursues, the development of a relationship with an expert provider who takes the time to listen to you and provide mutually respectful, caring, and honest feedback leads people to become motivated to make healthy behavior change – whether it is in learning how to manage pain or diabetes, overcome depression, develop healthy relationships, or change problematic teenage behaviors. In other words, the therapeutic relationship that you have with a healthcare provider is what leads, in part, to making healthy changes that can improve health.

So, in a study aiming to determine how CBT is effective for managing pain, Salomons, et al., needed to make sure that they were measuring what is unique to CBT for pain and not the general effectiveness that all the psychotherapies have in common. To do so, they compared CBT to a psychotherapy that was not for pain, but which would have the general therapeutic factors that are common to all therapies, including the CBT for pain. This study design thus allows the researchers to conclude that if CBT for pain is in fact more effective, then what’s making it more effective are those things that are unique to CBT. In other words, the therapeutic relationship might play a role in both psychotherapies equally, but if one is more effective, such as the CBT, then what’s pushing it over the top are those things that are unique to CBT.

So, let’s get back to what Salomons, et al., found.

Cognitive behavioral therapy and central sensitization

While both groups of study subjects reported less pain intensity, those who underwent CBT reported that the pain they had was less unpleasant and therefore more tolerable. These findings that CBT reduces pain and makes pain more tolerable are largely similar to most clinical trials of CBT for pain.

The more interesting and important finding was that the subjects who received CBT exhibited a 38% reduction in the area of secondary hyperalgesia. Recall that secondary hyperalgesia is a form of central sensitization in which the nerves around the site of pain become more reactive in a widening area. In this increasing area around the original site of pain, less and less stimuli are required to generate pain. Secondary hyperalgesia is thought to be one of the ways an acute injury can transition to chronic pain even after the acute injury has healed. In their study, Salomon, et al., experimentally induced secondary hyperalgesia and subsequently showed that CBT can reduce it.

To my knowledge, no previous study has directly demonstrated a reduction in a form of central sensitization with CBT interventions.

A possible explanation for this finding is that CBT reduces the stress response that occurs with pain. By coming to think about pain differently, the change in thinking corresponds to changes in the neural network of the brain. These changes in the brain might subsequently alter the hormonal and inflammatory responses of the stress response, which subsequently makes the nerves in the peripheral area around the site of the original pain less reactive. As such, the cognitive restructuring corresponds to changes in the brain that reduce the stress response, which lead to downstream reductions in nerve reactivity.

Whatever is the explanation, the findings of Salomons, et al., are important as they can lead us to greater confidence as to why CBT and CBT-based chronic pain rehabilitation programs are effective at reducing chronic pain.

References

Salomons, T. V., Moayedi, M., Erpelding, N., & Davis, K. D. (2014). A brief cognitive-behavioral intervention for pain reduces secondary hyperalgesia. Pain, 155, 1446-1452. doi: 10.1016/j.pain.2014.02.012

Author: Murray J. McAllister, Psy.D.

Date of last modification: 9-2-2014

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Cognitive Behavioral Therapy Mon, 01 Sep 2014 20:54:35 +0000
Abdominal Pain https://www.instituteforchronicpain.org/common-conditions/abdominal-pain https://www.instituteforchronicpain.org/common-conditions/abdominal-pain

What is chronic abdominal pain?

Abdominal pain is common and occurs to most people on occasion. It usually occurs for a brief period of time and can have many benign causes, such as indigestion, stress and anxiety. Sometimes, such as when having appendicitis, it is serious and requires the attention of a healthcare provider. Abdominal pain can also become chronic. Healthcare providers consider it chronic when it last longer than six months.

Is there a cure for chronic abdominal pain?

Chronic abdominal pain is often identified as a problem in the gastrointestinal, endocrine, or reproductive systems of the body. However, chronic abdominal pain commonly has no identifiable cause. An example is chronic pancreatitis. Healthcare providers are able to identify that the pancreas is involved, but are often unable to understand why it is happening. Conditions, like chronic pancreatitis, that have no identifiable cause are called idiopathic.

Most patients with idiopathic chronic abdominal pain have had numerous tests and procedures. Common tests are the following:

  • MRI scans
  • CT scans
  • Endoscopies
  • Colonoscopies
  • Blood, urine and fecal tests
  • Endoscopic retrograde cholangiopancreatographies (ERCP’s)
  • Magnetic resonance cholangiopancreatographies (MRCP’s)
  • Ultrasound

These tests are ways to assess the health and functioning of the different bodily systems that lie in the abdomen, such as the gastrointestinal and reproductive systems. It is important to rule-out potential causes of pain in these systems, such as cancers, endometriosis, Crohn’s disease, irritable bowel syndrome, among others. Oftentimes, however, as stated above, the cause of chronic abdominal pain remains unknown.

Therapies & Procedures for chronic abdominal pain

Similarly, patients with idiopathic chronic abdominal pain often have had numerous procedures that fail to cure the condition. When a cause is not readily identifiable, recommendations for therapies and procedures tend to get made on a trial-and-error basis. Patients with chronic abdominal pain commonly have had multiple procedures and surgeries. Examples are the following:

  • Appendectomies
  • Cholecystectomies (i.e., removal of the gall bladder)
  • Oopherectomies (i.e., removal of the ovaries)
  • Hysterectomies
  • Ablations
  • Stent insertions
  • Biliary and pancreatic sphincterectomies
  • Scar tissue removal
  • Exploratory surgeries

Pursuit of these procedures assumes that the primary cause of pain is some problem in the gastrointestinal, endocrine, or reproductive system. Patients and their healthcare providers tend to try one procedure after another in attempt to cure the pain condition. These procedures are often worth trying, particularly in the acute phases of having abdominal pain. However, they are often unsuccessful once pain has become chronic.

It is well-established that central sensitization is a factor in chronic abdominal pain.1, 2, 3 Central sensitization is a highly reactive state of the nervous system, which causes pain. It can occur with any pain disorder, including chronic abdominal pain. It is not known whether central sensitization can be an initial cause of abdominal pain or whether it is a secondary cause, which maintains abdominal pain on a chronic course. Either way, it is important to address in treatment.

Chronic pain rehabilitation programs focus on reducing the central sensitization associated with any type of chronic pain condition, including chronic abdominal pain. They are an intensive, interdisciplinary approach that combines lifestyle changes, coping skills training, and medication management. The overall goal of these treatment approaches is to reduce central sensitization by down-regulating the nervous system. The original problem in the gastrointestinal or reproductive system that initially caused the pain may remain unresolved or unknown. However, by reducing central sensitization, pain is reduced to tolerable levels.

There is hope even if the original cause of pain remains unknown. There is hope even if there is no cure.

References

1. Dengler-Crish, C. M., Bruehl, S., & Walker, L. S. (2011). Increased wind-up to heat pain in women with a childhood history of functional abdominal pain. Pain, 152, 802-808.

2. Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152, S2-S15.

3. Mayer, E. A., & Tillisch, K. (2011). The brain-gut axis in abdominal pain syndromes. Annual Review of Medicine, 62. doi: 10.1146/annurev-med-012309-103958.

Date of publication: April 27, 2012

Date of last modification: October 13, 2018

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:34:36 +0000
What is Central Sensitization? https://www.instituteforchronicpain.org/understanding-chronic-pain/what-is-chronic-pain/central-sensitization https://www.instituteforchronicpain.org/understanding-chronic-pain/what-is-chronic-pain/central-sensitization

Central sensitization is a condition of the nervous system that is associated with the development and maintenance of chronic pain. When central sensitization occurs, the nervous system goes through a process called wind-up and gets regulated in a persistent state of high reactivity. This persistent, or regulated, state of reactivity lowers the threshold for what causes pain and subsequently comes to maintain pain even after the initial injury might have healed.

Nervous SystemCentral sensitization has two main characteristics. Both involve a heightened sensitivity to pain and the sensation of touch. They are called allodynia and hyperalgesia. Allodynia occurs when a person experiences pain with things that are normally not painful. For example, chronic pain patients often experience pain even with things as simple as touch or massage. In such cases, nerves in the area that was touched sends signals through the nervous system to the brain. Because the nervous system is in a persistent state of heightened reactivity, the brain doesn't produce a mild sensation of touch as it should, given that the stimulus that initiated it was a simple touch or massage. Rather, the brain produces a sensation of pain and discomfort. Hyperalgesia occurs when a stimulus that is typically painful is perceived as more painful than it should. An example might be when a simple bump, which ordinarily might be mildly painful, sends the chronic pain patient through the roof with pain. Again, when the nervous system is in a persistent state of high reactivity, it produces pain that is amplified.

Chronic pain patients can sometimes think they must be going crazy because they know intellectually that touch or simple bumps shouldn’t be as uncomfortable or painful as they experience them. Other times, it’s not the patients themselves who think they are crazy, but their friends and loved ones. Friends and loved ones can witness the chronic pain patient grimacing at the slightest touch or crying out at the simplest bump and they think that the chronic pain patient must really be a hypochondriac or something. After all, the contrast between them and the chronic pain patient is stark: the friends and loved ones can be touched or get a bump and it doesn’t send them through the roof. The difference, though, is that the friends and loved ones don’t have a nervous system that is stuck in a persistent state of heightened reactivity, called central sensitization.

In addition to allodynia and hyperalgesia, central sensitization has some other characteristics, though they may occur less commonly. Central sensitization can lead to heightened sensitivities across all senses, not just the sense of touch. Chronic pain patients can sometimes report sensitivities to light, sounds and odors.1 As such, normal levels of light can seem too bright or the perfume aisle in the department store can produce a headache. Central sensitization is also associated with cognitive deficits, such as poor concentration and poor short-term memory.2 Central sensitization also corresponds with increased levels of emotional distress, particularly anxiety.3 After all, the nervous system is responsible for not only sensations, like pain, but also emotions. When the nervous system is stuck in a persistent state of reactivity, patients are going to be literally nervous – in other words, anxious. Lastly, central sensitization is also associated with sick role behaviors, such as resting and malaise,4 and pain behavior.5, 6 

Central sensitization has long been recognized as a possible consequence of stroke and spinal cord injury. However, it has become increasingly clear that it plays a role in many different chronic pain disorders. It can occur with chronic low back pain,7, 8 chronic neck pain,9 whiplash injuries,10 chronic tension headaches,11, 12 migraine headaches,13 rheumatoid arthritis,14 osteoarthritis of the knee,15 endometriosis,16 injuries sustained in a motor vehicle accident,17 and after surgeries.18 Fibromyalgia,19 irritable bowel syndrome,20 and chronic fatigue syndrome,21 all seem to have the common denominator of central sensitization as well.

What causes central sensitization?

Central sensitization involves specific changes to the nervous system. Changes in the dorsal horn of the spinal cord and in the brain occur, particularly at the cellular level, such as at receptor sites.3, 22 

As stated above, it has long been known that strokes and spinal cord injuries can cause central sensitization. It stands to reason. Strokes and spinal cord injuries cause damage to the central nervous system – the brain, in the case of strokes, and spinal cord, in the case of spinal cord injuries. These injuries alter the parts of the nervous system that are directly involved in central sensitization.  

But what about the other, more common, types of chronic pain disorders, listed above, like headaches, chronic back pain, or limb pain? The injuries or conditions that lead to these types of chronic pain are not direct injuries to the brain or spinal cord. Rather, they involve injuries or conditions to the peripheral nervous system – that part of the nervous system that lies outside the spinal cord and brain. How do injuries and conditions associated with the peripheral nervous system lead to changes in the central nervous system, which, in turn, lead to chronic pain in the isolated area of the original injury? In short, how do isolated migraine headaches become chronic daily headaches? How does an acute low back lifting injury become chronic low back pain? How does an injury to a hand or foot become a complex regional pain syndrome?

There are likely multiple factors that lead to the development of central sensitization in these so-called ‘peripheral’ chronic pain disorders. These factors might be divided into two categories:

  • Factors that are associated with the state of the central nervous system prior to onset of the original injury or pain condition
  • Factors that are associated with the central nervous system following onset of the original injury or pain condition

The first group involves those factors that might predispose patients to developing central sensitization once an injury occurs and the second group involves antecedent factors that foster central sensitization once pain starts.

Predisposing factors

There are likely both biological, psychological, and environmental predisposing factors.

Low and high sensitivity to pain, or pain thresholds, are likely in part due to multiple genetic factors.1 While there is no research as of yet to support a causal link between pre-existing pain thresholds and subsequent development of central sensitization following an injury, it is largely assumed that one will be found.

Psychophysiological factors, such as the stress-response, are also apt to play a role in the development of central sensitization. Direct experimental evidence on animals23, 24 and humans,25, 26 as well as prospective studies on humans,27 have shown a relationship between stress and lowering of pain thresholds. Similarly, different types of pre-existing anxiety about pain is consistently related to higher pain sensitivities.28, 29 All these psychophysiological factors suggest that the pre-existing state of the nervous system is an important determinant of developing central sensitization following the onset of pain. It stands to reason. If the stress response has made the nervous system reactive prior to injury, then the nervous system might be more prone to become centrally sensitized once onset of pain occurs.  

There is considerable indirect evidence for this hypothesis as well. A prior history of anxiety, physical and psychological trauma, and depression are significantly predictive of onset of chronic pain later in life.30, 31, 32, 33 The common denominator between chronic pain, anxiety, trauma, and depression is the nervous system. They are all conditions of the nervous system, particularly a persistently altered, or dysregulated, nervous system.

It's not that such pre-existing problems make people more prone to injury or the onset of illness -- as injury or illness is apt to occur on a somewhat random basis across the population. Rather, these pre-existing problems are apt to make people prone to the development of chronic pain once an injury or illness occurs.  The already dysregulated nervous system, at the time of injury, for instance, may interfere with the normal trajectory of healing and thereby prevent pain from subsiding once tissue damage heals.

Factors leading to central sensitization following onset of pain

Antecedent factors can also play a role in the development of central sensitization. The onset of pain is often associated with subsequent development of conditions such as depression, fear-avoidance, anxiety and other stressors. The stress of these responses can, in turn, further exacerbate the reactivity of the nervous system, leading to central sensitization.3, 34 

Poor sleep is also a common consequence of living with chronic pain. It is associated with increased sensitivity to pain as well.35, 36 

In what’s technically called operant learning, interpersonal and environmental reinforcements have long been known to lead to pain behaviors, but it is also clear that such reinforcements can lead to the development of central sensitization.37, 38, 39 

Treatments of central sensitization

Treatments for chronic pain syndromes that involve central sensitization typically target the central nervous system or the inflammation that corresponds with central sensitization. These are antidepressants,40 and anticonvulsant medications,41, 42, 43 and cognitive behavioral therapy.44, 45, 46 While usually not considered to target the central nervous system, regular mild aerobic exercise alters structures in the central nervous system47, 48 and leads to reductions in the pain of many conditions that are mediated by central sensitization. As such, mild aerobic exercise is used to treat chronic pain syndromes marked by central sensitization.49 Non-steroidal anti-inflammatories are used for the inflammation associated with central sensitization.3

Lastly, chronic pain rehabilitation programs are a traditional, interdisciplinary treatment that uses all of the above-noted treatment strategies in a coordinated fashion. They also take advantage of the research on the role of operant learning in central sensitization and have developed behavioral interventions to reduce the associated pain and suffering.50, 51  Such programs are typically considered the most effective treatment option for chronic pain syndromes.52, 53, 54, 55 

More information

For more information, please see these related topics: definition of pain, the neuromatrix of pain, the changing paradigms in chronic pain management, and the mission of the Institute for Chronic Pain to educate the public about empirical-based conceptualizations of pain and its treatments. 

References

1. Phillips, K. & Clauw, D. J. (2011). Central pain mechanisms in chronic pain states – maybe it is all in their head. Best Practice Research in Clinical Rheumatology, 25, 141-154.

2. Yunus, M. B. (2007). The role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Practice Research in Clinical Rheumatology, 21, 481-497.

3. Curatolo, M., Arendt-Nielsen, L., & Petersen-Felix, S. (2006). Central hypersensitivity in chronic pain: Mechanisms and clinical implications. Physical Medicine and Rehabilitation Clinics of North America, 17, 287-302.

4. Wieseler-Frank, J., Maier, S. F., & Watkins, L. R. (2005). Immune-to-brain communication dynamically modulates pain: Physiological and pathological consequences. Brain, Behavior, & Immunity, 19, 104-111.

5. Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome. Clinical Journal of Rheumatology, 26, 465-473.

6. Melzack, R., Coderre, T. J., Kat, J., & Vaccarino, A. L. (2001). Central neuroplasticity and pathological pain. Annals of the New York Academy of Sciences, 933, 157-174.

7. Flor, H., Braun, C., Elbert, T., & Birbaumer, N. (1997). Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neuroscience Letters, 224, 5-8.

8. O’Neill, S., Manniche, C., Graven-Nielsen, T., Arendt-Nielsen, L. (2007). Generalized deep-tissue hyperalgesia in patients with chronic low-back pain. European Journal of Pain, 11, 415-420.

9. Chua, N. H., Van Suijlekom, H. A., Vissers, K. C., Arendt-Nielsen, L., & Wilder-Smith, O. H. (2011). Differences in sensory processing between chronic cervical zygapophysial joint pain patients with and without cervicogenic headache. Cephalalgia, 31, 953-963.

10. Banic, B, Petersen-Felix, S., Andersen O. K., Radanov, B. P., Villiger, P. M., Arendt-Nielsen, L., & Curatolo, M. (2004). Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and fibromyalgia. Pain, 107, 7-15.

11. Bendtsen, L. (2000). Central sensitization in tension-type headaches – possible pathophysiological mechanisms. Cephalalgia, 20, 486-508.

12. Coppola, G., DiLorenzo, C., Schoenen, J. & Peirelli, F. (2013). Habituation and sensitization in primary headaches. Journal of Headache and Pain, 14, 65.

13. Stankewitz, A., & May, A. (2009). The phenomenon of changes in cortical excitability in migraine is not migraine-specific – A unifying thesis. Pain, 145, 14-17.

14. Meeus M., Vervisch, S., De Clerck, L. S., Moorkens, G., Hans, G., & Nijs, J. (2012). Central sensitization in patients with rheumatoid arthritis: A systematic literature review. Seminars in Arthritis & Rheumatism, 41, 556-567.

15. Arendt-Nielsen, L., Nie, H., Laursen M. B., Laursen, B. S., Madeleine P., Simonson O. H., & Graven-Nielsen, T. (2010). Sensitization in patients with painful knee osteoarthritis. Pain, 149, 573-581.

16. Bajaj, P., Bajaj, P., Madsen, H., & Arendt-Nielsen, L. (2003). Endometriosis is associated with central sensitization: A psychophysical controlled study. The Journal of Pain, 4, 372-380.

17. McLean, S., Clauw, D. J., Abelson, J. L., & Liberzon, I. (2005). The development of persistent pain and psychological morbidity after motor vehicle collision: Integrating the potential role of stress response systems into a biopsychosocial model. Psychosomatic Medicine, 67, 783-790.

18. Fernandez-Lao, Cantarero-Villanueva, I., Fernandez-de-Las-Penas, C, Del-Moral-Avila, R., Arendt-Nielsen, L., Arroyo-Morales, M. (2010). Myofascial trigger points in neck and shoulder muscles and widespread pressure pain hypersensitivity in patients with post-mastectomy pain: Evidence of peripheral and central sensitization. Clinical Journal of Pain, 26, 798-806.

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Date of publication: March 23, 2013

Date of last modification: May 29, 2017

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) What is Chronic Pain Fri, 27 Apr 2012 13:12:35 +0000