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PRIVACY / DISCLAIMER https://www.instituteforchronicpain.org Tue, 31 Jan 2023 09:32:46 +0000 Joomla! - Open Source Content Management en-gb Chronic Hip Pain https://www.instituteforchronicpain.org/common-conditions/hip-pain https://www.instituteforchronicpain.org/common-conditions/hip-pain

What is chronic hip pain?

Hip pain is common, particularly as people grow older. Sometimes, it occurs in an acute manner, such as when someone falls and has a hip fracture. Other times, it comes and goes, such as when people have bursitis. Sometimes, it lasts longer and can become chronic.

The most common cause of chronic hip pain is osteoarthritis. Osteoarthritis is a common form of arthritis. It is a pain condition marked by inflammation of the joints. The inflammation causes pain, swelling, and stiffness.

Osteoarthritis might best be considered the result of general wear and tear. It can occur from injuries, overuse, and age. It results from a loss of cartilage, which ordinarily provides cushioning for the bones in the joints. The loss of cartilage causes inflammation when the hip joint is used. In turn, the inflammation leads to pain, swelling, and stiffness.

Is there a cure for chronic hip pain?

When due to osteoarthritis, hip pain is a chronic condition. Typically, chronic health conditions are also conditions that have no cure and last indefinitely.

Therapies & Procedures for chronic hip pain

In the absence of a cure, patients and their healthcare providers typically pursue therapies with the goals of reducing pain and its impact on the patient's life. In our healthcare system, patients can commonly get many different therapies and procedures for chronic hip pain. Common treatments are anti-inflammatory medications, physical therapy, cortisone injections, hip replacement surgery, and chronic pain rehabilitation programs.

Anti-inflammatory medications

Anti-inflammatory medications are likely the most commonly used medication for chronic hip pain. Anti-inflammatory medications (as well as acetaminophen) have been shown to be mildly effective in reducing the pain of osteoarthritis.1, 2 

Physical therapy

Physical therapy is also commonly used. Physical therapy is proven beneficial in reducing pain for osteoarthritis of the hip.3 

Cortisone injections

Many patients also try cortisone injections for hip pain. Kruse4 reviewed four clinical trials of cortisone injections for osteoarthritic hip pain. Three out of the four trials showed that cortisone injections were able temporarily reduce pain at the two to three month follow-up periods.

Total Hip Replacement Surgery

For a select group of patients with chronic hip pain, total hip replacement is a surgical procedure that can substantially reduce pain. The procedure is also called total hip arthroplasty. It involves removing portions of the hip bones and replacing them with artificial components to form an artificial hip joint.

Conventionally, in healthcare, total hip replacement surgery is thought of as an effective surgery. It is important to note, however, that being effective does not necessarily mean curative. Total hip replacement tends to reduce pain but on average patients tend to continue having pain.5 

In a long-term follow-up study of outcomes more than three years after obtaining a total hip replacement, a third of patients had no reduction in pain or even worse pain. Now, of course, two-thirds of patients who received total hip replacement surgery did improve. However, when compared to a matched group of patients who did not receive total hip replacement, this rate of success did not differ.6 

Rasanen, et al.,7 also found total hip replacement surgeries to be effective on average, but not fully curative.

Chronic pain rehabilitation programs

Chronic pain rehabilitation programs are also a common therapy for patients with chronic hip pain. They are not a cure, but rather help patients to live well despite having chronic pain of a osteoarthritic hip. Chronic pain rehabilitation programs focus on reducing pain, returning to work or other life activities, reducing the use of pain medications, and reducing the need for obtaining healthcare services. It is an intensive, interdisciplinary approach that combines lifestyle changes, coping skills training, and medication management. Research consistently shows that for the goals of reducing pain, returning to work, and reducing the need for pain medications, these programs are highly effective for patients with chronic pain in general.8, 9 (Gatchel & Okifuji, 2006; Turk, 2002).

References

1. Bradley, J. D., Brandt, K. D., Katz, B. P., Kalasinski, L. A., & Ryan, S. I. (1991). Comparison of anti-inflammatory dose of ibuprofen, an analgesic dose of ibuprofen, and acetaminophen in the treatment of patients with osteoarthritis of the knee. New England Journal of Medicine, 325, 87-91.

2. Bjordal, J. M., Ljunggren, A. E., Klovning, A., & Slordal, L. (2004). Non-steroidal anti-inflammatory drugs, including cyclo-oxygenase-2 inhibitors, in osteoarthritic knee pain: Meta-analysis of randomized, placebo-controlled trials. British Medical Journal, 329, 1317-1323.

3. Hernandez-Molina, G., Reichenbach, S., Zhang, B., Lavalley, M., Felson, D. T. (2008). Effect of therapeutic exercise on hip osteoarthritis pain: Results of a meta-analysis. Arthritis Care & Research, 59, 1221-1228.

4. Kruse, D. W. (2008). Intraarticular cortisone injection for osteoarthritis of the hip: Is it effective? Is it safe? Current Review of Musculoskeletal Medicine, 1, 227-233.

5. Fortin, P. R., et al. (1999). Outcomes of total hip and knee replacement: Preoperative functional status predicts outcomes at six months after surgery. Arthritis & Rheumatism, 42, 1722-1728.

6. Nilsdotter, A. K., Petersson, I. F., Roos, E. M., & Lohmander, L. S. Predictors of patient relevant outcome after total hip replacement for osteoarthritis: A prospective study. Annals of Rheumatic Diseases, 62, 923-930.

7. Rasanen, P., Paavolainen, P., Sintonen, H., Koivisto, A. M., Blom, M., Ryynanen, O. P., & Roine, R. P. (2007). Effectiveness of hip or knee replacement surgery in terms of quality-adjusted life years and costs. Acta Orthopaedica, 78, 108-115.

8. Gatchel, R., J., & Okifuji, A. (2006). Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic non-malignant pain. Journal of Pain, 7, 779-793.

9. Turk, D. C. (2002). Clinical effectiveness and cost-effectiveness of treatments for patients with chronic pain. The Clinical Journal of Pain, 18, 355-365.

Date of publication: April 27, 2012

Date of last modification: October 23, 2015

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:38:08 +0000
Headache https://www.instituteforchronicpain.org/common-conditions/headache https://www.instituteforchronicpain.org/common-conditions/headache

What is headache?

Headache is a condition marked by pain in the head. There are multiple kinds of headache: tension headache; migraine; cluster; trigeminal neuralgia; and rebound headache.

Tension headache

Tension headache is a headache that usually starts in the neck or lower part of the back of the head and progresses around to the front of the head. It is often on both sides of the head. Pain can also occur in the shoulders, neck, or jaw. Often described as a tight band or even a vice-like grip, the pain of tension headaches can range in intensity from mild to very severe.

Tension headaches are the most common form of headache.1

The cause of tension headaches is muscle tension, usually due to stress. Anxiety and depression can also lead to persistent muscle tension, which then produces a headache.Photo by Nik Shuliahin courtesy of Unsplash

Sometimes, tension headaches develop as a result of having another type of headache. For instance, someone having a migraine can subsequently develop a tension headache. The body’s response to the pain of the migraine is for the muscles to become tense. If the migraine is long lasting, then the persistent muscle tension that occurs as a result of the pain of the migraine can itself generate a tension headache.

Many chronic daily headaches develop in this manner. Whether the primary headache is tension-related or migraine or what have you, the pain of the primary headache leads to muscle tension, which generates a tension headache. In turn, the pain of the secondary tension headache leads to further muscle tension, which generates yet again another tension headache. A vicious cycle of pain causing pain by way of recurrent muscle tension occurs. As such, many chronic daily headaches are either completely tension-related or what’s called a ‘mixed headache,’ such as mixed migraine and tension headache.

Migraine

Migraine headaches are a type of headache that usually centers on one side of the head. Sensitivity to light and sound, nausea and vomiting are also common with migraine headaches. The pain of migraine headaches is typically severe.

An aura often precedes the onset of pain in migraines. An aura is a visual disturbance marked by a temporary blind spot or seeing stars or distinct blurry lines that cut across the visual field.

Onset of a migraine headache can be abrupt. Different foods, drinks, and activities can trigger a migraine. Some of the more common are the following:

  • Bright lights
  • Red wine
  • Aged cheeses
  • Abrupt caffeine withdrawal
  • Rigorous exercise
  • Relaxing after a stressful period of time
  • Going too long without eating
  • Hormonal changes during the menstrual cycle

The cause of migraine headaches is not known.

Cluster headaches

Cluster headaches are a type of headache that centers in and around one eye. The eye often gets tearful. Sometimes, the nostril on the same side as the pain can also become stuffy. The pain is typically intense and severe.

Cluster headaches occur on a repetitive basis over a month or more, followed by a period of being headache-free.

The cause of cluster headaches is not known.

Trigeminal neuralgia

Trigeminal neuralgia (TN) is a condition that causes pain in the face and head. The pain is usually on one side of the face. The pain is related to the trigeminal nerve, which runs from the brain to the side of the face.

The pain of TN is often intense and short-lived. Patients often describe the pain as electrical in quality. While often the pain occurs in a burst that lasts for seconds, sometimes the pain can occur in repetitive bursts that last for hours to days.

There is no single cause of TN. It is thought that compression of the trigeminal nerve by an enlarged blood vessel can cause it. It is also associated with aging. Multiple sclerosis is also sometimes associated with it.

Rebound headache

Rebound headache (also referred to as medication overuse headache) is a type of headache that occurs as a result of frequent use of medications, which are taken for other types of headaches. Some medications tend to produce rebound headaches more often than other medications. As a general rule, medications that are used on an as-needed basis once a headache starts tend to produce rebound headache, particularly if they are used frequently. Medications that prevent headaches from occurring in the first place do not tend to produce rebound headaches.

Medications that can cause rebound headache when taken too often are the following:

  • Barbiturates
  • Opioids, like oxycodone or hydrocodone
  • Ergotamines
  • Triptans
  • Acetaminophen
  • Non-steroidal anti-inflammatories
  • Over-the-counter medications containing caffeine

This list is not exhaustive. Conventional wisdom suggests that barbiturates, opioids, ergotamines, and triptans have the greatest capacity for developing rebound headache.

Rebound headache is a common way headaches of all types become chronic daily headaches. A person may have, for instance, migraine headaches on a periodic basis and in response he or she takes an as-needed medication. If it occurs too often, a rebound headache results and the medication is again taken. Another rebound headache occurs and a vicious cycle begins. The very thing that the patient takes to treat headache is itself causing headache.

Central sensitization

Central sensitization is a highly reactive state of the nervous system, which causes pain. It can occur with most any pain disorder. It is likely to play a role in the occurrence of all forms of headache as well as their possible progression to chronic daily headaches. It is apt to be an important factor in tension headaches.It is likely to play a role in migraine headache.3, 4 Central sensitization has been implicated in cluster headachesand trigeminal neuralgia.6, 7

Is there a cure for headache?

As traditionally defined, there are no cures for the different types of headaches. Goals of care are to reduce the frequency and intensity of headache.

Therapies & Procedures for headache

Treatment for headaches is dependent on the type of headache.

Common treatments for tension headaches are acetaminophen, non-steroidal anti-inflammatory medications, stress management and relaxation therapies. Common treatments for chronic daily tension headaches are the afore-mentioned treatments but also antidepressant medications, muscle relaxants, opioid medications, mild aerobic exercise, cognitive behavioral therapy, and chronic pain rehabilitation programs.

Common treatments for migraine headache are acetaminophen, non-steroidal anti-inflammatory medications, triptan medications, ergotamine medications, avoidance of triggers, stress management, and relaxation therapies. Common treatments for chronic daily migraines or mixed migraine-tension headaches are the afore-mentioned treatments but also antidepressant medications, anticonvulsant medications, opioid medications, mild aerobic exercise8, cognitive behavioral therapy, and chronic pain rehabilitation programs.

Common treatments for cluster headache are acetaminophen, non-steroidal anti-inflammatory medications, triptan medications, stress management, and relaxation therapies. Common treatments for chronic cluster headaches or mixed cluster-tension headaches are the afore-mentioned treatments but also antidepressant medications, anticonvulsant medications, opioid medications, mild aerobic exercise, cognitive behavioral therapy, and chronic pain rehabilitation programs.

Common treatments for TN are anticonvulsant medications, neuroablation procedures, surgery, and chronic pain rehabilitation programs.

Treatment for rebound headache is to taper off the medication that is suspected to be causing the headache and to do so under the guidance of a prescribing provider. Typically, such tapering is done in the context of the patient participating in a chronic pain rehabilitation program or, at least, within the context of engaging in cognitive behavioral therapy with a chronic pain rehabilitation psychologist.

References

1. Stovner, L. J., Hagen, K., Jensen, R., Katsarava, Z., Lipton, R. B., Scher, A. I., Steiner, T. J., & Zwart, J.-A. (2007). The global burden of headache: A documentation of headache prevalence and disability worldwide. Cephalalgia, 27, 193-210. doi: 10.1111/j.1468-2982.2007.01288.x

2. Jensen, R. (2003). Peripheral and central mechanisms in tension-type headache: An update. Cephalalgia, 23, 49-52.

3. Chen, W., Wang, S., Fuh, J., Lin, C., Ko, Y., & Lin Y. (2011). Persistent ictal-like visual cortical excitability in chronic migraine. Pain, 152, 254-258.

4. 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.

5. Donnet, A., et al. (2007). Chronic cluster headache: A French clinical descriptive studyJournal of Neurology, Neurosurgery, and Psychiatry, 78, 1354-1358.

6. Hu, W. H., Zhang, K., & Zhang, J. G. (2010). A typical trigeminal neuralgia: A consequence of central sensitization? Medical Hypotheses, 75, 65-66.

7. Watson, J. C. (2007). From paroxysmal to chronic pain in trigeminal neuralgia: Implications of central sensitization. Neurology, 69, 817-818.

8. Lemmons, J., De Pauw, J., Van Soom, T., Michiels, S., Versijpt, J., van Breda, E., Castien, R., & De Hertogh, W. (2019). The effect of aerobic exercise on the number of migraine days, duration and pain intensity in migraine: A systematic literature review and meta-analysisJournal of Headache Pain, 20(1), 16. doi: 10.1186/s10194-019-0961-8

Date of publication: April 27, 2012

Date of last modification: January 13, 2019

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:37:54 +0000
Foot & Leg Pain https://www.instituteforchronicpain.org/common-conditions/foot-leg-pain https://www.instituteforchronicpain.org/common-conditions/foot-leg-pain Foot & Leg Pain

What is foot and leg pain?

Pain in the feet or legs is common. It can be caused by a number of different conditions. The most common conditions that cause pain in the feet and/or legs are the following:

  • Plantar fasciitis
  • Arthritis
  • Neuropathy
  • Sciatica

Some of these conditions are commonly short-lived, while others are chronic.

If you have a new onset of pain in your legs or feet, it is important to have it evaluated by a healthcare provider. Many acute conditions, such as sprains, bone fractures, or blood clots, can be successfully treated. Some conditions, however, are chronic.

Plantar fasciitis

Plantar fasciitis causes pain in the heel and bottom of the foot. It is due to inflammation of the plantar fascia. The plantar fascia is a muscle-like connective tissue at the bottom of the foot.

Plantar fasciitis is associated with overuse, such as with runners, or in cases of obesity.

Treatments are anti-inflammatory medications, heel stretches, supportive footwear, and weight loss.

With treatment or on its own, plantar fasciitis usually improves within months to a year or two.

Arthritis

Arthritis is a common pain condition marked by inflammation of the joints. The inflammation causes pain, swelling, and stiffness. Arthritis can occur in any joint of the body.

There are different types of arthritis. The two most common are osteoarthritis and rheumatoid arthritis.

Osteoarthritis might best be considered the result of general wear and tear. It can occur from traumatic injuries, overuse, and age. It Photo by How Soon Ngu courtesy of Unsplashresults from a loss of cartilage, which ordinarily provides cushioning for the bones in the joints. With the loss of cartilage, the bones can rub together in the joints, causing inflammation. In turn, the inflammation leads to pain, swelling, stiffness, and tenderness. Osteoarthritis most commonly occurs in the hips, knees, ankles and feet.

Common treatments for osteoarthritis are anti-inflammatory medications, physical therapy, cortisone injections, arthroscopic and joint replacement surgeries, and chronic pain rehabilitation programs.

Rheumatoid arthritis is the result of the immune system mistaking healthy cartilage for being diseased, and consequently it attacks the cartilage of the joints. Over time, the immune system erodes the cartilage. The subsequent loss of cartilage causes inflammation when the joints are used. In turn, the inflammation causes pain, joint stiffness, and swelling. In advanced stages, the joints become deformed. Rheumatoid arthritis most commonly occurs in the hands and feet.

Common treatments for rheumatoid arthritis are anti-inflammatory medications, chemotherapies, physical therapy, and chronic pain rehabilitation programs.

Neuropathy

Neuropathy is damage to nerves and causes pain, numbness and/or tingling. While technically many conditions are a form of neuropathy, the term ‘neuropathy’ usually refers to peripheral neuropathy.

Peripheral neuropathy is nerve damage in the peripheral nerves. It usually starts in the hands or feet as numbness or tingling. Over time, these symptoms can progress to pain. Patients most often describe the pain as a burning type of pain.

The most common cause of peripheral neuropathy in the hands or feet is diabetes. It is then commonly referred to as ‘diabetic neuropathy.’ Other causes can be kidney disease, HIV, or alcohol dependence. It can also occur for unknown reasons. In the latter case, it is called ‘idiopathic peripheral neuropathy.’

If the cause of neuropathy is diabetes, therapy involves aggressive treatment of diabetes. In such cases, treatment consists of medications to control glucose, dietary changes, exercise, and weight loss.

In all cases of neuropathy, therapies also focus on symptom management. Common symptom management therapies include antidepressant medications, anticonvulsant medications, opioid medications, mild aerobic exercise, cognitive behavioral therapy, and chronic pain rehabilitation programs.

Sciatica

Sciatica is a common pain condition marked by pain, numbness and/or tingling, beginning in the buttock and oftentimes extending down the leg, all the way to the foot and toes.

The vast majority of acute cases of sciatica resolve on their own within a few weeks to months. Sometimes, it continues and becomes chronic. It’s considered chronic when lasting longer than six months.

Sciatica is the result of either inflammation or irritation of the sciatic nerve. The sciatic nerve is a nerve which starts at the spinal cord in the low back, extends through the piriformis muscle in the buttock, and branches down the back of the leg, and into the foot. Causes of sciatica are disc herniations or other forms of degenerative disc disease in the lower part of the spine, piriformis syndrome, and, rarely, tumors along the spine. Stress can also play a role, particularly in exacerbations of sciatica.

The cause of sciatica is often difficult to identify in actual practice. The use of MRI’s to identify the cause is common, but problematic in many cases. While tumors are typically readily seen on an MRI, it is often difficult to identify degenerative changes of the spine that might cause sciatica. Some patients will have MRI’s that show, for example, a disc herniation and nerve root irritation that is consistent with their symptoms. Many patients, however, have sciatica without any objective findings on MRI. Still others commonly have findings on MRI that are inconsistent with their symptoms. For these reasons, providers often pursue epidural steroid injections and nerve blocks in an attempt to identify the cause of sciatica. However, these procedures can also provide unreliable results. As such, with the exception of tumor-related sciatica, healthcare providers typically presume the cause of the condition without ever obtaining definite confirmation.

Common therapies for sciatica are the following:

  • Spine surgeries
  • Interventional procedures: epidural steroid injections, nerve blocks, rhizotomies, and spinal cord stimulator implants
  • Physical therapies: stretching and strengthening exercises, mild aerobic exercises
  • Chronic pain rehabilitation programs

Date of publication: April 27, 2012

Date of last modification: September 21, 2021

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:37:41 +0000
Fibromyalgia https://www.instituteforchronicpain.org/common-conditions/fibromyalgia https://www.instituteforchronicpain.org/common-conditions/fibromyalgia

What is fibromyalgia syndrome?

Fibromyalgia syndrome (FMS) is a common widespread pain condition. It occurs in about 3.4% of women and 0.5% of men.1 It has a typical set of symptoms:

While not considered part of FMS per se, patients commonly also report irritable bowel symptoms, Reynaud’s symptoms, dysmenorrhea, urinary urgency, and depression.

Photo by Syarafina Yusof courtesy of Unsplash

FMS has long been considered a diagnosis of exclusion, meaning all other conditions, such as rheumatoid arthritis or osteoarthritis, must first be ruled out. For this reason, FMS is sometime referred to pejoratively as ‘a wastebasket’ diagnosis.

However, there is increasing consensus among healthcare providers that FMS is an actual condition and that it is a disorder of central sensitization.2, 3, 4 Central sensitization is a condition of the nervous system. The nervous system becomes stuck in a state of high reactivity. Central sensitivity involves multiple changes to the nervous system, including the brain, and leads to all of the above-mentioned symptoms.

There is no definitively known cause of FMS. Likely, there are multiple types of causes across different individuals with FMS as well as multiple factors leading to the condition within any one individual. FMS has some known risk factors that may lead to FMS: traumatic injury, surgery, illness; interpersonal trauma and anxiety; sleep disturbance; and perfectionistic personality traits. There may also be some genetic predisposition that must be in place before the other factors can lead to the condition.

The course of FMS can vary across different individuals. While it can get worse, it is not inevitable that it worsens. Moreover, with treatment, it can get better.

Is there a cure for fibromyalgia syndrome?

FMS has no cure. It is a chronic pain disorder. Chronic conditions are health conditions that tend to last indefinitely. Healthcare for chronic conditions focuses on the following:

  • Reducing symptoms
  • Reducing the impact that the condition has on the patient’s life

The goal is to live well despite having the condition.

Therapies & procedures for fibromyalgia syndrome

Common treatments for FMS are anti-inflammatory medications, antidepressant medications, anticonvulsant medications, opioid medications, physical therapy, trigger point injections, cognitive behavioral therapy, and chronic pain rehabilitation programs.

These therapies are not equally effective. In fact, their relative effectiveness varies quite a bit. Additionally, conventional agreement suggests that no one therapy, even when it is in fact helpful, is sufficient by itself for patients to dramatically improve. As such, most clinicians agree that effective treatment for FMS requires a multidisciplinary approach.

Anti-inflammatory medications

Non-steroidal, anti-inflammatory medications are either over-the-counter or prescribed pain medications. FMS patients commonly take them. In preparation for developing treatment guidelines for the American Pain Society, Goldenberg5 reviewed the research literature on all common treatments for FMS, including the use of non-steroidal, anti-inflammatory medications. They found no evidence to support the use of these medications for FMS.

Antidepressants medications

Because some antidepressants are heavily advertised for use in FMS, patients are frequently familiar with them. When considering their use, it is important to understand the different types of antidepressants and their relative effectiveness.

Roughly, there are three types of antidepressant medications. Serotonin norepinephrine reuptake inhibitors (SNRI’s) are the newest types of antidepressant medications. SNRI’s are typically the ones that are advertised for use in FMS. Selective serotonin reuptake inhibitors (SSRI’s) are the second type and are a little older. They were originally developed for use in depression. They are now sometimes also used for FMS. Tricyclic antidepressants are the third type. They are the oldest type of antidepressants. They too were originally developed for use in depression. However, they also have a long history of use for FMS, as well as chronic pain in general, and also sleep disturbances.

Surprisingly, the newest type of antidepressant medications, the SNRI’s, are not the most effective, despite having been specifically developed for use in FMS.6 The most effective type of antidepressant are the tricyclics. These are the oldest type. They are moderately effective in reducing pain and sleep disturbance. They are also mildly effective in reducing fatigue. Unfortunately, they also tend to have the most side effects.

The SNRI’s, the newest type of antidepressants, are at most mildly effective in reducing pain. Neusch, et al.,7 in their meta-analysis, found that the effectiveness of SNRI's is statistically significant, when compared to a placebo, but the improvement is so small that it is questionable whether it is clinically relevant. What that means is that there was a positive difference in symptoms when taking these medications, but the difference was so small that it wouldn't really matter in the everyday lives of someone taking it. The effect of SNRI's on reducing sleep disturbance, fatigue, and depression is not substantial.6

The SSRI’s are also mildly effective for reducing pain and depression. Their effect on sleep disturbance is also not substantial.6

All antidepressants tend to have high rates of discontinued use because of intolerable side effects.

Anticonvulsants medications

Anticonvulsant medications are also commonly prescribed for FMS. Patients might know of at least some of these medications as they are also frequently advertised. Meta-analyses,7, 8, 9, 10  which combine all known clinical trials of the medications into one large study, show that they are statistically better than placebo, but likely only mildly effective. Let's cite the studies specifically and explain what they mean.

Hauser, et al.,8 in their meta-analysis, reported effect sizes with use of gabapentin and pregabalin in the mildly effective range. What this means is that there was a noticable positive difference, but they were only mildly helpful. Straube, et al.,9 and Tzellos, et al.,10 did not cite standard effect sizes, but rather a different statistic called, number needed to treat (NNT). This statistic represents how many people on average need to be treated before one of them achieves at least a 50% reduction in their symptoms. Both studies show that the NNT for anticonvulsant medications is 7 to 8. That is to say, on average, seven to eight FMS patients will have to be treated with anticonvulsants before one of them will have a 50% or greater reduction in pain. Both of the latter studies cite high rates of discontinuing the medications because of intolerable side effects.

Opioid medications

Opioid medications are narcotic pain medications. Their use is controversial for FMS, or for any type of noncancer, chronic pain. They are addictive. They also increase the risk of death in certain individuals. In their review of the research literature, Goldenberg, et al.,5 found no studies showing that opioid medications are effective for FMS.

Physical therapy

Physical therapy is generally considered a necessary therapy for FMS. It is consistently shown to be moderately effective in reducing pain and depression, and in increasing functioning. Specifically, low impact aerobic exercise is typically considered the gold standard, when compared to other forms of exercise.5, 7, 11 However, Hooten, et al.,12 found that strengthening exercises were similarly effective as low impact aerobic exercise.

Trigger point injections

In their review of the research, Goldenberg, et al.,5 found no evidence to suggest that trigger point injections are effective in the management of FMS.

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) is a common type of treatment that teaches patients what they can do to manage pain well. This emphasis on what the patient can do to get better is what the Photo by Geetanjal Khanna Courtesy of Unsplash healthcare system refers to as self-management. Self-management is a catchall phrase for a number of health behaviors and ways of coping which, when done by the patient over time, can have positive effects on FMS. The positive effects are the following:

  • Reducing symptoms of FMS (by reducing the reactivity of the nervous system)
  • Getting better at coping with the symptoms that remain so that they are less distressing and impairing

A health psychologist or a pain psychologist who specializes in chronic pain rehabilitation usually provides CBT.

A meta-analysis of clinical trials of CBT for FMS shows that CBT is mildly to moderately effective in reducing pain, fatigue, sleep disturbances, and disability.13 Moreover, unlike any other treatment for FMS, these effects are long-lasting. A second and later meta-analysis also found CBT effective for FMS.7

Interdisciplinary chronic pain rehabilitation

Interdisciplinary chronic pain rehabilitation consists of cognitive behavioral therapy, mild aerobic exercise and other types of physical therapy as needed, and non-narcotic pain medication management. The latter usually consists of the use of antidepressant medications or anticonvulsant medications.

In their meta-analysis, Hauser, et al.,14 found that interdisciplinary care as described above was moderately effective in reducing pain, and very effective in reducing fatigue and depression, and very effective in increasing quality of life.

Numerous investigators conclude that interdisciplinary chronic pain rehabilitation is the gold standard for treatment of FMS.5, 7 15, 16 

References

1. Wolfe, F., & Cathey, W. (1983). Prevalence of primary and secondary fibrositis. Journal of Rheumatology, 10, 965-968.

2. Martinez-Lavin, M. (2007). Biology and therapy of fibromyalgia: Stress, stress response, and fibromyalgia. Arthritis Research and Therapy, 9, 216.

3. Clauw, D. J. (2009).Fibromyalgia: An overview. Pain, 122(12), S3-S13.

4. 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.

5. Goldenberg, D. L., Burckhardt, C., & Crofford, L. (2004). Management of fibromyalgia syndrome. Journal of the American Medical Association, 292, 2388-2395. doi: 10.1001/jama.292.19.2388{

6. Hauser, W., Wolfe, F., Tolle, T., Uceyler, N. & Sommer, C. (2012). The role of antidepressants in the management of fibromyalgia: A systematic review and meta-analysis. CNS Drugs, 26, 297-307.

7. Neusch, E., Hauser, W., Bernardy, K., Barth, J. & Juni, P. (2013). Comparative efficacy of pharmacological and non-pharmacological interventions in fibromyalgia syndrome: Network meta-analysis. Annals of the Rheumatic Diseases, 72, 955-962.

8. Hauser, W., Bernardy, K., Uceyler, N., & Sommer, C. (2009). Treatment of fibromyalgia syndrome with gabapentin and pregabalin – A meta-analysis of randomized controlled trials. Pain, 145, 169-181.

9. Straube, S., Derry, S., Moore, R. A., & McQuay, H. J. (2010). Pregabalin in fibromyalgia: Meta-analysis of efficacy and safety from company clinical trial reports. Rheumatology, 49, 706-715. doi: 10.1093/rheumatology/kep432

10. Tzellos, T. G., Toulis, K. A., Goulis, D. G., Papazisis, G., Zampellis, Z. A., Vakfari, A., & Kouvelas, D. (2010). Gabapentin and pregabalin in the treatment of fibromyalgia: A systematic review and meta-analysis. Journal of Clinical Pharmacy and Therapeutics, 35, 639-656. doi: 10.1111/j.1365-2710.2009.01144.x

11. Busch, A. J., Barber, K. A., Overend, T. J., Peloso, P. M., & Schachter, C. L. (Updated August 17, 2007). Exercise for treating fibromyalgia. In Cochrane Database Reviews, 2007, (4). Retrieved May 16, 2011, from The Cochrane Library, Wiley Interscience.

12. Hooten, W. M., Qu, W., Townsend, C. O., & Judd, J. W. (2012). Effects of strength vs aerobic exercise on pain severity in adults with fibromyalgia: A randomized equivalence trial. Pain, 153, 915-923.

13. Glombiewski, J. A., Sawyer, A. T., Guterman, J., Koenig, K., Reif, W., & Hofmann, S. G. (2010). Psychological treatments for fibromyalgia: A meta-analysis. Pain, 151, 280-295.

14. Hauser, W., Bernardy, K., Arnold, B., Offenbacher, M., & Schiltenwolf, M. (2009). Efficacy of mulicomponent treatment in fibromyalgia syndrome: A meta-analysis of randomized controlled clinical trials. Arthritis & Rheumatism, 61, 216-224.

15. Rossy, L. A., Buckelew, S. P., Dorr, N., Hagglund, K. J., Thayer, J. F., McIntosh, M. J., Hewett, J. E., & Johnson, J. C. (1999). A meta-analysis of fibromyalgia treatment interventions. Annals of Behavioral Medicine, 21, 180-191.

16. Sarzi-Pattuni, P., Buskila, D., Carrabba, M., Doria, A., & Atzeni, F. (2008). Treatment strategy in fibromyalgia syndrome: Where are we now? Seminars in Arthritis and Rheumatism, 37, 353-365.

Date of publication: April 27, 2012

Date of last modicification: October 12, 2018

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:37:26 +0000
Facial Pain https://www.instituteforchronicpain.org/common-conditions/facial-pain https://www.instituteforchronicpain.org/common-conditions/facial-pain

What is facial pain?

Facial pain is a catchall term for any type of pain in the face. Facial pain can be either acute or chronic. Acute pain is pain that lasts less than six months. Acute pain usually resolves either on its own or with treatment. Examples are sinusitis, infections of the mouth or gums, or injuries to the face, such as a black eye or broken nose. Chronic facial pain is pain that either lasts continuously for over six months or occurs on a fluctuating basis over a period of six months or longer. Examples are trigeminal neuralgia and temporomandibular joint disorder.

Is there a cure for facial pain?

Typically, there are no cures for chronic facial pain. Healthcare providers and their patients focus onmanagement of the chronic pain. Chronic pain management has two broad goals:

  • Reduce symptoms to the extent possible
  • Reduce the emotional distress and functional impairments that are associated with the symptoms

The first goal involves reducing pain and any other symptoms associated with facial pain. The second goal is two-fold: to reduce the fear, anger, anxiety, depression or sleep problems that tend to go along with living with chronic facial pain, and reducing the sense of disability that tends to occur with pain. Overall, these goals amount to assisting the patient to live well, work, and be involved in life, despite having some chronic pain symptoms.

The healthcare system has different ways it pursues chronic pain management. Broadly speaking, there are many and different types of chronic pain clinics in our healthcare system:

  • Pain clinics that focus on surgeries
  • Pain clinic that focus on interventional procedures (steroid injections, nerve-burning procedures, and the like)
  • Pain clinics that focus on long-term medication management (such as long-term use of narcotic pain medications)
  • Pain clinics that focus on chronic pain rehabilitation (such as interdisciplinary chronic pain rehabilitation programs)

All four types of clinics treat chronic facial pain.

There are different types of chronic facial pain. The most common are trigeminal neuralgia and temporomandibular joint disorder.

Trigeminal neuralgia

Trigeminal neuralgia (TN) is a pain disorder that affects the face, usually on one side. The pain is related to the trigeminal nerve, which runs from the brain to the side of the face.

The pain of trigeminal neuralgia is often intense and short-lived. Patients often describe the pain as electrical in quality. While often the pain occurs in a burst that lasts for seconds, sometimes the pain can occur in repetitive bursts that lasts for hours to days. The intermittent frequency of pain can often lead patients to a persistent sense of vigilance and alarm in anticipation of the next burst of pain. This combination of intermittent pain and persistent fear can lead to difficulties with coping. In turn, these difficulties can lead to impairments, such as staying home from work or other activities as a way of attempting to cope with it all.

There is no single cause of TN. Moreover, the known possible causes are not clearly defined. It is thought that compression of the trigeminal nerve by an enlarged blood vessel can cause it. It is also associated with aging. Multiple sclerosis is also sometimes associated with TN. Central sensitization may also play a role in the progression of TN.1, 2 Central sensitization is a highly reactive state of the nervous system, which amplifies pain. It can occur with most any pain disorder.

Therapies & procedures

Common treatments for TN are anticonvulsant medications, neuroablation procedures, surgery, and chronic pain rehabilitation programs.

Anticonvulsant Medications

Anticonvulsant medications, particularly carbamazepine, is typically a first-line treatment. A Cochrane Review concluded that carbamazepine is effective in reducing TN pain.3 Gabapentin, another anticonvulsant medication, may also reduce the pain of TN.4 However, the long-term efficacy of these medications remains largely unknown.

Yang, et al.,5 reviewed clinical trials for other medications, which are not anticonvulsants. They found clinical trials only for tizanidine, tocainide, and pimozide. They concluded that none of these medications provide substantial benefit over carbamazepine.

Neuroablation Procedures & Surgeries

Zakrzewska and Akram6 reviewed clinical trials of different neuroablation procedures as well as decompression surgeries. They found no clinical trials for decompression surgeries, despite how commonly they are done. In terms of neuroablation procedures, they concluded that established clinical trials showed reductions in pain, though sensory side effects were common. They also observed that the published clinical trials were of poor quality and often demonstrated bias.

Chronic Pain Rehabilitation Programs

Failing to obtain sufficient pain reduction through the use of medications or surgical and interventional procedures, patients with TN often seek care in chronic pain rehabilitation programs. TN pain can easily lead to suffering in terms of emotional distress and functional impairments.7 Chronic pain rehabilitation programs are designed to reduce such distress and impairments for patients with any type of chronic pain, including TN. They are effective in doing so, and there is high quality research evidence demonstrating this effectiveness.8 However, there are no clinical trials assessing the effectiveness of chronic pain rehabilitation programs solely for TN.

Temporomandibular joint disorder

Temporomandibular joint disorder (TMJ) is a pain disorder that occurs in the joints of the jaws, on either side of the face. Specifically, it occurs in the joints located in front of the ears, where the lower jaw joins the face. The pain is usually described as a tension-related ache, though in more advanced stages, it can sometimes be a sharp pain.

The cause of pain is due to orthopedic changes of the jaw from persistent wear and tear. The wear and tear is usually associated with stress-related clenching and tension of the jaw muscles. It can also sometimes start with a trauma to the jaw joints.

Therapies & Procedures

Common treatments for TMJ are biofeedback, cognitive behavioral therapies, anti-inflammatory medications, antidepressant medications, bite guards or occlusal adjustments, botox injections, surgical procedures, and chronic pain rehabilitation programs.

Biofeedback

Biofeedback is a method of teaching patients to reduce the chronic jaw muscle tension that leads to TMJ. In their meta-analysis, Crider and Glaros9 determined that biofeedback was effective in reducing TMJ pain. Indeed, they found that 69% of patients who underwent biofeedback were symptom free after treatment.

Cognitive behavioral therapies

Cognitive behavioral therapy (CBT) is a collection of therapies delivered by a psychologist. CBT essentially teaches patients ways to reduce pain, reduce the emotional distress associated with pain, and reduce the impact that pain has on their lives. In a clinical trial, Litt, et al.,10 randomized 101 men and women into either standard care or standard care with cognitive behavioral therapy. Standard care was defined by use of splints, a diet of soft foods, and anti-inflammatory medications. They found that the group with cognitive behavioral therapy had significantly less pain, less depressive symptoms, and less interference in their lives by pain, particularly for those who had a high readiness or motivation for treatment.

Turner, et al.,11 randomly assigned 79 patients with TMJ to cognitive behavioral therapy and 79 patients with TMJ to a control group who underwent an educational class. At one-year follow-up, patients in the cognitive behavioral therapy group had significantly better improvements on all measures. For example, half the cognitive behavioral group had at least 50% improvement in pain. Less than a third of the control group had such improvement. The cognitive behavioral therapy group reported no interference from their TMJ at a rate three times higher than the control group.

Anti-inflammatory medications

There are few data that supports the effectiveness of anti-inflammatory medications for TMJ pain. Lauren & Dionne12 showed that naproxen reduced pain significantly better than either celecoxib or a placebo.

Antidepressant medications

There is a lack of well-designed research supporting the use of antidepressant medications for the pain of TMJ. Their use tends to be supported because of their demonstrated effectiveness with other chronic pain disorders. The only published randomized clinical trial of an antidepressant looked at the use of amitriptyline. Rizatti-Barbosa, et al.,13 found that amitriptyline was significantly better than placebo in reducing pain. However, the trial was very small and the medication was used only for two weeks. Consequently, it is hard to make generalizations to how effective it is in actual clinical practice.

Bite guards or occlusal adjustments

In their Cochrane review, Koh and Robinson14 reviewed 660 published articles on the use of bite guards, only six of which were clinical trials. Upon their review of these six clinical trials, they concluded that bite guards provide no benefit over the comparison or control groups.

Botox injections

In a double-blind, placebo-controlled clinical trial, Nixdorf, et al.,15 found no difference in pain or other measures between patients who were treated with botox injections and those who were treated with an injection filled with placebo.

Surgeries

In their Cochrane review, Rigon, et al.,16 eviewed all published outcome studies for surgery related to TMJ. They found seven clinical trials. They found that there was no difference in any outcome measure, including pain, between those patients getting surgery and those who did not get surgery.

References

1. Hu, W. H., Zhang, K., & Zhang, J. G. (2010). Atypical trigeminal neuralgia: A consequence of central sensitization? Medical Hypotheses, 75, 65-66.

2. Watson, J. C. (2007). From paroxysmal to chronic pain in trigeminal neuralgia: Implications of central sensitization. Neurology, 69, 817-818.

3. Wiffen P. J., Derry S., Moore R. A., McQuay, H. J. (Updated September 15, 2011). Carbamazepine for acute and chronic pain in adults. In Cochrane Database Reviews, 2011, (1). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

4. Moore, R. A., Wiffen P. J., Derry S., & McQuay, H. J. (Updated February 16, 2011). Gabapentin for chronic neuropathic pain and fibromyalgia in adults. In Cochrane Database Reviews, 2011, (3). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

5. Yang, M., Zhou, M., Chen, N., & Zakrzewska, J. M. (Updated April 30, 2010). Non-epileptic drugs for trigeminal neuralgia. In Cochrane Database Reviews, 2011, (1). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

6. Zakrzewska, J. M., & Akram, H. (Updated May 13, 2010). Neurosurgical interventions for the treatment of classical trigeminal neuralgia. In Cochrane Database Reviews, 2011, (9). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

7. Carlson, C. R. (2007) Psychological factors associated with orofacial pain. Dental Clinics of North America, 51, 145-160.

8. Gatchel, R., J., & Okifuji, A. (2006). Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic non-malignant pain. Journal of Pain, 7, 779-793.

9. Crider, A. B., & Glaros, A. G. (1999). A meta-analysis of EMG biofeedback treatment of temporomadibular disorders. Journal of Orofacial Pain, 13, 29-37.

10. Litt, M. D, Shafer, D. M., & Kreutzer, D. L. (2010). Brief cognitive-behavioral treatment of TMD pain: Long-term outcomes and moderators of treatment. Pain, 151,110-116. doi:10.1016/j.pain.2010.060.030

11. Turner, J. A., Mancl, L. & Aaron, L. A. (2006). Short- and long-term efficacy of brief cognitive-behavioral therapy for patients with chronic temporomandibular disorder pain: A randomized, controlled trial. Pain, 121, 181-194.

12. Lauren, E. T. & Dionne, R. A. (2004). Treatment of painful temporomandibular joints with a cyclooxygenase-2 inhibitor: A randomized placebo-controlled comparison of celecoxib to naproxen. Pain, 111, 13-21.

13. Rizatti-Barbosa, C. M., Nogueira, M. T., de Andrade, E. D., Ambrosano, G. M., & de Barbosa, J. R. (2003). Clinical evaluation of amitriptyline for the control of chronic pain caused by temporomandibular joint disorders. Cranio, 21, 221-225.

14. Koh, H., & Robinson, P. G. (Updated November 12, 2002). Occlusal and adjustment for treating and preventing temporomandibular joint disorders. In Cochrane Database Reviews, 2003, (1). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

15. Nixdorf, D. R., Heo, G., & Major, P. W. (2002). Randomized controlled trial of botulinum toxin A for chronic myogenous orofacial pain. Pain, 99, 465-473.

16. Rigon, M., Pereira, L. M., Bortoluzzi, M. C., Loguercio, A. D., Ramos, A. L. & Cardosa, J. R. (Updated April 10, 2010). Arthroscopy for temporomandibular joint disorders. In Cochrane Database Reviews, 2011, (5). Retrieved May 11, 2011, from The Cochrane Library, Wiley Interscience.

Date of publication: April 27, 2012

Date of last modification: October 23, 2015

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:37:13 +0000
Degenerative Disc Disease https://www.instituteforchronicpain.org/common-conditions/degenerative-disc-disease https://www.instituteforchronicpain.org/common-conditions/degenerative-disc-disease

What is degenerative disc disease?

Degenerative disc disease is one of the most common diagnoses for people with back pain. The diagnosis is often alarming to patients. It sounds terrible. It sounds like they have a disease that is deteriorating the discs in their spine. It also sounds like it’s inevitably going to get worse. These reactions to the diagnosis are common.

Degenerative disc disease is a catchall phrase for a number of structural changes of the spine, such as lossof disc height, disc bulges, and impingement of nerves in the spine, among other changes. Certain healthcare providers and their patients typically presume that such changes of the spine are the cause of back pain. As such, it is one of the most commonly used diagnoses to explain back pain. Degenerative disc disease is also one of the most common reasons for undergoing spine surgeries1 and interventional procedures.2 

Given how frequently the diagnosis is made in clinical practice, and given how commonly it is used as a reason to proceed with spine surgery or interventional procedures, it is important for patients to know that the diagnosis of degenerative disc disease is a controversial diagnosis within the healthcare community. There is by no means agreement that it is understood accurately across all healthcare providers. There is also no agreement that it should be diagnosed as often as it is.

Common misunderstandings of degenerative disc disease

Degenerative disc disease is commonly misunderstood. Given its name, patients with a diagnosis of degenerative disc disease often believe that they have a condition that is deteriorating their spine and which is inevitably going to get worse. Despite what its name implies, however, it is neither a disease nor a condition that inevitably worsens.

It is not considered a disease because degenerative changes of the spine are normal and common in the general population. By mid-adulthood, most people will have degenerative changes of the spine. Most degenerative changes are not painful. These facts are consistent findings in research.

Powell, et al.,3 had 302 women with no history of back pain undergo MRI scans of the lumbar spine. More than a third of women aged 18 to 40 had at least one degenerative disc. The percentage was higher for those older than 40 years of age.

Jensen, et al.,4 essentially repeated this study with 98 men and women who had no history of back pain. 64% of the sample had degenerative changes at one disc and 38% of the sample had degenerative changes at more than one disc.

Takatalo, et al.,5 performed essentially the same study on a much larger sample of 558 young men and women ages 20-22. They found that almost half of the young men and women had at least one degenerative disc.

The results of these studies show that degenerative disc disease is common and it is commonly not painful. Indeed, most of the time, degenerative changes of the spine are not painful.

Degenerative disc disease is therefore no longer considered a disease. The name is a misnomer and degenerative changes of the spine might better be thought of as a normal condition. Upwards of half of all adults (or more) have it and most of these people have no pain.

Moreover, degenerative changes of the spine do not inevitably get worse. Numerous studies over the years have shown that, while degenerative changes of the spine can get worse, most of the time they remain the same or get better.

Symmons, et al.,6 reviewed X-rays of 742 women aged 45 or older and then repeated the X-rays 8 to 11 years later. They divided the women into two groups, those with back pain and those without back pain. They found that 40% of those with back pain had degenerative disc disease, which did not get worse. They also found that 70% of the women without back pain had degenerative disc disease, which did not get worse.

Using MRI scans on a repeated basis, Matsubara, et al.,7 followed 32 patients with herniated discs in their lumbar spine. They found that, over the course of a year, 62% of disc herniations spontaneously reduced in size. The remaining 38% herniations did not progressively worsen.

Using repeated MRI scans over time, Hutton, et al.,8 reviewed two groups of patients with lumbar-related endplate changes. Endplate changes are another type of degenerative change in the spine. The first group was 36 patients with a low level of endplate changes and the second group was 22 patients with a more advanced stage of such changes. In the first group, half remained the same; a little less than half got worse; and two patients reversed back to normal. In the second group with the more advanced changes, most remained the same; some got better and none got worse.

Humphreys, et al.,9 looked at still other degenerative changes of the spine. They found that foraminal stenosis did narrow with age but found no progression of disc height, lordosis, or reduced width of the central canal.

In clinical practice, healthcare providers often attribute the progression of degenerative changes of the spine to injuries and accidents. However, even injuries and accidents do not inevitably lead to a progression of degenerative changes. Carragee, et al.,10 gave MRI’s to 200 working adults without any history of low back pain and then repeated the scans every six months for five years. They also kept track of different injuries and accidents that occurred in the intervening five years. Examples of what they tracked were sports and lifting injuries, traffic accidents, slips and falls. They found that, as long as the injury or accident was not severe enough to cause bone fracture or joint dislocation, everyday accidents and injuries did not cause pre-existing degenerative disc disease to worsen.

Jarvik, at al,11 performed essentially the same study on 123 Veteran's Affairs (VA) patients over a three-year period. Their subjects had no recent history of back pain at the beginning of the study. Over the course of the three years, 67% of their sample reported having an onset of back pain. Upon MRI scanning, only 9% showed evidence of adverse change in their spine – whether it was onset of degenerative disc disease or progression of a pre-existing degenerative disc disease.

Scientific certainty is based on different investigators coming to the same finding. What all these studies show is that degenerative changes of the spine can get worse, but it is far from inevitable that they will get worse. These studies also show that the name ‘degenerative disc disease’ is a misnomer and leads to misunderstanding of the condition.

Controversy in the use of the diagnosis of degenerative disc disease

In clinical practice, the diagnosis of degenerative disc disease is a common explanation for why a patient has back or neck pain. Healthcare providers commonly use X-ray, CT or MRI scans to find evidence of degenerative changes. Once found, they use the results of these tests to explain the cause of pain. The diagnosis also forms the basis of treatment decisions. Procedures like spine surgeries and epidural steroid injections aim to modify degenerative changes in the spine. Many healthcare providers and patients confidently proceed with these kinds of procedures in the belief that the MRI or CT scan has identified the cause of pain – degenerative disc changes in the spine.

The confidence seems well founded. The pain is in the back or neck and so it seems reasonable to look for some type of structural abnormality in the spine. If a CT or MRI scan shows degenerative changes in the spine, then the pain must be caused by the degenerative changes. Patients and healthcare providers, particularly spine surgeons and interventional pain physicians, understand the cause of back pain in this manner.

There is, however, no way to be certain that degenerative changes of the spine are the cause of back or neck pain in any particular individual.

When a patient with back pain presents to a healthcare provider, and the patient undergoes a scan, such as an MRI, one of three types of findings will occur. The scan might show a normal spine, as far as degenerative changes go. This type of finding happens up to half the time.12 Another possibility, of course, is that the scan shows degenerative changes of the spine. Sometimes, the changes are not in the right place to possibly cause the pain (i.e., the degenerative disc is in the mid-back, for instance, when the pain is in the low back). These are considered ‘incidental’ findings. Incidental findings of non-painful degenerative changes are common, as many if not most adults have degenerative changes in their spine, whether they have pain or not. If, however, the scan shows degenerative changes in a place that could be the cause of pain, healthcare providers often conclude that the degenerative changes are the cause of pain. They subsequently proceed to treat the degenerative disc through interventional or surgical procedures.

How confident should they be? How do they know that these findings aren’t incidental too? What if the degenerative changes are in fact non-painful, like the other ones that so often occur, and the true cause of pain is something else entirely? Just because they are in the right location to possibly cause pain, doesn’t prove that they are in fact causing the pain. There is no way to reliably identify when a disc is painful through any of the available scans.

Because of this problem, discography has become more widely used in recent years. Discography is a procedure that attempts to provoke pain and, by doing so, identify degenerative discs. The procedure is controversial because of its unreliability – it can too often identify degenerative discs as painful when they really aren’t or otherwise fail to find the true cause of pain. Despite its common use, professional and governmental organizations recommend against using it.13, 14 

As a result, there is no way to know for certain when a degenerative change of the spine is painful or not, even when they are found on a scan.

Research, too, consistently finds that the presence of degenerative findings on scans cannot fully explain why pain occurs. In a recent review of this research, Endean, et al.15 found statistically significant correlations between degenerative changes of the spine and having back pain. After all, sometimes, degenerative changes of the spine are painful. However, the associations were weak because, as described above, they are also sometimes not painful. So, what this means is that back pain is only partly attributable to the presence of degenerative changes of the spine. There must be other reasons for back pain and imaging scans do not identify them. As such, these investigators did not recommend using findings from scans as the sole means of determining why an individual has pain.

Recent practice guidelines developed by the American Pain Society and American College of Physicians took even a stronger stance.16 Unless patients show signs of severe neurological problems, infection or cancer, they recommend against obtaining routine imaging scans, like MRI’s or CT’s, for acute back pain. Numerous countries around the world have come to a similar conclusion.17 A different group of researchers recently recommended against routine use of scans in chronic back pain too.18

These guidelines might initially surprise patients. However, there is significant concern in the healthcare community about the diagnosis of degenerative disc disease by means of imaging scans or discography. The reason is that it can lead to poor outcomes for surgical and interventional procedures.19 After all, if there really is no way to determine when a degenerative change in the spine is truly painful or not, then treatments like back surgeries and interventional procedures are likely to be unnecessary at times. It might also be a reason why such treatments are so often unsuccessful in reducing pain.20, 21, 22, 23, 24, 25 

Therapies and Procedures for degenerative disc disease

For degenerative disc disease, the American Pain Society and American College of Physicians recommend the use of anti-inflammatory and antidepressant medications, chiropractic care, physical therapy, cognitive behavioral therapy, and chronic pain rehabilitation programs.26, 27 

Conclusion

Degenerative disc disease is a commonly misunderstood and controversial diagnosis. Its name is a misnomer, as it leads to misunderstanding. Degenerative changes of the spine are neither inevitably degenerative nor a disease. It really acts as a catchall phrase for a number of conditions of the spine that are common in the general population and are usually not painful. Sometimes, of course, they can cause pain. However, there is currently no way to determine with any certainty when a degenerative change in the spine is painful or not. Practice guidelines developed by professional and governmental organizations recommend against the routine use of imaging scans and discography to diagnose degenerative disc disease. The reason is that their use can lead to over-diagnosis of degenerative disc disease, which, in turn, leads to unnecessary and unsuccessful treatments.

References

1. Deyo, R. A., Cherkin, D. C., Loeser, J. D., Bigos, S. J., & Ciol, M. A. (1992). Morbidity and mortality in association with operations on the lumbar spine. Journal of Bone and Joint Surgery, 74, 536-543.

2. Friedrich, J. M., & Harrast, M. A. (2010) Lumbar epidural steroid injections: Indications, contraindication, risks, and benefits. Current Sports Medicine Reports, 9, 43-49.

3. Powell, M. C., Szypryt, P., Wilson, M., Symonds, E. M., & Worthington, B. S. (1986). Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women. Lancet, 328, 1366-1367

4. Jensen, M. C., Brant-Zawadzki, M. N., Obuchowski, N., Modic, M. T., Malkasian, D., Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. New England Journal of Medicine, 331, 69-73.

5. Takatalo, J., Karppinen, J., Niinimaki, J., Taimela, S., Nayha, S., Jarvelin, M. R., Kyllonen, E., Tervonen, O. (2009). Prevalence of degenerative imaging findings in lumbar magnetic imaging among young adults. Spine, 34, 1716-1721.

6. Symmons, D. P., van Hemert, A. M., Vandenbroucke, J. P., & Valkenburg, H. A. (1991). A longitudinal study of back pain and radiological changes in the lumbar spines of middle aged women. II. Radiographic findings. Annals of the Rheumatic Diseases, 50, 162-166.

7. Matsubara, Y. Kato, F. Mimatsu, K., Kajino, G., Nakamura, S., & Nitta, H. (1995). Serial changes on MRI in lumbar disc herniations treated conservatively. Neuroradiology, 37, 378-383.

8. Hutton, M. J., Baker, J. H., & Powell, J. M. (2011). Modic vertebral body changes: The natural history as assessed by consecutive magnetic resonance imaging. Spine, 36, 2304-2307.

9. Humphreys, S. C., Hodges, S. D., Patwardhan, A., Eck, J. C., Covington, L. A., & Sartori, M. (1998). The natural history of the cervical foramen in symptomatic and asymptomatic individuals aged 20-60 years as measured by magnetic resonance imaging: A descriptive approach. Spine, 23, 2180-2184.

10. Carragee, E., Alamin, T., Cheng, I., Franklin, T., & Hurwitz, E. (2006). Does minor trauma cause serious low back illness? Spine, 31, 2942-2949.

11. Jarvik, J. G., Hollingsworth, W., Martin, B., Emerson, S. S., Gray, D. T., Overman, S., Robinson, D. Staiger, T., Wessbecher, F., Sullivan, S. D., Kreuter, W., & Deyo, R. A. (2006). Rapid magnetic resonance imaging vs radiographs for patient with low back pain. Journal of the American Medical Association, 289, 2810-2818.

12. Savage, R. A., Whitehouse, G. H., & Roberts, N. (1997). The relationship between magnetic resonance imaging appearance of the lumbar spine and low back pain, age, and occupation in males. European Spine Journal, 6, 106-114.

13. Agency for Healthcare Research and Quality. (2007). Total expenses and percent distribution for selected conditions by type of service: United States, 2009. Washington DC: Government Printing Office. Retrieved from http://guidelines.gov/content.aspx?id=12540.

14. Chou, R. Loeser, J. D., Owens, D. K., Rosenquist, R. W., Atlas, S. J., Baisden, J., Caragee, E. J., Grabois, M., Murphy, D. R., Resnick, D. K., Stanos, S. P., Shaffer, W. O., & Wall, E. R. (2009). Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain. Spine, 34, 1066-1067.

15. Endean, A., Palmer, K. T., & Coggon, D. (2011). Potential of MRI findings to refine case definition for mechanical low back pain in epidemiological studies: A systematic review. Spine, 36, 160-169.

16. Chou, R., Aseem, A., Snow, V., Casey, D., Cross, T., Shekelle, P., & Owens, D. K. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147, 478-491.

17. Koes, B. W., van Tulder, M. W., Ostelo, R., Kim, B. A., & Waddell, G. (2001). Clinical guidelines for the management of low back pain in primary care: An international comparison. Spine, 26, 2504-2513.

18. Chou, D., Samartzis, D., Bellabarba, C., Patel, A., Luk, K., Kisser, J. M., & Skelly, A. C. (2011). Degenerative magnetic resonance imaging changes in patients with chronic low back pain: A systematic review. Spine, 36, S43-S53.

19. Modic, M. T., Obuchowski, N. A., Ross, J. S., Brant-Zawadzki, M. N., Groof, P. N., Mazanec, D. J., & Benzel, E. C. (2005). Acute low back pain and radiculopathy: MR imaging findings and their prognostic role and effect on outcome. Radiology, 237, 597-604.

20. Arden, N. K., Price, C., Reading, I., Stubbing, J., Hazelgrove, J., Dunne, C., Michel, M., Rogers, P., & Cooper C. (2005). A multicentre randomized controlled trial of epidural corticosteroid injections for sciatica: The WEST study. Rheumatology, 44, 1399-1406.

21. Gibson J. N. & Waddell, G. (Updated January 6, 2007). Surgical intervention for lumbar disc prolapse. In Cochrane Database of Systematic Reviews, 2007 (2). Retrieved November 25, 2011, from The Cochrane Library, Wiley Interscience.

22. Mirza, S. K. & Deyo, R. A. (2007). Systematic review of randomized trials comparing lumbar fusion surgery to nonoperative care for treatment of chronic back pain. Spine, 32, 816-823.

23. Ng, L., Chaudhary, N., & Sell, P. (2005). The efficacy of corticosteroids in periradicular infiltration in chronic radicular pain: A randomized, double-blind, controlled trial. Spine, 30, 857-862.

24. Staal, J. B., de Bie, R., de Vet, H. C., Hildebrandt, J., & Nelemans, P. (Updated March 30, 2007). Injection therapy for subacute and chronic low back pain. In Cochrane Database of Systematic Reviews, 2008 (3). Retrieved April 22, 2012.

25. van Tulder, M. W., Koes, B., Seitsalo, S., & Malmivaara, A. (2006). Outcomes of invasive treatment strategies in low back pain and sciatica: An evidence based review. European Spine Journal, 15, S82-S89.

26. Chou, R., Atlas, S. J., Stanos, S. P., & Rosenquist, R. W. (2009). Nonsurgical interventional therapies for low back pain: A review of the evidence for the American Pain Society clinical practice guideline. Spine, 34, 1078-1093.

27. Chou, R. & Huffman, L. H. (2007). Medications for acute and chronic low back pain: A review of the evidence for an American Pain Society/American College of Physicians clinical practice guideline. Annals of Internal Medicine, 147, 505-514.

Date of publication: April 27, 2012

Date of last modification: January 29, 2017

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:37:01 +0000
Conversion Disorder https://www.instituteforchronicpain.org/common-conditions/conversion-disorder https://www.instituteforchronicpain.org/common-conditions/conversion-disorder

What is conversion disorder?

A conversion disorder is a nerve-related condition that is due to psychological stress or trauma. While not fully understood, the symptoms develop in response to stress or trauma that lead to intolerable conflict. The psychological cause may occur in one instance or on a repetitive basis prior to onset of symptoms. Onset of this type of nerve-related symptom can occur immediately after the stressor or trauma, or it can occur after a delay of many years.

The symptoms are neurological in nature:

  • Weakness or paralysis
  • Parathesias (i.e., numbness and/or tingling)
  • Pain
  • Blindness
  • Loss of speech abilities
  • Loss of hearing
  • Non-epileptic or psychogenic seizures
  • Fainting spells

These symptoms can occur singularly or in combination.

Despite having a relationship to stress, conversion disorders differ from most stress-related health problems. Many stress-related health problems are common and will occur to most everyone at some point in their lives. Most everyone, for instance, has had a tension headache or an upset stomach. As their descriptions suggest, these conditions are manifestations of emotional stress. Conversion disorders are different and much less common.

An important characteristic differentiates conversion disorders from other stress-related health problems. Conversion disorder symptoms tend to reflect an intolerable conflict in a way that is unique to the particular stressor or trauma. For example, suppose a man witnesses the violent deaths of innocent children in war; because of the intolerable nature of this trauma, he develops blindness; after all possible medical explanations are exhausted, the blindness is diagnosed as a conversion disorder. Another example might be a woman who was unsuccessful in her attempts to save her children in a house fire and ended up having to run out to save her own life; the intolerable conflict inherent in this trauma leads to paralysis of her legs; after no viable medical explanation is found, the paralysis is diagnosed as a conversion disorder. Notice how the symptoms tend to manifest the conflict that each individual experienced and seems essentially unique to the conflict itself. The unique way that conversion disorders manifest the stressful problem is different from most common stress-related health problems. There is nothing unique about a tension headache or an upset stomach. Countless stressful problems can lead to them. In conversion disorders, however, the symptoms tend to be unique to the stressful problem that the patient experienced.

Sometimes, with conversion disorders, there isn't such a direct one-to-one relationship between the intolerable conflict and the nerve-related symptom, such as witnessing trauma and becoming blind or running out of burning house and becoming paralyzed. Nonetheless, the symptom continues to have a unique relationship to the intolerable conflict in that it prevents the patient from having to come to terms with the intolerable conflict. Non-epileptic, or psychogenic seizures, can occur in this manner. An example might be a young professional who develops non-epileptic seizures at about the same time as it has become clear that he has been promoted too early and is insufficiently prepared for his position and so is on the verge of being let go; the non-epileptic seizures inhibit him from having to deal with the intolerable conflict within his career. As such, conversion disorders don't always have a direct, one-to-one relationship to the intolerable conflict, but they nonetheless inhibit the patient from having to face the intolerable conflict and come to terms with it.

It is important to recognize that patients with a conversion disorder do not intentionally make up their symptoms. They do not decide to have the symptoms and cannot simply decide to stop having the symptoms.

Diagnosis of a conversion disorder is based on a) the presence of symptoms which are neurological in nature, b) the symptoms have some relationship to a stressor or trauma that led to intolerable conflict, c) all other viable medical explanations have been exhausted or ruled-out, and d) the person with the symptoms are not making them up.1 

Healthcare providers are often reluctant to diagnose a conversion disorder.2 Many factors lead to such reluctance:

  • Concern about stigmatizing the patient
  • Concern that the patient will have difficulty accepting the diagnosis and will subsequently become angry with the healthcare provider
  • Concern about legal action and/or licensing board complaints if a patient is angry with the diagnosis; even if unfounded, responding to such actions require time and money
  • Concern about the possibility of having the diagnosis proven wrong by medical testing down the road

Because of their reluctance, healthcare providers tend to refrain from diagnosing a conversion disorder and instead proceed with either a) lots of further testing which assess for medical explanations that are unlikely to occur, b) create cycles of false-hope and disappointment for the patient when further and further testing continue to come back with negative results, and c) are expensive to the patient and the healthcare system.

It is important to recognize that stress and trauma are just as legitimate a way of becoming ill as any other possible cause of health problems.

Is there a cure for conversion disorder?

The course of a conversion disorder can vary across different individuals. A conversion disorder can sometimes resolve either on its own or in treatment. It can also become chronic. In simple tracking studies, roughly 50% of patients had recovered at four and ten year follow-ups.3, 4 

Therapies & procedures for conversion disorders

Clinical knowledge of conversion disorders suffers from a notable lack of well-designed research studies.5 As such, treatment is typically guided by conventional wisdom within the healthcare community and clinical judgment of the particular healthcare provider.

Conventional wisdom in the healthcare community is that conversion disorders are best treated psychologically, through psychodynamic psychotherapy. This type of psychotherapy provides a safe and empathic relationship with a trusted provider who can assist the patient in working through the following issues:

  • Acceptance of the diagnosis
  • Understanding of how such symptoms can occur
  • Coming to a meaningful resolution of the intolerable conflict

Without shame or guilt, the patient comes to find meaning in the stressful event that brought about the symptoms and consequently the patient comes to be able to ‘move on’ with the rest of his or her life. It is often a difficult process. Initially, motivational interviewing interventions may be necessary to assist the patient in coming to accept the diagnosis.

There is limited evidence that antidepressant medications might be mildly helpful.6, 7

Conventional wisdom suggests that physical therapy and occupational therapy can be helpful in managing the symptoms.

References

1. American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington DC: Author.

2. Gratten-Smith, P., Fairly, M., & Procopic, P. (1988). Clinical features of conversion disorder. Archives of Disease in Childhood, 63, 408-414.

3. Couprie, W, Wijdicks, E. F., Rooijmans, H. G., & van Gijn, J. (1995). Outcome in conversion disorder: A follow up. Journal of Neurology, Neurosurgery, and Psychiatry, 58, 750-752.

4. Mace, C. J., & Trimble, M. R. (1996). Ten-year prognosis of conversion disorder. British Journal of Psychiatry, 196, 282-288.

5. Ruddy R., & House, A. (Updated August 22, 2005). Psychosocial interventions for conversion disorder. In Cochrane Database of Systematic Reviews, 2005 (4). Retrieved May 3, 2012, from The Cochrane Library, Wiley Interscience.

6. Fishbain, D. A., Cutler, R. B., Rosomoff, H. L., & Rosomoff, R. S. (1998). Do antidepressants have an analgesic effect in psychogenic pain and somatoform pain disorder? A meta-analysis. Psychosomatic Medicine, 60, 503-509.

7. Voon, V. & Lang, A. E. (2005). Antidepressant treatment outcomes of psychogenic movement disorder. Journal of Clinical Psychiatry, 66, 1529-1534.

Date of publication: April 27, 2012

Date of last modification: September 8, 2016

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:36:34 +0000
Back Pain https://www.instituteforchronicpain.org/common-conditions/back-pain https://www.instituteforchronicpain.org/common-conditions/back-pain

What is chronic back pain?

Back pain affects most everyone at some point. At any given time, 25% of the population will have had low back pain in the previous three months. It is one of the most common reasons for medical visits.1, 2 Fortunately, the vast majority of cases of new back pain will resolve within a few weeks to months.3 

Some people have back pain that does not go away. Back pain is considered chronic when it lasts longer than six months. Chronic low back pain affects about 10% of the population.4 It is one of the most common reasons for disability. Additionally, among all health conditions, back pain is one of the highest costs to the healthcare system.5, 6 

Despite these alarming statistics, it is important to recognize that most people with chronic back pain live well and do not seek healthcare for it on a regular basis. Roughly, three quarters of people with chronic back pain fit this description.7 They are neither distressed nor impaired enough to seek care for it. Or, they recognize that medical options for chronic back pain are limited and not very effective. So, they self-manage their chronic back pain. Either way, it is possible to self-manage chronic back pain and live well enough to have no need to seek care for it. In fact, the majority of people with chronic back pain are not seeking care for it.

Common causes of back pain are varied. Broadly speaking, the many common causes of back pain can be divided into three categories: muscular, orthopedic, and nervous. Muscle strain and tears can cause back pain. Degenerative changes of the spine are commonly thought to cause pain. Changes in the nervous system, commonly referred to as central sensitization, can also cause pain. Less common causes of back pain are spinal fractures, infection and cancer.

It is often difficult to know the cause of back pain in an individual case. There are no examinations or tests that can definitively prove a cause of pain for any of the three most common categories of causes mentioned above.

Take, for example, orthopedic causes of back pain. CT or MRI scans are commonly used to identify degenerative changes of the spine as possible causes of back pain. When found, it is easy to assume that these findings provide a definitive diagnosis of the cause. However, most healthcare providers know that the research does not support this assumption.

To understand this point, it is helpful to know something about how science goes about finding a cause of pain in general. In order to find a cause of pain, scientific inquiry tries to find something that is unique to those who have pain and which subsequently differentiates those who have pain from those who do not have pain. Findings of degenerative changes of the spine on MRI or CT scans are not unique to patients with back pain in this way. Numerous studies consistently show that people without back pain have degenerative changes of the spine at just as high a rate or higher than people with back pain.8, 9, 10 There currently is no way of knowing what differentiates degenerative changes of the spine that are painful from those that are not painful. Another possibility is that there is no difference and the findings of degenerative changes of the spine on MRI or CT scans are simply irrelevant. There is currently no test that can tell for certain.

As such, in the individual case, it is difficult to know what is causing pain, even if an MRI or CT scan shows degenerative changes of the spine. Are these changes relevant to the patient’s pain when we know that people without back pain are likely to have the same findings? Healthcare providers don’t ultimately know.

Is there a cure for chronic back pain?

In the absence of a known cause, healthcare providers and their patients often proceed through various therapies and procedures on a trial-and-error basis. There are many common treatments for chronic back pain:

  • Anti-inflammatory medications
  • Muscle relaxant medications
  • Antidepressant medications (used for pain)
  • Anticonvulsant medications (used for pain)
  • Opioid, or narcotic, medications
  • Chiropractic care
  • Physical therapy
  • Cognitive behavioral therapy
  • Epidural steroid injections
  • Rhizotomy
  • Back surgeries – laminectomies, disctectomies, and fusions
  • Implantable pain control devices – spinal cord stimulators and intrathecal drug delivery devices (aka, “pain pumps”)
  • Chronic pain rehabilitation programs

Many of these therapies and procedures have been shown in research to be effective in reducing pain and increasing functioning. However, in this regard, effective does not mean curative. Unfortunately, there are no known cures for chronic back pain.

Therapies & procedures for chronic back pain

In 2007, the American College of Physicians and the American Pain Society developed clinical practice guidelines for chronic back pain.11 They determined that providers should first recommend self-management for patients with back pain. Moreover, they recommended that healthcare providers educate patients on how to self-manage back pain. They do not recommend the use of immediate CT or MRI scans for back pain unless there is evidence of severe neurological problems or evidence of other severe conditions like cancer or infection. If back pain continues and becomes chronic, they recommend the use of medications and chronic pain rehabilitation therapies.

In terms of medications, they note that even the most effective medications only moderately reduce pain. They recommend the use of acetaminophen and non-steroidal anti-inflammatory medications first. If these fail to reduce pain, they recommend using tricyclic antidepressant medications. They note that these three classes of medications have the most and highest quality evidence supporting their effectiveness. They also note that the poor quality of evidence for the use of opioid and anticonvulsant medications.12 

In terms of chronic pain rehabilitation therapies, they recommend the use of exercise, cognitive behavioral therapy, and chronic pain rehabilitation programs (which put the two previous types of therapies together in a coordinated fashion).

The clinical practice guidelines recommend MRI or CT scans and possible referral for surgical evaluation only if patients meet two criteria: a) when patients fail to progress from the above-mentioned treatments and b) they show evidence of neurological problems, such as referred pain.

It is important to recognize that the order of these recommendations reflect the likelihood of their being effective. That is to say, based on the available research evidence, the first recommendation is the one that is most likely to be helpful, the second recommendation is the second most likely to be helpful, the third is the third most likely to be helpful, and so on.

It is also important to recognize how often these guidelines do not get followed in actual practice.13 While many patients have acetaminophen and non-steroidal anti-inflammatory medications recommended to them, most patients do not get tricyclic antidepressant medications, exercise, cognitive behavioral therapy, or chronic pain rehabilitation programs recommended to them. When they do, it is only after they have undergone MRI or CT scans and have tried multiple interventional and surgical procedures, all of which have either poor quality research supporting their effectiveness or are known to be less effective.

References

1. Deyo, R. A., Mirza, S. K., & Martin, B. I. (2006). Back pain prevalence and visit rates: Estimates from U. S. national surveys, 2002. Spine, 31, 2724-277.

2. Hart, L. G., Deyo, R. A., & Cherkin, D. C. (1995). Physician office visits for low back pain: Frequency, clinical evaluation, and treatment patterns from a U. S. national survey. Spine, 20, 11-19.

3. Andersson, G. B. (1999). The epidemiologic features of chronic low back pain. Lancet, 354, 581-585.

4. Freburger, J. K., Holmes, G. M., Agans, R. P., Jackman, A. M., Darter, J. D., Wallace, A. S., Castel, L. D., Kalsbeeck, W. D., & Carey, T. S. (2009). The rising prevalence of chronic low back pain. Archives of Internal Medicine, 169, 251-258.

5. Agency for Healthcare Research and Quality. (2009). Total expenses and percent distribution for selected conditions by type of service: United States, 2009. Washington DC: Government Printing Office. 

6. Center for Disease Control. (2009). Prevalence and most common causes of disability among adults – United States, 2005. Washington DC: Government Printing Office. Retrieved from http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5816a2.htm

7. Cote, P., Cassidy, J. D., & Carroll, L. (2001). The treatment of neck and low back pain: Who seeks care? Who goes where? Medical Care, 39, 956-967.

8. Jensen, M. C., Brant-Zawadzki, M. N., Obuchowski, N., Modic, M. T., Malkasian, D., Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. New England Journal of Medicine, 331, 69-73.

9. Powell, M. C., Szypryt, P., Wilson, M., Symonds, E. M., & Worthington, B. S. (1986). Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women. The Lancet, 328, 1366-1367.

10. Takatalo, J., Karppinen, J., Niinimaki, J., Taimela, S., Nayha, S., Jarvelin, M. R., Kyllonen, E., Tervonen, O. (2009). Prevalence of degenerative imaging findings in lumbar magnetic imaging among young adults. Spine, 34, 1716-1721.

11. Chou, R., Aseem, A., Snow, V., Casey, D., Cross, T., Shekelle, P., & Owens, D. K. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147, 478-491.

12. Chou, R., & Huffman, L. H. (2007). Medications for acute and chronic low back pain: A review of the evidence for an American Pain Society/American College of Physicians clinical practice guideline. Annals of Internal Medicine, 147, 505-514.

13. Carey, T. S., Freburger, J. K., Holmes, G. M., Castel, L., Darter, J., Agans, R., Kalsbeek, W., & Jackman, A. (2009). A long way to go: Practice patterns and evidence in chronic low back care. Spine, 34, 718-724.

Date of publication: April 27, 2012

Date of last modification: October 23, 2015

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:36:07 +0000
Rheumatoid Arthritis https://www.instituteforchronicpain.org/common-conditions/arthritis/rheumatoid https://www.instituteforchronicpain.org/common-conditions/arthritis/rheumatoid

What is rheumatoid arthritis?

In general, arthritis is a common pain condition marked by inflammation of the joints. The inflammation causes pain, swelling, and stiffness. Such inflammation is largely common to all types of arthritis.  

Rheumatoid arthritis is a specific type of arthritis. Rheumatoid arthritis is the result of the immune system mistaking healthy cartilage for being diseased, and consequently it attacks the cartilage of the joints. Over time, the immune system erodes the cartilage. The subsequent loss of cartilage causes inflammation when the joints are used. In turn, the inflammation causes pain, joint stiffness, and swelling. In advanced stages, the joints become deformed.

Rheumatoid arthritis most commonly occurs in the hands and fingers, but can occur in any joint.

Because it involves the immune system reacting to normal tissue, rheumatoid arthritis is considered an autoimmune disorder.  

Central sensitization is a common complication of rheumatoid arthritis.1 Central sensitization is a highly reactive state of the central nervous system, which amplifies pain. It also can cause sensitivity to touch or mild pressure, fatigue, poor sleep, anxiety, and sometimes depression. It can occur with any pain disorder, including rheumatoid arthritis. It is important to address in treatment when it occurs.  

Is there a cure for rheumatoid arthritis?

It is important to know that there is no cure for rheumatoid arthritis. It is considered a chronic condition. Just because there is no cure, patients should not become hopeless.  Persons with chronic health conditions need to redefine what having hope means. Hope in the context of a chronic health condition, like rheumatoid arthritis, means having a realistic plan to get better and “better” is defined by the following:

  • Having less pain and other symptoms
  • Being able to do more activities, like stay at work or return to work
  • Needing less pain medications
  • Being less distressed about pain
  • Needing to seek healthcare less

Therapies and procedures for rheumatoid arthritis

Common treatments for rheumatoid arthritis are anti-inflammatory medications, corticosteroid medications, chemotherapies, physical therapy, cortisone injections, and chronic pain rehabilitation programs. Treatments that address central sensitization are antidepressant medications (which are used for pain), anti-seizure medications (which also are used for pain), and chronic pain rehabilitation programs.  

References

1. 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. 

Date of publication: April 27, 2012

Date of last modification: October 23, 2015

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Arthritis Fri, 27 Apr 2012 13:35:52 +0000
Osteoarthritis https://www.instituteforchronicpain.org/common-conditions/arthritis/osteo https://www.instituteforchronicpain.org/common-conditions/arthritis/osteo

What is osteoarthritis?

Osteoarthritis is a common form of arthritis. It is a pain condition marked by inflammation of the joints. The inflammation causes pain, swelling, and stiffness. Osteoarthritis can occur in any joint of the body.

Osteoarthritis might best be considered the result of general wear and tear. It can occur from injuries, overuse, and age. It results from a loss of cartilage, which ordinarily provides cushioning for the bones in the joints. With the loss of cartilage, inflammation occurs when the joints are used. In turn, the inflammation leads to pain, swelling, and stiffness. Osteoarthritis most commonly occurs in the hips, knees, ankles and feet.

Osteoarthritis is commonly considered to be the cause of pain in joints, such in the knees or hips. Surprizingly, however, the correlation between pain and osteoarthritic changes as identified on scans is poor. Recent scientific evidences indicates that pain in the joints is more apt to be due to both osteoarthic changes in the joints and central sensitization.1 

Patients often mistake osteoarthritis for rheumatoid arthritis. While each condition causes inflammation and pain in the joints, the two types of arthritis are different. Rheumatoid arthritis occurs when the immune system mistakes healthy cartilage for being diseased, and consequently attacks the cartilage of the joints. Over time, the immune system erodes the cartilage. This loss of cartilage causes inflammation and subsequently pain, swelling, and stiffness. In osteoarthritis, the immune system has no such role. Indeed, there is no disease process at all which erodes the cartilage in osteoarthritis. The loss of cartilage in osteoarthritis comes simply from the wear and tear of injuries, use, and age over time.

Is there a cure for osteoarthritis?

Osteoarthritis is a chronic condition. Chronic health conditions are conditions that have no cure. As such, chronic conditions typically last indefinitely. However, it is not considered terminal as it does not cause death.

Therapies & Procedures for osteoarthritis

In the absence of a cure, patients and their healthcare providers typically pursue therapies with the goals of reducing pain and increasing the ability to do more things in life. In our healthcare system, patients can commonly get many different therapies and procedures for osteoarthritis. Common treatments for osteoarthritis are anti-inflammatory medications, physical therapy, injection therapies, arthroscopic and joint replacement surgeries, and chronic pain rehabilitation programs.

Some of these therapies and procedures have been shown in research to be helpful in reducing pain and increasing functioning. Others have been shown to be unhelpful, even though they are done quite a bit in our healthcare system.

Anti-inflammatory medications

Anti-inflammatory medications are likely the most commonly used medication for osteoarthritis. Anti-inflammatory medications (as well as acetaminophen) have been shown to be mildly effective in reducing pain.2, 3 

Physical therapy

Physical therapy is also commonly used to treat osteoarthritis. Physical therapy is proven beneficial in reducing pain for osteoarthritis of the knee4 and the hip.5 

Injection therapies

Many patients also try cortisone injections into the osteoarthritic joint. Research shows that cortisone injections are, on average, mildly helpful in reducing pain for one to two weeks.6, 7 

Hyaluronan injections are also sometimes used to treat osteoarthritis of the knee. The outcome research for hyaluronan injections is mixed: some studies show no benefit,8, 9 whereas other studies show a small benefit.10, 11 

Arthroscopic and joint replacement surgeries

Arthroscopic knee surgeries are often performed for osteoarthritis of the knee. Despite the frequency with which they are pursued, arthroscopic knee surgeries have consistently been shown to be ineffective on average.12, 13 

Total knee and total hip replacement surgeries are commonly pursued for patients with advanced forms of osteoarthritis. These surgeries are largely effective in reducing pain and increasing quality of life, though many patients will continue to have some level of pain.14, 15, 16 

Chronic pain rehabilitation programs

Chronic pain rehabilitation programs are also a common therapy for patients with osteoarthritis, among other types of chronic pain. They are not a cure, but rather help patients to live well despite having chronic pain of osteoarthritis. Chronic pain rehabilitation programs focus on reducing pain, returning to work or other life activities, reducing the use of pain medications, and reducing the need for obtaining healthcare services. It is an intensive, interdisciplinary approach that combines lifestyle changes, coping skills training, and medication management. Research consistently shows that for the goals of reducing pain, returning to work, and reducing the need for pain medications, these programs are highly effective.17, 18, 19 

References

1. Arendt-Nielsen, L. (2017). Joint pain: More to it than just structural damage? Pain, 158, S66-S73.

2. Bradley, J. D., Brandt, K. D., Katz, B. P., Kalasinski, L. A., & Ryan, S. I. (1991). Comparison of anti-inflammatory dose of ibuprofen, an analgesic dose of ibuprofen, and acetaminophen in the treatment of patients with osteoarthritis of the knee. New England Journal of Medicine, 325, 87-91.

3. Bjordal, J. M., Ljunggren, A. E., Klovning, A., & Slordal, L. (2004). Non-steroidal anti-inflammatory drugs, including cyclo-oxygenase-2 inhibitors, in osteoarthritic knee pain: Meta-analysis of randomized, placebo-controlled trials. British Medical Journal, 329, 1317-1323.

4. Jamtvedt, G., Dahm, K. T., Christie, A., Moe, R. H., Haavardholms, E., Holm, I., & Hagen, K. B. (2008). Physical therapy interventions for patients with osteoarthritis of the knee: An overview of systematic reviews. Physical Therapy, 88, 123-136.

5. Hernandez-Molina, G., Reichenbach, S., Zhang, B., Lavalley, M., Felson, D. T. (2008). Effect of therapeutic exercise on hip osteoarthritis pain: Results of a meta-analysis. Arthritis Care & Research, 59, 1221-1228.

6. Arroll, B., & Goodyear-Smith, F. (2004). Corticosteroid injections for osteoarthritis of the knee: Meta-analysis. British Medical Journal, 328, 869-874.

7. Bellamy N., Campbell, J., Welch, V., Gee, T. L., Bourne, R., & Wells, G. A. (2006). Intraarticular corticosteroid for treatment of osteoarthritis of the knee. [Cochrane Review]. In Cochrane Database of Systematic Reviews, 2006 (2). Retrieved April 13, 2012, from The Cochrane Library, Wiley Interscience.

8. Arrich, J, Piribauer, F., Mad, P., Schmid, D., Klaushofer, K., & Mullner, M. (2005). Intra-articular hyaluronic acid for the treatment of osteoarthritis of the knee: Systematic review and meta-analysis. Canadian Medical Association Journal, 172, 1039-1043.

9. Karlsson, J., Sjogren, L. S., & Lohmander, L. S. (2002). Comparison of two hyaluronan drugs and placebo in patients with knee osteoarthritis: A controlled, randomized, double-blind, parallel-design multicentre study. Rheumatology, 41, 1240-1248.

10. Lo, G. H., LaValley, M., McAlindon, T., & Felson, D. T. (2003). Intra-articular hyaluronic acid in treatment of knee osteoarthritis: A meta-analysis. Journal of the American Medical Association, 290, 3115-3121.

11. Bannuru, R. R., Natov, N. S., Obadan, I. E., Price, L. L., Schmid, C. H., & McAlindon, T. E. (2009). Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: A systematic review and meta-analysis. Arthritis Care & Research, 61, 1704-1711.

12. Kirkley, A., Birmingham, T. B., Litchfield, R. B., Giffin, R., Willits, K. R., Wong, C. J., Feagan, B. G., Donner, A., Griffin, S. H., D’Ascanio, L. M., Pope, J. E., & Fowler, P. J. (2008). A randomized trial of arthroscopic surgery for osteoarthritis of the knee. New England Journal of Medicine, 359, 1097-1107.

13. Moseley, J. B., O’Malley, K., Petersen, N. J., Menke, T. J., Brody, B. A., Kuykendall, D. H., Hollingsworth, J. C., Ashton, C. M., & Wray, N. P. (2002). A controlled trial of arthroscopic surgery for osteoarthritis of the knee. New England Journal of Medicine, 347, 81-88.

14. Agency for Healthcare Research and Quality. (December, 2003). Total knee replacement. AHRQ Publication No. 04-E006-2. Washington DC: Government Printing Office. Retrieved from http://www.ahrq.gov/downloads/pub/evidence/pdf/knee/knee.pdf

15. Chang, R. W., Pellissier, J. M., & Hazen, G. B. (1996). A cost-effectiveness analysis of total hip arthroplasty for osteoarthritis of the hip. Journal of the American Medical Association, 275, 858-865.

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Date of publication: April 27, 2012

Date of last modification: August 7, 2017

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joemcallister4@gmail.com (Murray J. McAllister, PsyD) Arthritis Fri, 27 Apr 2012 13:35:37 +0000