TEMPOROMANDIBULAR JOINT

Mechanical Force, Manually Assisted Adjustments to the Temporomandibular Joint

: Are They Safe?

By Darryl Curl

I was looking through the daily mail one day recently, and I ran across an interesting letter from a dentist, D.D. Sommers, who writes to me through the recommendation of his chiropractic friend, J.

Schuler, D.C. Both of these fine doctors are from Minot, North Dakota. Dr. Sommers writes: "As a practicing orthodontist, I have seen several patients on referral who have been undergoing chiropractic care for the management of craniomandibular disorders. Some of these patients have undergone mandibular 'adjustments.' Others have received 'activator' [sic] adjustments ... over the lateral aspect of the temporomandibular (TM) joint. I am concerned that such blows may result in sufficient insult to the capsular tissues to elicit inflammation ... compounding or exacerbating TM pain and dysfunction.

"Having had a limited exposure to chiropractic concepts, I am not clear as to the intent of the delivery of what appears to be a traumatic blow to the lateral aspect of the TM joint. Having experience in both dentistry and chiropractic care, I am interested in knowing your thoughts relating to this matter as well."

Dr. Sommers' letter points to a subject that I find most interesting; it's also one of the subjects I'm asked most often about. The subject, in this case, can be stated: "Is there a potential for injury to the TM joint when performing mechanical force, manually assisted adjustments?

The Delivery

First of all, we need to define the type of delivery of the adjustment being used in this situation. Dr. K.M. Bartol developed a model for the categorization of chiropractic treatment procedures used within the chiropractic profession.¹ In this model, which was used in the June 1991 Consensus Conference in Monterey, California, we find that there is a category for the chiropractic procedure that uses the piston device which Dr. Sommers refers to (i.e., an adjustment assisted by some form of mechanical device). This procedural category is titled, Mechanical Force, Manually Assisted.

The Anatomy

Before we can begin to address Dr. Sommers' estimable concern we need to establish some anatomical boundaries. In order to do so we will take the position of the tip of the mechanical piston as being over the lateral aspect of the TM joint. When this position is taken, it is important to ask, "What are all the tissues that are being impacted when the force from the mechanical device is delivered through the piston?

For the sake of brevity, let us leave out all those structures which may lie under the piston (e.g., preauricular lymph nodes, auriculotemporal nerve, portions of the facial nerve, and the superficial temporal artery and vein) and go directly to the joint itself. Here we can see that the lateral and second-most superficial structure is the articular capsule. (The most superficial structure is the TM ligament; not shown.) The fact that the capsule is situated as it is means that it is not designed to withstand "point-blank" insults.

Improperly delivered procedures, no matter what kind, always increase the patient's exposure to potential injury. This is particularly true for the TM joint when a mechanical device is used on it. Of particular concern is a crushing type injury to the lateral portion of the articular capsule as it crosses the lateral pole of the mandibular condyle.

Dr. Sommers' concern for insult injury to the capsular tissues is quite correct. The inflammation and edema he refers to are just two of the physiologic events that occur in capsulitis. Capsulitis has many causes (we saw one last month -- remember?) with one of the more common being trauma. Capsulitis can be a serious condition in-and-of itself and is formally classified as one of the many types of TM disorders. If a TM disorder was already present, capsulitis can compound the difficulty in treatment, and at a minimum it will exacerbate the symptom of pain and the signs of dysfunction.

The Prevention of Injury

Whenever possible, insult injury to the TM joint must be avoided during the deliver of mandibular adjustments. This is particularly true when a piston device is used over the joint. Fortunately, there are many ways in which the doctor can safeguard against crushing type injuries when using a piston device over the TM joint. In order to keep our discussion from getting too long, let's confine the safeguards for when the placement of the piston's tip is to the lateral aspect of the TM joint.

Insult injury to the tissues covering the TM joint can be prevented by using one of the following procedures: 1) Use a very soft tip on the end of the piston, preferably one that has a large flat surface. When using this method, the doctor should set the piston device to the lower amplitude setting. High settings or small tips should not be used when placing the piston in direct contact with the TM joint. 2) When a higher amplitude is needed, the piston should never be placed in direct contact over the TM joint. Instead, the doctor can place his thumb over the joint and then place the piston over the thumbnail. The piston's force is then delivered through the doctor's thumb.

1. Bartol KM: A model for the categorization of chiropractic treatment procedures. J Chiro Tech., 3(2):78-80, May 1991.

EXERCICE OF ANY DURATION,INTENSITY AFFEETS WEIGHT LOSS SIGNIFICANTLY

Exercise-Weight loss

Exercise of Any Duration, Intensity Affects Weight Loss Significantly

Considerable evidence points to exercise as an important component of a behavioral weight loss program; however, the optimal amount of exercise needed to maximize long-term weight loss remains unclear.

The Centers for Disease Control and Prevention (CDC) and the American College of Sports Medicine recommend 30 minutes (minimum) of moderate-intensity activity on "most days of the week" to improve health; the Institute of Medicine (IOM) suggests 60 minutes minimum of exercise on most days to control body weight.






This study compared the effects of different durations and intensities of exercise on weight loss and overall cardiovascular fitness in 201 sedentary women (average age: 37) involved in a university-based weight control program. Participants were assigned to one of four exercise groups:

1) vigorous intensity/high duration
2) moderate intensity/high duration
3) moderate intensity/moderate duration
4) vigorous intensity/moderate duration

All women were also instructed to reduce energy intake to 1,200-15,00 kcal/day and to limit dietary fat to 20-30% of total daily energy intake. Each participant completed a detailed medical history and a physical activity readiness questionnaire prior to entry, and provided documentation from her physician indicating that the proposed 12-month intervention was not contraindicated. Main outcome measures were body weight, cardiorespiratory fitness, and exercise participation.

Following 12 months in the program (completed by 94% of the participants), weight loss and increased cardiovascular fitness was significant in all four groups, but with no significant differences noted between any of the groups.

"The results of this study have implications for prescription of exercise for sedentary, overweight adults engaging in weight loss efforts," conclude the study authors. "Moderate to high doses of exercise in combination with a decrease in energy intake resulted in 8% to 10% reductions in body weight following a 12-month intervention."

Recommending Exercise for Patients With Diabetes:

Diabetes mellitus affects an estimated 150 million people worldwide, including 16 million Americans; according to estimates, by the year 2025, the number of patients suffering from the condition will exceed 300 million.

Type 1 diabetes, which afflicts 10% of sufferers, is characterized by insulinopenia, requiring that patients take insulin for survival.
This overview of type I diabetes provides the clinician with an introduction to its etiology and how it is diagnosed, then explores the influence of exercise on patients with the condition, including the many general effects of a consistent exercise regimen:

* improving glucose tolerance by augmenting insulin sensitivity;
* decreasing muscle capillary basement membrane thickening and arterial pulse volume recordings;
* increasing lean body mass and work capacity;
* improving overall weight management;
* reducing serum total cholesterol, low-density lipoprotein (LDL) and very low-density lipoprotein levels (VLDL), while raising high-density lipoprotein (LDL) levels; and
* increasing cardiac function.

Numerous management strategies and guidelines for exercise are included and can be obtained from the Internet, along with steps clinicians should take in evaluating patients with type I diabetes (prior to recommending any exercise regimen); specific considerations in terms of diet, exercise intensity and duration, and energy requirements; and potential risks and complications.

The authors emphasize that caring for diabetes patients requires that all clinicians be responsible for education about blood glucose self-monitoring; proper exercise prescription; appropriate dietary and insulin management plans; pre-participation clearance; and ongoing education. With respect to exercise, they note: "Exercise has risks and benefits that must be understood so that participation yields a safe, enjoyable outcome. ..."

TMJ ANATOMY

Temporo mandibular joint 

Keywords; tmj anatomy, trigeminal neuralgia, chiropractic help, jaw joint exercises, migraine headaches.

This page is not designed to be a highly academic tour of this complex joint; however it is a difficult topic that has had chiropractors scratching their heads. The sensory nucleus of the large nerve that supplies the jaw is located in the cervical spine, and hence the strong connection between migraine headache, neck and facial pain. 

It will give you some insights if you can struggle with the anatomy, and provide some understanding of how the temporo mandibular joint cancause severe

• Facial pain 
• Migraine headaches 
• Referral to the upper neck
• Tinnitus or ringing in the ears

It is also the joint that contributes to a complex and extremely painful condition called trigeminal neuralgia. You can go to our TMJ ear pain page for more information.

Shall we sully forth on our TMJ anatomy tour? It will help you understand any jaw joint symptoms you may be having and how it can cause such misery. 

Two cranial structures form the joint.

• The temporal bone lies on the side of your head. It has a neat little socket into which the jawbone fits.
• The mandible is the anatomical name of the jawbone.

Hence temporo mandibular and then, of course, joint to get TMJ. 

TMJ anatomy

The pterygoid pocket is a cul de sac behind the upper molars; it can be very painful.

This picture is taken from a book called Grays Anatomy. Come back later and take a short tour about this amazing man. A real pioneer. Click here for more about Henry Grays Anatomy tour.

Notice the mandible has two prongs.

1. The posterior prong (hidden in the picture above behind some ligaments which hold the jawbone firmly in place) fits snuggly into a hollow in the Temporal bone, just in front of the ear.
2. The anterior prong is for the attachment of the Temporalis muscle, the main biting muscle. See how much leverage this gives the Temporalis muscle which covers the side of the head? - hence its awesome power.

TMJ muscles

Notice two features in this second picture of our temporo mandibular joint anatomy tour.

The actual joint, where the posterior prong fits into a socket in the temporal bone.

The three muscles that slam the jaw closed.

1. The huge flat temporalis muscle that is attached to the other prong (or condyle), and another jaw closer,
2. the masseter muscle.
3. The third, the internal pterygoid we'll come to later.

A very powerful trio, strong enough to bite your own finger off! Literally. As we will see in due course, these muscles can contribute to your headache and facial pain, and neck pain if the temporo mandibular joint is not functioning as it should.

You will discover four primary jaw muscles on your tmj anatomy tour. They open, close, protrude and move the jaw sideways, enabling you to talk, chew, and swallow, kiss and many other things we do with our mouths. We'll come to the fourth muscle in due course.

There are three kinds of tmj anatomy pain:

1. Primary muscle pain is not really common but overuse, as in chewing gum or in South Africa, biltong, in association with disc malfunction can commonly causes jaw pain, facial pain headache and sometimes neck pain.

If the jaw joints are functioning optimally then muscle overuse is not usually a problem. But if the jaw joints are not moving in sinc then the more you chew, the greater the problem.

The important feature on this leg of our TMJ anatomy tour is the disc, ormeniscus as it is known, that rides in the joint, which functions as a moving shock absorber between the condyle and the fossa, or, socket, separating the two bony structures.

It's unique, quite different to any other joint in the body. As you open your jaw, the condyle first rotates and then slides forward in the fossa.

When the disc malfunctions, often after the jaw has been opened too wide, or taken a blow as in a punch, then it gives the familiar clicking and popping sound so often associated with temporo mandibular joint pain.

Please, please, do not slap your child's face, your spouse, even your enemy. You may just cause them a life time's temporo mandibular joint anatomy pain.

Joint related pain may occasionally result from inflammation, as in rheumatoid arthritis, but more usually from degeneration of the tissues within the temporo mandibular joint. 

This wear and tear in the joint, and dislocation of one of the menisci, are the two most common joint disorders of the temporo mandibular joint. The two joints then no longer work together in harmony causing facial pain, jaw joint pain and migraine headache. And, upper neck referred pain. 

Note two things here. How the condyle (posterior prong) sits in its fossa, and the position of the normal disc. See how the disc is attached another very important muscle, the lateral pterygoid? Because of this attachment to the disc, this muscle can become supremely, exquisitely, extremely painful.

This is the muscle that opens the jaw, pulling the condyle forwards out of its fossa, protected by the disc from grinding bone on bone. Used on one side only, it moves the jaw from side to side when chewing the cud. Juggle your jaw from side to side - that's the Lateral Pterygoid you are using. Now protrude the jaw, push it forwards. That's the two Lateral Pterygoids working together. See in the next picture how the condyle has slid forwards out of its fossa? That's normal.

Dislocated disc (meniscus)

Notice in the next picture how the disc has been displaced forwards. This is definitely not normal. Should you now open your jaw there will be a popping sound as the disc pops back behind the prong of the jawbone (the condyle). When this happens repeatedly the disc starts to wear, and sets up a pain pattern in the muscles around the jaw joint.

Try placing the pads of your index fingers in your ear, and slowly open your mouth. Do they open nicely together? Any clicks or pops?

Often patients are terrified of words like disease and degenerationsometimes used in describing this wear-and-tear process. No need, it's no different to your hair turning grey. What is now clearly recognised in the literature though is that, untreated, joint malfunctions, or fixations as we call them, lead to unnecessary, premature degeneration. Every time the displaced disc has to pop over the condyle, it is probably equivalent in terms of wear and tear to 100 openings of a healthy jaw.

Nerve pain or Trigeminal Neuralgia

This information about the jaw joint, its position, clicking and pain is then fed back to the brain via the largest cranial nerve, theTrigeminal nerve which supplies the face and has a spinal nucleus deep in the neck. This is how the pain from a clicking jaw causes facial pain, and can be referred to the neck. It's the reason why TMJ sufferers also usually have upper neck pain.

This facial pain can be very severe and is sometimes set off by a stimulus a slight as brushing the cheek or a breath of wind.

See that long black structure in the picture below? (in the next pic it's highlighted in green). That is the huge trigeminal nucleus extending right down into the spinal cord in the neck.

Facial Pain

It's called the TRI-geminal nerve, because it has three different sensory branches, seen here in green, blue and brown, supplying primarily the face, teeth, sinuses and TMJ. It is by far the largest cranial nerve.

Whilst I don't want to overdo the complexity of TMJ anatomy, this next slide will show you how the TMJ can cause neck pain, perhaps CAUSE subluxations, and how subluxations in the cervical spine can make the TMJ vulnerable to injury.

On the right hand side you have the four functions of the Trigeminal nerve. Focus only on the one labelled "Pain and Temperature". If you follow it along the "Spinal Trigeminal Tract" you will see that its sensory nucleus (called the "Spinal Trigeminal nucleus") is right down in the neck. From there a dark-coloured tract reaches up into the sensory cortex of the brain (those two dark arrows) where the pain is perceived.

So, noxious pain and temperature signals from the TMJ feed right down into the neck, where they meet up with other nerves from the neck, swapping messages. Pain!

Enough, right! Well done, you're a perseverer!

There's nothing simple about the human body. Nothing! and certainly not the TMJ anatomy. "Fearfully and wonderfully made" as one great surgeon named his book. Amen!

I said there are four jaw muscles. The fourth, the Internal Pterygoid is also a jaw closer. I include it here, partly for completeness, but also so that you can see the four branches of the Trigeminal nerve in situ. One motor branch to the muscles of the jaw, and three sensory nerves (labelled 1st Div, 2nd and 3rd). See the proximity of the nerve to the Internal Pterygoid muscle? This is why jaw muscle pain can so readily become intense nerve pain.

For anatomy students only: See the tiny branches supplying the Tensor Tympani muscle in the inner ear (dampens overly loud sounds) and the Tensor Veli palatini muscle that has two vital functions: in swallowing it helps raise the soft palate so food doesn't enter the sinuses, and opens the auditory tube, allowing for equalising the pressure between the inner ear and the outside air. Vital for example when driving up a steep hill, or ascending in an aeroplane. That pop in the ear... Tensor Veli Palatini doing its job.

So, the very complex fifth cranial nerve, the Trigeminal nerve, is almost continuously in use in chewing, speaking, swallowing, hearing and bringing sensory information from the teeth, face, jaw joints to the brain. 

Tinnitus 

Not a pain, but there is an irritating condition, sometimes it becomes extreme, ringing in the ears, that is common and sometimes associated with vertigo, and sometimes a result of a TMJ anatomy problem. But not usually, alas. But if you have crackling sounds, pain and stiffness coming from your jaw, then your tinnitus MAY be coming from the TMJ. May. If there is hearing loss, then Meniere's disease also needs to be considered.
Vertigo, similar to but not quite the same as dizziness, is a dreadful condition that we will consider elsewhere at Chiropractic Help.

Chiropractic Help

Like all other chronic joint conditions there is no real permanent cure for TMJ anatomy wear and tear. An acute pain or click which has just begun, correctly addressed should pass over, and the trick is not to allow it to become chronic. Like any other condition, once you know it's not going to get better on its own, then it's better to contact the relevant health professional sooner rather than later.

Not unlike the neck and back, good care of chronic TMJ pain aims at reducing the ache, restoring normal function, and avoiding known factors that provoke symptoms; like biting a whole apple and chewing gum.

The pain and dysfunction is often temporary, lasting a few days or weeks, even a month or two perhaps, so adventurous surgery which cannot be reversed should only be contemplated when all else has failed. Your first port of call, of course should be your chiropractor.

I have done no research in my practice, but I would guess at least 75 percent of patients have good to excellent results with chiropractic treatment of the TMJ.

What will your chiropractor do? Firstly a good history of how the pain or clicking started, how long it's been there, what aggravates it and so on; whether you are getting headaches, and any of the sharp stabbing pain associated with trigeminal neuralgia. Are there any definite sinus symptoms?

Then there will be an examination of the TMJ anatomy, and your neck. Treatment will include mobilising the joint, treating any active trigger points, and stretching of the muscles and joint capsule.

So, what's the good news? This is a very treatable condition. You don't have to live with TMJ anatomy pain for months.

Is there any bad news? If the pterygoids have active trigger points, they can only be reached from inside the mouth, and the treatment may be wretchedly painful, sometimes lasting a few days. Hang in with your chiroprator, that too will pass. It's very effective.

What can you do for yourself? Are there any jaw exercises for TMJ? An ice block rubbed directly on the painful spot, followed by moist heat; do it in the shower.  Now that you've taken your TMJ anatomy tour, you know where to find these muscles, right? Gently massage them. Your chiropractor will give you some stretches and, for more tips about TMJ exercises, scroll down.

If appropriate, your chiropractic treatment may include cervical spine adjustments too, if there are associated fixations. For more about the neck adjustments, scroll down to neck pain treatment.

For an interesting case from the coalface, click on this link and scroll down to Mrs Hol. 

There is a tool for self treatment of the internal pterygoid muscle; I regret I've seen no research on how effective it is, but you might like to try it

CHRONIC PAIN

Is defined as pain that has lasted longer than three to six months

Is defined as pain that has lasted longer than three to six months,^[1][2] though some theorists and researchers have placed the transition from acute to chronic pain at 12 months.^[3] Others apply acute to pain that lasts less than 30 days, chronic to pain of more than six months duration, and subacute to pain that lasts from one to six months.^[4] A popular alternative definition ofchronic pain, involving no arbitrarily fixed duration, is "pain that extends beyond the expected period of healing".^[2]

There is little evidence for treating most types of chronic pain with opioids.^[5] An exception is chronic pain due to cancer. While they may improve pain in the short term there is no evidence of improved long term pain or functioning.^[6] Risks include overdose and addiction.^[6] In the United States about 100 million people have chronic pain, with 25% of those having more or severe chronic pain.^[5]

Chronic pain may be divided into "nociceptive" (caused by activation of nociceptors), and "neuropathic" (caused by damage to or malfunction of the nervous system).^[7]

Nociceptive pain may be divided into "superficial" and "deep", and deep pain into "deep somatic" and "visceral". Superficial pain is initiated by activation of nociceptors in the skin or superficial tissues. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Visceral pain originates in the viscera (organs). Visceral pain may be well-localized, but often it is extremely difficult to locate, and several visceral regions produce "referred" pain when damaged or inflamed, where the sensation is located in an area distant from the site of pathology or injury.^[8]

Neuropathic pain is divided into "peripheral" (originating in the peripheral nervous system) and "central" (originating in the brain or spinal cord).^[9] Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".^[10]

Pathophysiology

Under persistent activation nociceptive transmission to the dorsal horn may induce a pain wind-up phenomenon. This induces pathological changes that lower the threshold for pain signals to be transmitted. In addition it may generate nonnociceptive nerve fibers to respond to pain signals. Nonnociceptive nerve fibers may also be able to generate and transmit pain signals. The type of nerve fibers that are believed to propagate the pain signals are the C-fibers, since they have a slow conductivity and give rise to a painful sensation that persists over a long time.^[11] In chronic pain this process is difficult to reverse or eradicate once established.^[12] In some cases, chronic pain can be caused by genetic factors which interfere with neuronal differentiation, leading to a permanent reduction in the threshold for pain.^[13]

Chronic pain of different etiologies has been characterized as a disease affecting brain structure and function. Magnetic resonance imaging studies have shown abnormal anatomical^[14] and functional connectivity, even during rest^[15][16] involving areas related to the processing of pain. Also, persistent pain has been shown to cause grey matter loss, reversible once the pain has resolved.^[17][18]

These structural changes can be explained by the phenomenon known as neuroplasticity. In the case of chronic pain, the somatotopic representation of the body is inappropriately reorganized following peripheral and central sensitization. This maladaptive change results in the experience of allodynia and/or hyperalgesia. Brain activity in individuals with chronic pain, measured via electroencephalogram (EEG), has been demonstrated to be altered, suggesting pain-induced neuroplastic changes. More specifically, the relative beta activity (compared to the rest of the brain) is increased, the relative alpha activity is decreased, and the theta activity both absolutely and relatively is diminished.^[19]

Management

Complete and sustained remission of many types of chronic pain is rare, though some can be done to improve quality of life.^[20]

Pain management is the branch of medicine employing an interdisciplinary approach to the relief of pain and improvement in the quality of life of those living with pain.^[21] The typical pain management team includes medical practitioners (particularly anesthesiologists), clinical psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners.^[22] Acute pain usually resolves with the efforts of one practitioner; however, the management of chronic pain frequently requires the coordinated efforts of the treatment team.^[23][24][25]

Psychological treatments including cognitive behavioral therapy^[26][27] and acceptance and commitment therapy^[28][29][30] have been shown effective for improving quality of life in those with chronic pain.

Alternative medicine

Hypnosis, including self-hypnosis, has tentative evidence.^[31] Evidence does not support hypnosis for chronic pain due to a spinal cord injury,

Epidemiology

In a recent large-scale telephone survey of 15 European countries and Israel, 19% of respondents over 18 years of age had suffered pain for more than 6 months, including the last month, and more than twice in the last week, with pain intensity of 5 or more for the last episode, on a scale of 1(no pain) to 10 (worst imaginable). 4839 of these respondents with chronic pain were interviewed in depth. Sixty six percent scored their pain intensity at moderate (5–7), and 34% at severe (8–10); 46% had constant pain, 56% intermittent; 49% had suffered pain for 2–15 years; and 21% had been diagnosed with depression due to the pain. Sixty one percent were unable or less able to work outside the home, 19% had lost a job, and 13% had changed jobs due to their pain. Forty percent had inadequate pain management and less than 2% were seeing a pain management specialist.^[32]

In a systematic literature review published by the International Association for the Study of Pain (IASP), 13 chronic pain studies from various countries around the world were analyzed. (Of the 13 studies, there were three in the United Kingdom, two in Australia, one each in France, the Netherlands, Israel, Canada, Scotland, Spain, and Sweden, and a multinational.) The authors found that the prevalence of chronic pain was very high and that chronic pain consumes a large amount of healthcare resources around the globe. Chronic pain afflicted women at a higher rate than men. They determined that the prevalence of chronic pain varied from 10.1% to 55.2% of the population.^[33]

In the United States, the prevalence of chronic pain has been estimated to be approximately 30%. According to the Institute of Medicine, there are about 116 million Americans living with chronic pain, which suggests that approximately half of American adults have some chronic pain condition.^[1][34] The Mayday Fund estimate of 70 million Americans with chronic pain is slightly more conservative.^[35] In an internet study, the prevalence of chronic pain in the United States was calculated to be 30.7% of the population: 34.3% for women and 26.7% for men.^[36] These estimates are in reasonable agreement and indicate a prevalence of chronic pain in the US that is relatively comparable to that of other countries.^{[citation needed]}

Outcomes

Chronic pain is associated with higher rates of depression and anxiety.^[37] Sleep disturbance, and insomnia due to medication and illness symptoms are often experienced by those with chronic pain.^[38] Chronic pain may contribute to decreased physical activity due to fear of exacerbating pain, often resulting in weight gain.^[37] Such comorbid disorders can be very difficult to treat due to the high potential of medication interactions, especially when the conditions are treated by different doctors.

Severe chronic pain is associated with increased 10 year mortality, particularly from heart disease and respiratory disease.^[39] Several mechanisms have been proposed for the increased mortality, e.g. abnormal endocrine stress response.^[40] Additionally, chronic stress seems to affect cardiovascular risk by acceleration of the atherosclerotic process. However, further research is needed to elucidate the relationship between severe chronic pain, stress and cardiovascular health.^[39]

Psychology

Personality

Two of the most frequent personality profiles found in chronic pain patients by the Minnesota Multiphasic Personality Inventory (MMPI) are the conversion V and the neurotic triad. The conversion V personality, so called because the higher scores on MMPI scales 1 and 3, relative to scale 2, form a "V" shape on the graph, expresses exaggerated concern over body feelings, develops bodily symptoms in response to stress, and often fails to recognize their own emotional state, including depression. The neurotic triad personality, scoring high on scales 1, 2 and 3, also expresses exaggerated concern over body feelings and develops bodily symptoms in response to stress, but is demanding and complaining.^[41]

Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels.^{[42][43][44][45]} Self-esteem, often low in chronic pain patients, also shows striking improvement once pain has resolved.^[45]

Social Support

Social support has important consequences for individuals with chronic pain. In particular, pain intensity, pain control, and resiliency to pain has been implicated as outcomes influenced by different levels and types of social support. Much of this research has focused on emotional, instrumental, tangible and informational social support. Research has examined a wide range of social support including, but not limited to, online social networks, romantic partners, friends, and even complete strangers. A meta-analysis conducted by Zaza and Baine (2002) revealed moderate effect sizes between chronic pain variables and social support.^[46] Across a majority of studies investigated, there was a direct significant association between social activities and/or social support and pain. Higher levels of pain were associated with a decrease in social activities, lower levels of social support, and reduced social functioning.

Recent neuroimaging studies have supported this link between the experience of pain and social support. Eisenberger and colleagues (2011) conducted a study that investigated the role attachment figures serve as safety signals for individuals experiencing pain.^[47] The researchers had participants view pictures of a significant other while receiving painful stimuli during an fMRI procedure. The study demonstrated that viewing partner pictures during a painful experience led to reductions in self-reported pain intensity and reductions in pain-related neural activity as indicated by dorsal anterior cingulate cortex, and anterior insula activity and increased activity in the ventromedial prefrontal cortex (VMPFC) compared to individuals who did not view a picture of a partner. Activity in the VMPFC has been shown to be related to safety signaling and fear extinction, and greater activity was associated with the participant’s perception that the significant other was a greater source of support. Additionally, it has been shown that interaction with a romantic partner activates several reward-processing regions of the brain including the caudate head, nucleus accumbens, lateral orbitofrontal cortex, amygdala, and dorsolateral PFC.^[48] While distraction tasks such as word association tasks were also shown to significantly reduce perceived pain, the tasks did not activate these reward areas. Taken together, these results suggest that companionship support may buffer the pain experience such that the greater the perceived sense of support the less intensity an individual will rate their pain.

In addition to the above findings, recent studies have demonstrated that the size and quality of a person’s social network also impacts pain sensitivity. Molton and Terrill (2014) discussed research conducted by Martin and colleagues (2012) demonstrating that smaller social networks are more sensitive to losses and strain.^[49][50] According to their study, those with persistent pain conditions tend to rely on their social support as a coping mechanism and therefore have better outcomes when they are a part of larger more supportive social networks. Brown and colleagues (2003) further demonstrated that both passive and active forms of social support reduce experimental pain.^[51] The aforementioned work was extended by Vigil and colleagues (2013) who demonstrated sex differences in how social networks and intimate relationships influence experimental pain sensitivity.^[52] Females displayed higher pain sensitivity when their social networks contained a higher proportion of more intimate relationships while males displayed patterns in the opposite direction. Males displayed lower pain sensitivity when they received higher levels of support from their social networks.

A common way an individual with chronic pain communicates their pain is by catastrophizing (a tendency to misinterpret and exaggerate situations that may be threatening) as a way to elicit emotional and/or tangible support from others.^[53] Pain catastrophizing has been associated with greater levels of supportive solicitation and higher observer ratings of pain behaviors in the presence of painful stimuli.^[54] While pain catastrophizing often functions as a way to communicate pain, it has also been consistently shown to be associated with punishing responses from significant others.^[55] These punishing responses (i.e., irritation or frustration) have been shown to be related to higher levels of pain severity and depressed mood.^[56] Quartana, Campbell, & Edwards (2009) point out that individuals with chronic pain may be attempting to solicit supportive responses, yet may unintentionally causing interpersonal stress and difficulty.^[55] Further research on social support and chronic pain has shown that too much sympathy and help may lead to increased pain and disability.^[57] This indicates that there is an optimal level of interpersonal effectiveness for social support for individuals with chronic pain.

The type of support an individual with chronic pain receives has also been shown to be associated with pain controllability. A study by Cho, Zunin, Chao, Heiby, and McKoy (2012) attempted to determine differences in social support for individuals with high and low pain controllability for patients seeking treatment at two outpatient pain management clinics.^[58] The results showed that individuals with low pain controllability had greater preference for informational, instrumental, and emotional social support. This demonstrates that individuals with lower pain control attempt to seek support, but may not be effective in doing so. Thus, these individuals may indirectly communicate their desire for support and fail to obtain their preferred level of support.

It is also important to consider the strong associations the have been demonstrated between social support and chronic pain resilience (i.e., the ability to cope with adversity and adjust to chronic pain symptoms). Newton-John, Mason, and Hunter (2014) conducted a study investigating the role of resilience in adjustment and coping with chronic pain.^[59]The results of their study revealed positive associations between the ability to recover from adversity and/or stress and social support in individuals from a pain rehabilitation clinic. The researchers also found that resilient individuals were more likely to be employed compared to less resilient individuals. This finding indicates that integration into social systems and having support resources are valued aspects of chronic pain adjustment and coping. These findings also support previous research conducted by Sturgeon and Zautra (2010) who explained that social engagement noticeably improves the ability to cope with pain among those who suffer from chronic pain.^[60] They also suggest that those who are more proactive in their efforts to engage with their social networks demonstrate higher levels of resilience to pain.

Effect on cognition

Chronic pain's impact on cognition is an under-researched area, but several tentative conclusions have been published. Most chronic pain patients complain of cognitive impairment, such as forgetfulness, difficulty with attention, and difficulty completing tasks. Objective testing has found that people in chronic pain tend to experience impairment in attention, memory, mental flexibility, verbal ability, speed of response in a cognitive task, and speed in executing structured tasks. In 2007, Shulamith Kreitler and David Niv advised clinicians to assess cognitive function in chronic pain patients in order to more precisely monitor therapeutic outcomes, and tailor treatment to address this aspect of the pain experience.^[61]

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