Myofascial Pain Syndrome (MPS) And Fibromyalgia

Myofascial Pain Syndrome (MPS) And Fibromyalgia

Source: fibromyalgia-symptoms.org

“Many of those already suffering from the pain of fibromyalgia also suffer from myofascial pain syndrome. Myofascial pain syndrome is another form of chronic pain that can affect the entire body, particularly the face and jaw. Myofascial pain can add to the already annoying symptoms of fibromyalgia, and can contribute to disability and a poor quality of life if not diagnosed properly. If you think that you may be suffering from myofascial dysfunction, visit with your health care provider to discuss your treatment options.

What is Myofascial Pain Syndrome?

Myofascial syndrome is a pain disorder that affects the muscles and fascia throughout your body. Fascia is like a web that surrounds the bones, tissues, organs, and blood vessels throughout the body. Myofascial pain syndrome can attack and cause degeneration of certain areas of the fascia, resulting in chronic pain and a variety of other symptoms.

Pain usually originates in specific areas of the body, called myofascial trigger points (TrPs), which feel like tiny nodules under the skin. These trigger points commonly develop throughout the body, typically where the fascia comes into contact with a muscle.

Myofascial pain syndrome is a very common illness, and most people will develop at least one trigger point in their body at some point in their lives. The majority of these people will not develop severe symptoms and will be able to continue on with their normal routines. However, about 14% of the population will develop a chronic form of the syndrome, resulting in persistent pain and discomfort.

Myofascial pain disorder is very common in fibromyalgia sufferers. It was once thought that myofascial pain syndrome was actually a kind of fibromyalgia. However, this is now known not to be the case. It is possible to have both fibromyalgia and chronic myofascial syndrome, and therefore it is important to be diligent when analyzing your symptoms. If you notice myofascial syndrome symptoms, record them and report them to your doctor.

Signs and Symptoms of Myofascial Pain Syndrome:

The most common sign of myofascial pain is the presence of palpable trigger points in your muscles. Trigger points are areas of extreme tenderness and sensitivity, and usually form in bands of muscle underneath your skin. They are similar to the tender points caused by fibromyalgia, only trigger points can be felt beneath the skin. When touched, trigger points will produce pain and twitching in the muscles. Often, pain is felt in an area distinct from the trigger point that is actually affected – this is called referred pain.

The pain of myofascial syndrome is typically a dull ache, but can also produce a throbbing, stabbing, or burning sensation. Pain is often located in the jaw area, though any part of the body can be affected. One-third of myofascial pain sufferers report localized pain, while two-thirds report having pain all over their bodies.

Myofascial pain can also produce a variety of other symptoms, many of which may appear unrelated. These include:

* numbness in the extremities
* popping or clicking of the joints
* limited movement of joints, particularly the jaw
* muscle weakness (manifested in dropping things)
* migraine or headache
* disturbed sleep
* balance problems
* tinnitus and ear pain
* double vision or blurred vision
* problems with memory
* unexplained nausea, dizziness, and sweating

Aggravating Factors

Symptoms are often aggravated by specific factors. Stress and anxiety contribute to muscle tension and can irritate trigger points. Changes in the weather, including sudden coldness, high humidity, or extreme dryness can also exacerbate symptoms. Physical activity can also trigger symptoms.

Causes of Myofascial Pain Syndrome

There are numerous proposed causes of myofascial pain:

Muscle and Skeletal Problems:
The causes of myofascial pain dysfunction syndrome can be numerous and depend upon the individual. Generally, myofascial pain is caused by some sort of trauma to the muscles and skeleton in the body. Overworking of the muscles can cause damage to certain areas resulting in the development of a trigger point. Poor posture can also trigger myofascial pain in certain individuals. Skeletal abnormalities, such as having different sized feet, toes, or legs, can also contribute to the development of myofascial pains. Frequent exposure to cold weather may also increase the risk of developing chronic myofascial pain syndrome.

Chronic Fibromyalgia Pain:
People with fibromyalgia may get myofascial pain syndrome as a result of their fibromyalgia pain. Compensating for pain can often cause reduced movement or an unhealthy posture, leading to the formation of trigger points. The severe pain caused by fibromyalgia also causes muscle contractions around tender points, referred to as guarding. Eventually these muscle contractions cause trigger points to form in addition to the tender points of fibromyalgia.

Depression Associated with Fibromyalgia:
The depression associated with fibromyalgia may also cause myofascial pain to develop. At least 30% of fibromyalgia patients suffer from depression, which causes low levels of serotonin in the brain. Serotonin is a neurotransmitter responsible for regulating mood and pain in the body. Depression may interfere with the process of regulating pain, causing MPS.

Effects of MPS on Fibromyalgia:

Having both myofascial pain syndrome and fibromyalgia can be quite trying at times. Symptoms of MPS and fibromyalgia are very similar, making it difficult for medical professionals to properly diagnose many people. Without proper diagnosis, a patient may not receive appropriate treatment, causing his or her symptoms to become even worse. In addition, myofascial pain can often contribute to the pain caused by fibromyalgia, making life much more difficult to enjoy.

 

Wear Purple for Fibromyalgia

Wear Purple for Fibromyalgia

One Day I Will Wake…

We are not alone.

Isolation

Here I stand alone again, waiting for the pharmacology train.
Misplaced by mistrust, thrown away among the muck.
I stare at the tracks, that bled my arms dry.
The only train to keep appearance, says destination goodbye.

I stand then sit at the station, I wait in anguish at the situation.
All the trains pass by me, there not for me to ride.
Quarantined inside my body, like a caged animal I solemnly.
Await for the conductor to call, my ticket of pain-free divorce.

Far away from buildings or places, out of phase I stare aimless.
At the faces that pass on by, so fast, without care, am I even there.
Cut off from the world around me, but I still feel the people surround me.
Will the train of destitution arrive, if not, how will I strive?

Like a diseased patient I lay in wait, a guessing game from a doctor’s fate.
Food to which I should not have eaten, side effects that fill my plate.
How do I change my state, it’s too late for contemplation.
So I isolate my self, from you, from me, and all that the world can be.

By Stuart Otway-Smith

An attempt to describe in poetry what Isolation feels like, a symptom of Fibromyalgia / Chronic Pain Syndrome.

National Fibromyalgia & Chronic Pain Association
Mark the date for May 12 National Fibromyalgia Awareness Day!

Spasm Chasm

Ache-1437

Deep within a dark dank place, hidden from the human race.

I sit.

I feel alone.

The pain is deep and winding.
My muscles ache and twitch.
No drugs flow through my veins.
If they did, they’d only make me itch.

These oddities often manifest, quite simply on their own.

My legs are locked, my arms are torn, it even hurts to smile.
A locked jaw, I want no more, I’m no longer mobile.
A sudden jerk of pre convulsion, pain of mind without emotion.
A limb, my face, but no trace, left for anyone to see.

The abyss of fibres rip, without sound, people pass by unnoticeably.

The Spasm Chasm I not implore, consumes all of my being.
Although I feel it deep within, it’s not for all, too seeing!
On my own, I sit at home, without choice or empathy.
I really want this to end, it’s been like this days.

When will it end?
Will I mend?

My body, convolutes, a random dance.

Confusion of verse betrays me, Fibro Fog, belated me.

The mountain of stairs, not that there’s many, is simply to hard to climb.
It’s times like these that make me ache, with throbbing and pulsation.
Pins like bladed needles walk my back, where art though compassion oh great creator.
My words like medicine heal my soul, the Spasm Chasm has its hold.

This verse, full of gaping, nonsensical confusion.
This is how the Spasm Chasm consumes you!

My world, its illusion.

By Stuart Otway-Smith

An attempt to describe in poetry what Muscle Spasms feel like, a symptom of Fibromyalgia / Chronic Pain Syndrome.

National Fibromyalgia & Chronic Pain Association
Mark the date for May 12 National Fibromyalgia Awareness Day!

10 Reasons To Increase Fibromyalgia Awareness

10 Reasons To Increase Fibromyalgia Awareness

by Purple Law Lady

Fibromyalgia Awareness Day May 12th 2012

  1. As we all know, it takes some people years and years to find out what is wrong and finally be diagnosed. If everyone knew all about fibromyalgia, then people could be diagnosed earlier. There would be  less of those depressing years of searching for answers.
  2. Sufferers will feel less alone – they will see posters and information booklets EVERYWHERE, giving them tips on how to cope.
  3. Doctors will become more interested in our condition and start investigating (and keeping up to date with) the newest medications and treatments, rather than ‘It’s Fibromyalgia – there’s nothing I can do.’
  4. Medical researchers and scientists will be more interested in finding a cure! Nobody wants to spend their time looking for a cure for something that no-one has heard of, they all want to cure the illnesses that people know about!
  5. We will no longer have to answer questions such as ‘Fibro-my-WHAT?’, ‘Fibromyalgia? What on Earth is that?’ or ‘Is that even real?’ No more long difficult explanations of the never-ending symptoms.
  6. People may even become more understanding! Relatives and friends will understand why you don’t feel up to partying. Employers understand why you have limitations and will be able to give you suitable arrangements because they will know what they are dealing with.
  7. Advertising companies will realise that there are a LOT of us and will design fibro-friendly products such as ride-on vacuum cleaners, ergonomically designed car seats, etc.
  8. More support groups will be formed as a result of more people realising that they have fibromyalgia.
  9. More people will donate money to research to find new treatments and… dare I say it… maybe even a cure!
  10. Because it makes you feel good about yourself!! You aren’t just doing this for yourself; we are doing this as a TEAM EFFORT! We need to reach as many people as possible to make this a success.

Related articles

Fibro Haze

#Fibro - Awareness Day

Fibro Haze

Once again, I spend my days, floating in a fibro haze.
My minds a mess, my thoughts a vapour, I can hardly put pen to paper.
An indistinct or billowing mass, my heads in the clouds again; Alas!
A transparent word, not rude nor absurd, gives rise to a frowning aggravation.

Once again, I spend my days, floating in a fibro haze.
Vague, indistinct, is that right, I’m sure; I think?
Obscure thoughts fog my mind, until the perceived I suddenly remind.
Misunderstood flushes of trance, a waking sleep of sleight of hand!

Once again, I spend my days, floating in a fibro haze.
Withered and torn, wish not I was born, especially in the winter.
On a cold day, please go away, or I am likely to eat ya!
It’s not that I hate you, it’s not that I don’t care, it’s more like my mind, just isn’t there.

Once again, I spend my days, floating in a fibro haze.
Running on empty, without any diesel, that’s not an excuse for hurting people.
And why do you sit there, hating yourself, does not your family, not give you self wealth?
It’s cold out here, it’s dark and it’s lonely, it wouldn’t be so bad, if someone would hold me.

By Stuart Otway-Smith

An attempt to describe in poetry what Fibro Fog feels like, a symptom of Fibromyalgia / Chronic Pain Syndrome.

National Fibromyalgia & Chronic Pain Association
Mark the date for May 12 National Fibromyalgia Awareness Day!

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Neurobiology Underlying Fibromyalgia Symptoms

Review Article

Neurobiology Underlying Fibromyalgia Symptoms

1Alan Edwards Centre for Research on Pain, McGill University, 3640 University Street, Room M19, Montreal, QC, H2A 1C1, Canada
2Department of Neurology & Neurosurgery, McGill University, 3640 University Street, Room M19, Montreal, QC, H2A 1C1, Canada
3Department of Anesthesia, McGill University, 3640 University Street, Room M19, Montreal, QC, H2A 1C1, Canada
4Center for Neurosensory Disorders, University of North Carolina, CB No. 7280, 3330 Thurston Building, Chapel Hill, NC 27599, USA

Received 27 April 2011; Accepted 23 August 2011

Academic Editor: Muhammad B. Yunus

Copyright © 2012 Marta Ceko et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Fibromyalgia is characterized by chronic widespread pain, clinical symptoms that include cognitive and sleep disturbances, and other abnormalities such as increased sensitivity to painful stimuli, increased sensitivity to multiple sensory modalities, and altered pain modulatory mechanisms. Here we relate experimental findings of fibromyalgia symptoms to anatomical and functional brain changes. Neuroimaging studies show augmented sensory processing in pain-related areas, which, together with gray matter decreases and neurochemical abnormalities in areas related to pain modulation, supports the psychophysical evidence of altered pain perception and inhibition. Gray matter decreases in areas related to emotional decision making and working memory suggest that cognitive disturbances could be related to brain alterations. Altered levels of neurotransmitters involved in sleep regulation link disordered sleep to neurochemical abnormalities. Thus, current evidence supports the view that at least some fibromyalgia symptoms are associated with brain dysfunctions or alterations, giving the long-held “it is all in your head” view of the disorder a new meaning.

1. Introduction

In order to examine the neurobiology underlying the symptoms of fibromyalgia, we must first determine what those symptoms are. Until recently, fibromyalgia (FM) was diagnosed based on the ARC1990 criteria [1], which were widespread pain in combination with tenderness at 11 or more of 18 specific tender point sites. The provisional ACR 2010 FM diagnostic criteria [2], suggested as an alternative method of diagnosing FM, do not require the presence of tenderness, but rather include a list of several other symptoms, including fatigue, unrefreshing sleep, and cognitive symptoms, as well as a mix of some other symptoms that could include headache, depression, and lower abdominal pain/cramping. The hallmark symptom is still widespread pain, and a diagnosis of fibromyalgia requires this symptom. However, a patient must also have some of the other symptoms that are common among FM patients in order to reach a composite score that would lead to a diagnosis of FM. In addition to clinical symptoms that make up the diagnosis of FM, experimental studies have identified a number of other abnormalities in FM patients, including increased sensitivity to multiple types of painful stimuli, increased sensitivity to other sensory modalities, and alterations in pain modulatory mechanisms. Further, neuroimaging studies have found functional, anatomical, and neurochemical differences in the brains of FM patients compared to healthy control subjects. Most of the clinical symptoms associated with FM have not been systematically studied in the experimental setting, but there are a number of studies that have provided an objective evaluation of the altered cognitive functioning and sleep disturbances reported in FM patients. Thus, this paper will focus on the experimental evidence related to FM symptoms and connect these perceptual and cognitive signs to abnormalities observed in the brains of FM patients.

1.1. Altered Pain Perception in FM Patients

The hallmark symptom of FM is widespread ongoing musculoskeletal pain. In addition, FM patients have been distinguished from other patients with widespread pain syndromes primarily by the presence of tenderness that has been assessed clinically by finding pain evoked by 4 kg manual pressure in at least 11 of 18 defined tender points. This tender point concept was not based on an understanding of the underlying pathophysiology, but rather on empirical observation. Thus, although the ARC-90 diagnostic criteria provided an important uniform tool for defining the FM syndrome, they did not validate the tender point concept, due to the circular evidence on which the criteria were based [3]. In fact, much evidence indicates that tender points are just sites normally more sensitive to pressure pain in all individuals [47] and that FM patients have an increased pressure sensitivity at non-tender-point sites as well [8]. Accumulating evidence now shows that FM patients have increased sensitivity to many types of painful stimulation, including pressure at non-tender-point sites [9], heat and cold pain [6,1014], electrical stimulation [6], and intramuscular hypertonic saline injection [15]. Despite the plethora of evidence for hypersensitivity to painful stimuli, there is less evidence that FM patients are more sensitive to innocuous somatosensory stimuli. Detection thresholds for tactile and electrical stimuli are not altered in FM [61213], but Hollins et al. [16] found that FM patients rated innocuous pressure as more intense than did healthy controls, although the effects in the innocuous range were weaker than in the noxious range. The evidence for changes in cool or warm detection also is mixed, with most investigators finding no differences between FM and controls for heat [610] or cold [1012], whereas one study found FM patients to have reduced heat detection thresholds [12], and one study found patients to have reduced cold detection thresholds [6]. Thus, it appears that the altered sensitivity within the somatosensory system is more profound in the noxious range than in the innocuous range.

1.2. Evidence for Generalized Hypersensitivity to Unpleasant Stimuli

The hypersensitivity of FM patients to painful stimuli has led some investigators to propose that fibromyalgia involves a hypervigilance to pain and pain-associated information [1719]. However, there is now evidence that the hypersensitivity to unpleasant stimuli extends beyond the somatosensory system, which has led to the hypothesis that there is a generalized hypervigilance for sensory stimuli in FM [162021]. A few studies have examined the sensitivity of FM patients in modalities other than pain and found perceptual amplification. FM patients have been shown to have decreased tolerance of unpleasant noise [20] and increased sensitivity to loud unpleasant auditory stimuli that parallels their increased pressure pain sensitivity [22]. Similarly, FM patients perceive unpleasant olfactory stimuli to be more intense and more unpleasant than do matched control subjects [23]. On the other hand, when pleasant odors were tested, FM patients and controls perceived the odors as equally intense, consistent with another evidence that the hypersensitivity across perceptual modalities may be confined to stimuli in the unpleasant range [24]. Nevertheless, for pleasant odors, although FM patients did not rate them as more intense, they did evaluate the pleasant odors as less pleasant than did control subjects. Further, a range of auditory stimuli were rated as more intense by FM patients than by controls, and auditory stimuli rated as mildly pleasant by healthy subjects were rated as somewhat unpleasant by FM patients [16]. The finding of hypersensitivity in multiple modalities of stimulation, particularly for unpleasant stimuli, suggests that the evoked pain sensitivity of FM may be related to an altered hedonic appreciation for sensory stimuli, rather than to peripheral tissue abnormalities.

1.3. Other Phenomena Related to Altered Pain Perception

Other types of evidence from experimental pain studies in FM patients support the idea of a centrally mediated up-regulation of nociceptive activity in the CNS. A central pathophysiological process that appears to be disturbed in FM patients is the “windup” of central nociceptive processing of C-fibre input to the spinal cord, resulting in the perceptual phenomenon of temporal summation of pain. Windup of nociceptive activity is dependent on activation of the NMDA receptor complex in the spinal cord by input from C-nociceptors [2526]. Some FM patients show increased temporal summation of pain and increased aftersensations at the termination of noxious stimulation [27]. These enhanced responses could be related to one or more of several possible factors: (1) an ongoing peripheral source of input from C nociceptors other than the applied stimulus; (2) sensitized NMDA receptors on central nociceptive neurons; (3) abnormalities in descending modulation; (4) abnormal processing at supraspinal levels. Evidence of increased sensitivity in multiple sensory modalities suggests that ongoing C-nociceptor input cannot alone account for FM symptoms, indicating that there probably also are either sensitized NMDA receptors, abnormalities in modulatory systems in the brain, or abnormal sensory processing at spinal or supraspinal levels. Increased sensitivity has been demonstrated at the spinal level in FM [11]. Staud et al. [28] showed that an NMDA inhibitor reduced temporal summation in both healthy people and FM patients, suggesting that NMDA receptors probably are not sensitized in FM. On the other hand, experimental evidence shows that there are abnormalities in pain modulatory systems in FM patients that could account for altered temporal summation and other putative spinal effects.

1.4. Altered Pain Inhibition in FM Patients

For hundreds of years, clinicians have known that pain inhibits pain, a phenomenon termed “counterirritation.” More recently, a physiological basis of this phenomenon has been identified; the application of noxious stimulation activates an endogenous analgesic system involving supraspinal descending control of dorsal horn nociceptive activity. This system is termed “diffuse noxious inhibitory control” or DNIC and its physiological basis in the spinal cord has been studied extensively in anesthetized animals [2930]. Nevertheless, when competing noxious stimuli are presented in conscious humans, other systems that modulate pain, such as distraction, also are probably in effect, so that care must be taken in inferring that perceptual effects are due to DNIC. Accordingly, a group of interested researchers has suggested that the term “conditioned pain modulation” be used in humans studies to avoid the mechanistic implication [31]. Studies that have examined conditioned pain modulation in FM patients show that conditioning stimuli that produce an analgesic response to experimental pain stimuli in healthy control subjects fail to have an effect on FM patients [133234]. One of these studies controlled for the effects of distraction and habituation and found a similar lack of conditioned pain modulation in FM patients [33], suggesting the possibility that the DNIC system is in fact impaired in these individuals. Alternatively, DNIC and other descending inhibitory systems could be activated by the widespread pain of FM, and the failure to demonstrate DNIC in FM could represent a ceiling effect in which these activated systems cannot be further engaged by the experimental manipulations [8]. In addition, distraction can have a powerful pain-inhibiting effect [3539], and some researchers have suggested that FM patients have altered attentional focusing, with a hypervigilance to unpleasant stimuli (see discussion above).

2. Other Symptoms of FM

2.1. Altered Cognitive Function in FM Patients

In addition to pain, many patients with fibromyalgia complain of problems with memory and concentration, often referred to as “fibrofog” [4043]. This clinical symptom has received a large amount of experimental study, and studies using objective cognitive tests substantiate patients’ subjective reports of cognitive dysfunctions, most commonly related to speed of information processing, attention, and memory [4356]. The most robust deficits in tests of memory and attention have so far been observed in paradigms involving a prominent distraction from a competing source of information, wherein FM patients are less capable than healthy controls to retain new information when rehearsal is prevented by a distraction [495057]. Milder deficits have been observed in memory free of distraction at encoding [43444849515859]. FM patients frequently display greater impairments in the ability to actively retrieve past episodic events in the absence of a cue (free recall) than on recognition tests, which serve to evaluate the retrieval of remembered information and are more resistant to the effects of impaired attention and concentration [43444851]. It has thus been proposed that memory impairments in FM are more highly related to attentional factors that modulate the efficiency of memory functioning than to primary memory processes per se [486061]. Thus, the inability to manage distraction seems to be a particular problem in fibromyalgia patients and is reflected in patients’ reports of difficulty concentrating and dealing with complex, rapidly changing environments [61] and by memory tests showing performance decrements in the presence of distraction. Impaired cognitive performance is evident even after controlling for anxiety and depression and the influence of medications that might affect cognitive functioning [43505258]. Another area of cognitive functioning that has been shown to be abnormal in FM is that of emotional decision making [6263]. A similar deficit has been shown in chronic back pain patients, suggesting that this is not unique to FM [64].

2.2. Sleep Disturbances in FM Patients

Many FM patients complain of unrefreshed sleep. Several laboratory studies using objective measures of sleep physiology such as EEG substantiate these reports by showing disordered sleep architecture in FM patients, including delayed onset to sleep, altered sleep stage dynamics, and reduced slow wave sleep (deep sleep) and rapid-eye movement (REM) sleep [6568]. The intrusion of EEG frequencies characteristic of wakefulness (alpha waves) in the deep non-REM sleep (delta waves) seems to be a prominent feature of the nonrestorative sleep of FM patients [656971]. Further, patients with FM often have fragmented sleep resulting from periodic intrusions such as involuntary limb movements (restless legs), sleep apnea, and arousal disturbances [687274]. Although FM patients tend to report greater disturbances in sleep duration and quality than shown in laboratory studies, and their subjective reports correlate better with the severity of clinical symptoms [75], objectively measured sleep disturbances have been associated with pain and subjective daily sleepiness in several studies [6768,7173].

3. Brain Changes That Could Underlie Symptoms

3.1. Neural Basis of Pain Amplification and Altered Pain Modulation

Functional brain imaging studies support psychophysical findings of increased pain perception in FM, in that there is an augmentation of sensory processing throughout pain-related brain regions [97681]. This is important, since laboratory findings of increased sensitivity could be interpreted as a reporting bias, rather than evidence of increased activation in pain pathways. The functional imaging studies have found that fibromyalgia patients show significantly more activity in response to pressure and thermal stimuli compared to controls in a number of brain regions. Increased activations were observed not only in limbic structures, but also in brain regions involved in sensory-discriminative processing, such as primary and secondary somatosensory cortices, which supports the view that neural responses to afferent signals are amplified in fibromyalgia.

Although the increased pain-evoked brain activations corroborate patients’ reports, the correlation between increased brain activity and increased pain perception does not explain how the afferent signal is amplified. As discussed above, there is psychophysical evidence of dysfunctions in pain modulation as well as pain perception. There is now much evidence that the activation of descending control circuitry is involved in pain modulation and that this circuitry includes parts of prefrontal, cingulate, and insular cortices [2336378283]. A number of anatomical imaging studies in FM patients reveal decreased brain gray matter in these regions [8490]. Although the cellular basis of decreased gray matter in FM patients is not known, it is possible that due to neuronal loss, decreased dendritic arborisation, or changes in glial activation, pain inhibitory systems do not work in FM patients as well as in healthy individuals.

Consistent with the idea that pain modulatory systems may be disturbed in fibromyalgia are data showing that some FM patients have abnormalities in neurochemical systems involved in pain control, including the forebrain opioid and dopamine systems. A positron emission tomography (PET) competitive binding study using the D2/D3 receptor antagonist [11C] raclopride showed that striatal dopamine is released in response to painful muscle stimulation in healthy subjects, but not in FM patients [1591], which might partially explain the increased sensitivity of FM patients to the painful muscle stimulation. For the opioid system, investigators using PET found that FM patients had decreased binding potentials at rest for the exogenously administered 𝜇-opioid receptor agonist carfentanil in several brain areas, including the ventral striatum, the anterior cingulate cortex, and the amygdala [92]. These areas are implicated in pain and its emotional modulation, and correspondingly, the binding potentials showed a negative relationship with the magnitude of affective pain scores relative to the sensory scores. Although results of this study do not tell us whether levels of endogenous opioids were increased or whether receptor availability was decreased, the findings support the notion that disturbances in the opioidergic system might be related to the increased pain sensitivity in fibromyalgia. For both dopamine and opioids, the ongoing widespread pain of FM could lead to a tonic activation within these systems and thus be a main factor in altering receptor availability and associated responsiveness to externally applied painful stimuli.

3.2. Neural Basis of Cognitive Symptoms

It is well known that cognitive capabilities such as attention and memory functions decline continuously across the adult lifespan [93], which, together with findings of accelerated age-related decline of brain gray matter observed in FM patients [84], suggests that there may be a relationship between gray matter reductions in FM and cognitive deficits in these patients. Two recent studies have linked FM to impaired emotional decision making [6263]. Anatomical imaging studies have reported that FM patients have decreased gray matter in the medial prefrontal and insular cortices [848589], areas implicated in emotional decision making [9499]. Together, these data suggest a possible association between gray matter loss and emotional decision making in FM. One study has directly examined the relationship between performance on working memory tasks and gray matter in FM patients and found that an individual’s performance was positively correlated with gray matter values in medial frontal and anterior cingulate cortices, thereby providing direct evidence for an association between altered working memory and gray matter morphology in fibromyalgia [51]. Both of these brain regions, together with lateral premotor cortex, lateral prefrontal cortex, frontal poles, and posterior parietal cortex, are areas known to be related to working memory processes [100105]. In terms of the neurochemical abnormalities in FM discussed above, dopamine plays an important role for cognitive functioning. Multiple lines of evidence demonstrate the importance of mesocortical and striatal dopaminergic pathways in memory tasks, perceptual speed, and response inhibition (see [106] for review). Thus, there is an overlap between tasks in which fibromyalgia patients perform poorly and tasks that are related to dopamine functioning, suggesting that a dysfunctional dopamine system could contribute to the cognitive symptoms of fibromyalgia.

3.3. Neural Basis of Sleep Disturbances

While many studies have used EEG and related methods to show various aspects of disordered sleep physiology in FM patients, little is known about the neurobiology underlying these disturbances. Several neurotransmitters have been proposed to influence CNS hypersensitivity associated with sleep alterations. For example, inhibition of the CNS serotonin synthesis has been linked to insomnia and increased pain sensitivity [107]. Accordingly, in FM there is evidence for low serum and cerebrospinal fluid serotonin levels [108109]. Injecting amounts of substance P into the CNS of rats has been shown to reduce sleep efficiency, increasing latency to onset to sleep and provoking awakenings from sleep [110], and there is evidence for elevated cerebrospinal fluid levels of substance P in FM patients [111,112].

3.4. What Do the Psychophysical, Cognitive, and Neuroimaging Studies Tell Us about the Neurobiology Underlying FM Symptoms?

The wealth of experimental evidence showing that FM patients are hypersensitive to painful stimuli, as well as unpleasant stimuli from other sensory modalities, in conjunction with functional brain imaging data showing increased stimulus-evoked activation throughout nociceptive pathways, shows that the defining symptom of FM—increased pain—is in fact real and not just a response bias of the patients. The finding that perception is increased in multiple modalities speaks against the hypothesis that FM pain is due to an upregulation of peripheral nociceptive processes. Further, psychophysical evidence that descending modulatory systems are altered in FM patients supports the opposing idea that FM symptoms are at least in part caused by alterations in CNS processing of the pain signal, including a dysregulation of pain modulatory systems. Nevertheless, the apparent dysregulation within these systems could be caused and/or perpetuated by a tonic activation related to the presence of ongoing widespread pain, so that the systems are saturated and cannot regulate further in response to external stimuli.

Since similar descending control systems, including attentional and emotional regulatory circuitry, affect multiple sensory modalities [113119], a dysfunction (or saturation) in these systems could lead to the hypersensitivity in multiple sensory modalities. FM patients show reduced habituation to nonpainful tactile stimuli and increased cortical response to intense auditory stimuli, both of which have been linked to deficient inhibition of incoming sensory stimuli [120121]. Also in support of the idea of a central dysregulation or saturation of pain modulation are changes in the opioid and dopamine neurotransmitter systems, both known to be involved in hedonic regulation [122].

Finally, the findings that FM patients not only perceive themselves to have altered memory and concentration (“fibrofog”), but also in fact perform poorly on multiple cognitive tests, even when depression is excluded as a contributing factor, suggest that there are alterations in brain function. The anatomical brain imaging studies that show reductions in gray matter in frontal regions important for cognitive function further indicate that this common symptom of FM is based on altered brain function. Together, the experimental evidence provides strong support for the idea that FM symptoms are related to dysfunctions in the central nervous system. The cause of these changes cannot be deduced from the available evidence, as it is correlational in nature. Did long-term ongoing pain cause the changes or did the changes cause the pain? Without a relevant animal model or long-term longitudinal studies, we cannot answer these questions. Nevertheless, we can at least say that fibromyalgia is real and that it is associated with multiple changes in the brain.

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