Fibromyalgia

Fibromyalgia Explored

2008-04-09T12:11:00.000-07:00

Fibromyalgia
From Wikipedia, the free encyclopedia

Classification and external resources
ICD-10
M 79.7
ICD-9
729.1
MedlinePlus
000427
eMedicine
med/790 med/2934 ped/777 pmr/47
MeSH
D005356

Fibromyalgia (FM) is a disorder classified by the presence of chronic widespread pain and tactile allodynia.[1] An example of tactile allodynia is when a person perceives light pressure or the movement of clothes over the skin as painful, whereas a healthy individual would not feel pain. Fibromyalgia patients are often affected by a number of symptoms other than pain, including debilitating fatigue, abnormal sleep architecture [2] meaning the brain does not reach all the restorative levels of sleep necessary for overall health, functional bowel disturbances[3] and a variety of neuropsychiatric problems including cognitive dysfunction [4] which can mean short and/or long term memory problems, slowed information processing ability, diminished attention span and anxiety and depressive symptoms[5]. While the criteria for such an entity have not yet been thoroughly developed, the recognition that fibromyalgia involves more than just pain has led to the frequent use of the term “fibromyalgia syndrome.” It is not contagious, and recent studies suggest that people with fibromyalgia may be genetically predisposed.[6] It affects more females than males, with a ratio of 9:1 by American College of Rheumatology (ACR)criteria.[7] Fibromyalgia is seen in about 2% of the general population.[8] It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.

The disorder is not directly life-threatening. The degree of symptoms may vary greatly from day to day with periods of flares (severe worsening of symptoms) or remission; however, the disorder is generally perceived as non-progressive.[9]

The validity of fibromyalgia as a unique clinical entity is a matter of some contention among researchers in the field. For example, it has been proposed that the pathophysiology responsible for the symptoms that are collectively classified as representing "fibromyalgia" is poorly understood, thereby suggesting that the fibromyalgia phenotype which is the difference between an individual’s heredity and what that heredity produces, may result from several different disease processes that have global hyperalgesia - an increased sensitivity to pain - and allodynia in common, [10][11][12] an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other.[13] Alternatively, there is evidence for the existence of differing pathophysiological - which is the study of the disturbance of normal mechanical, physical, and biochemical functions of the body - within the greater fibromyalgia construct[14][15], which may be interpreted to represent evidence for the existence of biologically distinct "sub-types" of the disorder akin to conditions such as epilepsy, schizophrenia and major depressive disorder. In a January 14, 2008 article in the New York Times, the controversy of the reality of the disease and its proposed cures are discussed, while citing that the American College of Rheumatology, the Food and Drug Administration and insurers recognize fibromyalgia as a diagnosable disease. Drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.[16]

History
Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis.[17] The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra (fiber)[18] and the Greek words myo (muscle)[19] and algos (pain).[20]

In 1981, Dr. Muhammad B. Yunus published the "first controlled study of the clinical characteristics" of the fibromyalgia syndrome, for which he is considered "the father of our modern view of fibromyalgia."[21][22] His work was the "first controlled clinical study" of fibromyalgia with validation of known symptoms and tender points, and he also proposed "the first data-based criteria." In 1984, he proposed the important concept that the fibromyalgia syndrome and other similar conditions are interconnected. In 1986, he showed serotonergic and norepinephric drugs to be effective.[23]

Yunus later emphasized a "biopsychosocial perspective" of fibromyalgia, which is considered the "only way to synthesize the disparate contributions of such variables as genes and adverse childhood experiences, life stress and distress, posttraumatic stress disorder, mood disorders, self-efficacy for pain control, catastrophizing, coping style, and social support into the evolving picture of central nervous system dysfunction vis-a-vis chronic pain and fatigue."[21][22]

Fibromyalgia was recognized by the American Medical Association as an illness and a cause of disability in 1987.[citation needed] In an article the same year, in the Journal of the American Medical Association, a physician named Dr. Don Goldenberg also called the disorder fibromyalgia.[citation needed] The ACR published a criteria for fibromyalgia in 1990, and developed neurohormonal mechanisms with central sensitization in the 1990s.[23]

Symptoms
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch. There is also typically moderate to severe fatigue. Those affected may also experience heightened sensitivity of the skin (also called allodynia), tingling of the skin (often needle-like), achiness in the muscle tissues, prolonged muscle spasms, weakness in the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of fibromyalgia. Indeed, studies suggest that sleep disturbance are related to a phenomenon called alpha-delta sleep, a condition in which deep sleep (associated with delta EEG waves) is frequently interrupted by bursts of brain activity similar to wakefulness (i.e. alpha waves). Deeper stages of sleep (stages 3 & 4) are often dramatically reduced.
In addition, many patients experience cognitive dysfunction (known as "brain fog" or "fibrofog"), which may be characterized by impaired concentration and short-term memory consolidation, impaired speed of performance, inability to multi-task, and cognitive overload.[24][25] Many experts suspect that "brain fog" is directly related to the sleep disturbances experienced by sufferers of fibromyalgia.[citation needed]
Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome (possibly linked to lower levels of ghrelin [2], genitourinary symptoms and interstitial cystitis), dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although fibromyalgia is classified based on the presence of chronic widespread pain, pain may also be localized in areas such as the shoulders, neck, low back, hips, or other areas. Many sufferers also experience varying degrees of facial pain and have high rates of comorbid temporomandibular joint disorder. Not all patients have all symptoms.
Symptoms can have a slow onset, and many patients have mild symptoms beginning in childhood, that are often misdiagnosed as growing pains.[citation needed] Symptoms are often aggravated by unrelated illness or changes in the weather.[citation needed]They can become more tolerable or less tolerable throughout daily or yearly cycles; however, many people with fibromyalgia find that, at least some of the time, the condition prevents them from performing normal activities such as driving a car or walking up stairs. The disorder does not cause inflammation as is characteristic of rheumatoid arthritis, although some NSAIDs may temporarily reduce pain symptoms in some patients. Their use, however, is limited, and often of little to no value in pain management.[26]

[edit] Variability of symptoms
The following factors have been proposed to exacerbate symptoms of pain in patients:
Increased psychosocial stress[citation needed]
Excessive physical exertion (exercise seems to decrease the pain threshold of people with fibromyalgia but increase it in healthy individuals)[27]
Lack of slow-wave sleep
Changes in humidity and barometric pressure[citation needed]

[edit] Proposed causes and pathophysiology
The cause of fibromyalgia is unknown. Fibromyalgia can, but does not always, start as a result of some trauma such as a traffic accident, major surgery, or disease. Some evidence shows that Lyme Disease may be a trigger of fibromyalgia symptoms.[28] Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic inflammatory process to clinical depression [29]

[edit] Genetics
By using self-reported "Chronic Widespread Pain" (CWP) as a surrogate marker for fibromyalgia, the Swedish Twin Registry found that a modest genetic contribution may exist:[30][31]
Monozygotic twins with CWP have a 15% chance that their twin sibling has CWP
Dizygotic twins with CWP have a 7% chance that their twin sibling has CWP

[edit] Stress
Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia,[32] and that PTSD is linked with fibromyalgia.[33][34] The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.
A non-mainstream hypothesis that fibromyalgia may be a psychosomatic illness has been described by John E. Sarno's "tension myositis syndrome". He believes many cases of chronic pain result from changes in the body caused by the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, (and in some cases, psychotherapy) are treatments proposed to stop the brain from using that strategy.[35][36][37][38]

[edit] Dopamine abnormality
Dopamine is a catecholamine neurotransmitter perhaps best known for its role in the pathology of schizophrenia, Parkinson's disease and addiction. There is also strong evidence for a role of dopamine in restless leg syndrome [39], which is a common co-morbid condition in patients with fibromyalgia. [40] In addition, dopamine plays a critical role in pain perception and natural analgesia. Accordingly, musculoskeletal pain complaints are common among patients with Parkinson's disease [41], which is characterized by drastic reductions in dopamine owing to neurodegeneration of dopamine-producing neurons, while patients with schizophrenia, which is thought to be due (in part) to hyperactivity of dopamine-producing neurons, have been shown to be relatively insensitive to pain.[42][43] Interestingly, patients with restless legs syndrome have also been demonstrated to have hyperalgesia to static mechanical stimulation.[44]
Fibromyalgia has been commonly referred to as a "stress-related disorder" due to its frequent onset and worsening of symptoms in the context of stressful events.[45][46] It was therefore proposed that fibromyalgia may represent a condition characterized by low levels of central dopamine that likely results from a combination of genetic factors and exposure to environmental stressors, including psychosocial distress, physical trauma, systemic viral infections or inflammatory disorders (e.g. rheumatoid arthritis, systemic lupus erythematosus).[47] This conclusion was based on three key observations: (1) fibromyalgia is associated with stress; (2) chronic exposure to stress results in a disruption of dopamine-related neurotransmission[48]; and (3) dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia [49] including the nucleus accumbens [50], insular cortex [51], anterior cingulate cortex [52], thalamus [53], periaqueductal gray [54], and spinal cord [55] [56].
In support of the 'dopamine hypothesis of fibromyalgia', a reduction in dopamine synthesis has been reported by a study that used positron emission tomography (PET) and demonstrated a reduction in dopamine synthesis among fibromyalgia patients in several brain regions in which dopamine plays a role in inhibiting pain perception, including the mesencephalon, thalamus, insular cortex and anterior cingulate cortex.[57] A subsequent PET study demonstrated that, whereas healthy individuals release dopamine into the caudate nucleus and putamen during a tonic experimental pain stimulus (i.e. hypertonic saline infusion into a muscle bed)[58], fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation. [59] Moreover, a substantial subset of fibromyalgia patients respond well in controlled trials to pramipexole, a dopamine agonist that selectively stimulates dopamine D2/D3 receptors and is used to treat both Parkinson's disease and restless legs syndrome.[60] Trials of other dopamine agonists are currently ongoing.

[edit] Serotonin
Serotonin is a neurotransmitter that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration and descending inhibition of pain. Accordingly, it has been hypothesized that the pathophysiology underlying the symptoms of fibromyalgia may be a dysregulation of serotonin metabolism, which may explain (in part) many of the symptoms associated with the disorder. This hypothesis is derived in part by the observation of decreased serotonin metabolites in patient plasma [61] and cerebrospinal fluid.[62] However, selective serotonin reuptake inhibitors (SSRIs) have met with limited success in alleviating the symptoms of the disorder, while drugs with activity as mixed serotonin-norepinephrine reuptake inhibitors (SNRIs) have been more successful[63]. Accordingly, duloxetine (Cymbalta), a SNRI originally used to treat depression and painful diabetic neuropathy, has been demonstrated by controlled trials to relieve symptoms of some patients. Eli Lilly and Company, the manufacturer of duloxetine has submitted a supplementary new drug application (sNDA) to the FDA for approval of it use in the treatment of FM. The relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.[64] Ironically, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin 5-HT3 antagonists) actually block some of the effects of serotonin.[65]

[edit] Sleep disturbance
Electroencephalography studies have shown that people with fibromyalgia lack slow-wave sleep and circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may cause or worsen the condition.[66] According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The hypothesis supposes that stage 4 sleep is critical to the function of the nervous system, as it is during that stage that certain neurochemical processes in the body 'reset'. In particular, pain causes the release of the neuropeptide substance P in the spinal cord which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound to become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect.
The sleep disturbance/substance P hypothesis could explain "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures.[citation needed] The hypothesis proposes that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. This hypothesis could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system. The sleep disturbance hypothesis could also provide a possible connection between fibromyalgia, chronic fatigue syndrome (CFS) and post-polio syndrome through damage to the ascending reticular activating system of the reticular formation. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.
Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.[citation needed]

[edit] Human growth hormone
An alternate hypothesis suggests that stress-induced problems in the hypothalamus may lead to reduced sleep and reduced production of human growth hormone (HGH) during slow-wave sleep. People with fibromyalgia tend to produce inadequate levels of HGH. Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.[citation needed]
This view is supported by the fact that those hormones under the direct or indirect control of HGH, including IGF-1, cortisol, leptin and neuropeptide Y are abnormal in people with fibromyalgia,[67] In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep[68][69][70][71] though there is disagreement about the proposition.[72]

[edit] Deposition disease
The 'deposition hypothesis of fibromyaglia' posits fibromyalgia is due to intracellular phosphate and calcium accumulations that eventually reaches levels sufficient to impede the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the removal of excess phosphates from the blood stream. Accordingly, proponents of this hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is required for the excess phosphate to enter the cells.[citation needed]The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.[73]
Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the muscles to detect lumps and areas of spasm thought to be caused by an excess of calcium in the cytosol of the cells. The mapping technique is notably different from the manual tenderpoint examination[74] upon which a diagnosis of fibromyalgia depends and is purportedly different from the detection of trigger points that characterize the myofascial pain syndrome.[citation needed]
While this hypothesis does not identify the causative mechanism in the kidneys, it proposes a treatment known as guaifenesin therapy. This treatment involves administering the drug guaifenesin to a patient's individual dosage, avoiding salicylic acid in medications or on the skin. Often products for salicylate sensitivity are very helpful. If the patient is also hypoglycemic, a diet is designed to keep insulin levels low.
The phosphate build-up hypothesis explains many of the symptoms present in fibromyalgia.[citation needed]and proposes an underlying cause. The guaifenesin treatment, based on this hypothesis, has received mixed reviews, with some practitioners claiming many near-universal successes[citation needed] and others reporting no success. Of note, guaifenesin is also a central acting muscle relaxant used in veterinary anaesthesia[75] that is structurally related to methocarbamol, a property that might explain its utility in some fibromyalgia patients. A controlled trial of guaifenesin for the treatment of fibromyalgia demonstrated no evidence for efficacy of this medication. [76] However, this study has been criticized by the chief proponent of the deposition hypothesis for not limiting salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method.[77] As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the hypothesis. It should be noted that nothing in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.

[edit] Other hypotheses
Other hypotheses have been proposed related to various toxins from the patient's environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to intestinal bacteria,[78][79] neurotransmitter disruptions in the central nervous system, and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule.[80][81] This association has not repeated in a number of related studies,[82] and the US-FDA concluded "the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants."[83] Due to the multi-systemic nature of illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging branch of medical science called psychoneuroimmunology (PNI) is looking into how the various hypotheses fit together.
Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from vasomotor dysregulation causing improper vascularflow and hypoperfusion (decreased blood flow to a given tissue or organ).[84]

[edit] Always a comorbid disease?
Cutting across several of the above hypotheses is the proposition that fibromyalgia is almost always a comorbid disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia,[85] and a large coeliac support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurrence with chronic fatique.[86]
According to this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery. In other cases the two disorders coexist.

[edit] Diagnosis
There is still debate over what should be considered essential diagnostic criteria. The most widely accepted set of classification criteria for research purposes were elaborated in 1990 by the Multicenter Criteria Committee of the the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990" define fibromyalgia according to the presence of the following criteria:
A history of widespread pain lasting more than three months—affecting all four quadrants of the body, i.e., both sides, and above and below the waist.
Tender points—there are 18 designated possible tender or trigger points (although a person with the disorder may feel pain in other areas as well). During diagnosis, four kilograms-force (39 newtons) of force is exerted at each of the 18 points; the patient must feel pain at 11 or more of these points for fibromyalgia to be considered.[87] Four kilograms of force is about the amount of pressure required to blanch the thumbnail when applying pressure. This set of criteria was developed by the American College of Rheumatology as a means of classifying an individual as having fibromyalgia for both clinical and research purposes. While these criteria for classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis, they have become the de facto diagnostic criteria in the clinical setting. It should be noted that the number of tender points that may be active at any one time may vary with time and circumstance.

[edit] Differentials
A number of other disorders can produce similar symptoms to fibromyalgia:
Chronic fatigue syndrome
Depression
Ehlers-Danlos syndrome
Gulf War syndrome
Influenza
Lead poisoning
Lupus erythematosus
Lyme disease
Mercury poisoning
Myofascial pain syndrome
Tendinitis
Thyroid disease
Vitamin B12 deficiency
Vitamin D deficiency
Whiplash-associated disorder
Multiple chemical sensitivity

[edit] Treatment
As with many other syndromes, there is no universally accepted cure for fibromyalgia, though some physicians claim to have found cures.[88] However, a steady interest in the disorder on the part of academic researchers as well as pharmaceutical interests has led to improvements in its treatment, which ranges from symptomatic prescription medication to alternative and complementary medicine.

[edit] Medications
Many medications are used to treat specific symptoms of fibromyalgia, such as muscle pain and insomnia.

[edit] Pain Relief
A number of pain relievers have been prescribed for fibromyalgia. This includes NSAID medications over the counter, COX-2 inhibitors, and tramadol in prescription form for more advanced cases. Recently, pregabalin (marketed as Lyrica) has been given FDA approval for the treatment of diagnosed Fibromyalgia.[16]

[edit] Muscle Relaxants
Muscle relaxants, such as cyclobenzaprine (Flexeril) or tizanidine (Zanaflex), may be used to treat the muscle pain associated with the disorder.[89][90][91]

[edit] Tricyclic antidepressants (TCAs)
Traditionally, low doses of sedating antidepressants (e.g. amitriptyline and trazodone) have been used to reduce the sleep disturbances that are associated with fibromyalgia and are believed by some practitioners to alleviate the symptoms of the disorder. Because depression often accompanies chronic illness, these antidepressants may provide additional benefits to patients suffering from depression. Amitriptyline is often favoured as it can also have the effect of providing relief from neuralgenic or neuropathic pain.[citation needed] It is to be noted that Fibromyalgia is not considered a depressive disorder; antidepressants are used for their sedating effect to aid in sleep.

[edit] Selective serotonin reuptake inhibitors (SSRIs)
Research data consistently contradict the utility of agents with specificity as serotonin reuptake inhibitors for the treatment of core symptoms of fibromyalgia. [92][93][94] Moreover, SSRIs are known to aggravate many of the comorbidities that commonly affect patients with fibromyalgia including restless legs syndrome and sleep bruxism[95][96][97].

[edit] Anti-seizure drugs
Anti-seizure drugs are also sometimes used, such as gabapentin [98] and pregabalin (Lyrica). Pregabalin, originally used for the nerve pain suffered by diabetics, has been approved by the American Food and Drug Administration for treatment of fibromyalgia. A randomized controlled trial of pregabalin 450 mg/day found that a number needed to treat of 6 patients for one patient to have 50% reduction in pain.[99]

[edit] Dopamine agonists
Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip)) have been studied for use in the treatment of fibromyalgia with good results. [100] A trial of transdermal rotigotine is currently on going [101].

[edit] Combination therapy
A controlled clinical trial of amitriptyline and fluoxetine demonstrated utility when used in combination.[102]

[edit] Cannabis and cannabinoids
Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disorder.[103] Writing in the July 2006 issue of the journal Current Medical Research and Opinion, investigators at Germany's University of Heidelberg evaluated the analgesic effects of oral THC (∆9-tetrahydrocannabinol) in nine patients with fibromyalgia over a 3-month period. Subjects in the trial were administered daily doses of 2.5 to 15 mg of THC, but received no other pain medication during the trial. Among those participants who completed the trial, all reported a significant reduction in daily recorded pain and electronically induced pain.[104] Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,[105] particularly in the treatment of cancer pain and neuropathic pain,[106][107] both of which are poorly treated by conventional opioids. As a result, some experts have suggested that cannabinoid agonists would be applicable for the treatment of chronic pain conditions unresponsive to opioid analgesics such as fibromyalgia, and they propose that the disorder may be associated with an underlying clinical deficiency of the endocannabinoid system.[108][109]

[edit] Topical Remedies
Users of Epsom Salts in the gel form (Magnesium Sulfate), have reported significant and lasting relief from pain associated with fibromyalgia. Epsom Salts have long been touted for its ability to reduce pain and swelling. [110]

[edit] Non-drug treatment

[edit] Physical treatments
Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[111] Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy, massage, or acupuncture may find them beneficial.[112] Most patients find exercise, even low intensity exercise to be extremely helpful.[113] Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.[114]
A holistic approach—including managing diet, sleep, stress, activity, and pain—is used by many patients. Dietary supplements, massage, chiropractic care, managing blood sugar levels, and avoiding known triggers when possible means living as well as it is in the patient's power to do.[citation needed]

[edit] Psychological/Behavioral Therapies
As the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.[115] Although there is no universally accepted cure, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.[116]
Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain.[8] Neurofeedback has also shown to provide temporary and long-term relief.
Treatment for the "brain fog" has not yet been developed, however biofeedback and self-management techniques such as pacing and stress management may be helpful for some patients. The use of medication to improve sleep helps some patients, as does supplementation with folic acid and ginkgo biloba.[citation needed]

[edit] Dietary treatment
In a 2001 review of four case studies, symptom alleviation was found by minimizing consumption of monosodium glutamate.[117]

[edit] Investigational treatments
Milnacipran, a serotonin-norepinephrine reuptake inhibitor (SNRI), is available in parts of Europe where it has been safely prescribed for other disorders. On May 22nd, 2007, a Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as a treatment of fibromyalgia syndrome. At this time, only initial top-line results are available and further analyses will be completed in the coming weeks. If ultimately approved by the FDA, Milnacipran could be distributed in the United States as early as summer, 2008.[118]
Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol [73] the efficacy of guaifenesin in treating fibromyalgia has not been proven in properly designed research studies. Indeed, a controlled study conducted by researchers at Oregon Health Science University in Portland failed to demonstrate any benefits from this treatment,[76] and the lead researcher has suggested that the annecdotaly reported benefits where due to placebo suggestion.[119] The results of the study have since been contested by Dr St. Amand, who was a co-author or the original research report.[120]
Dextromethorphan is an over-the-counter cough medicine with activity as an NMDA receptor antagonist. It has been used in the research setting to investigate the nature of fibromyalgia pain[121][122]; however, there are no controlled trials of safety or efficacy in clinical use.

[edit] Living with fibromyalgia
Fibromyalgia can affect every aspect of a person's life. While neither degenerative nor fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can severely curtail social activity and recreation, and as many as 30% of those diagnosed with fibromyalgia are unable to maintain full-time employment.[citation needed] Like others with disabilities, individuals with FMS often need accommodations to fully participate in their education or remain active in their careers.
In the United States, those who are unable to maintain a full-time job due to the condition may apply for Social Security Disability benefits. Although fibromyalgia has been recognized as a genuine, severe medical condition by the government, applicants are often denied benefits, since there are no formal diagnostic criteria or medically provable symptoms. Because of this, if an applicant does have a medically verifiable condition that would justify disability benefits in addition to fibromyalgia, it is recommended that they not list fibromyalgia in their claim. However, most are awarded benefits at the judicial level; the entire process often takes two to four years.[citation needed]
In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistance.[123]
Fibromyalgia is often referred to as an "invisible" illness or disability due to the fact that generally there are no outward indications of the illness or its resulting disabilities. The invisible nature of the illness, as well as its relative rarity and the lack of understanding about its pathology, often has psychosocial complications for those that have the disorder. Individuals suffering from invisible illnesses in general often face disbelief or accusations of malingering or laziness from others that are unfamiliar with the disorder.
There are a variety of support groups on the Web that cater to fibromyalgia sufferers.

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^ Staud R, Vierck CJ, Robinson ME, Price DD (2005). "Effects of the N-methyl-D-aspartate receptor antagonist dextromethorphan on temporal summation of pain are similar in fibromyalgia patients and normal control subjects". The journal of pain : official journal of the American Pain Society 6 (5): 323-32. doi:10.1016/j.jpain.2005.01.357. PMID 15890634.
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^ The Fibromyalgia Association of the UK

[edit] Further reading
Fibromyalgia for Pharmacists, a medication guide

[edit] See also
Somatosensory Amplification

[edit] External links
American College of Rheumatology Fibromyalgia factsheet
US Food and Drug Administration Living with Fibromyalgia, First Drug ApprovedJune 21, 2007
Fibromyalgia at the Open Directory Project
National Institute of Arthritis and Musculoskeletal and Skin Diseases. Questions and Answers About Fibromyalgia. Retrieved on 2008-03-18.
The National Fibromyalgia Association U.S (2007). Retrieved on 2007-06-01.
Fibromyalgia Resource Information (2005). Retrieved on 2007-06-01.
[hide]
v • d • eDiseases of the musculoskeletal system and connective tissue (M, 710-739)
Arthropathies
Arthritis (Septic arthritis, Reactive arthritis, Rheumatoid arthritis, Psoriatic arthritis, Felty's syndrome, Juvenile idiopathic arthritis, Still's disease) - crystal (Gout, Chondrocalcinosis) - Osteoarthritis (Heberden's node, Bouchard's nodes)
acquired deformities of fingers and toes (Boutonniere deformity, Bunion, Hallux rigidus, Hallux varus, Hammer toe) - other acquired deformities of limbs (Valgus deformity, Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot, Unequal leg length, Winged scapula)
patella (Luxating patella, Chondromalacia patellae)Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte
Systemic connectivetissue disorders
Polyarteritis nodosa - Churg-Strauss syndrome - Kawasaki disease - Hypersensitivity vasculitis - Goodpasture's syndrome - Wegener's granulomatosis - Arteritis (Takayasu's arteritis, Temporal arteritis) - Microscopic polyangiitis - Systemic lupus erythematosus (Drug-induced) - Dermatomyositis (Juvenile dermatomyositis) - Polymyositis - Scleroderma - Sjögren's syndrome - Behçet's disease - Polymyalgia rheumatica - Eosinophilic fasciitis - Hypermobility
Dorsopathies
Kyphosis - Lordosis - Scoliosis - Scheuermann's disease - Spondylolysis - Torticollis - Spondylolisthesis - Spondylopathies (Ankylosing spondylitis, Spondylosis, Spinal stenosis) - Schmorl's nodes - Degenerative disc disease - Coccydynia - Back pain (Radiculopathy, Neck pain, Sciatica, Low back pain)
Soft tissue disorders
muscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva)
synovium and tendon: Synovitis/Tenosynovitis (Calcific tendinitis, Stenosing tenosynovitis, Trigger finger, DeQuervain's syndrome) - Irritable hip - Ganglion cyst
bursa: bursitis (Olecranon, Prepatellar, Trochanteric) - Baker's cyst
fibroblastic disorders (Dupuytren's contracture, Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis, Fasciitis, Fibromatosis)
shoulder lesions: Adhesive capsulitis - Rotator cuff tear - Subacromial bursitis
enthesis: enthesopathies (Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis)other, NEC: Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia
Osteopathies
disorders of bone density and structure: Osteoporosis - Osteomalacia - continuity of bone (Pseudarthrosis, Stress fracture) - Monostotic fibrous dysplasia - Skeletal fluorosis - Aneurysmal bone cyst - Hyperostosis - Osteosclerosis Osteomyelitis - Avascular necrosis - Paget's disease of bone - Algoneurodystrophy - Osteolysis - Infantile cortical hyperostosis
Chondropathies
Juvenile osteochondrosis (Legg-Calvé-Perthes syndrome, Osgood-Schlatter disease, Köhler disease, Sever's disease) - Osteochondritis - Tietze's syndrome
See also congenital conditions (Q65-Q79, 754-756)

Retrieved from "http://en.wikipedia.org/wiki/Fibromyalgia"
Categories: Rheumatology Diseases involving the fasciae Syndromes Ailments of unknown etiology

For information on another disease, click on Digestive Diseases Library.

Nerve Pain

2008-04-06T13:00:00.000-07:00

Neuropathy
From Wikipedia, the free encyclopedia

Classification and external resources
ICD-10
G 56. - G 63.,G 90.0, G 99.0
ICD-9
337.0-337.1,356-357, 377
eMedicine
topic list
Neuropathy is usually short for Peripheral Neuropathy. Peripheral neuropathy is defined as deranged function and structure of peripheral motor, sensory, and autonomic neurons, involving either the entire neuron or selected levels.[1]

Classification
The four cardinal patterns of peripheral neuropathy are polyneuropathy, mononeuropathy, mononeuritis multiplex and Autonomic Neuropathy . The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs.

A radiculopathy involves spinal nerve roots, but if peripheral nerves are also involved the term radiculoneuropathy is used.

The form of neuropathy may be further broken down by cause, or the size of predominant fiber involvement, i.e. large fiber or small fiber peripheral neuropathy. Frequently the cause of a neuropathy cannot be identified and it is designated idiopathic.

Neuropathy may be associated with varying combinations of weakness, autonomic changes and sensory changes. Loss of muscle bulk or fasciculations, a particular fine twitching of muscle may be seen. Sensory symptoms encompass loss of sensation and "positive" phenomena including pain. This wikipedia entry will focus on the painful aspects of neurological conditions. Readers interested in a more detailed discussion of peripheral neuropathy should follow the links to the main entry.

Neuropathic pain
According to the most widely accepted definition, neuropathic pain is "initiated or caused by a primary lesion or dysfunction in the nervous system."[2] As much as 3% of the population is affected.[3]

Neuropathic pain may result from disorders of the peripheral nervous system or the central nervous system (brain and spinal cord). Thus, neuropathic pain may be divided into peripheral neuropathic pain, central neuropathic pain or mixed (peripheral and central) neuropathic pain.
Central neuropathic pain is found in spinal cord injury, multiple sclerosis, and some strokes. Fibromyalgia, a disorder of chronic widespread pain, is potentially a central pain disorder and is responsive to medications effective for neuropathic pain.[4]

Aside from diabetes (see Diabetic neuropathy) and other metabolic conditions, the common causes of painful peripheral neuropathies are herpes zoster infection, HIV-related neuropathies, nutritional deficiencies, toxins, remote manifestations of malignancies, genetic and immune mediated disorders.[5][6]

Neuropathic pain is common in cancer as a direct result of cancer on peripheral nerves (e.g., compression by a tumor), as a side effect of some chemotherapy drugs, and as a result of radiation injury.

Symptoms
Neuropathy often results in numbness, abnormal sensations called dysesthesias and allodynias that occur either spontaneously or in reaction to external stimuli, and a characteristic form of pain, called neuropathic pain or neuralgia, that is qualitatively different from the ordinary nociceptive pain one might experience from stubbing a toe.

Neuropathic pain may have continuous and/or episodic (paroxysmal) components. The latter are likened to an electric shock. Common qualities of the pain include burning or coldness, "pins and needles" sensations, numbness and itching. "Ordinary" pain results from exclusive stimulation of pain fibers, while neuropathic pain often results from the firing of both pain and non-pain (touch, warm, cool) sensory nerve fibers serving the same area. The result is signals that the spinal cord and brain do not normally receive.

Treatments for neuropathic pain
Neuropathic pain can be very difficult to treat with only some 40-60% of patients achieving partial relief.[7]

Deciding on the best treatment for individual patients challenges both the art and science of medicine. Attempts to synthesize scientific studies into best practices are limited by such factors as differences in reference populations and a lack of head-to-head studies. Furthermore, there are few studies evaluating treatment combinations or the special needs of children.
It is common practice in medicine to designate classes of medication according to their most common or familiar use e.g. as "antidepressants" and "anti-epileptic drugs" (AED's). These drugs have alternate uses to treat pain because the human nervous system employs common mechanisms for different functions, for example ion channels for impulse generation and neurotransmitters for cell-to-cell signaling.

In addition to the work of Dworkin, O'Connor and Backonja et al., cited above, there have been several recent attempts to derive guidelines for pharmacological therapy.[8][9] These have combined evidence from randomized controlled trials with expert opinion.

Favored treatments are certain antidepressants e.g tricyclics and selective serotonin-norepinephrine re-uptake inhibitors (SNRI's), anticonvulsants, especially pregabalin (Lyrica) and gabapentin (Neurontin), and topical lidocaine. Opioid analgesics and tramadol are recognized as useful agents but are not recommended as first line treatments.

Many of the pharmacologic treatments for chronic neuropathic pain decrease the sensitivity of nociceptive receptors, or desensitize C fibers such that they transmit fewer signals.

Antidepressants
Antidepressants function differently in neuropathic pain than in depression. Activation of descending norepinephrinergic and serotonergic pathways to the spinal cord limit pain signals ascending to the brain. Antidepressants will relieve neuropathic pain in non-depressed persons.
In animal models of neuropathic pain it has been found that compounds which only block serotonin reuptake do not improve neuropathic pain.[10][11][12][13][14][15][16][17] Similarly, compounds that only block norepinephrine reuptake also do not improve neuropathic pain. Compounds such as duloxetine, venlafaxine, and milnacipran that block both serotonin reuptake and norepinephrine reuptake do improve neuropathic pain.

Tricyclic antidepressants may also work on sodium channels in peripheral nerves.

Anticonvulsants
Pregabalin (Lyrica) and gabapentin (Neurontin) work by blocking specific calcium channels on neurons. The actions of the anticonvulsants carbamazepine (Tegretol) and oxcarbazepine (Trileptal), especially effective on trigeminal neuralgia, are principally on sodium channels.
Lamotrigine may have a special role in treating two conditions for which there are few alternatives, namely post stroke pain and HIV/AIDS-related neuropathy in that subgroup on antiretroviral therapy.[18]

Opioids
Opioids, also known as narcotics, are increasingly recognized as important treatment options for chronic pain. They are not considered first line treatments in neuropathic pain but remain the most consitently effective class of drugs for this condition. Opioids must be used only in appropriate individuals and under close medical supervision.

Several opioids, particularly and methadone have NMDA antagonist activity in addition to their µ-opioid agonist properties.

Methadone and ketobemidone possess NMDA antagonsism. Methadone does so because it is a racemic mixture; only the l-isomer is a potent µ-opioid agonist.[19]

There is little evidence to indicate that one strong opioid is more effective than another. Expert opinion leans toward the use of methadone for neuropathic pain, in part because of NMDA antagonism. It is reasonable to base the choice of opioid on other factors.[20]

Topical agents
In some forms of neuropathy, especially post-herpes neuralgia, the topical application of local anesthetics such as lidocaine can provide relief. A transdermal patch containing Lidocaine is available commercially in some countries.

Repeated topical applications of capsaicin, are followed by a prolonged period of reduced skin sensibility referred to as desensitization, or nociceptor inactivation. Capsaicin not only deplete substance P but also results in a reversible degeneration of epidermal nerve fibers. [21] Nevertheless, benefits appear to be modest. [22]

Marijuana and cannabinoids
Cannabinoids are modestly effective in reducing chronic pain. Nabilone is a synthetic cannabinoid which is significantly more potent than delta-9-tetrahydrocannabinol (THC). Nabilone produced less relief of chronic neuropathic pain and had more side effects than a weak opioid. [23]

The predominant adverse effects are CNS depression and cardiovascular effects which are mild and well tolerated but, psychoactive side effects limit their use.[24] A complicating issue may be a narrow therapeutic window; lower doses decrease pain but higher doses have the opposite effect.[25]

Sativex, a fixed dose combination of delta-9-tetrahydrocannabinol (THC) and cannabidiol, is sold as an oromucosal spray. It has some limited effect on multiple sclerosis pain. There are high rates of adverse effects (92%), especially dizziness and nausea and intoxication. About half the users will stop the drug after one year. [26]

Nabilone has some positive effects on the pain and other symptoms of fibromyalgia, at least in the short term.[27] Long-term studies are need to assess the probability of weight gain and other adverse effects.

A recent study showed smoked marijuana is beneficial in treating HIV-associated peripheral neuropathy.[28]

NMDA antagonism
The N-methyl-D-aspartate (NMDA) receptor seems to play a major role in neuropathic pain and in the development of opioid tolerance.

[Dextromethorphan]] is an NMDA antagonist at high doses.

Experiments in both animals and humans have established that NMDA antagonists such as ketamine and dextromethorphan can alleviate neuropathic pain and reverse opioid tolerance.[29] Unfortunately, only a few NMDA antagonists are clinically available and their use is limited by unacceptable side effects.

Reducing sympathetic nervous stimulation
In some neuropathic pain syndromes, "crosstalk" occurs between descending sympathetic nerves and ascending sensory nerves. Increases in sympathetic nervous system activity result in an increase of pain; this is known as sympathetically-mediated pain.

Lesioning operations on the sympathetic branch of the autonomic nervous system are sometimes carried out.

Dietary supplements
There are two dietary supplements that have clinical evidence showing them to be effective treatments of diabetic neuropathy; alpha lipoic acid and benfotiamine.[30]

A 2007 review of studies found that injected (parenteral) administration of alpha lipoic acid (ALA) was found to reduce the various symptoms of peripheral diabetic neuropathy.[31] While some studies on orally administered ALA had suggested a reduction in both the positive symptoms of diabetic neuropathy (including stabbing and burning pain) as well as neuropathic deficits (paresthesia),[32] the metanalysis showed "more conflicting data whether it improves sensory symptoms or just neuropathic deficits alone".[31] There is some limited evidence that ALA is also helpful in some other non-diabetic neuropathies.[33]

Benfotiamine is a lipid soluble form of thiamine that has several placebo controlled double blind trials proving efficacy in treating neuropathy and various other diabetic comorbidities.[34][35]

Other modalities
In addition to pharmacological treatment several other modalities are commonly recommended.[36] While lacking adequate double blind trials, these have shown to reduce pain and improve patient quality of life for chronic neuropathic pain: chiropractic, massage, meditation, cognitive therapy,[37] and prescribed exercise. Some pain management specialists will try acupuncture, with variable results.

Transcutaneous electrical nerve stimulation (TENS) may be worth considering in chronic neurogenic pain. TENS, with certain electrical waveforms, appears to have an acupuncture-like function.

Infrared photo therapy has been used to treat neuropathic symptoms.[38] However, recent work has cast doubt on the value of this approach.[39]

See also

References

^ Dyck PJ (1982). "Current concepts in neurology. The causes, classification, and treatment of peripheral neuropathy". N. Engl. J. Med. 307 (5): 283-6. PMID 6283352.
^ Bogduk, Nikolai; Merskey, Harold (1994). Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms, 2nd edition, Seattle: IASP Press, 212. ISBN 0931092051.
^ Gilron I, Watson CP, Cahill CM, Moulin DE (2006). "Neuropathic pain: a practical guide for the clinician". CMAJ 175 (3): 265-75. doi:10.1503/cmaj.060146. PMID 16880448.
^ Dworkin RH, Fields HL (2005). "Fibromyalgia from the perspective of neuropathic pain". J Rheumatol Suppl 75: 1-5. PMID 16078355.
^ Portenoy RK (1989). "Painful polyneuropathy". Neurol Clin 7 (2): 265-88. PMID 2566901.
^ Vaillancourt PD, Langevin HM (1999). "Painful peripheral neuropathies". Med. Clin. North Am. 83 (3): 627-42, vi. PMID 10386118.
^ Dworkin RH, O'Connor AB, Backonja M, et al (2007). "Pharmacologic management of neuropathic pain: evidence-based recommendations". Pain 132 (3): 237-51. doi:10.1016/j.pain.2007.08.033. PMID 17920770.
^ Attal N, Cruccu G, Haanpää M, et al (2006). "EFNS guidelines on pharmacological treatment of neuropathic pain". Eur. J. Neurol. 13 (11): 1153-69. doi:10.1111/j.1468-1331.2006.01511.x. PMID 17038030.
^ Moulin DE, Clark AJ, Gilron I, et al (2007). "Pharmacological management of chronic neuropathic pain - consensus statement and guidelines from the Canadian Pain Society". Pain Res Manag 12 (1): 13-21. PMID 17372630.
^ Bennett G, Xie Y (1988). "A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man". Pain 33 (1): 87-107. PMID 2837713.
^ Seltzer Z, Dubner R, Shir Y (1990). "A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury". Pain 43 (2): 205-18. PMID 1982347.
^ Kim S, Chung J (1992). "An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat". Pain 50 (3): 355-63. PMID 1333581.
^ Malmberg A, Basbaum A (1998). "Partial sciatic nerve injury in the mouse as a model of neuropathic pain: behavioral and neuroanatomical correlates". Pain 76 (1-2): 215-22. PMID 9696476.
^ Sung B, Na H, Kim Y, Yoon Y, Han H, Nahm S, Hong S (1998). "Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats". Neurosci. Lett. 246 (2): 117-9. PMID 9627194.
^ Lee B, Won R, Baik E, Lee S, Moon C (2000). "An animal model of neuropathic pain employing injury to the sciatic nerve branches". Neuroreport 11 (4): 657-61. PMID 10757496.
^ Decosterd I, Woolf C (2000). "Spared nerve injury: an animal model of persistent peripheral neuropathic pain". Pain 87 (2): 149-58. PMID 10924808.
^ Vadakkan K, Jia Y, Zhuo M (2005). "A behavioral model of neuropathic pain induced by ligation of the common peroneal nerve in mice". The journal of pain : official journal of the American Pain Society 6 (11): 747-56. PMID 16275599.
^ Wiffen PJ, Rees J. Lamotrigine for acute and chronic pain.Cochrane Database Syst Rev. 2007;(2):CD006044.
^ Davis AM, Inturrisi CE (1999). "d-Methadone blocks morphine tolerance and N-methyl-D-aspartate-induced hyperalgesia". J. Pharmacol. Exp. Ther. 289 (2): 1048-53. PMID 10215686.
^ Bruera E, Palmer JL, Bosnjak S, et al (2004). "Methadone versus morphine as a first-line strong opioid for cancer pain: a randomized, double-blind study". J. Clin. Oncol. 22 (1): 185-92. doi:10.1200/JCO.2004.03.172. PMID 14701781.
^ Nolano M, Simone DA, Wendelschafer-Crabb G, Johnson T, Hazen E, Kennedy WR (1999). "Topical capsaicin in humans: parallel loss of epidermal nerve fibers and pain sensation". Pain 81 (1-2): 135-45. PMID 10353501.
^ Finnerup NB, Otto M, Jensen TS, Sindrup SH (2007). "An evidence-based algorithm for the treatment of neuropathic pain". MedGenMed 9 (2): 36. PMID 17955091.
^ Frank B, Serpell MG, Hughes J, Matthews JN, Kapur D (2008). "Comparison of analgesic effects and patient tolerability of nabilone and dihydrocodeine for chronic neuropathic pain: randomised, crossover, double blind study". BMJ 336 (7637): 199-201. doi:10.1136/bmj.39429.619653.80. PMID 18182416.
^ Campbell FA, Tramèr MR, Carroll D, Reynolds DJ, Moore RA, McQuay HJ (2001). "Are cannabinoids an effective and safe treatment option in the management of pain? A qualitative systematic review". BMJ 323 (7303): 13-6. PMID 11440935.
^ Wallace M, Schulteis G, Atkinson JH, et al (2007). "Dose-dependent effects of smoked cannabis on capsaicin-induced pain and hyperalgesia in healthy volunteers". Anesthesiology 107 (5): 785-96. doi:10.1097/01.anes.0000286986.92475.b7. PMID 18073554.
^ Rog DJ, Nurmikko TJ, Young CA (2007). "Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial". Clin Ther 29 (9): 2068-79. doi:10.1016/j.clinthera.2007.09.013. PMID 18035205.
^ Skrabek RQ, Galimova L, Ethans K, Perry D (2008). "Nabilone for the treatment of pain in fibromyalgia". J Pain 9 (2): 164-73. doi:10.1016/j.jpain.2007.09.002. PMID 17974490.
^ Abrams D, Jay C, Shade S, Vizoso H, Reda H, Press S, Kelly M, Rowbotham M, Petersen K (2007). "Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial". Neurology 68 (7): 515-21. PMID 17296917.
^ Nelson KA, Park KM, Robinovitz E, Tsigos C, Max MB (1997). "High-dose oral dextromethorphan versus placebo in painful diabetic neuropathy and postherpetic neuralgia". Neurology 48 (5): 1212-8. PMID 9153445.
^ Head KA (2006). "Peripheral neuropathy: pathogenic mechanisms and alternative therapies" (PDF). Altern Med Rev 11 (4): 294-329. PMID 17176168.
^ a b Foster TS (2007). "Efficacy and safety of alpha-lipoic acid supplementation in the treatment of symptomatic diabetic neuropathy". Diabetes Educ 33 (1): 111-7. doi:10.1177/0145721706297450. PMID 17272797. “ALA appears to improve neuropathic symptoms and deficits when administered via parenteral supplementation over a 3-week period. Oral treatment with ALA appears to have more conflicting data whether it improves sensory symptoms or just neuropathic deficits alone.”
^ Ziegler D, Ametov A, Barinov A, et al (2006). "Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial". Diabetes Care 29 (11): 2365-70. doi:10.2337/dc06-1216. PMID 17065669.
^ Patton LL, Siegel MA, Benoliel R, De Laat A (2007). "Management of burning mouth syndrome: systematic review and management recommendations". Oral Surg Oral Med Oral Pathol Oral Radiol Endod 103 Suppl: S39.e1-13. doi:10.1016/j.tripleo.2006.11.009. PMID 17379153.
^ Stracke H, Lindemann A, Federlin K (1996). "A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy". Exp. Clin. Endocrinol. Diabetes 104 (4): 311-6. PMID 8886748.
^ Thornalley PJ (2005). "The potential role of thiamine (vitamin B(1)) in diabetic complications". Curr Diabetes Rev 1 (3): 287-98. PMID 18220605.
^ Chen H, Lamer TJ, Rho RH, et al (2004). "Contemporary management of neuropathic pain for the primary care physician". Mayo Clin. Proc. 79 (12): 1533-45. PMID 15595338.
^ Kerns JW, White A, Nashelsky J, Sherman S (2006). "Does psychiatric treatment help patients with intractable chronic pain?". J Fam Pract 55 (3): 235-6. PMID 16510058.
^ Burke T. Part 9. How Light (Photo Energy) May Increase Local NO and Vasodilation. Nitric Oxide and Its Role in Health and Diabetes. Diabetes In Control. Retrieved on 2008-03-28.
^ Lavery LA, Murdoch DP, Williams J, Lavery DC (2008). "Does anodyne light therapy improve peripheral neuropathy in diabetes? A double-blind, sham-controlled, randomized trial to evaluate monochromatic infrared photoenergy". Diabetes Care 31 (2): 316-21. doi:10.2337/dc07-1794. PMID 17977931.

Neuropathy related organizations

External links

v • d • e Nervous system pathology, primarily PNS (G50-G99, 350-359)
Nerve, nerve rootand plexus disorders
cranial nerve: V (Trigeminal neuralgia) - VII (Facial nerve paralysis, Bell's palsy, Melkersson-Rosenthal syndrome, Central seven) - XI (Accessory nerve disorder)
nerve root and plexus: Brachial plexus lesion - Thoracic outlet syndrome - Phantom limb mononeuropathy: Carpal tunnel syndrome - Ulnar nerve entrapment - Radial neuropathy - Causalgia - Meralgia paraesthetica - Tarsal tunnel syndrome - Morton's neuroma - Mononeuritis multiplex
Polyneuropathiesand other disorders of the PNS
Hereditary and idiopathic (Charcot-Marie-Tooth disease, Dejerine Sottas syndrome, Refsum's disease, Morvan's syndrome) - Guillain-Barré syndrome - Alcoholic polyneuropathy - Neuropathy
Diseases of myoneural junctionand muscle
Myasthenia gravis - Lambert-Eaton myasthenic syndrome - Myopathy - Primary disorders of muscles (Muscular dystrophy, Myotonic dystrophy, Myotonia congenita, Thomsen disease, Neuromyotonia, Paramyotonia congenita, Centronuclear myopathy, Nemaline myopathy, Mitochondrial myopathy, Central core disease) - Periodic paralysis (Hypokalemic, Hyperkalemic) - Infantile neuroaxonal dystrophy
Autonomic
Familial dysautonomia - Horner's syndrome - Multiple system atrophy (Shy-Drager syndrome, Olivopontocerebellar atrophy)

Retrieved from "http://en.wikipedia.org/wiki/Neuropathy"
Categories: Neurological disorders Neurology

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Fibromyalgia

2006-12-08T14:32:00.000-08:00

Some researchers think that the symptoms of Fibromyalgia might be due to sleep disorders, and others believe that fibromyalgia may be caused by a microorganism. Even others suspect changing skeletal muscle metabolism or chronic overreaction of the immune system to be the cause. Still, many believe that fibromyalgia is “all in the head” in a sense – not due to depression or stress but to altered pain processing and to changes in neurochemicals in the brain. (When someone suffers chronic pain for a long period of time, such as from Crohn's Disease, Lupus, MS, or Pancreatitis this causes altered pain processing and neurochemicle changes in the brain.) While answers to what is causing this condition might still be years away, doctors can now identify patients with fibromyalgia and try to help them live relatively normal lives.
..
Symptoms
There are many symptoms associated with fibromyalgia, but the condition always starts with chronic widespread pain and pain when in particular areas called “tender points” are palpated. Most people with fibromyalgia also have some degree of chronic fatigue and interrupted sleep. Other symptoms may include:

Body stiffness, especially in the morning and with prolonged sitting
Chest pain, irregular heartbeat, shortness of breath
Constipation
Depression and anxiety (may coexist)
Diarrhea
Difficulty concentrating, memory lapses
Difficulty swallowing
Dizziness, balance problems
Dry eyes, difficulty focusing
Dry mouth
Gas and cramping, abdominal pain
Headaches
Heartburn
Irritable bowel syndrome (IBS)
Itchy, dry, or blotchy skin
Localized edema (such as swollen fingers)
Blood pressure that lowers when standing
Painful menstruation
Painful sexual intercourse
Parasthesia (numbness and tingling in hands and feet)
Pelvic pain
Restless legs syndrome and periodic limb movement during sleep
Rhinitis consisting of nasal congestion/discharge and sinus pain (but no allergic immune response)
Sensitivity to light, sound, touch, temperature, and odors
Sensitivity to medications (more likely to have side effects)
Temporomandibular joint dysfunction (TMD), pain in jaw joints and surrounding muscles
Urinary frequency, urge, and irritation

Fibromyalgia can and does co-exist with many other chronic illnesses such as chronic fatigue syndrome, rheumatoid arthritis, Sjögren’s syndrome, thyroid disease, multiple sclerosis, and lupus. The symptoms of these conditions may be similar with those associated with fibromyalgia, making diagnosis more of a challenge.
..
Tender points
Tender points are specific places on the body (18 specific points at 9 bilateral locations) that are exceptionally sensitive to the touch in people with fibromyalgia upon examination by a doctor.

The American College of Rheumatology also has designated 18 sites on the body as possible tender points. For a fibromyalgia diagnosis, a person must have 11 or more tender points.

The 18 Tender Points of Fibromyalgia

Tender points of fibromyalgia exist at these nine bilateral muscle locations:

Low Cervical Region: (front neck area) at anterior aspect of the interspaces between the transverse processes of C5-C7.
Second Rib: (front chest area) at second costochondral junctions.
Occiput: (back of the neck) at suboccipital muscle insertions.
Trapezius Muscle: (back shoulder area) at midpoint of the upper border.
Supraspinatus Muscle: (shoulder blade area) above the medial border of the scapular spine.
Lateral Epicondyle: (elbow area) 2 cm distal to the lateral epicondyle.
Gluteal: (rear end) at upper outer quadrant of the buttocks.
Greater Trochanter: (rear hip) posterior to the greater trochanteric prominence.
Knee: (knee area) at the medial fat pad proximal to the joint line.

Rheumatism, Rheumatic Disease, and Arthritis
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Rheumatism, Rheumatic Disease, and Arthritis...

Are They All the Same?
What Is Rheumatism?

Rheumatism refers to various painful medical conditions which affect bones, joints, muscles, tendons. (see illustration.)

Rheumatism may also involve internal organs including:

The term "rheumatism" is not frequently used in current medical text, but is more often found in historical medical text. Rheumatism does not refer to a single disease or condition. There are over 100 conditions commonly referred to as rheumatism.

Rheumatism has been more specifically classified, based on location and characteristics of symptoms, as:

localized rheumatism (e.g. zSB(3,3)
regional rheumatism (e.g. temporo mandibular joint pain)
generalized rheumatism (e.g. fibromyalgia)
psychogenic rheumatism (e.g. muscle and joint pain expressed is inconsistent with actual physiology and patient is thought to have psychological reasons for the symptoms)

What Are Rheumatic Diseases/Conditions?

Rheumatic diseases and conditions primarily affect joints, tendons, ligaments, bones, and muscles (see illustration).

Joints, particularly hinge joints like the elbow and the knee, are complex structures made up of bone, muscles, synovium and cartilage and ligaments, designed to bear weight and move the body through space. The knee consists of the femur (thigh bone) above, and the tibia (shin bone) and fibula below. The patella, or kneecap rides on top of the lower portion of the femur and the top portion of the tibia. The muscles and ligaments connect these bones and the space between them is cushioned by fluid-filled capsules (synovia) and cartilage. When muscles are exercised, they pull on the bones, strengthening them. The range of motion of a joint represents how far it can be flexed (bent) and extended (stretched).

Rheumatic diseases are characterized by the signs of inflammation - redness, heat, swelling, and pain.
Rheumatic diseases are characterized by loss of function among one or more connective or supportive structures of the body.
Rheumatic diseases can also affect internal organs.

Common Rheumatic Diseases

What Is Arthritis?
Some people use the word arthritis to refer to all rheumatic diseases. Arthritis, which literally means joint inflammation (see illustration of joint), is just part of the rheumatic diseases. Arthritis primarily involves:

joint pain
joint stiffness
joint inflammation
joint damage

Common Types of Arthritis

Conclusion About Rheumatism, Rheumatic Disease, and Arthritis
Rheumatism and rheumatic disease are terms which can be used interchangeably. Rheumatism is recognized as an older term though. The various types of arthritis, however, are just part of the rheumatic diseases.

Treatment
In general, treatment for fibromyalgia includes both medication and self-care. The emphasis is on minimizing symptoms and improving general health.

Medications
Medications can help reduce the pain of fibromyalgia and improve sleep. Common choices include:

Analgesics. Acetaminophen (Tylenol, others) may ease the pain and stiffness caused by fibromyalgia. However, its effectiveness varies. Tramadol (Ultram) is a prescription pain reliever that may be taken with or without acetaminophen. Your doctor may recommend nonsteroidal anti-inflammatory drugs (NSAIDs) — such as aspirin, ibuprofen (Advil, Motrin, others) or naproxen sodium (Anaprox, Aleve) — in conjunction with other medications. NSAIDs haven't proved to be effective in managing the pain in fibromyalgia when taken by themselves.
Antidepressants. Your doctor may prescribe antidepressant medications such as amitriptyline, nortriptyline (Pamelor) or doxepin (Sinequan) to help promote sleep. Fluoxetine (Prozac) in combination with amitriptyline has also been found effective. Sertraline (Zoloft) and paroxetine (Paxil) may help if you're experiencing depression.

Some evidence exists for a newer class of antidepressants known as serotonin and norepinephrine reuptake inhibitors or dual uptake inhibitors, which regulate two brain chemicals that may transmit pain signals. Studies have found that duloxetine (Cymbalta) may help control pain better than placebo in people with fibromyalgia. Small trials of venlafaxine (Effexor) suggest the same, though more study is needed to confirm these findings.

Muscle relaxants. Taking the medication cyclobenzaprine (Flexeril) at bedtime may help treat muscle pain and spasms. Muscle relaxants are generally limited to short-term use.
Anticonvulsants. Drugs approved to treat epilepsy have shown some effectiveness in people with chronic pain. Pregabalin (Lyrica) decreased pain and fatigue and improved sleep in people with fibromyalgia in trials.
Prescription sleeping pills, such as zolpidem (Ambien), may provide short-term benefits for some people with fibromyalgia, but doctors usually advise against long-term use of these drugs. These medications tend to work for only a short time, after which your body becomes resistant to their effects. Ultimately, using sleeping pills tends to create even more sleeping problems in many people.
Benzodiazepines may help relax muscles and promote sleep, but doctors often avoid these drugs in treating fibromyalgia. Benzodiazepines can become habit-forming, and they haven't been shown to provide long-term benefits.
Doctors don't usually recommend narcotics for treating fibromyalgia because of the potential for dependence and addiction. Corticosteroids, such as prednisone, haven't been shown to be effective in treating fibromyalgia.

Cognitive behavior therapy
Cognitive behavior therapy seeks to strengthen your belief in your abilities and teaches you methods for dealing with stressful situations. Therapy is provided through individual counseling, classes, and with tapes, CDs or DVDs, and may help you manage your fibromyalgia.

Treatment programs
Programs that combine a variety of treatments may be effective in improving your symptoms, including relieving pain. These interdisciplinary programs can combine relaxation techniques, biofeedback and receiving information about chronic pain. There isn't one combination that works best for everybody. Your doctor can create a program based on what works best for you.

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This page last updated September 17, 2007

Stomach Virus a Culprit in Chronic Fatigue Syndrome

2006-09-04T11:05:00.000-07:00

http://www.everydayhealth.com/publicsite/ShowArticle.aspx?IsP=news/608/news608181.xml&cen=HC:%20Digestive%20Health
Stomach Virus a Culprit in Chronic Fatigue Syndrome
Published: 09/13/07

THURSDAY, Sept. 13 (HealthDay News) -- A father's concern for his son led to research that now sheds new light on a disease that has long been shrouded in mystery.
Andrew Chia, now 24, was diagnosed with debilitating chronic fatigue syndrome in 1997.
This week he is co-author with his father, Dr. John Chia, of a study which links chronic fatigue syndrome (CFS) with enteroviruses, which cause acute respiratory and gastrointestinal infections.

"This is sort of a new beginning. Now we can have development of antiviral drugs," said the elder Chia, an infectious disease specialist in private practice in Torrance, Calif. "We don't have anything for these poor people, although we've tried a number of things. Now we can study how these viruses behave and how we can kill them."

"Dr. Chia's data was on a substantial number of patients," said Dr. Nancy Klimas, a professor of medicine at the University of Miami Miller School of Medicine and director of the Gulf War Illness Center at the VA Medical Center. "This could send the field in a new direction."

The findings are published in the Sept. 13 online issue of the Journal of Clinical Pathology.
More than 1 million people in the United States are estimated to suffer from CFS, costing the nation some $9 billion annually. The condition is more common in women aged 40 to 60 and is marked by a cluster of debilitating symptoms, including unexplained fatigue, problems sleeping, problems with memory and concentration, and pain. CFS can be as disabling as multiple sclerosis.

The illness was first recognized in the late 1980s and, initially dubbed the "yuppie flu," has suffered from a credibility crisis. The causes of chronic fatigue syndrome (CFS) remain unclear.
Several different viruses, including Epstein-Barr virus, Cytomegalovirus and parvovirus have been implicated, along with enteroviruses. There are more than 70 different types of enteroviruses that can affect the central nervous system, heart and muscles, all of which is consistent with the symptoms of CFS.

It was, however, difficult to find definitive proof of the viruses' presence. "That's how we judge a disease, if it causes organ damage or death, then it's a real disease," Chia said. "But if it doesn't show up, it doesn't mean it's not there."

Chia started on a Herculean task of drawing some 3,000 blood samples from patients, looking for viral genes. Over a period of five to six years, he found evidence of enteroviruses in 35 percent of patients, but this was after multiple samples from each patient. "If we were to take one sample from each patient, it would be less than 5 percent," Chia said. "We realized this wasn't the way to look at it. The assumption we made about CFS that we have to find the virus in their blood is totally wrong, so we started looking for the viruses in tissue, meat."

A team of European investigators had found enteroviruses in the brain, muscle and heart of a CFS patient who had committed suicide. But brain and heart biopsies are virtually impossible to perform in living people.

Chia started looking in the viruses' "area of replication," meaning the stomach. The viruses are resistant to stomach acids.

They eventually took stomach biopsies and performed endoscopies on 165 CFS patients, all of whom had had longstanding gastrointestinal complaints (these are common in CFS patients).
Eighty-two percent of the specimens from CFS patients tested positive for enteroviral particles, compared with just 20 percent of the samples from healthy people. In many patients, the initial infection had taken place years earlier (up to 20 years).

Partly, Chia's work was possible because of technological breakthroughs, Klimas pointed out. He also looked in the right "compartment."

"People were busy looking in the bloodstream, but he looked in the gut. He looked in the right compartment and, lo and behold, he found the viruses," she said. "It depends where you look, what you see."

Chia believes that enteroviruses may cause half of cases of CFS. The disease can also be triggered by other infections.

"It makes sense to me as an infectious disease. This makes all the sense in the world," he said. "If this is a virus, it doesn't destroy the cells, it hides inside the cells. It's one smart little virus."
Chia's son has recovered from the disease although, the elder Chia reported, "he spent a lot of time in the laboratory. Without him, I would not have done this."

More information
For more on chronic fatigue syndrome, visit the CFIDS Association of America.Last reviewed: 09/13/2007 Last updated: 09/13/2007

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