Author: Genisio Marianna
Date: 08/02/2009



Fibromyalgia (FM), meaning muscle and connective tissue pain, is a disorder classified by the presence of chronic widespread pain and a heightened and painful response to gentle touch (tactile allodynia).
Fibromyalgia is seen in about 2% of the general population and affects more females than males, with a ratio of 9:1 by ACR criteria.
It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.
FM involves many more invalidant symptoms than just pain and so is more often called “Fibromyalgia syndrome (FMS)” . Not all affected people experience all the symptoms associated with the greater syndrome.
FMS include:

 Moderate severe fatigue
 Needle-like tingling of the skin
 Muscle aches
 Prolonged muscle spasms
 Weakness in limbs
 Nerve pain
 Sleep disturbances, that may be related to a phenomenon called alpha-delta sleep, a condition in which deep sleep (associated with delta waves) is frequently interrupted by bursts of alpha waves, which normally occur during wakefulness. Slow-wave sleep is often dramatically reduced).
 Typical areas of localized pain:
 Shoulders
 Neck
 Low back
 Hips
 Face
 Temporomandibular jointer
 Cognitive dysfunction ( known as “brain fog” or “fibrofog”, probably related to the sleep disturbances), which may be characterized by:
 Impaired concentration
 Problem with short and long –term memory
 Impaired speed of performance
 Anxiety
 Depressive symptoms
 Eye problems, such as:
 Eye pain
 Sensitivity to light
 Blurred vision

Other symptoms often attributed to FM that may possible due to a comorbid disorder include:

 Myofascial pain syndrome
 Diffuse non dermatomal paresthesias
 Functional bowel disturbances and irritable bowel syndrome
 Genitourinary symptoms and cystitis
 Dermatological disorder
 Headaches
 Myoclonic twitches
 Symptomatic hypoglycaemia
The diagnosis of FM is often difficult because, in most cases, laboratory testing appears normal and many of the symptoms mimic those of other rheumatic conditions such as arthritis or osteoporosis.
In general, most doctors diagnose patients with a process called differential diagnosis.

The most widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the the American College of Rheumatology (“the ACR 1990”).
These criteria include:

 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). The patient must feel pain at the pressure of 11 or more of these points for fibromyalgia to be considered.
The cause of FM is currently unknown but is certainly multifactorial.
Several hypotheses have been developed:
1. Genetic predisposition:
The genetic factors plays a role in the development of FM, demonstrated by high aggregation of FM in families.
The mode of inheritance is most probably polygenic.
Research has demonstrated that patients affected by FM can show a particular COMT gene haplotype, associated with a faulty cathecolamine-clearing enzyme , a consequent hyperadrenergic state and a more pain sensitivity.

Furthermore, FM is common in autoimmune diseases and there is some evidence for immunological aberrations in FM.
2. Environmental factors:
A number of triggers are temporally associated with the development of FM, including physical trauma, emotional stress and certain infections (HCV, HIV, Borrelliosis).
The mechanism with which these factors act is in dorsal root ganglia sodium channels (DRG).
Dorsal root ganglia are potential sympathetic-nociceptor short-circuit sites.
Sodium channels, in particular an isoform encoded in gene SCN9A of chromosome 2q24.3, located in DRG, acts as molecular gatekeepers of pain detection, at peripheral nociceptors.
Several cytokine, including nerv growth factor (NGF), are able to up-regulate this sodium channel; individuals at high risk of developing FM would be those with a genetically determined sympathetic-hyperactivity due to faulty COMT enzymes.
Trauma, stress, infection or SCN9A mutation may trigger sympathetic sprouting in DRG through NGF over-espression and this may facilitate nociceptive signals.


The same environmental stressors can act with another mechanism , determining a disorder called Central dopamine dysfunction, characterized by low levels of central dopamine.
Dopamine is a catecholamine neurotransmitter that plays a critical role in pain perception and natural analgesia

Furthermore, the environmental factors can cause sleep disturbances and possibly initial chronic pain that may initiate the disorder.
In particular they could interfere with stage IV of sleep, that is critical to the function of SNC; during this stage certain neurochemical processes in the body “reset”.
3. Altered coenzyme Q10 distribution in blood:
CoQ10 plays a crucial role in cellular metabolism, acting as the electron carrier of the mitochondrial respiratory chain and is a major antioxidant factor , with α-tocopherol, in plasma and prevent oxidative damage.
In FM, the muscles present different abnormalities such as higher plasma levels of coenzyme Q10 (CoQ10) , but a decreased levels of CoQ10 in blood mononuclear, indicating a dysfunction of CoQ10 distribution in the blood of FM patients, resulting in increased ROS production.
The oxidative stress could be the cause of the abnormality in muscle pain, characterized by disorganization of Z bands, altered number shape of mitochondria and altered of ATP and phosphocreatine levels.
Interestingly, patients with CoQ10 deficiency display improvement of symptoms, sometimes dramatic, after oral CoQ10 supplementation.
4. Abnormal serotonin metabolism:
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.
A dysregulation of serotonin metabolism could be explain in part many of the symptoms of FM.
This hypothesis is supported by the observation of decreased serotonin metabolites in patient plasma and cerebrospinal fluid.


Long-chain polyunsaturated fatty acids and the pathophysiology of myalgic encephalomyelitis (chronic fatigue syndrome). 2006

Evidence is put forward to suggest that myalgic encephalomyelitis, also known as chronic fatigue syndrome, may be associated with persistent viral infection. In turn, such infections are likely to impair the ability of the body to biosynthesize n-3 and n-6 long-chain polyunsaturated fatty acids by inhibiting the delta-6 desaturation of the precursor essential fatty acids alpha-linolenic acid and linoleic acid. In turn, this would impair the proper functioning of cell membranes, including cell signalling, and have an adverse effect of the biosynthesis of eicosanoids from the long-chain polyunsaturated fatty acids dihomo-a-linolenic acid, arachidonic acid and eicosapentaenoic acid. These actions might offer an explanation for some of the symptoms and signs of myalgic encephalomyelitis. A potential therapeutic avenue may be offered by bypassing the inhibition of the enzyme delta-6-desaturase by administering both virgin cold-pressed non-raffinated evening primrose oil and eicosapentaenoic acid. The former would supply gamma-linolenic acid and lipophilic pentacyclic triterpenes. The gamma-linolenic acid can readily be converted into dihomo-a-linolenic acid and thence arachidonic acid, while triterpenes have important free radical scavenging, cyclooxygenase and neutrophil elastase inhibitory activities. Furthermore, both arachidonic acid and eicosapentaenoic acid are, at relatively low concentrations, directly virucidal.

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