Diagnostics up to date
The fibromyalgia syndrome is a symptom complex with the property of an exclusion diagnosis. Somatically largely inexplicable pain is often accompanied by vegetative complaints such as tiredness and other general unspecific body symptoms. The following presents the current diagnostic criteria.
The pain in fibromyalgia syndrome are typically located by the affected in many (even changing) body parts, preferably musculature and tendon-bone transitions. They are accompanied by more or less pronounced social and psychological disabilities and, characteristically, psychophysical symptoms such as tiredness, depression and insomnia. The importance of these “accompanying phenomena” is now more fully reflected in the updated ACR criteria (American College of Rheumatology) of 2010 . The leading symptom of fibromyalgia, namely the (un) typical pain manifestation as large-scale pain, is now presented as a number from 19 defined affected body regions (Widespread Pain Index, WIP). Closely related to this are other important and characteristic symptoms, which are measured on a symptom severity scale (SS). This includes fatigue, unawakened awakenings, cognitive disorders, and somatic general symptoms (see Table 1).
Symptom constellations are weighted more heavily
Compared to the “old” diagnostic criteria of the 1990 ACR , it is no longer compulsory to require a widespread pain in at least three out of four body quadrants over three months plus pain in the axial skeleton (cervical, lumbar, thoracic) plus eleven out of 18 defined tender points painful to pressure of 4 kg must be present. Rather, regional pain syndromes can now meet the criteria if the extent of characteristic accompanying symptoms is correspondingly impressive. Conspicuous radiological or laboratory findings do not rule out fibromyalgia syndrome.
According to the new diagnostic criteria, the fibromyalgia syndrome is therefore defined by extensive pain in at least one body quadrant / body side and additionally in one or more areas of the axial skeleton (WS rib cage). The most significant change is the increased weighting of the characteristic symptom constellation of tendon muscle pain with non-restorative sleep, fatigue, and impaired cognitive function in combination with additional symptoms over the previous week’s assessment period. The number of defined "tender Points" is therefore no longer a central criterion, because their qualifiability and quantifiability were apparently too much investigator-dependent. The most important criterion, however, is still that no specific medical cause can be found for the pain complained that could explain the complaints.
A WPI >7 and SS >5 or a WPI 3 – 6 and SS >9 are considered to be highly significant suspects of fibromyalgia. The further pain analysis, anamnesis and physical examination then confirms the diagnosis.
It certainly remains to be seen whether these new criteria in their broad practical application will meet their own requirements for high specificity and sensitivity. In any case, the revised version of the Guideline of the German Interdisciplinary Association for Pain Therapy (DIVS) “Fibromyalgia, Diagnosis and Therapy”, recommended in 2012, advises against using the new ACR criteria and instead recommends remaining with the old criteria (see illustration on next page)..
Differential diagnosis and further medical clarification
Patients with fibromyalgia syndrome should first be examined for inflammatory diseases, especially those of the rheumatic type, as such diseases may cause similar symptoms or may be associated with a fibromyalgia syndrome (RA, polymyalgia rheumatica, systemic lupus erythematosus). Endocrine disorders that can cause muscle and joint pain (hypothyroidism, hyperparathyroidism and Addison’s disease) should also be investigated. In addition to the history and clinical findings, a routine laboratory should be included, which should include the erythrocyte sedimentation reaction, rheumatoid factor, creatine kinase and CRP / CCP / ANA, as well as differential blood counts, thyroid scores and serum iron transferrin. According to the latest findings, almost half of the fibromyalgia patients appear to respond positively to anti-polymer antibodies in the screening test . This may be the result of specific therapeutic approaches.
In addition, the definition of subgroups is discussed on the basis of symptom severity [5, 6, 7]. By the differential weighting of physical and psychological symptoms one wants to come to efficient therapeutic approaches. Special emphasis is placed on the psychological (co-) morbidities in fibromyalgia, the presence of which indicates drug and / or behavioral therapeutic approaches, depending on their severity. Whether it is actually subgroups can be sharply demarcated, however, is less crucial. The importance, however, seems to be in the special rating of the leading symptoms for the respective individualized mechanism-oriented therapy . However, the special medical history with the help of questionnaire inventories (eg German Pain Questionnaire and the new ACR criteria 2010) should be made much easier.
Fibromyalgia as a central sensitization syndrome
Fibromyalgia is a syndrome that is becoming ever more common in the daily routine of treatment, and is becoming increasingly important from a socio-legal point of view in that sufferers often suffer from severe disabling symptoms but are not acknowledged.
In the absence of objective findings, too many physicians still find it difficult to accept that there may still be a subjective impairment. Perhaps this would be easier if one followed the aetiological classifications of recent research. After that, the most obvious explanation is where pain is transmitted and processed: in the central nervous system. According to Smith, fibromyalgia is primarily a processing disorder of the pain affection. He classifies fibromyalgia as a central sensitization syndrome (CSS) .
In the biopsychosocial model of pain, there are specific indications of biological and psychosocial contexts, which increasingly explain the typical clinical picture of fibromyalgia syndrome, especially in its phenomenological colourfulness. But none of these variables, whether biological or psychosocial, can yet be held to be the sole condition responsible for the onset or maintenance of the fibromyalgia syndrome. In the overall view, however, the connections become much clearer. Basic research and clinical studies show: there is apparently
- sensitization and plasticity of central NMDA receptors (which also play an important role in opioid-associated hyperalgesia),
- a dysregulation of cortical dopaminergic neurotransmission,
- a decrease in the central nervous serotonin level and an increase in the substance P concentration,
- a hypothalamic-pituitary-adrenocortical axis disorder characterized by altered levels of cortisone, ACTH, growth hormone, and IGF-1,
- a massive disturbance of deep sleep phases associated with the aforementioned humoral alterations,
- a genetic disposition, z. For example, in fibromyalgia subgroups proven for the serotonin transporter gene, the catecholamine methyltransferase gene, the expression of beta-2 adrenoceptors,
- a hitherto barely specified influence of sex hormones, which might explain why fibromyalgia affects predominantly the female sex.
Thus, the main symptoms of the fibromyalgia syndrome move into a new (explainable) light: neuroendocrine and neuroimmunological functional disorders are becoming more and more prominent as drivers and markers of the central sensitization of pro-algesic pain perception.
If the actual pain-triggering factors are to be found in the neuro-immuno-humoral system, this at least theoretically results in therapeutic approaches that could have a chance of success. You will not be able to change a genetic disposition. However, one can certainly attack the psychosocial stressors and the stress response, the neurotransmitter systems as well as deconditioning regarding pain experience and attention control.
Multimodal strategies that combine medical treatment and psychotherapeutic interventions with educational elements and athletic rehabilitation are consequently the leading therapeutic approach in the literature . Monotherapy of any kind, however, are clearly inferior and probably even promote the chronification.
The first important option in patients with suspected or diagnosed fibromyalgia syndrome is to avoid what these patients all too often expect, namely incomprehension. Equally ineffective are remarks like “it all just happens in your head” or “you probably have a mental health problem”. It is important to pick up the patient where he stands: pain-stricken and with little plan, why.
The second important option is to seriously consider the importance and potential treatability of psychosocial implications and interweave them into the therapeutic concept. With high activity of tender points and high levels of pain without significantly predominant depression / anxiety psychotherapy makes little sense. This is where somatic therapies are needed. These may consist in education, physiotherapy and activation, eg. As a training program, in which one must often ensure the feasibility even by specific pain-medical measures (acupuncture, medication, etc.). On the other hand, leading behavioral / psychological co-morbidities require the primary therapeutic approaches.
The differential indication of therapeutic treatment plans and therapy settings thus essentially requires a pain analysis that largely evaluates all facets of chronic pain patients (eg German Pain Questionnaire). Because only on the basis of the evaluation of these data is an overall view of the severity of pain with regard to possible therapeutic options meaningful. Especially as minor episodes of paraplegia, such as lack of sleep and daytime fatigue, play a prominent role especially in fibromyalgia patients. In addition to depression and anxiety, they are the very first therapy address . The latter are “aggressive” to treat. If you get the depression and anxiety not sufficiently under control, all other therapeutic approaches are little or not promising. Behavior therapy strategies are able to significantly improve the symptoms of almost every second patient . On the other hand, antidepressant therapy alone does not cure fibromyalgia.
The drug therapy in fibromyalgia at most a (small) part of the therapeutic options. The evidence for the efficacy of antidepressant medications, such as tricyclics (e.g., amitriptyline), selective serotonin reuptake inhibitors (eg, citalopram), and mixed serotonin / norepinephrine reuptake inhibitors (eg, duloxetine), is now sufficient. These medications can also reduce pain, as well as relieve disturbed sleep . Here is a practical note: “Start low and go slow”. Nevertheless, if tricyclics are poorly tolerated, which is not at all uncommon, certain anticonvulsants such as gabapentin, clonazepam and non-benzodiazepine hypnotics (eg zolpidem) are an alternative. Their sometimes higher habituation potential, however, is noteworthy. An American guideline even recommends the combination of zolpidem / zopiclone and zaleplon (Sonata®) in severe cases of insomnia, d. H. so-called “Z-substances” .
Genuine anti-inflammatory drugs, such as NSAIDs and corticosteroids, are useful only when there is significant inflammation. The potential risks (cardiovascular, gastrointestinal, renal) usually exceed the expected benefits here.
Muscle relaxants are also rarely indicated, for example, when the leading finding is an increased, peripherally detectable tender and trigger activity. As a rule, however, fibromyalgia patients do not have a morbid muscle finding, which then makes the use of muscle relaxants theoretically and practically very questionable. Moreover, none of these preparations has been able to provide convincing proof of efficacy.
The use of opioids also lacks a usable study situation. Only tramadol, a weak μ-opioid receptor agonist with additional effects on serotonin and norepinephrine receptors, is described as being positive for pain in fibromyalgia. Although other opioids are often used because of severe pain, they are theoretically of less benefit because of the reduced opioid receptor density in fibromyalgia patients.
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