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The Tender Point Test for healthcare professionals

Fri, 30 May 2008 12:00:00 +0100

The Tender Point test is the only test for Fibromyalgia Syndrome (as opposed to for excluding differential diagnoses) that is routinely carried out in the clinical setting. However little or no training in performing the test is often given and variations in carrying it out impact heavily on its effectiveness as a diagnostic tool.

It should be noted that the choice of 11 out of the standard 18 tender points as a diagnostic for Fibromyalgia Syndrome was originally devised as an inclusion test for research and that 11 is an arbitary number. Examiners should also take into account that tender point test scores are typically lower in men than in women. [1]

According to the 1990 ACR Criteria for the Classification of Fibromyalgia, "digital palpation should be performed [on the standard tender point sites] with an approximate force of 4 kg. For a tender point to be considered "positive" the subject must state that the palpation was painful. "Tender is not to be considered "painful." [2]

The thumb pad of the examiner's dominant hand can be used to apply pressure to the evaluation sites during the tender-point examination. This allows the examiner to detect important tactile cues, such as the existence of myofascial trigger points around a tender point site which can lead to a false positive.

There are some common sense guidelines, based on the requirements of the ACR Criteria, for conducting a tender point examination, including:

Taking into account that the patient's position during examination, the amount of force applied at the evaluation site, the number of times the evaluation site is palpated, and the method of applying force (instrument vs finger pad) may influence tender-point sensitivity.
Ensuring that they (the examiner) know how to recognise myofascial trigger points so as to differentiate between these and tender points. The most obvious signs are that a myofascial trigger point, unlike a tender point, will likely feel like a knot in the muscle and should refer pain or other symptoms elsewhere.
Telling the patient before beginning the examination that they need to respond to each tender point examination. The patient should respond with a “yes” or “no” if they have any pain at the site being examined. If the patient's response is “yes,” the examiner should ideally get them to rate the pain on a scale of 0 (no pain) to 10 (worst pain), and record each response.
Only palpating each tender point once. It will be easier for the examiner if the patient is in a standard, easy access hospital gown and is in a comfortable position, either sitting or lying down. The examiner should locate the tender point position visually before applying any pressure and should then apply a force equivalent to 4kg, which should be sufficient to blanch the nail bed of the thumb used. The tender point should be palpated for long enough for the patient to respond: some doctors recommend a constant palpation for 4 seconds.
There are control sites that can be palpated and recorded to provide baseline documentation of the patient's pain perception. These sites should be less painful and include the nail of the thumbs and the forehead.

The 1990 ACR criteria for the location of tender points are as follows:

Occiput: Bilateral, at the suboccipital muscle insertions.
Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7.
Trapezius: bilateral, at the midpoint of the upper border.
Supraspinatus: bilateral, at origins, above the scapula spine near the medial border.
Second rib: bilateral, at the second costochondral junctions, just lateral to the junctions on upper surfaces.
Lateral epicondyle: bilateral, 2 cm distal to the epicondyles.
Gluteal: bilateral, in upper outer quadrants of buttocks in anterior fold of muscle.
Greater trochanter: bilateral, posterior to the trochanteric prominence.
Knee: bilateral, at the medial fat pad proximal to the joint line.

References:

Clauw, DJ. Fibromyalgia: Update on Mechanisms and Management. Journal of Clinical Rheumatology: Volume 13(2)April 2007pp 102-109.
Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicenter criteria committee. Arthritis Rheum 1990;33:160---72.

EULAR Guidelines for Fibromyalgia

Sun, 08 Jun 2008 12:00:00 +0100

In July 2007, the European League Against Rheumatism (EULAR) published the first set of evidence based recommendations for the management of Fibromyalgia Syndrome. E-published in July 2007, the article describing the development of these recommendations then appeared in the April 2008 edition of the Annals of the Rheumatic Diseases.

With the objective of developing evidence-based recommendations for the management of Fibromyalgia Syndrome, a multidisciplinary task force was formed representing 11 European countries. The researchers, including a number of Britons, said that:

"Although effective treatments are available no guidelines exist for management of [Fibromyalgia Syndrome]"

The task force carried out a systematic review of the literature with the keywords "fibromyalgia", "treatment or management" and "trial". Studies were excluded from consideration if they did not use the American College of Rheumatology (ACR) criteria for the classification of Fibromyalgia Syndrome, were not clinical trials, or included patients with chronic fatigue syndrome or myalgic encephalomyelitis. The primary outcome measures looked for were change in pain assessed by visual analogue scale and fibromyalgia impact questionnaire. The task force categorised the quality of the studies based on randomisation, blinding and allocation concealment and only the highest quality studies were used to base recommendations on.

One hundred and forty-six studies were found to be eligible for the review and 39 pharmacological intervention studies and 59 non-pharmacological were included for the final recommendations after those of a lower quality or with insufficient data were separated.

Identified categories of treatment were antidepressants, analgesics, and "other pharmacological" and exercise, cognitive behavioural therapy, education, dietary interventions and "other non-pharmacological". Nine recommendations for the management of fibromyalgia syndrome were developed using a systematic review and expert consensus. However, in many studies the sample size was small and the quality of the study was insufficient for strong recommendations to be made. EULAR intends to update the recommendations every 5 years, incorporating findings from good-quality clinical trials that will add to the currently available evidence.

The task force said in summary that:

"These recommendations are the first to be commissioned for FMS, although previous reviews have addressed the area ... [they] should assist health care providers, with asecondary intention to incorporate information into materials for patients."

Specific recommendations in these guidelines regarding general considerations for management of FMS are as follows:

Comprehensive evaluation of pain, function, and psychosocial context is needed to understand FMS completely, because it is a complex, heterogeneous condition involving abnormal pain processing and other secondary features (level of evidence, IV D).

Optimal treatment of FMS mandates a multidisciplinary approach, which should include a combination of nonpharmacologic and pharmacologic interventions. After discussion with the patient, treatment modalities should be specifically tailored based on pain intensity, function, and associated features such as depression, fatigue, and sleep disturbance (level of evidence, IV D).

Specific recommendations on nonpharmacologic management of FMS are as follows:

Heated pool treatment, with or without exercise, is effective (level of evidence, IIa B).

For some patients with FMS, individually tailored exercise programs can be helpful. These may include aerobic exercise and strength training (level of evidence, IIb C).

For certain patients with FMS, cognitive behavioral therapy may be beneficial (level of evidence,IV D).

Based on the specific needs of the patient, relaxation, rehabilitation, physiotherapy, psychological support, and other modalities may be indicated (level of evidence, IIb C).

Specific recommendations on pharmacologic management are as follows:

Tramadol is recommended for management of pain (level of evidence, Ib A). Although other treatment options may include simple analgesics (eg, paracetamol) and other weak opioids, corticosteroids and strong opioids are not recommended (level of evidence, IV D).

Antidepressants are recommended for the treatment of FMS because they decrease pain and often improve function (level of evidence, Ib A). Appropriate options may include amitriptyline, fluoxetine, duloxetine, milnacipran, moclobemide, and pirlindole.

Tropisetron, pramipexole, and pregabalin are recommended for the treatment of FMS because they reduce pain (level of evidence, Ib A).

The limits of the recommendations include the small size of some studies and the use of other outcome measures in studies meaning that they were excluded from consideration. The assessment of strength of evidence tends to favour pharmacological studies as double blinding and placebo controls are impossible in many non-pharmacological studies. However, most non-pharmacological interventions are safe and have other health benefits and these important factors were taken into account. In some areas evidence was lacking due to the poor quality of the studies and expert opinion had to be used as a factor.

Reference: Carville SF, Arendt-Nielsen S, Bliddal H, Blotman F, Branco JC, Buskila D, Da Silva JA, Danneskiold-Samsøe B, Dincer F, Henriksson C, Henriksson KG, Kosek E, Longley K, McCarthy GM, Perrot S, Puszczewicz M, Sarzi-Puttini P, Silman A, Späth M, Choy EH; EULAR. EULAR evidence-based recommendations for the management of fibromyalgia syndrome. Ann Rheum Dis. 2008 Apr;67(4):536-41. Epub 2007 Jul 20.

Fibromyalgia Syndrome as a CNS Disorder

Tue, 30 Sep 2008 12:00:00 +0100

Fibromyalgia Syndrome has traditionally been classified as either a musculoskeletal disease or a psychological disorder. Accumulating evidence now suggests that fibromyalgia may be associated with CNS dysfunction. [1]

Here, we have collected some of the research from 2007 and 2008 that supports this view.

Accelerated brain gray matter loss in Fibromyalgia Syndrome patients [1]

In this study, anatomical changes in the brain associated with Fibromyalgia Syndrome were investigated. Using voxel-based morphometric analysis of magnetic resonance brain images, the brains of 10 female Fibromyalgia Syndrome patients and 10 healthy controls were examined.

It was found that Fibromyalgia Syndrome patients had significantly less total gray matter volume and showed a 3.3 times greater age-associated decrease in gray matter than healthy controls. The longer the individuals had had Fibromyalgia Syndrome, the greater the gray matter loss, with each year of Fibromyalgia Syndrome being equivalent to 9.5 times the loss in normal aging. In addition, Fibromyalgia Syndrome patients demonstrated significantly less gray matter density than healthy controls in several brain regions, including the cingulate, insular and medial frontal cortices, and parahippocampal gyri.

The neuroanatomical changes seen in Fibromyalgia Syndrome patients contribute additional evidence of CNS involvement in Fibromyalgia Syndrome. In particular, Fibromyalgia Syndrome appears to be associated with an acceleration of age-related changes in the very substance of the brain. Moreover, the regions in which objective changes are demonstrated may be functionally linked to core features of the disorder including affective disturbances and chronic widespread pain.

Reduced presynaptic dopamine activity in Fibromyalgia Syndrome [2]

For this pilot study, presynaptic dopaminergic function was investigated in 6 female Fibromyalgia Syndrome patients in comparison to 8 age- and gender-matched controls as assessed by positron emission tomography with 6-[(18)F]fluoro-L-DOPA as a tracer.

Semiquantitative analysis revealed reductions in 6-[(18)F]fluoro-L-DOPA uptake in several brain regions, indicating a disruption of presynaptic dopamine activity wherein dopamine plays a putative role in natural analgesia.

Although the small sample size made these findings preliminary, they showed that Fibromyalgia Syndrome might be characterized by a disruption of dopaminergic neurotransmission.

Abnormal dopamine response to pain [3]

Fibromyalgia Syndrome patients and matched healthy control subjects were subjected to deep muscle pain produced by injection of hypertonic saline into the anterior tibialis muscle. In order to determine the endogenous release of dopamine in response to painful stimulation, positron emission tomography was used to examine binding of [(11)C]-raclopride (D2/D3 ligand) in the brain during injection of painful hypertonic saline and nonpainful normal saline.

Fibromyalgia Syndrome patients experienced the hypertonic saline as more painful than healthy control subjects. Control subjects released dopamine in the basal ganglia during the painful stimulation, whereas Fibromyalgia Syndrome patients did not. In control subjects, the amount of dopamine release correlated with the amount of perceived pain but in Fibromyalgia Syndrome patients no such correlation was observed.

These findings provided the first direct evidence that Fibromyalgia Syndrome patients have an abnormal dopamine response to pain.

The disrupted dopaminergic reactivity in Fibromyalgia Syndrome patients could be a critical factor underlying the widespread pain and discomfort in Fibromyalgia Syndrome and suggests that the therapeutic effects of dopaminergic treatments for this intractable disorder should be explored.

Proton MR spectroscopy in the evaluation of cerebral metabolism in patients with Fibromyalgia Syndrome [4]

For this study, 21 patients with Fibromyalgia Syndrome and 27 healthy controls underwent conventional structural MR imaging and additional 2D-chemical shift imaging (CSI) MR-spectroscopy sequences.

For the 2D-CSI spectroscopy, larger volumes of interest (VOIs) were centered at the level of the basal ganglia and the supraventricular white matter. Within these larger areas, 16 smaller voxels were placed in a number of regions previously implicated in pain processing. N-acetylaspartate (NAA)/creatine(Cr), choline (Cho)/Cr and NAA/Cho ratios were calculated for each voxel. Subjects underwent clinical and experimental pain assessment.

Mean metabolite ratios and ratio variability for each region were analyzed by using repeated-measures analysis of variance (ANOVA). Correlations between clinical symptoms and metabolite ratios were assessed.

Cho/Cr variability in the right dorsolateral prefrontal cortex was significantly different in the 2 groups; a significant correlation between Cho/Cr in this location and clinical pain was present in the Fibromyalgia Syndrome group. Evoked pain threshold correlated significantly with NAA/Cho ratios in the left insula and left basal ganglia.

The data suggests that there are baseline differences in the variability of brain metabolite relative concentrations between patients with Fibromyalgia Syndrome and healthy controls, especially in the right dorsolateral prefrontal cortex. Furthermore, there are significant correlations between metabolite ratios and clinical and experimental pain parameters in patients with Fibromyalgia Syndrome.

Hippocampus dysfunction may explain symptoms of Fibromyalgia Syndrome [5]

The case-control study was performed in 15 female patients, who met American College of Rheumatology criteria for classification of Fibromyalgia Syndrome, and 10 healthy age-matched female controls. Patients and controls were receiving no medications known to affect cognitive functioning or central nervous system metabolites before their participation in the study.

In all patients and controls, proton magnetic resonance spectroscopy (1H-MRS) was used to assess N-acetylaspartate (NAA), choline (Cho), creatine (Cr), and their ratios from both hippocampi. Levels of metabolites and their ratios were determined and the findings compared between the groups. All patients and controls underwent psychological assessment to assess cognitive function, depression, and structured sleep interview with sleep diary; Fibromyalgia Impact Questionnaire (FIQ), number of tender points, and visual analog scale (VAS) for pain were assessed in all patients.

NAA levels of right and left hippocampi differed significantly between patients and controls. Cho levels in the right hippocampus were higher in the patient group than in controls, while no differences were found with respect to Cr levels in both hippocampi. NAA/Cho and NAA/Cr ratios differed significantly between patients and controls, while the Cho/Cr ratio showed no differences.

Significant correlations were found between language score and right Cho and right Cr levels, while no significant correlations were found between metabolites and their ratios with FIQ, VAS for pain, or number of tender points.

The hippocampus was dysfunctional in patients with Fibromyalgia Syndrome, as shown by lower NAA levels compared to controls, representing neuronal or axonal metabolic dysfunction. As the hippocampus plays crucial roles in maintenance of cognitive functions, sleep regulation, and pain perception, it was suggested that metabolic dysfunction of hippocampus may be implicated in the appearance of these symptoms in Fibromyalgia Syndrome.

Hippocampal Metabolite Abnormalities in Fibromyalgia Syndrome [6]

In this study, researchers interrogated the bilateral hippocampus of 16 premenopausal female Fibromyalgia Syndrome patients with no psychiatric comorbidity in comparison to 8 age- and gender-matched healthy control subjects using single voxel proton magnetic resonance spectroscopy.

The results demonstrate a significant reduction in the ratio of N-acetylaspartate to creatine (NAA/Cr) in Fibromyalgia Syndrome patients versus matched control subjects specifically in the right temporal lobe from a voxel centered on the right hippocampus. Moreover, correlation analysis demonstrated a significant negative correlation between patient scores on the Fibromyalgia Impact Questionnaire and NAA/Cr ratio within the right hippocampus.

The results indicate that Fibromyalgia Syndrome is associated with brain metabolite abnormalities within the right hippocampus that correlate with patient symptoms. A significant negative correlation between patient subjective experience of symptoms and a reduced NAA/Cr ratio suggests a role for hippocampal pathology in Fibromyalgia Syndrome.

References:

Kuchinad A, Schweinhardt P, Seminowicz DA, Wood PB, Chizh BA, Bushnell MC. Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain? J Neurosci. 2007 Apr 11;27(15):4004-7.
Wood PB, Patterson JC 2nd, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL. Reduced presynaptic dopamine activity in fibromyalgia syndrome demonstrated with positron emission tomography: a pilot study. J Pain. 2007 Jan;8(1):51-8. Epub 2006 Oct 4.
Wood PB, Schweinhardt P, Jaeger E, Dagher A, Hakyemez H, Rabiner EA, Bushnell MC, Chizh BA. Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 2007 Jun;25(12):3576-82.
Petrou M, Harris RE, Foerster BR, McLean SA, Sen A, Clauw DJ, Sundgren PC. Proton MR spectroscopy in the evaluation of cerebral metabolism in patients with fibromyalgia: comparison with healthy controls and correlation with symptom severity. AJNR Am J Neuroradiol. 2008 May;29(5):913-8. Epub 2008 Mar 13.
Emad Y, Ragab Y, Zeinhom F, El-Khouly G, Abou-Zeid A, Rasker JJ. Hippocampus dysfunction may explain symptoms of fibromyalgia syndrome. A study with single-voxel magnetic resonance spectroscopy. J Rheumatol. 2008 Jul;35(7):1371-7. Epub 2008 May 15.
Wood PB, Ledbetter CR, Glabus Deceased MF, Broadwell LK, Patterson JC 2nd. Hippocampal Metabolite Abnormalities in Fibromyalgia: Correlation With Clinical Features. J Pain. 2008 Sep 2. [Epub ahead of print]

Five Differential Diagnoses to Fibromyalgia Syndrome

Tue, 15 Dec 2009 12:00:00 +0000

Diagnosing Fibromyalgia Syndrome can be a complicated and protracted process. Tests that have shown abnormalities related to the condition in research are often not clinically available. A diagnosing physician has to rely on patient history, exclusion of differential diagnoses and the tender point examination to check for the widespread hyperalgesia characteristic of Fibromyalgia Syndrome.

There are a huge number of potential diferential diagnoses to Fibromyalgia Syndrome. Mis-diagnoses either way do occur and often patients need to re-assessed at a later stage.

Here are five differential diagnoses to Fibromyalgia Syndrome that may not have been fully investigated:

1. Sero-negative Systemic Lupus Erythematosus (SLE or Lupus) or other inflammatory conditions

Lupus patients can have a wide variety of symptoms and severity of symptoms, and may present with similar symptoms to Fibromyalgia Syndrome. No single test establishes the diagnosis of systemic lupus - 11 diagnostic criteria were established by the American Rheumatism Association, with 4 out of 11 strongly suggesting a diagnosis of SLE.

A positive antinuclear antibody test is only one of the possible criteria, with blood tests totalling 3 of the 11 possible criteria. Some patients suspected of having SLE may never develop enough criteria for a definite diagnosis and other patients accumulate enough criteria only after months or years of observation. Patients with SLE also often go on to develop Fibromyalgia Syndrome. It is therefore very important to consider more than just blood test results when considering whether a patient has Fibromyalgia Syndrome, an inflammatory connective tissue disorder or both conditions and to revisit the possibility in light of new or worsening symptoms.

Fibromyalgia Syndrome is not associated with elevated levels of ANA, RF, ESR or CRP. Nor is it commonly associated with significant swelling of joints. However, it is not uncommon for these findings to be dismissed if a diagnosis of Fibromyalgia Syndrome has already been made. A patient responding especially well to NSAIDs or steroids is another sign of an underlying inflammatory condition and should be fully investigated.

2. Myofascial Pain Syndrome

Myofascial Pain Syndrome is a relatively newly understood diagnosis, with much of the seminal work into this condition having been done by the American physicians Travell & Simons in the second half of the 20th century. Little training is given on the diagnosis and treatment of this condition, despite myofascial pain problems being widespread amongst the general population. With Fibromyalgia Syndrome, the situation is particularly complicated as patients with Fibromyalgia Syndrome often also have comorbid Myofascial Pain Syndrome. However, Myofascial Pain Syndrome requires a different treatment approach to Fibromyalgia Syndrome and can occur without Fibromyalgia Syndrome.

Signs that a patient may have Myofascial Pain Syndrome, whether or not they also have Fibromyalgia Syndrome, include: tight, "knotty" or hard muscles, which can easily be assessed through physical examination; referred pain or other symptoms, such as headaches, from areas of restrictions - this can manifest as neuropathic-type pain, recurrent or intractable headaches or migraine and even nausea; unusually fast build-up of lactic acid in the muscles upon slight exertion - often a particular problem in the legs; and restricted movement or stiffness, particularly after inactivity.

Some physiotherapists and a few consultants have done some post-graduate training in the diagnosis and treatment of Myofascial Pain. Treatment options include injections (often lidocaine, but saline & botox have also been used), muscle relaxants and physiotherapy, especially to help correct underlying postural problems and to peform direct trigger point release. However, the most effective treatment is often a course of myofascial release therapy and this is usually only available from private, specially trained massage therapists.

For more information, see the articles Tender points Trigger points and Pressure points and The Tender Point Test for healthcare professionals.

3. Vitamin D deficiency

Vitamin D deficiency is common in the UK and much of the Western World. As well as causing osteomalacia, vitamin D deficiency can cause symptoms of fatigue, muscle aches & pain, muscle weakness and bone pain. These symptoms can be mistaken for those of Fibromyalgia Syndrome, so vitamin D deficiency needs to be considered both as a possible differential diagnosis to Fibromyalgia Syndrome and as a comorbid condition that can seem to worsen the symptoms of Fibromyalgia Syndrome. Pregnant or breastfeeding women, and children, need extra vitamin D as it required for growth, so particular care should be taken to check for vitamin D deficiency in Fibromyalgia Syndrome patients who become pregnant, as they may not recognise the symptoms as being something other than their Fibromyalgia Syndrome.

Vitamin D deficiency can be checked for in a simple blood test and basic supplementation can help many patients, although some may require high doses by injection. One factor to consider, especially when supplementing vitamin D in patients with Fibromyalgia Syndrome or Irritable Bowel Syndrome, is that many of the more easily available supplements come as chewable tablets containing artifical sweeteners, which can cause diarrhoea & nausea in some patients, reducing both patient compliance and the absorption of the supplements.

For more information on vitamin D deficiency, see the patient.co.uk website here.

4. Magnesium deficiency

Magnesium is needed in the body for the correct function of the muscles and nervous system. Although a true, severe magnesium deficiency is rare, a relatively minor deficiency could impact on someone with Fibromyalgia Syndrome. Early symptoms of magnesium deficiency can include fatigue, muscle cramps & twitching, insomnia and cognitive dysfunction. Later symptoms may include continued muscle contraction, numbness, tingling and hallucinations.

Patients with Fibromyalgia Syndrome may struggle to eat a balanced diet if they are severely affected and aren't getting the help they need at home. They may also have problems with malabsorption through Irritable Bowel Syndrome or food intolerances causing chronic diarrhoea. This can lead to magnesium deficiency.

Diagnosing magnesium deficiency is complicated by the fact that serum magnesium levels may not accurately reflect intracellular levels. The simplest way to check for it in patient s with Fibromyalgia Syndrome who may have only a slight deficiency is to start the patient on a supplement of magnesium of 3 months and see if they improve and then see if they notice an increase in symptoms on stopping the supplement. As magnesium acts as a lazative if not absorbed, it is important that the patient realises that diarhhoea will mean the supplement is not being absorbed. Clinicians and patients report anecdotally that magnesium malate or chelated magnesium may be more readily absorbed than other varieties.

For more information, see this MedlinePlus article on Magnesium.

5. Lyme Disease

Lyme disease is a bacterial illness transmitted by ticks. It is rarely checked for in Europe - awareness of the condition is much higher in the USA, where an outbreak in children in 1975 kickstarted a lot of research.

Lyme disease is classically associated with a tick bite causing an expanding reddish rash, with accompanying flu-like symptoms. However, many people bitten by ticks do not notice the bite and more than 1-in-4 patients never get a rash, so relying on this symptom progression may mean Lyme Disease is missed. In the later stages, when Lyme Disease can become chronic, it can causes joint pain, peripheral neuropathy, fatigue and cognitive difficulties - symptoms which may be confused with Fibromyalgia Syndrome.

Generally, Lyme blood testing is helpful in a patient who has symptoms compatible with Lyme disease who has a history of a tick bite at least a month prior, or who has unexplained disorders of the heart, joints, or nervous system that are characteristic of Lyme disease, particularly if they are at high risk of having been bitten by a tick (e.g. lived/worked in the countryside or owned dogs or horses).

For more in-depth information see this Medicinenet article on Lyme Disease.