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Until recently, most clinicians and scientists believed that the experience of pain is perceptually proportional to the amount of incoming peripheral nociceptive drive due to injury or inflammation in the area perceived to be painful. However, many cases of chronic pain have defied this logic, leaving clinicians perplexed as to how patients are experiencing pain with no obvious signs of injury in the periphery. Conversely, there are patients who have a peripheral injury and/or inflammation but little or no pain. What makes some individuals experience intense pain with minimal peripheral nociceptive stimulation and others experience minimal pain with serious injury? It is increasingly well accepted in the scientific community that pain can be generated and maintained or, through other mechanisms, suppressed by changes in the central nervous system, creating a complete mismatch between peripheral nociceptive drive and perceived pain. In fact, there is no known chronic pain condition where the observed extent of peripheral damage reproducibly engenders the same level of pain across individuals. Temporomandibular disorders (TMDs) are no exception. This review focuses on the idea that TMD patients range on a continuum-from those whose pain is generated peripherally to those whose pain is centralized (i.e., generated, exacerbated, and/or maintained by central nervous system mechanisms). This article uses other centralized chronic pain conditions as a guide, and it suggests that the mechanistic variability in TMD pain etiology has prevented us from adequately treating many individuals who are diagnosed with the condition. As the field moves forward, it will be imperative to understand each person's pain from its own mechanistic standpoint, which will enable clinicians to deliver personalized medicine to TMD patients and eventually provide relief in even the most recalcitrant cases. [ABSTRACT FROM AUTHOR]

The publication of the American College of Rheumatology criteria for fibromyalgia syndrome (FMS) is often considered the starting point of a major paradigm shift. By establishing a standardized case definition for FMS, the criteria enabled researchers to move forward and changed the way clinicians and researchers think of FMS, and more broadly, chronic pain. Whereas chronic pain was once thought to be acute pain that merely lasted too long, it is now recognized that the mechanisms underlying acute and chronic pain are markedly different from each other, and that acute and chronic pain respond to entirely different treatments. This article reviews the paradigm shift that needs to occur to take care of chronic pain more effectively, as we appreciate intra-individual differences in the neural processing of pain and recognize that various pharmacologic and nonpharmacologic modalities are better at treating central pain states such as FMS than treatments such as nonsteroidal anti-inflammatory drugs, opioids, and surgery that work well for acute and 'peripheral' pain. The article also presents a recommended approach to the treatment of FMS and its associated comorbidities. [ABSTRACT FROM AUTHOR]

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Background: Sinus tenderness has not been quantitatively assessed. Objective: We sought to compare sinus and systemic tenderness in rhinosinusitis, allergic rhinitis, and chronic fatigue syndrome (CFS), and healthy (non-CFS) groups. Methods: Cutaneous pressures (kg/cm2) causing pain at 5 sinus and 18 systemic sites were measured in acute and chronic rhinosinusitis, active allergic rhinitis, healthy non-CFS/no rhinosinusitis, and CFS subjects. Results: Sinus thresholds differed significantly (P ≤ 10−11, ANOVA) between non-CFS/no rhinosinusitis (1.59 ± 0.14 kg/cm2, mean ± 95% CI, n = 117), allergic rhinitis (1.19 ± 0.31, n = 30), exacerbations of chronic rhinosinusitis (1.25 ± 0.26, n = 25), non-CFS/chronic rhinosinusitis (1.23 ± 0.27, n = 23), acute rhinosinusitis (1.10 ± 0.20, n = 22), CFS/no rhinosinusitis (0.98 ± 0.15, n = 70), and CFS/chronic rhinosinusitis (0.78 ± 0.12, n = 56). Systemic pressure thresholds were lower for CFS (1.46 ± 0.15) than for non-CFS (2.67 ± 0.22, P ≤ 10−11). Conclusions: The lower sinus thresholds of rhinosinusitis groups validated the sign of sinus tenderness. Sinus and systemic thresholds were both 44% lower in CFS than in non-CFS subjects, suggesting that systemic hyperalgesia contributed to CFS sinus tenderness and “rhinosinusitis” complaints. (Otolaryngol Head Neck Surg 2002;127:387-97.) [Copyright &y& Elsevier]

Complementary medical therapies are commonly used for the treatment and management of myofascial pain. No universally accepted therapy for this condition exists; consequently, patients often seek alternative and complementary therapies. Many complementary treatments are available.This article focuses on acupuncture, biofeedback, ultrasound, lasers, and massage. Although anecdotally claimed as effective, most of these modalities have not been rigorously investigated because of poor research quality. Appropriate controls, sample sizes, and blinding measures are often lacking. Despite these issues, the trend toward efficacy exists and further examination is warranted. [ABSTRACT FROM AUTHOR]

Background: The constituents of nasal mucus may be contaminated by plasma if there is epistaxis. Gross epistaxis is apparent as a red lavage fluid, while microepistaxis may yield a clear fluid. If gross or microepistaxis are present, it will be difficult to decide whether plasma protein concentrations are elevated because of plasma exudation or bleeding. In order to discriminate between these two possibilities, we measured erythrocyte-derived free hemoglobin (fHb) in nasal lavage fluids. Methods: Single-blinded subjects underwent standard hypertonic saline nasal provocation. Unilateral hypertonic nasal provocation was performed in normal, allergic rhinitis (AR) and nonallergic rhinitis (NAR) subjects (total of 1316 specimens). fHb was measured using the Sigma-Aldrich kit (St. Louis, MO). Grossly bloody specimens were analyzed separately from the remainder. Statistical analysis defined the means and 95th percentiles for fHb and albumin in the nonbloody normal group. Results: fHb concentrations ranged from below the limits of detection (< 1 µg/ml) to > 164 µg/ml fHb was 79.3 µg/ml ± 4.7 (mean ± SEM) in four normal, 31 AR and 25 NAR grossly bloody specimens. The 95th percentile of fHb in the nonbloody normal samples (n = 68 subjects, n = 681 specimens) was 16.5 µg/ml. This value was defined as the threshold to detect potential microepistaxis, and corresponded to approximately 245 000 erythrocytes per ml of lavage fluid. Total protein (P < 0.05) and albumin (P < 0.001), but not markers of glandular secretion, were significantly increased in samples with fHb > 16.5 µg/ml compared to those ≤ 16.5 µg/ml. Elevations of fHb without changes in albumin were more prevalent in nonallergic rhinitis. Conclusions: Significant bleeding into nasal lavage samples can contaminate the specimens and increase the concentrations of both fHb and plasma proteins. Increased albumin alone would indicate increased vascular... [ABSTRACT FROM AUTHOR]

Objectives: To describe the syndromes that share overlapping clinical features with fibromyalgia [FMS].Findings: There are a number of semantic terms currently used to described systemic syndromes that share overlapping features with FMS. These include chronic fatigue syndrome, multiple chemical sensitivity, somatoform disorders, and Gulf War Illnesses. There are also a number of regional or 'organ-specific' syndromes that overlap with these conditions that have as their common features regional pain, with and without dysfunction of internal organs.Conclusions: In aggregate, chronic multisymptom illnesses such as FMS are extremely common. Hallmarks of these syndromes include non-nociceptive pain, fatigue, memory difficulties, and dysfunction of visceral organs. [ABSTRACT FROM AUTHOR]

Objective: To assess potential mechanism(s) for the rhinitis found in Chronic Fatigue Syndrome (CFS) subjects. Methods: The concentration of mucus constituents were measured in basal nasal lavage fluids of 103 CFS and 92 non-CFS control subjects. Subjects were further characterized by their Rhinitis Score and allergy skin test results into nonallergic and allergic rhinitis, atopic, and negative subgroups to determine if differences were related to atopy. Other questionnaires of irritant sensitivity and medicine use were completed. Results: Mucin polysaccaride (p = 0.043, ANOVA), free hemoglobin (p = 0.0044), mucin/total protein (p = 0.039) and hemoglobin/total protein (p = 0.043) were much higher in CFS than controls. CFS subjects with positive Rhinitis Scores (p = 0.023) or skin tests (p = 0.047) had higher mucin levels than those with negative values. For all subjects, inceased mucin was correlated with total protein (Pearson's r2 = 0.188) and inhaled corticosteroid use (r2 = 0.082) and elevated Tobacco Scores (r2 = 0.061). Other correlations with demographic, medication, or questionnaire responses gave r2 < 0.05. Conclusions: CFS subjects have a higher level of complaints in many systems including the nose. They appear to have an irritant (nonallergic) rhinitis with increased mucin production and mucosal friability (epistaxis of hemoglobin). Nasal and systemic drugs do not explain these significant baseline changes. [ABSTRACT FROM PUBLISHER]

Hypothesis: Allergies have been proposed as a cause or contributing factor of chronic fatigue syndrome (CFS). If this is so, then the stigmata of atopy, such as symptoms of allergic rhinitis and high serum IgE, should be present in CFS subjects. Methods: Medical records from an allergy and immunology clinic were retrospectively reviewed. All subjects who had had a serum IgE measurement performed over a 4-year period were identified, and allergy history and skin test data reviewed. Patients were then classified as: (a) allergic rhinitis (n = 51), (b) CFS (n = 113, 1992 criteria), and (c) normal subjects without atopy, CFS or immunodeficiency (n = 76). IgE levels were compared between groups. Results: A clinical history of allergic rhinitis was present in 31% (35/113) of the CFS subjects. The IgE levels of allergic rhinitis subjects and the subset of CFS subjects with allergic rhinitis were 392 +/- 73 and 406 +/- 123 IU/ml, respectively. In contrast, normal subjects and CFS subjects who did not give a history of allergic rhinitis had normal IgE levels of 49 +/= 9 and 33 +/= 4 IU/ml, respectively. Conclusion: Atopy with clinically defined allergic rhinitis, high IgE, positive allergy skin tests and the presumed TH2 lymphocyte-IgE-mast cell-eosinophil axis overactivity and immediate hypersensitivity (Type 1) immune response was present in a minority of CFS subjects. While atopy may coexist in some CFS subjects, it is unlikely that atopy plays a causal role in CFS pathogenesis. [ABSTRACT FROM AUTHOR]

An abstract of the article "Differential acute effects of real and sham acupuncture on mu-opioid receptor availability in treatment naive and conditioned chronic pain patients," by N. Akbar, J. Zubieta, T. Love, D. Clauw, and R. Harris is presented.