[Non-inflammatory muscle pain]. / Nichtentzündliche Muskelschmerzen.

Muscle pain as a common symptom in daily practice frequently occurs as a non-specific accompanying symptom in multiple internal and neurological diseases. Primarily inflammatory or autoimmune muscular diseases are causing muscle pain. However, a number of non-inflammatory causes of pain can also be considered for differential diagnosis. These are presented in this article. In principle, a distinction must be made between focal and diffuse muscle pain. As an invasive diagnostic procedure, a muscle biopsy should only be performed as the last step in the diagnostic alogorithm. If diffuse muscle pain is only associated with slight muscle weakness or is completely absent, there is usually a primary rheumatic cause. Statins (HMG-CoA reductase inhibitors) can lead to rhabdomyolysis, muscle fiber atrophy and muscle necrosis by damaging the muscle fiber membrane. Myotonias are autosomal dominant or autosomal recessive inherited disorders of muscle function. The genetic defect leads to pronounced muscle stiffness. The cause of metabolic myopathies can be disorders of the carbohydrate, fat or purine metabolism. Fibromyalgia syndrome (FMS) is a non-inflammatory disease and, according to the current knowledge, recognized as the result of an exposure to physical, biological and psychosocial factors (biopsychological disease model). To help diagnosing FMS, pain regions and core symptoms (fatigue, sleep disturbances) can be detected using questionnaires (Widespread Pain Index [WPI] and Symptom Severity Scale [SSS]).

Short-Term Sensorimotor Effects of Experimental Occlusal Interferences on the Wake-Time Masseter Muscle Activity of Females with Masticatory Muscle Pain.

AIMS: To investigate the effects of the application of an acute alteration of the occlusion (ie, interference) on the habitual masseter electromyographic (EMG) activity of females with temporomandibular disorders (TMD)-related muscular pain during wakefulness. METHODS: Seven female volunteers with masticatory myofascial pain participated in a crossover randomized clinical trial. Gold foils were glued on an occlusal contact area (active occlusal interference, AI) or on the vestibular surface of the same molar (dummy interference, DI) and left for 8 days. The masseter electromyogram was recorded during wakefulness in the natural environment by portable recorders under interference-free, dummy-interference, and active-interference conditions. The number, amplitude, and duration of EMG signal fractions with amplitudes above 10% of the maximum voluntary contraction (activity periods, APs) were computed in all experimental conditions. Muscle pain, headache, and perceived stress were each assessed with a visual analog scale (VAS), and an algometer was used to assess masseter and temporalis pressure pain thresholds. Data were analyzed by means of analysis of variance. RESULTS: The frequency and duration of the recorded APs did not differ significantly between the experimental conditions (P>.05), but a small and significant reduction of the EMG mean amplitude of the APs occurred with AI (P<.05). Neither the VAS scores for muscular pain, headache, and perceived stress nor the pressure pain thresholds changed significantly throughout the entire experiment (P>.05). CONCLUSION: An active occlusal interference in female volunteers with masticatory muscle pain had little influence on the masseter EMG activity pattern during wakefulness and did not affect the pressure tenderness of the masseter and temporalis.

Phenotype standardization for statin-induced myotoxicity.

Statins are widely used lipid-lowering drugs that are effective in reducing cardiovascular disease risk. Although they are generally well tolerated, they can cause muscle toxicity, which can lead to severe rhabdomyolysis. Research in this area has been hampered to some extent by the lack of standardized nomenclature and phenotypic definitions. We have used numerical and descriptive classifications and developed an algorithm to define statin-related myotoxicity phenotypes, including myalgia, myopathy, rhabdomyolysis, and necrotizing autoimmune myopathy.

Correlation between bony changes measured with cone beam computed tomography and clinical dysfunction index in patients with temporomandibular joint osteoarthritis.

OBJECTIVES: To investigate the correlation between clinical dysfunction index (Di) and condylar bony changes, glenoid fossa bony changes and joint space changes. METHODS: Clinical data and cone beam computed tomography (CBCT) images of 240 patients with temporomandibular joint osteoarthritis (TMJ OA) were analyzed. The patients were assigned a score of Helkimo's clinical Di ranging from 1 to 25 and thereafter divided into 3 groups by the degree of Helkimo's Di. The condylar bony changes observed with CBCT were graded by the classification method of Koyama et al. Glenoid fossa bony changes and joint space changes were both classified as "positive" or "negative". Spearman's rank correlation test was used to correlate the score or degree of Helkimo's Di with the maximum condylar bony changes, glenoid fossa bony changes, and joint space changes. RESULTS: There was a significant correlation between the Helkimo's Di score and the maximum condylar bony changes (P ≤ 0.0001) and glenoid fossa bony changes (P ≤ 0.0001), and there was a poor correlation between the Helkimo's Di score and joint space changes (P = 0.184). Furthermore, there was a significant correlation between the degree of Helkimo's Di and the maximum condylar bony changes (P ≤ 0.0001) and glenoid fossa bony changes (P ≤ 0.0001), but there was a poor correlation between the degree of Helkimo's Di and joint space changes (P = 0.346). CONCLUSIONS: Both the score and degree of Helkimo's Di were highly correlated with maximum condylar changes and glenoid fossa bony changes, but not with joint space changes.