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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate changes in muscle soreness and serum enzyme activity following consecutive drop jumps. Seven male subjects (mean age 30.6 years) performed drop jumps from a 80-cm box height every 7 s until exhaustion (mean = 114 drop jumps). A questionnaire was used to assess muscle soreness (0 = no pain, 7 = unbearable painful) both pre- and post-exercise (0, 12, 24, 36 and 48 h, and 3, 4 and 5 days after the exercise). Blood samples were also taken from three subjects at each of these times. For the other four subjects, blood samples were taken pre-exercise and 0, 12 and 36 h and 5 days post-exercise only. Although there was large inter-subject variability in the development of muscle soreness, all the subjects reported muscle soreness in their lower extremity muscles, especially in the quadriceps femoris. Muscle soreness developed significantly (P less than 0.01) over time, its peak (mean +/- S.E. = 3.7 +/- 0.7) occurring 12-48 h post-exercise. Serum enzyme activity changed significantly over time (P less than 0.05), but the changes were small. Not one subject showed a large increase in creatine kinase, and the average increase was less than 1.3 times as much as the pre-exercise level throughout the period of study. These results suggest that the muscle damage that occurs after drop jumping is not associated with a large release of muscle enzymes into the blood, and muscle soreness is not necessarily related to enzyme elevation following drop jumps.
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PMID:Muscle soreness and serum enzyme activity following consecutive drop jumps. 189 57

Muscle biopsies of the descending portion of the trapezius muscle from female patients with chronic trapezius myalgia and from healthy women were analyzed with enzyme histochemical and immunohistochemical methods. Frequency, area, and capillarization of the muscle fiber types were determined. A biochemical analysis determined the lactate concentration of mixed muscle samples and the adenosine triphosphate (ATP) and phosphocreatine levels in single muscle fibers. The patients had larger type I fibers and a lower capillary:fiber area ratio for type I and type IIA fibers. The patients also exhibited lower levels of ATP and phosphocreatine in both type I and type II fibers. It is suggested that there might have been an imbalance between the capillary supply and the cross-sectional fiber area of type I and type IIA fibers in the patients. This imbalance might be of significance in the development of muscular fatigue and pain.
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PMID:Changes in muscle morphology in chronic trapezius myalgia. 194 20

Many of the hundreds of thousands of survivors of polio are now developing postpolio syndrome. Symptoms include progressive muscle weakness, fatigue, decreased endurance, joint and muscle pain, weight gain, respiratory difficulties, and sleep disturbance, often precipitated or exacerbated by a Type-A Personality pattern. A postpolio patient with Type-A Personality was taught self-hypnosis as a vital component of treatment. Pre-post testing included the Profile of Mood States, the State-Trait Anxiety Inventory, the State-Trait Anger Inventory, and the Personal Orientation Inventory; the patient's spouse was interviewed during the follow-up. At the 6-month follow-up, improvements were documented in pain level, depression, self-regard, self-acceptance, capacity for intimate contact, time competence (living in the present), confusion, anxiety, insomnia, and in trait and state anger. Only a mild improvement occurred in fatigue, and no improvement was found in weight control. Follow-up at 12 months confirmed the maintenance of improvements. Self-hypnosis training may prove extremely helpful for postpolio patients and may prove helpful in modifying central characteristics of Type-A Personality.
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PMID:Hypnosis for postpolio syndrome & Type-A behavior. 195 Nov 42

Myofascial pain (MFP) is a regional muscle pain disorder characterized by localized tenderness in taut muscle bands and referred pain. Frequently, MFP is overlooked as a common cause of chronic pain because of the frequent association with joint dysfunction and other pain disorders and the multiple behavioral and psychosocial contributing factors that are often present. Nonetheless, studies have reported that MFP is present in a significant number of people. This article describes current concepts for the diagnosis and management of MFP.
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PMID:Clinical care for myofascial pain. 199 46

This study examined the nature and extent of psychological differences among diagnostic subgroups of temporomandibular disorder (TMD) patients. Three subgroups were identified and labeled as: (1) primary myalgia, (2) primary temporomandibular joint (TMJ) problems, or (3) combination myalgia and TMJ problems. Patients' (n = 112) levels of pain and distress were measured using a VAS pain scale, the McGill Pain Questionnaire, the Beck Depression Inventory, the State-Trait Anxiety Scale and the MMPI. Patients with primary myalgia had the highest scores on the pain and distress measures while patients in the combination group scored between the myalgia and TMJ problem subgroups. When differences in pain levels were controlled, the differences among groups on measures of anxiety and depression were attenuated while the differences on measures of somatic overconcern remained significant. Discriminant function analysis using psychological variables to predict diagnostic grouping produced correct identification of 74% of the structural patients and 46% of the myalgia patients. Implications for different etiological factors among the 3 groups are discussed.
Pain 1991 Jan
PMID:Psychological distress and diagnostic subgroups of temporomandibular disorder patients. 203 85

Trauma history was studied for association with disease among six diagnostic subgroups of 230 patients with temporomandibular disorder (TMD) from a private practice setting with (1) disk displacement (DD) with reduction, (2) DD without reduction, (3) osteoarthrosis (OA) with prior derangement history, (4) primary OA, (5) myalgia only, and (6) subluxation only. Except for subluxation (29%), trauma history typified TMD patient groups 1 to 5 (63%, 79%, 44%, 53%, 54%) (p less than 0.001) compared with 13% and 18% of asymptomatic (n = 61) and symptomatic (n = 161) student control subjects, and 11% of general dental patients (n = 150). TMD groups 2 and 3 differed significantly (p less than 0.05). The high prevalence of trauma in the myalgia-only group complicates the concept of myofascial pain-dysfunction syndrome as solely a stress or centrally mediated disorder. DD without reduction (43%) and with reduction (38%) had the highest prevalences of motor vehicle accident trauma, myalgia and OA groups had less, and subluxation-only cases had none. On the other hand, patients with DD without reduction were also the only group to report multiple trauma (29%), suggesting that although specific traumatic events may seem to precipitate clinical symptoms, they may not always have initiated the problem. Trauma may be both an important cumulative and precipitating event in TMDs.
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PMID:Trauma history in diagnostic groups of temporomandibular disorders. 204 90

Painful crises in sickle cell anemia are associated with infarction and subsequent fibrosis of many different organs. Myonecrosis secondary to muscle infarction during a crisis and subsequent fibrosis are often not recognized as complications of sickle cell anemia. We describe four patients, all of whom had recurrent episodes of symmetric proximal muscle pain and swelling as prominent features of their crises. Muscle biopsies showed acute myonecrosis with a minimal inflammatory reaction as well as myofibrosis with abundant collagen deposition. Chronic sequelae consisted of muscle induration, atrophy, and contractures.
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PMID:Myonecrosis and myofibrosis as complications of sickle cell anemia. 192 31

Myopathies are not an unusual complication of drug therapy. The major symptoms in drug-induced myopathies are proximal muscle weakness, increased muscle enzyme levels, electromyographic changes and histological lesions. Some drug-induced myopathies are associated with neuropathy. Drug-induced myopathies can be classified according to the presence or absence of muscular pain and associated neuropathy. Among painless myopathies, we can distinguish myopathies without neuropathy (corticosteroids), myopathies with neuropathy (colchicine, chloroquine and hydroxychloroquine) and myasthenic syndromes (D-penicillamine, antibiotics, beta-blockers). Among painful myopathies, the classification is similar: painful myopathies may or may not be associated with neuropathies. Painful myopathies include polymyositis (D-penicillamine, cimetidine, zidovudine) and other myopathies without polymyositis (clofibrate, statines, cyclosporin). Among the painful neuromyopathies, eosinophilia-myalgia syndrome is a recently described disorder associated with the use of L-tryptophan. Combinations of drugs (for example, a fibrate and a statine or cyclosporin and colchicine) can induce severe myopathies. If such drugs are used together a vigorous surveillance to detect any sign of myopathy is warranted. Instead of classifying drug-induced myopathies according to clinical features, a histological classification can be proposed. Many drugs can induce vacuolar myopathy (colchicine, chloroquine, amiodarone, cyclosporin, drugs causing hypokalaemia and lipid-lowering agents), some others cause a mitochondrial myopathy (zidovudine) or a necrotizing myopathy as seen with vincristine. Overall, several criteria for reporting drug-induced myopathy can be recommended: lack of pre-existent muscular symptoms, a free period between the beginning of the treatment and the appearance of symptoms, lack of another cause accounting for the myopathy, and complete or incomplete resolution after withdrawal of the treatment. Rechallenge of the treatment is not advisable because of the risk of a serious relapse. The exact mechanisms by which drugs cause myopathies are unknown. Some cases may be due to metabolic changes, whereas others may be immune mediated. Nevertheless, the aspect these conditions have in common is the regression of the myopathy with the discontinuation of the drug.
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PMID:Drug-induced myopathies. 207 Apr 26

The chronic fatigue syndrome is a poorly defined symptoms complex characterized primarily by chronic or recurrent debilitating fatigue and various combinations of other symptoms, including psychological symptoms, sore throat, lymph node pain, headache, myalgia, arthralgias. Psychological disturbances, ranging from mild depression or anxiety to severe behavioral abnormalities, are always present. Chronic fatigue syndrome is the name that more accurately describes this symptom complex of unknown cause. A viral aetiology has long been hypothesized: many viruses are potential candidates, including any of the 23 Coxsackie A or 6 Coxsackie B viruses, herpes viruses, particularly Epstein-Barr virus and varicella. These studies, though interesting, remain unconvincing because of methodological flaws such as a poor case definition and inadequate control groups. This syndrome may represent an infection by a yet unidentified virus. It is more likely due to an abnormal immune response toward different intracellular pathogens. There is no treatment to ameliorate the chronic fatigue syndrome. Epidemiological studies are essential with explicit operational case definition before progress can be made in the management of this distressing disorder.
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PMID:[The chronic fatigue syndrome. A multifactorial approach and the treatment possibilities]. 207 78

The aim of this study was to observe the difference between patients of craniocervical muscle pain and nonpatients in head-neck posture, masticatory muscle activity, and the force exerted by the hand. Fifty-one patients and 28 nonpatients were observed. The electric activity of the masseter muscles was recorded when the subjects were doing pinching or grasping with the jaw in positions of rest, clenched, and clenched with gauze. Measurement of right and left tilting or extension and flexion of the head and neck was made from photographs of frontal and lateral views. It was found that the pinching and grasping force was much stronger in men than in women and in nonpatients than in patients with pain. The pinching and grasping force was more powerful with the teeth clenched. Clenching with gauze did not increase, but more often decreased the strength of the hand. The activity of the masseter muscle during clenching was about 10 to 26 times that of the resting activity. The activity decreased slightly when clenching with pinching or grasping. Patients were more likely to have a stretched neck with more extension of the head. Their masseter muscle activity and hand force were significantly weaker than that of the nonpatients.
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PMID:Body posture and hand strength of patients with temporomandibular disorder. 208 32


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