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Biomedical subjects

K G Henriksson

Publications and source records attributed to K G Henriksson.

At least 37 records · Page 2Linked to original sources

Fibromyalgia and disability. Report of the Moss International Working Group on medico-legal aspects of chronic widespread musculoskeletal pain complaints and fibromyalgia.

The present article is the result of a working group conference held in Moss, Norway, in June 1993, financed by the Royal Norwegian Ministry of Health and Social Affairs. Its purpose was to review and focus upon problems and needs related to the medico-legal aspects of fibromyalgia and chronic widespread musculoskeletal complaints: thus to define directions for future work on issues which have generally not been addressed within the medical community. Our report describes specific problems in this area in regard to definition, evaluation and recommendation, and in currently available work and disability statistics. We have recommended international efforts to establish research programs through organizations such as the International Social Security Association and the World Health Organization. While our recommendations call for research into medico-legal interactions, causes and pathogenic mechanisms, prevention and treatment are also key and relevant concerns in the medico-legal setting.

Chronic Disease↗

Isometric muscle strength and muscular endurance in normal persons aged between 17 and 70 years.

Isometric muscle strength was measured in 63 women and 65 men, randomly selected, aged 17-70 years, using Penny & Giles' hand-held dynamometer. Eight muscle groups as well as the hand grip strength were tested bilaterally. The muscular endurance was measured as time to exhaustion in the abductors of the shoulder and the flexors of the hip. Reference values for muscle strength and muscular endurance are given in the age groups 17-18, 20-29, 30-39, 40-49, 50-59 and 60-70 years of age. The mean strength of females was about 65-70% of that of the men, but when the results were related to weight, the differences almost disappeared. Both men and women seem to have the greatest muscle strength at the age of about 17-18. The strength is rather constant up to the age of about 40 years, after which a discrete decline is seen up to about 60, from where the decline is more obvious. Muscular endurance showed great variability between individuals. However, no decrease in endurance was seen in older ages. For both sexes, lower reference limits of endurance, with the methods used, for arm abductors are suggested as being 3 minutes and for hip flexors, 90 seconds.

Adolescent↗

Chronic muscular pain: aetiology and pathogenesis.

The conclusion is that no one single mechanism can explain FMS and is thus in that sense a compromise. FMS in some patients may start in the muscle, in other patients in the brain. The combination of peripheral and central factors is the key to the pathogenesis of FMS as long as FMS is defined as a pain syndrome.

Fibromyalgia↗

Mitochondrial myopathy with succinate dehydrogenase and aconitase deficiency. Abnormalities of several iron-sulfur proteins.

Recently, we described a patient with severe exercise intolerance and episodic myoglobinuria, associated with marked impairment of succinate oxidation and deficient activity of succinate dehydrogenase and aconitase in muscle mitochondria (1). We now report additional enzymatic and immunological characterization of mitochondria. In addition to severe deficiency of complex II, manifested by reduction of succinate dehydrogenase and succinate:coenzyme Q oxidoreductase activities to 12 and 22% of normal, respectively, complex III activity was reduced to 37% and rhodanese to 48% of normal. Furthermore, although complex I activity was not measured, immunoblot analysis of complex I showed deficiency of the 39-, 24-, 13-, and 9-kD peptides with lesser reductions of the 51- and 18-kD peptides. Immunoblots of complex III showed markedly reduced levels of the mature Rieske protein in mitochondria and elevated levels of its precursor in the cytosol, suggesting deficient uptake into mitochondria. Immunoreactive aconitase was also low. These data, together with the previous documentation of low amounts of the 30-kD iron-sulfur protein and the 13.5-kD subunit of complex II, compared to near normal levels of the 70-kD protein suggest a more generalized abnormality of the synthesis, import, processing, or assembly of a group of proteins containing iron-sulfur clusters.

Aconitate Hydratase↗

Quantification of extrajunctional acetylcholine receptors in human muscle biopsies.

Extrajunctional acetylcholine receptors were quantified in human muscle biopsies by in vitro autoradiography with 3H-alpha-bungarotoxin (alpha-Btx). Specific alpha-Btx binding was found in seven of eight biopsies with histological and/or histochemical signs of denervation. The highest binding (21 fmol/mg) was seen in the biopsy with the most pronounced signs of denervation. The specimens with co-existing signs of innervation had generally lower binding levels. Four of the control biopsies showed low binding (less than or equal to 1 fmol/mg) while no specific binding could be detected in the other six controls. The findings suggest that this method cannot only be used to demonstrate denervation in muscle biopsy specimens, but also to give a quantitative measure of the changes.

Adolescent↗

Fibromyalgia--a clinical entity?

Fibromyalgia (FM) is a syndrome characterized by widespread musculoskeletal pain and tenderness at specified sites, fatigue, and unrefreshing sleep. The American College of Rheumatology (ACR) has recently accepted diagnostic criteria for FM. The ACR criteria have high diagnostic specificity, sensitivity, and accuracy. Laboratory investigations show a disturbed microcirculation in painful muscles, a decrease in adenosine triphosphate and phosphocreatine, and a reduced relaxation rate. Pain analyses indicate that the pain is nociceptive. A characteristic physiological sleep disturbance has been described that is correlated to the symptoms. The etiology of FM is not known. The etiology may be different in different patients. FM is a clinical entity, but should be regarded as a syndrome rather than a disease.

Fibromyalgia↗

Deficiency of skeletal muscle succinate dehydrogenase and aconitase. Pathophysiology of exercise in a novel human muscle oxidative defect.

We evaluated a 22-yr-old Swedish man with lifelong exercise intolerance marked by premature exertional muscle fatigue, dyspnea, and cardiac palpitations with superimposed episodes lasting days to weeks of increased muscle fatigability and weakness associated with painful muscle swelling and pigmenturia. Cycle exercise testing revealed low maximal oxygen uptake (12 ml/min per kg; healthy sedentary men = 39 +/- 5) with exaggerated increases in venous lactate and pyruvate in relation to oxygen uptake (VO2) but low lactate/pyruvate ratios in maximal exercise. The severe oxidative limitation was characterized by impaired muscle oxygen extraction indicated by subnormal systemic arteriovenous oxygen difference (a-v O2 diff) in maximal exercise (patient = 4.0 ml/dl, normal men = 16.7 +/- 2.1) despite normal oxygen carrying capacity and Hgb-O2 P50. In contrast maximal oxygen delivery (cardiac output, Q) was high compared to sedentary healthy men (Qmax, patient = 303 ml/min per kg, normal men 238 +/- 36) and the slope of increase in Q relative to VO2 (i.e., delta Q/delta VO2) from rest to exercise was exaggerated (delta Q/delta VO2, patient = 29, normal men = 4.7 +/- 0.6) indicating uncoupling of the normal approximately 1:1 relationship between oxygen delivery and utilization in dynamic exercise. Studies of isolated skeletal muscle mitochondria in our patient revealed markedly impaired succinate oxidation with normal glutamate oxidation implying a metabolic defect at the level of complex II of the mitochondrial respiratory chain. A defect in Complex II in skeletal muscle was confirmed by the finding of deficiency of succinate dehydrogenase as determined histochemically and biochemically. Immunoblot analysis showed low amounts of the 30-kD (iron-sulfur) and 13.5-kD proteins with near normal levels of the 70-kD protein of complex II. Deficiency of succinate dehydrogenase was associated with decreased levels of mitochondrial aconitase assessed enzymatically and immunologically whereas activities of other tricarboxylic acid cycle enzymes were increased compared to normal subjects. The exercise findings are consistent with the hypothesis that this defect impairs muscle oxidative metabolism by limiting the rate of NADH production by the tricarboxylic acid cycle.

Aconitate Hydratase↗

Quantitative EMG and muscle tension in painful muscles in fibromyalgia.

Examinations were performed in 22 female fibromyalgic patients and in 9 healthy controls. The biceps brachii, trapezius, and tibial anterior muscles were examined electromyographically. The changes found were minor and non-specific. This implies that there is no important loss of motor units and no conspicuous muscle fiber degeneration in fibromyalgia. Our investigation also failed to demonstrate any electrically detectable muscle activity in muscles where the patients during the examination reported pain (paraspinal, trapezius and tibial anterior muscles). This means that muscle tension cannot be a prominent pathogenetic factor in fibromyalgia and that factors other than muscle tension are responsible for maintaining the pain in fibromyalgia.

Adult↗

Effect of sodium selenite and vitamin E treatment in myotonic dystrophy.

Fifteen patients with myotonic dystrophy, seven men and eight women, of age range 15-55 years, were treated with sodium selenite and vitamin E for 2 years. The patients were examined using a number of tests to assess muscle force and function at the start of the treatment period and 6, 12 and 24 months thereafter. Myotonia gives an increased relaxation time. The latter was measured in the adductor pollicis. There was a significant decrease in half relaxation time before treatment compared with the values during treatment. In summary, the results indicate that selenium and vitamin E therapy may have an effect on myotonia. The effects of treatment on motor functions were minimal, and overall motor performance was not improved.

Adult↗

Neuropathy and myopathy in primary Sjögren's syndrome: neurophysiological, immunological and muscle biopsy results.

Seventeen consecutive patients with primary Sjögren's syndrome (PSS) received neurophysiological examination, analysis of antibodies against peripheral nerve-myelin (PNM) and muscle biopsy, to show the prevalence and characteristics of peripheral neuropathy (PN) and myopathy; 3 PSS cases showed a clinical mild sensorimotor polyneuropathy, 1 of them had been treated with cytostatic drugs; 1 had mononeuropathia multiplex; and 1 clinical carpal tunnel syndrome. In these 5 patients neurophysiological investigation verified the clinical diagnosis of peripheral nerve involvement; 2 with PN had serum-antibodies against PNM; 1 of IgM-, and 1 of IgA-isotype. Muscle biopsies were taken from 15 PSS patients; 11 showed inflammatory myositis or inflammatory perivascular infiltrates and 3 showed signs of denervation. A combination of inflammation and morphological signs of myopathy, compatible with the biopsy diagnosis of polymyositis, was seen in 4, 1 of whom showed clinical signs of polymyositis. We conclude that the peripheral nervous and muscular systems are often involved in PSS, but commonly with relatively mild symptoms and laboratory findings. The common findings of inflammatory myopathy indicate an immune reaction in muscles in addition to other autoimmune manifestations of the disease.

Adult↗

Impaired oxidative metabolism increases adenine nucleotide breakdown in McArdle's disease.

Two patients with muscle phosphorylase deficiency [McArdle's disease (McA)] were studied during bicycle exercise at 40 (n = 2) and 60 W (n = 1). Peak heart rate was 170 and 162 beats/min, corresponding to approximately 90% of estimated maximal heart rate. Muscle samples were taken at rest and immediately after exercise from the quadriceps femoris. Lactate content remained low in both muscle and blood. Acetylcarnitine, which constitutes a readily available form of acetyl units and thus a substrate for the tricarboxylic acid cycle, was very low in McA patients both at rest and during exercise, corresponding to approximately 17 and 11%, respectively, of that in healthy subjects. Muscle NADH was unchanged during exercise in McA patients in contrast to healthy subjects, in whom NADH increases markedly at high exercise intensities. Despite low lactate levels, arterial plasma NH3 and muscle inosine 5'-monophosphate increased more steeply relative to work load in McA patients than in healthy subjects. The low postexercise levels of lactate, acetylcarnitine, and NADH in McA patients support the idea that exercise performance is limited by the availability of oxidative fuels. Increases in muscle inosine 5'-monophosphate and plasma NH3 indicate that lack of glycogen as an oxidative fuel is associated with adenine nucleotide breakdown and increased deamination of AMP. It is suggested that the early onset of fatigue in McA patients is caused by an insufficient rate of ADP phosphorylation, resulting in transient increases in ADP.

Acetylcarnitine↗

Chronic trapezius myalgia. Morphology and blood flow studied in 17 patients.

Bilateral open biopsies from the painful upper part of the trapezius muscle were studied in 17 patients with localized chronic myalgia related to static load during repetitive assembly work. Isolated pathologic ragged red fibers were related to the presence of myalgia. The phenomenon indicating disturbed mitochondrial function was confined to the Type 1 fibers. Using a laser-Doppler flowmeter, the muscle blood flow was recorded in the exposed muscle before a biopsy was taken. Pain was assessed and graded as the difference between the two sides, as was the presence of ragged red fibers. The myalgia correlated with reduced local blood flow: the greater the pain difference, the greater the reduction in blood flow. There was a correlation between the presence of mitochondrial changes and reduced muscle blood flow.

Adult↗

[Fibromyalgia--a new name for a syndrome with diffuse muscular disorders].

This new name for an old and common disease has introduced fresh criteria and initiated clinical and basic research. The present clinical knowledge of the diagnosis and treatment is reviewed. Morphological and biochemical findings in the muscle of fibromyalgia patients have shown an unevenly distributed reduction of the oxygen tension. Hypoxia in the muscle sensitizes nociceptors, resulting in hyperalgesia with a diffuse distribution of pain symptoms. These are difficult for the individual to localize and are often combined with muscle stiffness and increased fatigability. These symptoms correspond to complaints received from fibromyalgia patients.

Diagnosis, Differential↗