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Biomedical subjects

K G Henriksson

Publications and source records attributed to K G Henriksson.

At least 19 recordsLinked to original sources
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1990

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↗
PubMed1990

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↗
PubMed1990

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↗
PubMed1990

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↗
PubMed1990

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↗
PubMed1989

[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↗
PubMed1989

X-linked myotubular myopathy: clinical and pathological findings in a family.

A five-generation family with recessively inherited X-linked myotubular myopathy was investigated. Two of the affected boys, who were siblings and were verified by muscle biopsy to have the disease, died 3 days and 3 months, respectively, after birth. They showed marked hypotonus from birth, general muscle weakness and asphyxia. Three other boys, who were probably affected by the disease, had severe asphyxia and died shortly after birth. In three of the five cases there was polyhydramnios. The muscle biopsies of the two siblings revealed predominance of small fibres with central nuclei and accumulation of mitochondria in the central parts of the fibres. In one of the boys mainly the type 1 fibres were hypotrophic. The postmortem examination revealed variation in the involvement of different muscles, the anterior tibial muscle being the most severely affected. Intrafusal muscle fibres and myocardium were apparently unaffected. There was no involvement of the spinal cord. The clinical examination of two obligate carriers in the family revealed no muscle weakness but the muscle biopsy showed pathological changes including greatly increased variability of fibre size, and many fibres with central nuclei. The findings indicate that muscle biopsy is of value in genetic counselling to detect carriers although the observed changes were unspecific.

Adolescent↗
PubMed1989

The muscle in fibromyalgia--a review of Swedish studies.

In Sweden, several studies have been performed in patients with fibromyalgia to study muscle morphology, chemistry and physiology in order to understand the origin of the most prominent symptoms in fibromyalgia: muscle pain, muscle fatigue and muscle stiffness. These studies have shown changes indicating disturbed microcirculation, mitochondrial damage and a reduced content of high energy phosphates. Thus, there may be an energy deficiency state in the resting painful muscle in fibromyalgia. Pain analysis has supported the idea that there is a nociceptive origin of the pain. Our hypothesis is that any condition that could lead to constant muscle hypoxia, e.g., through establishment of abnormal motor patterns, might be a possible cause of fibromyalgic pain.

Adenosine Triphosphate↗
PubMed1989

Muscle pain in neuromuscular disorders and primary fibromyalgia.

Muscle fiber degeneration and regeneration, inflammation in the intramuscular connective tissue and hypoxia in resting muscle are not necessarily associated with pain. However, when sustained or dynamic muscle contractions are performed in an ischaemic muscle, severe pain develops. In the chronic muscle pain syndrome called fibromyalgia (or fibrositis) the most likely cause of the pain is a combination of muscle tension and muscle hypoxia. This conclusion is supported by the finding of a pathological distribution of tissue oxygen pressure in painful muscles and a subjective feeling of muscle tension and muscle stiffness in the majority of patients. A decrease of high energy phosphates is found in biopsies from painful muscle. The most characteristic morphological finding is the so-called ragged red fiber, a finding that can be seen in mitochondrial disorders. The morphological and chemical findings are possibly a consequence of a long standing hypoxia. The possibility that sympathetic nerve activity is important for the development of chronic muscle pain is discussed.

Fibromyalgia↗