[Hypercalcemia].
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Biomedical subjects
Publications and source records attributed to L Käser.
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Refractory hypertension is common in patients non-compliant with antihypertensive therapy, in obese and stroke patients, and due to drug interactions with nonsteroidal anti-inflammatory drugs or excessive alcohol intake. The evaluation and management of these pitfalls as well as the causes of secondary hypertension are discussed.
DESIGN: Randomized prospective study to compare the effects of three types of active therapy on the back muscle structure of chronic low back pain patients. OBJECTIVES: To analyze the effects of 3 months active therapy on gross back muscle size and muscle fiber type characteristics and their relationship to changes in muscle function. SUMMARY OF BACKGROUND DATA: Many studies have documented a diminished muscular performance capacity in cLBP patients, but few have supported this with evidence of alterations in either the macro- or microscopic structure of the paraspinal muscles. Investigations of the changes in muscle structure following active rehabilitation are even rarer. METHODS: Assessments of trunk muscle cross-sectional area (using MRI), erector spinae fiber size/type distribution and pathology (percutaneous biopsy), and muscle function (see Part 1) were made in a group of 59 individuals with cLBP, who were participating in a randomized trial of active therapies for cLBP (physiotherapy, muscle training on devices, aerobics). RESULTS: Fifty-three out of 59 patients (90%) completed the therapy. At baseline, significant correlations were observed between the size of the paraspinal muscles and isometric back extension strength (P=0.0001), and between the proportional area of the muscle occupied by each fiber type and the fatigability of the muscle (P=0.012). Following therapy, there were small (few percent) increases in trunk muscle size in the aerobics and physiotherapy groups and a similarly slight decrease in the devices group. Changes in erector spine size correlated only weakly and nonsignificantly with changes in back extension strength. There were no major changes in fiber type proportion or fiber size in any group following therapy. CONCLUSION: Three months active therapy is not sufficient to reverse the typical "glycolytic" profile of the muscles of cLBP patients or to effect major changes in backmuscle size. The alterations in muscle performance observed (increased strength and endurance; Part 1) werenot explainable on the basis of structural changes within the muscle.
Many studies have documented an association between chronic low back pain (LBP) and deficits in back muscle strength and endurance. The sub-optimal performance is believed to be the result of alterations in the size and structure of the muscle, although the long-standing issue of whether the observed changes precede or are a consequence of the pain remains unresolved. If consequent to the problem, and predominantly related to disuse of the muscles, then it may be expected that a relationship between muscle structure and symptom duration would exist. Lumbar paraspinal muscle samples were obtained from 59 chronic LBP patients using the percutaneous biopsy technique. The samples were subject to routine histochemical analysis for the examination of muscle fibre type characteristics and cytochemical architectural changes. In 55 of the patients, the gross cross-sectional areas of magnetic resonance images of the trunk muscles were also measured. Multivariate analysis showed that symptom duration was the strongest predictor of the individual proportions of the fast-fatigable type IIX fibres; with age and gender included in the model, nearly 30% of the variance in fibre type distribution could be accounted for. Duration of pain had no influence on fibre size. Gross muscle cross-sectional area correlated directly with lean body mass and inversely with age, but showed no relationship with symptom duration. Pathological changes in the internal fibre structure were more frequently encountered in older patients, and were independent of symptom duration. The results suggest that, over the long term, fibre type transformations rather than alterations in fibre size are the predominant changes to be found in the muscles of chronic LBP patients. The direction of change supports the results of many previous studies that have demonstrated corresponding differences in the fatigability of the muscles. There is a strong case for the early implementation of active measures to attempt to offset the development of these changes in back pain patients.
Parvalbumin (PV) is a high affinity Ca(2+)-binding protein found at high concentration in fast-contracting/relaxing skeletal muscle fibers of vertebrates. It has been proposed that PV acts in the process of muscle relaxation by facilitating Ca2+ transport from the myofibrils to the sarcoplasmic reticulum. However, on the basis of metal-binding kinetics of PV in vitro, this hypothesis has been challenged. To investigate the function of PV in skeletal muscle fibers, direct gene transfer was applied in normal and regenerating rat soleus muscles which do not synthesize detectable amounts of PV. Two weeks after in vivo transfection with PV cDNA, considerable levels of PV mRNA and protein were detected in normal muscle, and even higher amounts were detected in regenerating muscle. Twitch half-relaxation time was significantly shortened in a dose-dependent way in transfected muscles, while contraction time remained unaltered. The observed shortening of half-relaxation time is due to PV and its ability to bind Ca2+, because a mutant protein lacking Ca(2+)-binding capacity did not promote any change in physiology. These results directly demonstrate the physiological function of PV as a relaxing factor in mammalian skeletal muscle.
Following partial denervation motor units can increase (by self-reinnervation) as much as four to five times their normal size. To investigate the still unknown quantitative reinnervation capacity of a motor nerve in the case of foreign-reinnervation, in adult male rats the denervated sternomastoid muscle was either self-reinnervated by its original nerve or foreign-reinnervation by the omohyoid nerve, which had to reinnervate the three times the amount of muscle fibers and six times the amount of muscle mass. After survival times of 7, 8, 9, or 10 months, nerves and muscles were investigated histochemically and immunohistochemically. The omohyoid nerve could fully reinnervate the sternomastoid muscle, but at 7 and 8 months this muscle still revealed nearly the same proportions of IIA and IIB fibers as were seen in the self-reinnervated sternomastoid at all stages. However, in the following 2 months a shift of the fiber pattern toward that of the normal omohyoid was observed, as evidenced by a strong increase in type IIB fibers (from 24% to 62%), at the expense of type IIA fibers. These findings are in contrast to those after foreign (cross) reinnervation of leg muscles where the fiber transformation (according to the foreign motor input) occurs in parallel with the reinnervation process during the first 2-3 months. The delayed fiber transformation observed could be the consequence of the highly enlarged peripheral field of the omohyoid motoneuron pool or could merely reflect a general difference between limb and neck muscles.(ABSTRACT TRUNCATED AT 250 WORDS)