Subject(s)
Back Pain/therapy , Exercise Therapy , Lumbar Vertebrae , Muscle Denervation , Muscular Dystrophies/therapy , Osteochondritis/complications , Adolescent , Adult , Back Pain/etiology , Combined Modality Therapy , Humans , Isometric Contraction , Male , Middle Aged , Muscular Dystrophies/etiologyABSTRACT
The blood serum lactate dehydrogenase (LDH), creatine kinase (CK), and LDH isoforms activities have been measured in 103 patients with the compression neural and myodystrophic syndromes of lumbar osteochondrosis. The studies have revealed a relationship between the myodystrophic process severity and the intensity of LDH and CK ejection from the muscle into the blood, particularly in the trigger stage. The shift of LDH activity towards the predominance of slowly migrating isoforms augments and the total blood serum LDH and CK activities grow as the muscular syndrome progresses. These data permit a differentiation between the compression neural and the myodystrophic syndromes, as well as between the algic and the trigger stages of muscle involvement. Such a differentiation does not involve biopsy in many cases.
Subject(s)
Creatine Kinase/blood , L-Lactate Dehydrogenase/blood , Lumbar Vertebrae , Muscular Dystrophies/blood , Nerve Compression Syndromes/blood , Osteochondritis/blood , Adult , Humans , Middle Aged , Muscular Dystrophies/etiology , Nerve Compression Syndromes/etiology , Osteochondritis/complicationsABSTRACT
The state of skeletal muscles was subjected to a comprehensive study in 106 patients with verified rheumatoid arthritis. Kinesthetic, thermography, electromyography, tensometry and morphohistochemical methods were employed together with determination of serum activity of creatine phosphokinase. The muscular syndrome of the disease was characterized by the presence of foci of myofibrosis manifesting as local painful indurations of different size and consistency. It has been shown that one of the mechanisms of muscular injury in rheumatoid arthritis is the neural reflex one: under the influence of pathological impulses from the damaged joint there occur tonic and dystrophic alterations in the muscle, vasomotor dysfunctions and derangement of the neurotrophic control.
Subject(s)
Arthritis, Rheumatoid/complications , Muscular Diseases/diagnosis , Adolescent , Adult , Aged , Arthritis, Rheumatoid/physiopathology , Chronic Disease , Fibrosis/diagnosis , Fibrosis/etiology , Fibrosis/physiopathology , Histocytochemistry , Humans , Methods , Middle Aged , Muscles/enzymology , Muscles/physiopathology , Muscular Diseases/etiology , Muscular Diseases/physiopathology , Terminology as TopicSubject(s)
Peripheral Nervous System Diseases/physiopathology , Adult , Animals , Humans , Male , Middle Aged , RatsSubject(s)
Arthritis, Rheumatoid/diagnosis , Muscular Diseases/diagnosis , Adult , Humans , Middle Aged , SyndromeSubject(s)
Arthritis, Rheumatoid/enzymology , Creatine Kinase/blood , Adult , Enzyme Activation , Female , Humans , Male , Middle AgedABSTRACT
The authors performed pathomorphological examinations in 19 patients with compressional-neural and myodystrophic syndromes of lumbar osteochondritis and also in 16 experimental animals with an impaired axoplasmic current. In the light of the modern understanding of the neurodystrophic control the authors discuss the mechanisms of the denervational-reinnervational process in muscles of patients with vertebrogenic pathology and myodystrophic disorders.