Cases reported "Muscular Diseases"

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1/3. Familial fingerprint body myopathy.

    Muscle biopsy specimens from two half brothers with a congenital benign muscle disorder and from their mother, clinically unaffected, were studied by histochemistry and electron microscopy. In the children's biopsy specimens, the ultrastructural examination showed numerous fingerprint bodies located at the periphery of the muscle fibers. The histochemical pattern was different in these two specimens. In the mother's biopsy specimen, while fingerprint bodies were not found, the muscle fibers showed slight but definite changes. Even if the fingerprint bodies by themselves are not specific for a particular muscle disease, their occurrence in two half brothers is a valid argument in favor of the individalization of the fingerprint body myopathy, which has been previously described.
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2/3. Fingerprint inclusions. Ultrastructural demonstration of muscle fiber type specificity.

    Fingerprint inclusions were identified in the skeletal muscle of a child with severe hypotonia. The mean Z-line and M-line widths from each of 19 muscle fibers containing the fingerprint inclusions were calculated. The mean Z-line widths were 85-99 nm, and the mean M-line widths were 75-101 nm. According to out present system of fiber typing, all of these fibers would be classified as Type I. The possible pathogenesis and fiber type specificity of the fingerprint inclusion is discussed.
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3/3. Tubulomembranous and fingerprint-like inclusions in biopsied muscle of distal myopathy with rimmed vacuoles.

    Muscle biopsies from four patients were studied histochemically and electron-microscopically: they had myopathy of juvenile or early-adult onset, in which distal limb muscles were most severely affected but muscles supplied by cranial nerves were spared. Common histochemical findings included variation in fiber size, necrosis, phagocytosis, fiber splitting, central nuclei, endomysial fibrosis, and particularly rimmed vacuoles. Electron-microscopic examination revealed frequent autophagic vacuoles with numerous myeloid bodies. In addition, sarcoplasmic inclusion bodies with periodically laminated structures similar to the tubulomembranous structures (TMSs) first described by Fukuhara et al. (1981) in an atypical myopathy were found in all four cases, and in one, there were fingerprint-like structures resembling those described in neuronal ceroid-lipofuscinoses. These inclusions occasionally contained areas resembling lipofuscin pigment. They are certainly residual bodies of lysosomal origin, which might be related to the rimmed-vacuolar degeneration of the muscle, but whether or not they represent some specific metabolic abnormalities seems to remain an open question since the present cases differed clinically from either of the atypical myopathies with TMSs (Fukuhara et al. 1981) or any type of neuronal ceroid-lipofuscinosis.
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