Muscle fiber atrophy

Biopsy findings show disseminated muscle fiber atrophy which is confined to type 2 fibers, in many instances with type 2B (glycolytic) fibers most affected (Figure 23). Muscle necrosis is not seen, though at ultrastructural level focal myofibrillar disruption and myofilament loss may be evident. The muscle atrophy seems to be due to decreased protein synthesis, and at high doses, to increased catabolism. The reason for the selective effect on phasic, glycolytic fibers is not clear since, although steroids interfere with carbohydrate metabolism and oxidative capacity, there seems to be no overall effect on ATP levels. Nevertheless it has been... 

Ansved T, Odergren T, Borg K. Muscle fiber atrophy in leg muscles after botulinum toxin type A treatment of cervical dystonia. Neurology 1997 48(5) 1440-2. 

There are two major categories of muscle-fiber atrophy (a) ordinary denervation atrophy... 

Figures 1.1-1.3) and (b) type-2 muscle fiber atrophy (Figure 1.4), and other less frequently seen atrophies, including vacuolar atrophies. Conceptu-... 

In an individual patient the cause of type-2 fiber atrophy can be multifactorial. For example, possibilities are (a) in arthritic muscle atrophy, in which the commonly associated muscle-fiber atrophy is typically type-2 fiber atrophy [46], but whether the mechanism(s) is, speculatively, related to hypofunc-tion/disuse, or a putative pain reflex decreasing LMN function, and/or, in rheumatoid arthritis, a concomitant dysimmune mechanism (b) in HIV the atrophy could be dysschwannian dysimmune neuropathic, dysneuronal neuropathotoxic, cachectic, or possibly viral-myotoxic, or a combination of these. 

Intended for general treatment of muscle-fiber atrophy in aging and in several other settings, anti-myostatins are being developed as a new approach, but they have not yet become established for clinical use in any human muscle atrophy. 

Mendell JR, Engel WK. (1971) The fine structure of type n muscle fiber atrophy. Neurology 21, 358-365. 

Type-2 muscle fiber atrophy can be cansed by varions abnormalities, snch as cachexia, hypoactivity (disnse), glncocorticoid excess, hyperparathyroidism, a manifestation of recent pan-deinnervation [51, 52] or pan-dysinnervation, or npper-motor-nenron abnormality (for extensive discnssion, see Chapter 1). 

Vignette 1. Type-2 muscle-fiber atrophy, neoplasm-related cachectic atrophy, plus sensory-motor neuropathy... 

Proximal muscle weakness in an elderly patient associated with a normal electromyogram (EMG) can be caused by type-2 muscle fiber atrophy, which is diagnosable only on muscle biopsy. One should seek an identifiable cause, such as cachexia, disuse, glucocorticoid toxicity, a "remote" neoplasm, hyperparathyroidism, subtle denervation, or supra-segmental central nervous system (CNS) abnormality. This mainly-sensory nerve neuropathy can cause slowed sensory nerve conductions, if involving large diameter fiber, small diameter ones. 

Quadriceps muscle biopsy showed prominent type-2 muscle-fiber atrophy (especially of the type 2B fibers) prominent in degree and extent, and slight recent denervation (see Chapter 1 in this volume). Imaging of his chest disclosed a small lesion, which upon biopsy was a solitary bronchogenic small-cell carcinoma. Other studies did not disclose any me-tastases. Surgical resection of the chest lesion was considered complete. 

Waganat J, Cao Z, Pathare P, Aiken JM. (2001) Mitochondrial DNA deletion mutations colocahze with segmental electron transport system abnormalities, muscle fiber atrophy, fiber splitting, and oxidative damage in sarcopenia. FASEB J15, 322-332. 

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