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THE CONGENITAL NEUROMUSCULAR DISORDERS
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Included under this title are two sizable groups of muscle diseases one is an assemblage of old congenital deformities that involve muscle, and the other is a unique class of hereditary diseases called congenital myopathies Insofar as all of the disorders comprising these categories develop in utero, ie, are congenital, it may be helpful by way of introduction to summarize brie y the main facts about the natural development and aging of muscle Such diseases are of particular importance in pediatric neurology, for most of them attract notice at an early age
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The Development and Aging of Muscle
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The commonly accepted view of the embryogenesis of muscle is that muscle bers form by fusion of myoblasts soon after the latter differentiate from somatic mesodermal cells Muscle connective tissue derives from the somatopleural mesoderm The myoblasts, which are postmitotic, are spindle-shaped mononuclear cells that fuse to form muscle bers After fusion, a series of cellular events including the sequential activation of myogenic transcription factors leads to myo bril formation The newly formed bers are thin, centrally nucleated tubes (appropriately called myotubes) in which myo laments begin to be produced from polyribosomes As myo laments become organized into myo brils, the nuclei of the muscle ber are displaced peripherally to a subsarcolemmal position Once the nuclei assume a peripheral position, the myo ber is formed The detailed mechanisms whereby myoblasts seek one another, the manner in which each of a series of fused nuclei contribute to the myotube, the formation of actin and myosin brils, Z-discs, and the differentiation of a small residue of satellite cells on the surface of the bers are reviewed by Rubenstein and Kelly The mechanisms that determine the number and arrangement of bers in each muscle are not as well understood Presumably the myoblasts themselves possess the genetic information that controls the program of development, but within any given species there are wide familial and individual variations, which account for obvious differences in the size of muscles and their power of contraction The number of bers assigned to each muscle is probably attained by birth, and growth of muscle thereafter depends mainly on the enlargement of bers Although the nervous system and musculature develop independently, muscle bers continue to grow after birth only when they are active and under the in uence of nerve Measurements of muscle ber diameters from birth to old age show the growth curve ascending rapidly in the early postnatal years and less rapidly in adolescence, reaching a peak during the third decade After puberty, growth of muscle is less in females than in males, and such differences are greater in the arm, shoulder, and pelvic muscles than in those of the leg; growth in ocular muscles is about equal in the two sexes At all ages, disuse of muscle decreases ber size by as much as 30 percent (at the expense of myo brils), and overuse increases the size by about the same amount (work hypertrophy) Normally, type 1 (oxidative enzyme rich) bers are slightly smaller than type 2 (phosphorylative en1244
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zyme rich) bers; the numerical proportions of the two ber types vary in different muscles in accordance with their natural functions During late adult life, the number of muscle bers diminishes and variation in ber size increases The variations are of two types: group atrophy, in which clusters of 20 to 30 bers are all reduced in diameter to about the same extent, and random single- ber atrophy Also, there is enlargement of other bers The exercising of young animal muscle causes a hypertrophy of high-oxidative type 1 bers and an increase in the proportion of low-oxidative type 2 bers; aging muscle lacks this capacity exercise produces only an increase in the proportion of type 2 bers (Silbermann et al) No such data are available in humans, but clinical observation suggests that with aging, the capacity of muscle to respond to intense, sustained exercise is diminished Also, muscle cells, like other cells of postmitotic type, are subject to aging changes (lipofuscin accumulation, autophagic vacuolization, enzyme loss) and to death Group atrophy, present to a slight degree in 90 percent of gastrocnemii in individuals more than 60 years of age, represents denervation effect from an aging-related loss of lumbar motor neurons and peripheral nerve bers Further comments regarding muscle and aging can be found in Chap 29 Denervation from spinal motor neuron or nerve disease at every age has roughly the same effect namely, atrophy of muscle bers ( rst in random distribution, then in groups) and later, degeneration Muscle necrosis at all ages excites a regenerative response from sarcolemmal and satellite cells in any intact parts of the bers Presumably, if this occurs repeatedly, the regenerative potential wanes, with ultimate death of the ber leading to permanent depopulation of bers with the expected muscle weakness
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CONGENITAL DEFORMITIES INVOLVING MUSCLE Congenital Fibrous Contractures of Muscle and Joint Deformities
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Arthrogryposis (Arthrogryposis Multiplex Congenita) (Table 52-1) Multiple congenital contractures, multiple congenital articular rigidities, and amyoplasia congenita are some of the names that have been applied to congenital deformity and rigidity of many joints This disorder, now generally referred to as arthrogryposis
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Table 52-1 The main causes of arthrogryposis Werdnig-Hoffmann motor neuron disease Myotonic dystrophy Congenital myasthenia gravis (see Chap 53) Congenital polymyopathy Neonatal neuropathy Prader-Willi syndrome Amyoplasia (focal arthrogryposis)
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