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Restricted Nuclear Amyotrophies
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In another group of restricted palsies, the essential abnormality appears to lie in the central nervous system (nuclear amyotrophies) One of the most frequent is congenital ptosis due to an inborn defect of the innervation of the levator palpebrae muscles Complete paralysis of all muscles supplied by the oculomotor nerve, due apparently to hypoplasia of the third nerve nuclei, may be
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DISEASES OF SPINAL CORD, PERIPHERAL NERVE, AND MUSCLE
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observed in several members of a family and occasionally in only one member As discussed in Chap 14, congenital Horner syndrome may be familial; it is associated with depigmentation of the iris (heterochromia iridis) Bilateral abducens palsy is often associated with bifacial palsy in the newborn and is known as the Mob ius syndrome; this usually nonfamilial anomaly, the cause of which is thought to be a nuclear hypoplasia or aplasia, is discussed with the developmental disorders (page 873) In these familial nuclear amyotrophies the muscles develop independently of the nervous system but have no prospect of attaining their natural growth and function and indeed of surviving because of failure of innervation It is a kind of congenital denervation hypotrophy Of course, a primary muscle defect may also give rise to bifacial weakness, as in facioscapulohumeral muscular dystrophy
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RELATIVELY NONPROGRESSIVE AND SLOWLY PROGRESSIVE CONGENITAL POLYMYOPATHIES
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(See Table 52-2) Beginning in 1956, with the account by Shy and Magee of a patient whose muscle bers showed a peculiar central densi cation of sarcoplasm ( cores ), a new class of hereditary diseases of muscle was delineated The more common and better-de ned members of this group are the central core, nemaline (rod-body), centronuclear myopathies and myo brillar degeneration, and myopathy with tubular aggregates As the names imply, in each of these diseases there is no loss of muscle bers but within each ber there is a distinctive morphologic abnormality These illnesses may express themselves early in life by a lack of muscle bulk, hypotonia, weakness of the limbs, and often with additional mild dysmorphic features of other parts of the body A variety of other morphologic types of congenital myopathy have been described, but they are relatively uncommon and some are of dubious speci city; they are mentioned only brie y
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Further study has revealed that the diseases of this group are not con ned to infancy and early childhood and some of them, especially those present at birth, are not as benign as their early descriptions implied Each of the entities mentioned above has been observed at a later age, even in middle adult life Indeed, if the disease is mild, there is often no way of deciding whether it had been present since birth The characteristic feature of most of these myopathies is lack of progression or extremely slow progression, in contrast to the more rapid pace of many muscular dystrophies, of Werdnig-Hoffmann disease, and of other forms of hereditary motor system disease of childhood and adolescence Exceptionally, an example of more rapid progression of a congenital myopathy has been reported, and prior to the use of histochemical and electron microscopic techniques, such patients were usually considered to have a benign muscular dystrophy Familial occurrence has also been established in some types, so the clinical line of separation between this group of diseases and some of the more slowly progressive muscular dystrophies may in certain cases remain ambiguous There is no speci c treatment for any of the congenital myopathies As mentioned earlier, the characteristic lesions in the congenital myopathies are revealed most clearly by the systematic application of histochemical stains to frozen sections and by phase and electron microscopy Some of the abnormalities are also disclosed by the conventional stains used in light microscopy, but as a group their identi cation has been the product of newer histologic techniques A word of caution is in order about the speci city of some of the morphologic changes and the classi cations of the congenital myopathies based upon these changes It is inadvisable to assume that a change in a single organelle or a subtle change in the sarcoplasm of a muscle ber can be relied upon to characterize a pathologic process Indeed, as more careful studies were made of this class of disease, the speci city of the lesions came to be questioned For example, central cores are sometimes found in the same
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