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THE MUSCULAR DYSTROPHIES
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characteristic appearance, which allows immediate recognition of the disease in the newborn infant and child Dif culty in sucking and swallowing, bronchial aspiration (due to palatal and pharygeal weakness), and respiratory distress (due to diaphragmatic and intercostal weakness and pulmonary immaturity) are present in varying degrees of severity; the latter disorders are responsible for a previously unrecognized group of neonatal deaths (24 such deaths among siblings of affected patients in Harper s study) In surviving infants, delayed motor and speech development, swallowing dif culty, mild to moderately severe mental retardation, and talipes or generalized arthrogryposis are common Once adolescence is attained, the disease follows the same course as the later form As stated earlier, clinical myotonia in the congenital form of the disease becomes evident only later in childhood, although EMG study may disclose myotonic discharges in early infancy The diagnosis may be suspected by the simple test of eliciting myotonia in the mother Electrocardiographic changes occur in one-third of the patients In the congenital form of this disease the affected parent is always the mother, in whom the disease need not be severe Electrophysiologic testing will bring out the myotonia in the mother if it is inevident on percussion of muscle (In cases of adult onset, transmission is maternal or paternal) These data suggest that in addition to inheriting the myotonic dystrophy gene, the congenital cases also receive some maternally transmitted factor, the nature of which is presently unknown The prenatal diagnosis of myotonic dystrophy is readily accomplished by examination for CTG repeats in the amniotic uid or in a biopsy of chorionic villi However, it is not possible to predict whether a fetus with an expanded mutation will have congenital myotonic dystrophy or later onset myotonic dystrophy Proximal Myotonic Myopathy (PROMM; See Table 50-2) Under this name, Ricker and colleagues have described a myopathy characterized by autosomal dominant inheritance, proximal muscle weakness, myotonia, and cataracts Seventeen families, containing 50 affected members, have been studied by these authors Onset was between 20 and 40 years, with intermittent myotonic symptoms of the hands and proximal leg muscles, followed by a mild, slowly progressive weakness of the proximal limb muscles without signi cant atrophy Cataracts developed in one half the patients and cardiac arrhythmias in only two Onset in infancy; ptosis; weakness of facial, jaw, and distal limb muscles; and mental abnormalities were notably absent, thereby distinguishing PROMM from the conventional form of myotonic dystrophy Histologically the appearance was that of a nonspeci c myopathy, without ringbinden or subsarcolemmal masses Analysis of leukocyte and muscle DNA discloses no expansion of the CTG component of the myotonic dystrophy gene Rather, the gene defect for this disease has been mapped to chromosome 3q where there is an expansion of a CCTG repeat Like the expanded CTG repeat in myotonic dystrophy, the CCTG expansion in PROMM is associated with intranuclear accumulation of the expanded RNA transcript and like the CTG repeats of myotonic dystrophy, the CCTG segments do not code for a protein
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The Distal Muscular Dystrophies (Welander, Miyoshi Types) (See Table 50-3)
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Included in this group are several slowly progressive distal myopathies with onset principally in adult life Weakness and wasting
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of the muscles of the hands, forearms, and lower legs, especially the extensors, are the main clinical features Although such cases had been reported by Gowers and others, their differentiation from myotonic dystrophy and peroneal muscular atrophy was unclear until relatively recently Several types of distal dystrophy are inherited as autosomal dominant traits For example, Milhorat and Wolff studied 12 individuals from one family affected by a progressive muscular dystrophy of atrophic distal type The onset was between 26 and 43 years; within 5 to 15 years the patients had become disabled There was one autopsy, con rming the dystrophic nature of the disease A different dominantly inherited distal dystrophy was described by Welander in a study of 249 patients from 72 Swedish pedigrees (not to be confused with the Kugelberg-Welander juvenile spinal muscular atrophy affecting proximal muscles see page 946) Weakness developed rst in the small hand muscles and then spread to the distal leg muscles, causing a steppage gait Fasciculations, cramps, pain, sensory disturbances, and myotonia were notably absent Some patients have a low-grade sensory neuropathy, suggesting that pathology in this disorder may not be exclusively in muscle Senile cataracts appeared after the age of 70 in 3 patients and can be discounted as having special signi cance No endocrine disorders were detected Dystrophic changes were demonstrated in 3 autopsies and 22 biopsy specimens The central nervous system and peripheral nerves were normal Progression of the disease was very slow; after 10 years or so some wasting of proximal muscles was seen in a few of the patients Welander dystrophy has been linked to chromosome 2p13, near the locus for the below described Miyoshi myopathy Markesbery and colleagues reported a late-onset distal myopathy in which weakness began in the distal leg muscles (tibialis anterior) and later spread to the hands; there was also cardiomyopathy and heart failure Identical distal myopathies have been described in Finnish patients by Udd and colleagues and found to be caused by dominant mutations in the titin gene A form beginning in childhood described by Laing and colleagues was shown to be due to a mutation in the gene for myosin heavy chain The characteristic feature in all these cases is progressive bilateral foot drop Miyoshi Dystrophy A second type of distal dystrophy characterized by an autosomal recessive pattern of inheritance is particularly prevalent in Japan (Miyoshi et al, Nonaka et al), but numerous cases exist in all parts of the world Onset of the disease is in early adult life, with weakness and atrophy of the leg muscles, most prominent in the peroneal or the gastrocnemius and soleus muscles Over many years the weakness extends to the thighs, gluteal muscles, and arm muscles, including the proximal ones Serum CK concentrations are greatly increased in the early stages of the disease In this Miyosh type of dystrophy the mutation leads to an absence of the muscle protein dysferlin Dysferlin is a membrane protein that does not interact with any of the dystrophin-binding elements Whereas dystrophin and its binding partners are believed to confer tensile strength the muscle membrane, dysferlin and its associated proteins (eg, the annexins) function in calcium-mediated membrane repair (Lennon) Of interest is the fact, mentioned earlier, that one of the limb-girdle dystrophies (2B) has been linked to the same chromosomal locus and also lacks the dysferlin protein It is also striking that different family members with the same dysferlin mutation can have disease onset in either a proximal (LGMD) or distal (Miyoshi) pattern, suggesting that additional factors modify the pattern of weakness produced by dysferlin de ciency We
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