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LABORATORY FEATURES
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Serum CK is normal or slightly elevated Motor and sensory NCS are normal However, EMG is usually very abnormal, particularly in the severe X-linked infantile-onset form, revealing increased insertional and spontaneous activity in the form of positive sharp waves, brillation potentials, complex repetitive discharges, and even myotonic discharges6 Early recruitment of short-duration, small-amplitude MUAPs are evident in weak muscles Reduced amplitudes and mild slowing of motor and sensory NCS have been noted in some individuals with mutations in dynamin 2 gene (discussed in Pathogenesis section), which is not surprising as this is also a cause of dominant intermediate Charcot Marie Tooth disease type B(DI-CMTB)
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HISTOPATHOLOGY
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Muscle biopsies reveal myonuclei in the center of muscle bers, often forming chains when viewed longitudinally55 Occasionally, the nuclei cluster in the center of the ber rather than forming longitudinal chains On transverse section, the number of muscle bers with central nuclei range from 25% to 95% (Fig 25 8) The central nuclei appear in both ber types On ATPase stains, there is small perinuclear halo devoid of ATPase activity With oxidative enzyme stains, center of muscle bers appear dark and there is a radial arrangement of the intermyo brillar network, which resembles spokes on a wheel The type 1 bers predominate and appear hypotrophic, while the type 2 bers are normal in size Muscles biopsies of obligate female of X-linked myotubular myopathy may also show mild abnormalities57 On EM, there are reduced myo brils and an excess of mitochondria and glycogen granules in the center of muscle bers that are not occupied by nuclei
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MOLECULAR GENETICS AND PATHOGENESIS
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As noted previously, there is genetic heterogeneity between the different forms of centronuclear myopathy (Table 25 1) The severe X-linked neonatal form is caused by mutations in the myotubularin gene (MTM1)62,63 Myotubularin is a dual-speci city phosphatase, which plays a role in muscle cell growth and differentiation Terminal muscle ber differentiation is dependent on the hypophosphorylation of speci c gene-regulating proteins64 Myotubularin is thought to dephosphorylate these regulating proteins, and
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SECTION II
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Figure 25 8 Centronuclear myopathy Increased number of internalized nuclei often in the center of the muscle ber is appreciated (A), hematoxylin and eosin (H&E) Late childhood- and adult-onset cases often have increased nuclei more randomly located throughout the bers Central areas appear dark on NADH-TR (B)
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mutations in the myotubularin gene lead to loss of function of this phosphatase activity, resulting in maturational disturbances of muscle Some autosomal-dominant cases of late-onset centronuclear myopathy characterized by prominent distal limb weakness and ptosis have been linked to mutations in the DNM2 gene on chromosome 19p132, which encodes for dynamin-254,65 Recently, mutations in this gene have also been reported in 5 sporadic cases of severe neonatal centronuclear myopathy Of note, mutations in this gene cause dominant intermediate Charcot-Marie-Tooth disease B(DI-CMTB),66 thus explaining some of the overlapping features (distal weakness, mild sensory abnormalities) that might be seen Dynamin-2 belongs to the family of large GTPases and is important in endocytosis, membrane traf cking, actin assembly, and centrosome cohesion54 The autosomal-recessive forms of centronuclear myopathy have not been genetically linked
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a weak cry and suck in infancy6 Motor milestones are delayed, but muscle weakness is usually nonprogressive and functional status improves with age attained However, there are cases with a progressive and sometimes fatal course secondary to respiratory muscle insuf ciency67 Some children who are affected display dysmorphic facial features with a high-arched palate, congenital hip dislocations, kyphoscoliosis, arthrogryposis, and a rigid spine Muscle stretch re exes are reduced Approximately one-third of patients have some type of central nervous system abnormalities; some of these cases may represent forms of congenital muscular dystrophy with impaired glycosylation of alphadystroglycan (see 24)
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