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Juvenile MG represents a subclassi cation of autoimmune MG94 100 It is estimated that approximately 10% of acquired (non-neonatal) autoimmune MG cases will occur before 18 years of age, the majority subsequent to puberty 94 This statistic may be in ated, as some reported seronegative cases could easily represent congenital myasthenic syndromes (CMS) Few studies have been speci cally directed toward this patient population As a result, only modest data are available The mean age of onset for juvenile MG ranges from 7 to 14 years96,99 The distinction from adult MG may be arti cial, as all features seem identical except age The clinical features are similar to adult-onset MG, with the majority of patients initially presenting with primarily ocular symptoms99 Serum AChR antibodies are present in the majority of affected children The electrophysiologic ndings are also identical to the adult form of the disease100
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Transient neonatal autoimmune MG develops in approximately 10% of infants born to mothers with MG101 124
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autonomic neuropathy (eg, intestinal pseudoobstruction) with or without encephalopathy concomitant with the MG and thymoma142,145,146 Various autoimmune channelopathies occur in patient with MG Rare patients have a combination of MG and LEMS serologically and electrophysiologically147 151 Approximately 5% of patients with MG also have an in ammatory myopathy116,127 129,152,153,154 Most of these patients also have a thymoma with or without myocarditis The histopathology often reveals a giant cell or granulomatous myositis Serum CK levels are usually elevated with concomitant in ammatory myopathy, which would not be expected in MG alone A number of relatively rare conditions have been reported to coassociate with MG and thymoma These include acquired neuromyotonia or Isaacs syndrome,77,136,153,155 158 rippling muscle disease,69,70,153,155,159,160 stiff-persons syndrome161,162
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The following represents the current classi cation of these disorders based on the location of the NMT defect Mutations affecting epsilon subunit of AChR (primde ciency), rapsyn, and Dok-7 result in the most common forms of CMS Clinical features that are characteristic of individual disorders distinct from the general characteristics mentioned above are listed163
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CONGENITAL MYASTHENIC SYNDROMES
The congenital myasthenic syndromes (CMS) represent rare or at least uncommonly recognized genetic defects in speci c proteins, which, under normal circumstances, facilitate ef cient NMT at presynaptic, synaptic, or postsynaptic locations163 As in MG, their phenotype is typically dominated by fatiguing weakness Unlike MG of LEMS, these are not disorders of autoimmunity In general, the clinical manifestations of CMS may be somewhat heterogeneous, even within the limited phenotypic repertoire of the neonate and infant Reduced uterine motility may be recognized by the mother of the affected child Arthrogryposis multiplex congenita has been reported in at least three of the syndromes Most affected individuals will suffer from neonatal hypotonia in combination with a poor suck, weak cry, variable but usually symmetric ptosis, stridor, choking spells, and/or ventilatory dif culties that may include apnea Ophthalmoparesis may be observed As in other DNMT, the intensity of the children s problems may worsen as the day progresses, as the child ages, or with physical activity The natural history of these disorders varies both within and between the different syndromes Delayed motor milestones are the norm in those affected in infancy Some individuals have a seemingly static course, whereas slow disease progression is anticipated in two of the syndromes Most affected individuals are affected at birth or soon thereafter, but milder forms presenting later in life with fatigable limb or oculobulbar weakness do occur163,164 Identi cation of other family members in keeping with a recessive inheritance pattern or consanguinity is supportive of the diagnosis, but the absence of other affected family members does not preclude CMS from consideration Some forms of the slow channel syndrome are inherited in a dominant fashion165 168
Choline acetyltransferase de ciency This recessively inherited syndrome was originally designated as a familial infantile myasthenia Children affected by this tend to have an episodic rather than a static disorder characterized by feeding dif culties due to fatigue while sucking, a weak cry, intermittent ptosis, and spontaneous apnea episodes that may be provoked by fever, emesis, or excitement169 177 Children may expire due to these apneic periods, although these episodes tend to resolve if the child survives to adolescence or adult life CMS with paucity of synaptic vesicles and reduced quantal release The reported phenotype in this disorder included ptosis, ophthalmoparesis, facial weakness, and generalized fatigable extremity weakness beginning in infancy178,179 Other unde ned
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