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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

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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

the error code to an integer variable that a developer should test Any other type of exception will cause the process to panic This backward compatibility has several interesting consequences First, a developer should never mix the use of standard exceptions and SymbianOS leaves A function that leaves should not call a function that throws exceptions without enclosing it within a try/catch block in order to prevent propagation back to a TRAP macro Similarly, any function that may leave called from code using only standard exceptions should be wrapped with one of the TRAP/TRAPD macros

End-plate acetylcholinesterase (AChE) de ciency Patients born with a congenital de ciency of AChE present soon after birth or in early childhood with the phenotype described above172,173,180 184 In addition, there is mild slowing of the pupillary light response Patients do survive into adulthood but tend to have an overall reduced amount of muscle bulk and signi cant axial weakness leading to hyperlordosis and kyphoscoliosis and are often con ned to wheelchairs

Primary kinetic defect +/ AChR de ciency The slow channel syndrome is dominantly inherited in most cases There is a tendency toward a progressive course, although the severity of the phenotype can be quite variable Adult patients may have a pattern of weakness that frequently involves cervical, wrist, and nger extensor muscles accompanied by mild ophthalmoparesis, whereas infants may be wheelchair and ventilator dependent The natural history and the extent of af iction of the fast channel syndromes are variable as well Severe weakness may be present at birth

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