Neonatal Myasthenia Gravis

Abstract

An elegant chapter of recent medical history is the clarification of the pathogenesis of acquired myasthenia gravis.1 It is now recognized as an immunologic disorder, a principal aspect of which is antibody attack on the acetylcholine receptor protein.The muscle cell receptor apparatus is

Neuromuscular Junction Disorders and Floppy Infant Syndrome: A Comprehensive Review

“…Treatment is symptomatic; assisted ventilation, exchange transfusion, and intravenous immunoglobulins (IVIg) are rarely needed [19]. For the most part, the transmitted disease is short-lived (days to usually weeks), which reflects the biologic decay of circulating antibody and regeneration of normal binding protein at the myoneural junction of the baby, usually disappearing after six weeks [2,22]. In the meantime, the infant will benefit from symptomatic care and anticholinesterase drugs [2].…”

The Management of Myasthenia Gravis in Pregnancy

“…It is caused by transplacental passive transfer of circulating nicotinic acetylcholine receptor antibodies from the myasthenic mother to the fetus. 2,[27][28][29][30] It is not possible to precisely predict the occurrence and severity of neonatal MG; it is unclear why some infants are clinically affected and others remain asymptomatic, even though they have detectable acetylcholine receptor (AChR) antibodies. In general, a correlation between the occurrence and severity of neonatal MG and overall high AChR antibody titers in the mother as well as in the newborn has been observed; however, exceptions are not infrequent, and some myasthenic women without elevated AChR antibodies have had babies with neonatal MG. 31,32 The clinical severity of MG symptoms in the mother does not correlate with severity in the newborn, and neonatal MG has been reported in infants of myasthenic mothers who were in clinical remission.…”

Miastenia grave: avaliação clínica de 153 pacientes

“…A etiopatogênese é diferente nas formas neonatal e congênita. As adquiridas têm caráter auto-imune, com produção de auto-anticorpos anti-receptores de acetilcolina (AAChR) que bloqueiam os receptores de acetilcolina (AchR) na placa motora pós-sináptica, comprometendo sua função , 2,3,7,8,[13][14][15][16][17][18][19][20] . Com base etiopatogênica classifica-se a doença em dois grupos: miastenia grave não timomatosa e timomatosa.…”

“…A maioria dos autores relata que a doença pode ter início em qualquer idade, desde recém-nascidos até indivíduos com mais de 70 anos [2][3][4]6,8,10,[12][13][14][15]20,23,24,26,27,43 . Assis estudou 372 pacientes com média de idade de 23 anos para sexo feminino e 30 anos para o masculino 1 .…”