Caused by any one of more than 30 identified genes, the type of congenital myasthenic syndrome depends on which gene is affected.
Congenital myasthenic syndromes are classified by which location is affected in the neuromuscular junction ― the area that provides signals (impulses) between the nerve cells and the muscle cells to trigger movement (synapses). Disrupted signals that cause loss of muscle function can occur in different locations:
- Nerve cells where the impulse starts (presynaptic).
- Space between your nerve and muscle cells (synaptic).
- Muscle cells where the impulse is received (postsynaptic), the most common location.
Some types of congenital myasthenic syndromes are the result of congenital disorders of glycosylation. Glycosylation is a complex chemical process that plays a role in regulating communication between cells. Glycosylation defects can adversely affect the transmission of signals from nerve cells to muscles.
Congenital myasthenic syndromes are most commonly inherited in an autosomal recessive pattern. That means both parents must be carriers, but they do not typically show signs of the condition. The affected child inherits two copies of the abnormal gene — one from each parent. If children inherit only one copy, they won't develop the syndrome, but they'll be carriers and possibly pass the gene to their own children.
Rarely, congenital myasthenic syndromes can be inherited in an autosomal dominant pattern, meaning that only one parent passes on the affected gene. In some cases, the affected gene occurs randomly and is not inherited. In other cases, no gene can be identified.