Abstract
Patients affected with the severe infantile form of SMA die mostly in their early childhood due to respiratory insufficiency and bulbar paralysis. A homozygous deletion in the “Survival Motor Neuron” 1 gene (SMN1 gene) leads to deficiency of SMN protein and degeneration of the spinal motor neuron. But SMA is not only a motor neuron disease, other organs can be involved as clinical reports indicate. Reasons as secondary neuronal damage/muscle atrophy or the primary lack of SMN are discussed in literature.1
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