Fig. 6.

Proposed pathogenesis of gastrointestinal dysmotility in SSc suggests that SScIgGs initially block cholinergic neurotransmission by inhibition of ACh release by the MCN (neuropathy). With progression of the disease, SScIgGs lead to additional myopathy via inhibition of ACh action at the gastrointestinal smooth muscle proper (myopathy). This is followed by the last stage of intestinal fibrosis by yet unknown mechanisms. Dysmotility at the neuropathic and myopathic stages may be potentially reversible with IVIG, before smooth muscle fibrosis/atrophy ensue.