It does indeed has a dual mechanism.
Initially, Succinylcholine is a depolarizing, noncompetitive nicotinic agonist.
Succinylcholine is basically two molecules of Acetylcholine bound together which depolarizes the membrane by opening channels in the same manner as ACh.
This depolarization initially results in a brief period of repetitive muscle excitation (fasciculations) followed by NMJ block and flaccid paralysis (Phase I) as desensitization occurs due to Na channel blockade.
Since it is Ach like the NMJ block will not be reversed by AchE inhibitors. In fact AchE inhibitors potentiates Phase I.
This is followed by a non-depolarizing, phase II block which can be antagonized by AChE inhibitors.