The anesthetics propofol and sevoflurane have different binding sites even though they act on pretty much the same receptors. For this reason, their actions are additive, not competitive, which is a good thing. It is good because the two complement each other.
Equally important is that, due to genetic differences, different people have different sensitivity to a given anesthetic at its binding site. In other words, if propofol is not very effective in reducing symptoms in an ALS patient, it does not necessarily mean that anesthetics will not work for that patient. It is very likely that sevoflurane or some other anesthetic will do the trick.
In order for an anesthetic to be effective against ALS, it must potentiate all the right receptors, i.e., the receptors that are known to be deficient in ALS patients such as the GABA-A and glycine alpha-1 receptors. This is true for propofol and sevoflurane but not for the benzodiazepine sedatives (e.g., Versed).
Finally, the most important property of an effective anesthetic is something called potentiation. Sevoflurane and propofol both potentiate their target receptors. That is to say, they increase the receptors' affinity for their neurotransmitters, making them more efficient. This is important because potentiation does not disappear after the anesthetic is eliminated from the body. This is the reason PALS who have undergone an anesthetic treatment reported that the improvements lasted many days and weeks after the procedure.