Quote Originally Posted by tbone1004 View Post
his article was not about ICD, it was about IEDCS, two very different things, position of the C and D are important. One often causes the other, but you can get inner ear hits without helium.
The article proposes counter diffusion as the mechanism of isolated IEDCS:
In the intro:

the development of deeper diving techniques involving breathing of helium-oxygen gas mixtures has been associated with the occurrence of “pure” or “isolated” IEDCS (7), especially when switches to air or other nitrogen-rich breathing gas mixtures are made to accelerate decompression (3). Indeed, isobaric switches of inspired gas, made while the diver is held at a constant ambient pressure, have precipitated symptoms of IEDCS in the absence of any decompression.

In the discussion:
The case described here typifies the type of technical recreational diving that is becoming increasingly widespread. It also illustrates the potential for isolated IEDCS to occur in a seemingly random fashion during an otherwise uneventful deep technical dive that has gone according to plan. As we will discuss below, this case and others like it suggest that some decompression algorithms for deep technical dives, particularly those incorporating switches to nitrogen-rich breathing gas, may need to be modified to avoid such events. It certainly seems possible that isolated IEDCS will become more common as technical diving grows in popularity.
Quote Originally Posted by tbone1004 View Post
note that I said I'd be shocked if the gas switch was determined to be a contributing factor, ergo the gas switch was not relevant unless he dil flushed whcih there was no mention of.
The breathing-gas switch results in a transient elevation of vascular compartment and endolymph gas tensions above ambient pressure; such supersaturation is required for bubble formation. The peak vascular compartment gas tension was 37.8 atm (0.4 atm supersaturation) occurring at 2 min after the gas switch.

And later in the discussion section...
However, IEDCS is clearly associated with switching breathing gas from helium-rich to nitrogen-rich mixtures (4, 10), and the present model suggests that such gas substitution may cause bubble formation in the membranous labyrinth and endolymph. The model implicates transient supersaturation resulting from a counterdiffusion mechanism in which helium transfer from the perilymph to the other compartments temporarily exceeds the washout of helium in the venous blood.