This is an area that is still under investigation and is pretty complex. It stands to reason that "silent" venous gas emboli that become arterialized could cause small areas of infarction with effects being cumulative, but that has not been clearly demonstrated in the literature.
The first study (Balestra & Germonpre) you linked didn't find any correlation with PFO and the number and size of "Unidentified Bright Objects" (UBOs) found on MRI scans of diving subjects' brains, though PFO is not the only source of bubble shunting. They did find some evidence of performance decrements in divers vs control on a couple of the neuropsych tests, which would be correlated with the presence of those UBOs, but there's no demonstration of causality.
The Seyithonoglu et al. study looked at 11 divers, two of whom were saturation divers. Diffusion-weighted MRI is outside my wheelhouse so I'm not comfortable offering an in-depth critique of this study, though their statement, "These findings demonstrated the high sensitivity to hypoxia in the hippocampus, globus pallidus, and putamen[11]..." seems to indicate that they believe the changes in divers were related to hypoxia and I don't think they demonstrate this in their paper.
The Connolly & Lee meta-analysis reinforces the idea of white matter injury in divers vs controls.
The Hemelryck et al. group only did neuropsych testing, no imaging, but they had the largest "n" of the studies you linked. Their conclusion, "While it" *may* (emphasis mine) "be concluded that accident‐free SCUBA diving may have some long‐term adverse effects on short‐term memory, there is however, no evidence of general higher cognitive function deficiency..." is a good summary of what they found. I thought that the comparison with boxers (in whom chronic traumatic encephalopathy has been clearly demonstrated) was an interesting one. If there is a cumulative effect of diving on neurological functioning, it's much more subtle than CTE, but I think we're beginning to recognize that that the effect is probably there in at least some divers. It will be interesting to see research in this area evolve.
The Marinovic et al. study looked at vascular function in air divers, nitrox divers and controls. They looked at vascular "stiffness" after diving with two measurements: pulse wave velocity (PWV, higher velocity = more stiffness) and augmentation index (AI, higher AI = more stiffness). They found that PWV was higher in divers, but AI was lower, which they postulated was because of exercise while diving. I didn't see in the article where this was clearly elucidated, but these effects are transient. Higher inspired partial pressures of O2 result in vasoconstriction because the reactive oxygen species (free radicals) essentially scavenge circulating nitric oxide (NO), which is an endogenous vasodilator. The way I read the paper, the authors are wondering whether this could lead to effects similar to chronic hypertension in people who dive nitrox regularly. This has not been studied at all, and I think that the positive effects of nitrox far outweigh any of the theoretical negative effects, so I would not let this dissuade me from using nitrox to improve decompression efficiency and increase safety.
Tagging
@Dr Simon Mitchell for his take on this.
Best regards,
DDM
