Abstract
SCUBA diving exposes divers to decompression sickness (DCS). There has been considerable debate whether divers with a Patent Foramen Ovale of the heart have a higher risk of DCS because of the possible right-to-left shunt of venous decompression bubbles into the arterial circulation. Symptomatic neurological DCS has been shown to cause permanent damage to brain and spinal cord tissue; it has been suggested that divers with PFO may be at higher risk of developing subclinical brain lesions because of repeated asymptomatic embolization of decompression-induced nitrogen bubbles. These studies however suffer from several methodological flaws, including self-selection bias. We recruited 200 volunteer divers from a recreational diving population who had never suffered from DCS; we then randomly selected 50 of those for further investigation. The selected divers underwent brain Magnetic Resonance Imaging to detect asymptomatic brain lesions, contrast trans-oesophageal echocardiography for PFO, and extensive neuro-psychometric testing. Neuro-psychometry results were compared with a control group of normal subjects and a separate control group for subjects exposed to neurotoxic solvents. Forty two divers underwent all the tests and are included in this report. Grade 2 Patent Foramen Ovale was found in 16 (38%) of the divers; brain Unidentified Bright Objects (UBO's) were found in 5 (11.9%). There was no association between PFO and the presence of UBO's (P = 0.693) or their size (p = 0.5) in divers. Neuropsychometric testing in divers was significantly worse from controls in two tests, Digit Span Backwards (DSB; p < 0.05) and Symbol-Digit-Substitution (SDS; p < 0.01). Compared to subjects exposed to neurotoxic solvents, divers scored similar on DSB and SDS tests, but significantly better on the Simple Reaction Time (REA) and Hand-Eye Coordination (EYE) tests. There was no correlation between PFO, number of UBO's and any of the neuro-psychometric tests. We conclude that for uneventful recreational diving, PFO does not appear to influence the presence of UBO's. Diving by itself seems to cause some decrease of short-term memory and higher cognitive function, including visual-motor skills; this resembles some of the effects of nitrogen narcosis and we suggest that this may be a prolonged effect of diving.
Highlights
SCUBA diving on air exposes divers to possible nitrogen decompression problems upon their ascent and in the hours after the dive
It is accepted that these problems (DCS: Decompression Sickness) are caused by the formation of gas bubbles in the venous/arterial blood and/or supersaturated body tissues we will refer to circulating bubbles as Vascular Gas Emboli (VGE)
Using a randomized sample population of recreational divers who had extensive diving experience without a history or symptoms of decompression sickness, and using carefully selected reliable diagnostic techniques, we were not able to demonstrate a higher prevalence of cerebral MRI abnormalities in divers
Summary
SCUBA diving on air exposes divers to possible nitrogen decompression problems upon their ascent and in the hours after the dive. The lung acts as an efficient “bubble filter,” and only when too much bubbles are present, these could pass into the arterial circulation (Butler and Hills, 1979) In this respect, it is important to limit bubble production (Egi and Gurmen, 2000), and this is possible by using “lowbubble” decompression schedules (Dunford et al, 2002), one of the research areas explored by DAN Europe (Divers Alert Network Europe) during the recent years (Marroni et al, 2004; Bennett et al, 2007)
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