Why predominantly neurological decompression sickness in breath-hold divers?

It has been widely believed that human free divers were immune to decompression sickness because the only inert gas added during a breath-hold dive is the nitrogen (N2) that remains in the lungs from the inhalation before submerging. However, there has been anecdotal evidence from case reports of divers suffering neurological symptoms after repeated free dives. In breath-hold divers of the Tuamotu Archipelago a neurological syndrome called taravana had been described as early as 1958 (33). Paulev in 1965 reported symptoms such as nausea, dizziness, progressive visual disturbances, and unilateral paresis after repetitive free dives to 20 m (66 ft.) depth, and modeling of N2 tissue saturation supported the idea of reaching critical tissue nitrogen concentrations after frequent repetitive free dives with short surface intervals (31). These observations led to the hypothesis that decompression stress would be possible in humans performing extreme repetitive breath-hold dives (20). The possibility that free-diving humans could accumulate enough (N2) in the body tissues to suffer DCS after single deep breath-hold dives remained a controversial topic (29). More cases of stroke-like incidents after repeated shallow-water dives were reported more recently from professional Japanese breath-hold divers (Ama). Kohshi et al. (17) described a case of right homonymous hemianopsia in a 33-yrold man whose magnetic resonance imaging (MRI) of the brain showed signal intensities in the left occipital lobe and right basal ganglia. Another 39-yr-old man suffered right-sided motor weakness and sensory numbness, with his MRI showing increased signal intensities in the left parietal lobe and basal ganglia (17). These divers had neither vascular diseases nor risk factors for stroke, and the MRI findings were consistent with a vascular pathogenesis of the lesions, i.e., occlusion of cerebral arteries. Remarkably, in both cases the symptoms occurred in the afternoon during the second diving shift, performing repeated breath-hold dives to 20-25 m depth with 1-min surfacing intervals for several hours. More cases of acute neurological injury in Ama divers were published subsequently (18, 19), and a recent survey among professional Japanese Ama divers revealed that 6.9% of divers reported stroke-like neurological events during or immediately after repetitive breath-hold diving (38). A neuroimaging study investigated asymptomatic Japanese breath-hold divers using MRI (19). In that study, 11 of 12 divers displayed abnormalities of the brain consistent with ischemic lesions, indicating that even in the absence of overt neurological symptoms long term breath-hold diving can cause damage to the brain, probably through accumulation of repeated transient injury (19). Another study supports possible underestimation of the true damage to the brain. In that study elite breath-hold divers ( 30 m; 5 yr experience) with normal neurologic exams and normal brain MRIs, exhibited abnormal brain SPECT images in all five divers (32). Finally, stroke-like neurological events have been reported in competitive free divers after deep breath-hold dives 100 m depth (35). Remarkably, these cases occurred in young healthy subjects without a history of cardiovascular disease or pertinent risk factors.