Freediving and Taravana syndrome: DCS or PRES?

Michael Mutter

6. Sept.

5 Min. Lesezeit

Recent case reports, and in particular the MRI findings, raise an intriguing question: could what we refer to as cerebral DCS in freediving actually, in some cases, not be decompression sickness at all, but rather posterior reversible encephalopathy syndrome – or PRES for short (roughly translated as: a reversible brain disorder syndrome affecting the occipital region)?

Taravana syndrome

The term ‘Taravana’ originates from neurological incidents among the traditional mother-of-pearl divers of French Polynesia. Following repeated free-diving sessions, those affected developed, amongst other things, confusion, impaired consciousness, neurological deficits or epileptic seizures. The main risk factors are depth, the number and duration of dives, short surface intervals, and rapid ascents and descents.

The classic explanation is as follows: during repeated deep free dives, nitrogen is progressively absorbed into the tissues. During ascent, gas bubbles form, which ultimately cause neurological symptoms. In other words, cerebral DCS.

But this is precisely where the problem begins.

PRES rather than DCS?

In a classic case of arterial gas embolism, we would expect a gas bubble to occlude a cerebral vessel. The result would be local ischaemia (impaired blood flow) with a corresponding pattern on imaging. With PRES, something different happens.

The primary issue is a disturbance in cerebral vascular regulation and the blood-brain barrier. The vessels become more permeable, fluid leaks into the brain tissue, and vasogenic oedema develops (fluid accumulation in the tissue as a result of a vascular leak).

Typical symptoms include headaches, visual disturbances, confusion, impaired consciousness and seizures. MRI scans reveal characteristic oedema, often predominantly in the posterior region (at the back of the head), which may resolve as the condition progresses.

And it is precisely these findings that have now been described in freedivers who have experienced neurological incidents.

What does the MRI show?

Sánchez-Villalobos and colleagues reported on a freediver presenting with neurological symptoms following repeated dives. The imaging predominantly showed vasogenic oedema. The changes subsequently resolved. This is much more consistent with a PRES-like process than with a classic embolic cerebral infarction, as would be expected in cases of DCS.

Even more striking is a case published by Druelle and Castagna: a previously healthy 45-year-old freediver initially completed several short dives to a depth of 10 m, followed by four dives to around 41 m, with surface intervals of four to six minutes. He used an underwater scooter and reached extreme ascent speeds of up to 180 m/min. He subsequently lost consciousness and suffered an epileptic seizure.

A chest CT scan revealed no evidence of pulmonary barotrauma as the cause of an arterial gas embolism. In contrast, an MRI scan showed posterior cerebral oedema. Following hyperbaric oxygen therapy, his neurological condition returned to normal, and after just one week, the oedema had significantly subsided on a follow-up MRI scan. The clinical picture, and in particular the imaging findings, were remarkably consistent with PRES.

Do the bubbles form directly in the brain?

Druelle and Castagna hypothesised that, following deep repetitive apnea dives, microgas bubbles might form locally in the cerebral capillaries. These would damage the endothelium (the inner lining of the blood vessels), make the blood-brain barrier more permeable and thereby trigger vasogenic oedema.

The model would be:

deep repetitive free-dives → nitrogen supersaturation of the brain → local microgas bubbles → endothelial damage → disruption of the blood-brain barrier → vasogenic cerebral oedema → PRES

But is this really plausible?

De novo gas bubbles in the brain? – I’m sceptical

Due to its very high blood flow, the brain is actually one of the tissues that can release nitrogen particularly quickly. Even gas bubbles that have entered the brain can be eliminated relatively quickly due to the intense perfusion. We therefore typically see severe cerebral gas embolisms when large quantities of bubbles enter the arterial circulation – for example, via a pronounced right-to-left shunt in cases of catastrophic decompression sickness.

The idea that, of all things, significant quantities of gas bubbles should form de novo – that is, from scratch – in the brain during freediving seems highly questionable.

Furthermore, nitrogen supersaturation during freediving does not normally reach the levels we are familiar with from long or deep scuba dives.

The hypothesis of local gas bubble formation is therefore interesting, but by no means proven – and, in my view, highly debatable.

Perhaps the bubbles aren’t even necessary

A different link between freediving and PRES is far more interesting. During deep freediving, the brain is subjected to extreme physiological stress. The arterial oxygen partial pressure can drop dramatically, particularly during the ascent. At the same time, CO₂ levels rise, cerebral blood flow increases and the diving reflex causes pronounced peripheral vasoconstriction. Added to this are, in some cases, extreme spikes in arterial blood pressure, as have been measured during deep freedives.

With repetitive dives, a further problem arises: oxygen reserves may not yet have fully recovered during the short surface intervals. An increasing oxygen debt may develop.

Consequently, within a short period of time, massive changes in:

blood pressure + hypoxia + hypercapnia + cerebral perfusion + sympathetic activation

occur simultaneously.

It is precisely such stresses that could overwhelm cerebral autoregulation (the brain’s self-regulation of blood pressure) and lead to endothelial dysfunction (impaired vascular permeability). The blood-brain barrier becomes permeable. Fluid leaks into the brain tissue. Vasogenic oedema develops. And this brings us to PRES.

Interestingly, the endothelium also plays a role in DCS

The matter becomes even more intriguing because endothelial dysfunction is by no means discussed solely in the context of PRES. In the case of decompression sickness, too, it is becoming increasingly clear that gas bubbles are not simply small mechanical ‘vascular plugs’. They interact with the endothelium, trigger inflammatory processes and can impair vascular function.

DCS and PRES may therefore be closer together pathophysiologically than the two diagnoses might initially suggest. So perhaps the question is not simply: DCS or PRES? But rather:

Can the extreme physiology of repetitive apnea diving trigger a PRES-like clinical picture via endothelial dysfunction – possibly with, but perhaps also entirely without, significant gas bubble formation?

This suggests that the term ‘Taravana syndrome’ may in fact conceal several different pathophysiological mechanisms.

DCS, PRES – or something in between?

That, to me, is precisely the most fascinating aspect. We tend to automatically interpret neurological symptoms following a dive as decompression sickness. In freediving, we should perhaps be more cautious about this. Documented cases show that severe neurological symptoms can occur following extreme repetitive freedives. At the same time, individual MRI scans reveal vasogenic cerebral oedema, which is much more consistent with PRES than with a classic embolic cerebral infarction.

This does not prove that Taravana is, in principle, a PRES. Nor does it prove that gas bubbles play no role. But it does show that the equation

neurological symptoms following freediving = cerebral DCS

is probably too simplistic.

Conclusion

Taravana syndrome has been regarded for decades as a form of cerebral decompression sickness. However, its actual pathophysiology remains unclear to this day. Perhaps this is why Taravana syndrome is not, in fact, a single condition.

What we currently refer to as ‘cerebral DCS’ in freediving may in reality encompass a spectrum of different mechanisms – ranging from genuine decompression sickness and paradoxical gas embolism to a PRES-like syndrome without significant arterial gas embolisation.