I recently read an article in InDepth magazine about decompression sickness (DCS) in freediving. DCS in freediving is known as Taravana syndrome. In recent years, cases appear to be on the rise, which is thought to be related to the steady expansion of freediving limits. A case report raises the question of whether Taravana syndrome is actually a separate entity and what is known about it.
Taravana syndrome
Taravana syndrome was first described in 1956 by Dr. Truc, a French military doctor, and refers to neurological symptoms observed in mother-of-pearl divers in French Polynesia. The term “Taravana”, which means “going mad” in the local dialect, was coined in 1968.
It is difficult to collect reliable data on the syndrome. Most information comes from anecdotal reports or small case studies, which probably do not reflect the actual incidence. Diagnosis of the condition is difficult and subjective as criteria and methods vary. Key risk factors for Taravana syndrome include the number, depth, duration and frequency of free dives, as well as short surface intervals and rapid ascent and descent rates.
Truc explained the syndrome by the formation of nitrogen bubbles in the brain caused by repeated decompression during repetitive apnea dives and classified it as a form of cerebral decompression sickness (DCS). However, this is precisely where the problem lies: it is anything but certain whether this theory is actually true.
The case report
A remarkable case report in “frontiers of physiology” sheds light on Taravana syndrome from another perspective. A previously healthy 45-year-old freediver lost consciousness after several apnea dives and suffered an epileptic seizure. He had previously made several short dives to a depth of 10 m, followed by four dives to 41 m with surface intervals of 4 to 6 minutes and apnea times of up to 3 minutes 27 seconds. He was using an underwater scooter and had ascended and descended very quickly with ascent speeds of up to 180 (!) m/min.
The unconscious man was transported to hospital by air ambulance. A chest-CT-scan ruled out gas embolism caused by pulmonary barotrauma. An MRI (magnetic resonance imaging) showed posterior cerebral edema (swelling of the brain in the posterior region). Hyperbaric chamber therapy was initiated. The patient was oriented the next morning, but still showed slight speech disorders. Over nine days, he received further sessions of Heliox-based hyperbaric oxygen therapy, which completely normalized his neurological condition. An MRI check after one week showed a significant reduction in the cerebral edema.
The clinical picture and MRI findings indicate Posterior Reversible Encephalopathy Syndrome (PRES), a rare neurological disorder characterized by transient cerebral edema (swelling), especially in the posterior brain area. Typical symptoms include headaches, visual disturbances, confusion, seizures and increased blood pressure. Common triggers are excessive high blood pressure, kidney failure, autoimmune diseases or certain medications. PRES is usually reversible if the underlying cause is treated promptly. Diagnosis is typically made by MRI, which shows characteristic edema of the brain.
Possible mechanisms
Possible mechanisms of PRES include impaired cerebral autoregulation (blood pressure self-regulation of the brain), endothelial dysfunction or local ischemia (circulatory disorder). Endothelial dysfunction means damage to the inner layer of the vascular wall (endothelium), which leads to increased permeability of the blood-brain barrier. This allows fluid and proteins to leak into the brain tissue, which contributes to the formation of edema.
Endothelial dysfunction plays a role in DCS.
Endothelial dysfunction is increasingly coming to the foreground as an explanation for certain forms of decompression sickness (DCS). The fact that PRES occurs in connection with extreme freediving is particularly remarkable from this point of view.
The authors of the case study discuss possible pathophysiological mechanisms. Pulmonary barotrauma could be excluded. In addition, venous gas embolisms are rarely observed during freediving, which means that the mechanisms typical for a classic DCS such as pulmonary (arterio-venous anastomoses) or cardiac right-to-left shunts (open foramen ovale) do not play a role. For this reason, the authors favor the autochthonous (local) formation of gas bubbles directly in the brain as the trigger, which would lead to damage to the endothelium and thus the blood-brain barrier, which is the basic prerequisite for cerebral edema. But is this true?
De novo gas bubble formation in the brain during apnea diving? - Rather not.
The brain is generally considered to be excellently protected against DCS thanks to its excellent blood supply and active metabolism, which rapidly dissolve any gas bubbles that are entrapped. The brain is usually only affected in catastrophic cases of DCS, where massive amounts of gas bubbles enter the arterial system via right-to-left shunts. It therefore seems implausible that new bubbles could form in the brain of all places - especially in free diving, where the supersaturation levels of scuba diving are never reached. I would therefore dare to say that this explanation is hardly valid.
What is particularly interesting, however, is the link that the authors make between Taravana syndrome and PRES. In doing so, they open the focus far beyond DCS. During extreme or repeated free diving, conditions occur that are similar to the triggers of PRES. For example, extreme blood pressure spikes have been reported during free diving. It is also known today that repetitive freediving causes very accentuated oxygen deficiency situations. The latter lead to an “oxygen debt” that cannot be sufficiently compensated for even when taking the usual surface breaks, which could cause effects in the brain similar to a circulatory disorder (ischemia) (as already reported in the dekoblog).
Taravana syndrome = PRES?
Could Taravana syndrome actually be a special form of PRES, triggered by the physiological stresses of apnoea diving? This approach appears reasonable and offers a more convincing explanation than the theory of local gas bubble formation in the brain. It remains to be seen whether future research can confirm a connection.
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