Why Predominantly Neurological Decompression Sickness in Breath-Hold Divers?
Authors: J. D. Schipke, K. Tetzlaff
DOI / Source: 10.1152/japplphysiol.00840.2015
Date: 2016
Reading level: Intermediate
Why This Matters for Freedivers
Freediving DCS, when it shows up, often looks “neurological” (weird vision changes, numbness, weakness, vertigo, confusion) rather than the classic joint pain people associate with scuba. This article gives a plausible explanation for why: low oxygen during long/repetitive sessions may open “shortcut” blood pathways in the lungs that let venous bubbles slip into the arterial side and reach the brain.
Synopsis
For years, many divers assumed breath-hold divers were basically protected from decompression sickness because they only take one breath at the surface and don’t breathe compressed gas at depth. This viewpoint challenges that assumption and focuses on a very specific puzzle: when DCS-like problems happen in freedivers, why are they so often neurological.
The authors start by reviewing real-world reports: traditional working divers (like the Japanese Ama) and other repetitive breath-hold divers have documented stroke-like episodes after long sessions of repeated dives with short surface intervals. Competitive divers have also reported neurological events after very deep dives. These cases often occur in young, healthy people with no typical stroke risk factors, and brain imaging sometimes shows lesions consistent with reduced blood flow or small vessel blockages.
The core idea is about how bubbles could reach the brain in breath-hold diving. Normally, tiny venous bubbles (if they form) should be filtered out by the lung’s capillary network before they ever reach the arterial circulation. The authors propose that freediving has a special ingredient that may weaken that “lung filter”: hypoxia. During longer apneas—especially in repetitive diving—oxygen levels can drop very low. Hypoxia is known to recruit intrapulmonary arteriovenous pathways (think of them as larger “bypass channels” in the lung circulation). If these pathways open, venous bubbles can potentially pass through the lungs without being filtered and become arterialized, meaning they can travel to the brain.
Once bubbles reach the brain’s circulation, the clinical picture can look like a transient ischemic attack: sudden weakness, numbness, speech problems, vision disturbances, confusion, or vertigo that may resolve within minutes to hours. That “sometimes it resolves” pattern is one reason these cases can be under-recognized or dismissed as something else. The paper argues that this mechanism could help explain both dramatic neurological events and “silent” damage seen on imaging in some long-term breath-hold divers.
The authors also compare this to scuba-related mechanisms. In scuba, arterialization is often discussed in the context of a heart shunt (like PFO) or large bubble loads overwhelming the lung filter. In freediving, they suggest that hypoxia-driven opening of lung shunts could be an additional (and underappreciated) route for bubbles to reach the brain—helping explain why the clinical presentation skews neurological rather than “pain-only” DCS.
Bottom line: the paper doesn’t claim every neurological symptom after freediving is DCS, but it provides a coherent physiological story for why repeated or extreme breath-hold diving can produce brain-first decompression-type problems, and why those problems might be more common than we think if we only look for classic scuba-style symptoms.
Abstract
Breath-hold divers have long been thought to be largely protected from decompression sickness because inert gas uptake is limited to the nitrogen contained in the single breath taken before submersion. However, multiple reports describe stroke-like neurological events after repetitive breath-hold diving and after single extreme dives. This viewpoint discusses potential mechanisms that could explain why decompression illness in breath-hold divers appears predominantly neurological, focusing on arterialization of venous gas emboli through right-to-left pathways. The authors propose that hypoxia during breath-hold diving may recruit intrapulmonary arteriovenous shunts, allowing venous nitrogen bubbles to bypass the pulmonary capillary filter, enter the arterial circulation, and embolize cerebral vessels, producing transient or persistent neurological injury.