Neuroimaging of scuba diving injuries to the CNS

AJNR. American journal of neuroradiology

Diving-related decompression illness is classified into 2 main categories: arterial gas embolism and decompression sickness. The latter is further divided into types 1 and 2, depending on the clinical presentation. MR imaging is currently the most accurate neuroimaging technique available for the detection of brain and spinal cord lesions in neurologic type 2 decompression sickness. Rapid bubble formation in tissues and the bloodstream during ascent is the basic pathophysiologic mechanism in decompression illness. These bubbles can damage the central nervous system through different mechanisms, namely arterial occlusion, venous obstruction, or in situ toxicity. Neuroimaging studies of decompression sickness have reported findings associated with each of these mechanisms: some typical results are summarized and illustrated in this article. We also review the limitations of previous work and make practical methodologic suggestions for future neuroimaging studies.

Frontiers in Physiology, 2021

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mix...

Journal of Applied Physiology, 2016

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 (N 2) 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 N 2 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 (N 2) 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).

Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine, 1997

Scuba diving is associated with risk of severe decompression sickness (DCS type II), which results from rapid reduction of the environmental pressure sufficient to cause the formation into tissue or blood of inert gas bubbles previously loaded within tissues as a soluble phase. DCS type II constitutes a unique subset of ischemic insults to the central nervous system (CNS) with primarily involvement of the spinal cord. Ten patients with diving-related barotrauma underwent neurologic examination. Two of them presented progressive sensory and motor loss in the extremities at admission and were presumed affected by spinal cord DCS. Magnetic resonance imaging (MRI) demonstrated abnormalities in the white-matter tracts of the spinal cord in these patients, in each case corresponding to an area of the cord believed to be clinically involved. After a course of therapeutic recompressions, one patient was able to stand and walk a short distance, and MRI revealed a decreased extension of areas of spinal cord abnormalities. MRI has proved to be reliable in the detection of pathologic changes of spinal cord decompression sickness that were previously undetectable by other neuroimaging methods and also has proved to be useful in the follow-up during therapeutic hyperbaric recompressions.

Aviation Space and Environmental Medicine

We report a case of transient neurological disorder compatible with cerebral decompression illness in a breath-hold diver. A large right-to-left shunt was later detected with contrast transcranial Doppler ultrasound. While the mechanism of brain damage is unclear, this observation highlights the need for breath-hold divers to avoid excessive nitrogen loading and to refrain from forceful Valsalva maneuvers that may contribute to the opening of a patent foramen ovale and lead to paradoxical cerebral embolism. Because decompression illness is a possibility, anyone who experiences unusual symptoms after breath-hold diving should seek immediate medical attention.

Journal of Applied Physiology, 2016

TO THE EDITOR: Schipke and Tetzlaff (5) suggest breath-hold diving may recruit intrapulmonary arteriovenous anastomoses (IPAVA), providing a pathway for venous gas emboli to become arterialized leading to transient neurological injury consistent with transient ischemic attacks. To be a valid hypothesis there must be evidence of microbubbles in the right ventricle, left ventricle, carotid, or cerebral arteries of breath-hold divers after a typical dive profile with common dive times and surface intervals. Only one study could find evidence of microbubbles in the pulmonary infundibulum in a single subject (2) who had never even had symptoms of decompression sickness! With no evidence of arterialized microbubbles, the suggestion of IPAVA recruitment is premature. The recruitment of IPAVA by hypoxia is equally controversial, owing in part to an invalidated measurement technique that lacks a quantifiable assessment of IPAVA blood flow and involves a contrast agent that is susceptible to changes in transit time, blood gases, barometric pressure, and blood viscosity (1). Alternatively, we wondered if the dive profile of commercial breath-hold divers could be a sufficient intermittent hypoxic stimulus predisposing divers to the same cerebrovascular dysfunction observed in obstructive sleep apnea patients with similar presentations on neuroimaging studies (4). Progressive cerebrovascular dysfunction may underlie acute neurological injury, particularly if breath-hold diving acutely increases cerebrovascular transmural wall stress (through increased cerebral blood volume). The presence of vasogenic edema in breath-hold divers with neurological injury (3) supports a role for the breakdown of the blood-brain barrier, rather than gas emboli from IPAVA recruitment.

PLoS ONE, 2014

Background: Acute decompression illness (DCI) involving the brain (Cerebral DCI) is one of the most serious forms of divingrelated injuries which may leave residual brain damage. Cerebral DCI occurs in compressed air and in breath-hold divers, likewise. We conducted this study to investigate whether long-term breath-hold divers who may be exposed to repeated symptomatic and asymptomatic brain injuries, show brain damage on magnetic resonance imaging (MRI).

Journal of Applied Physiology, 2016

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 (N 2) 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 N 2 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 (N 2) 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).

Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc

Neurological signs and symptoms are common in recreational divers with decompression illness (DCI). The spectrum of neurological manifestations, temporal profile, and laboratory findings are described in a large series of 200 consecutive recreational divers treated for DCI. The Hyperbaric Medicine Unit charts of 200 recreational divers treated for DCI were reviewed and analyzed. The cohort was mainly male, with a median age of 40 years, and quite experienced, with a median of 100 prior dives. In 44 divers (22%) a rapid ascent was documented. The median time to onset of neurological symptoms was 60 minutes after surfacing. One hundred seventy-seven of 200 divers (88.5%) had at least one symptom of neurological DCI at presentation. The most common neurological manifestations were paresthesia, dysesthesia, incoordination, motor weakness, and dizziness. Paresthesias were associated with significantly younger (p = 0.003) and less experienced (p = 0.03) divers. Similar but less significan...

Neuroradiology, 2005

In the course of an ongoing study [1] on the value of post-mortem digital imaging in forensic pathology that is approved by both the local ethics committee and the juridical authorities, the deceased are examined by standard protocols with both multi-slice CT and MRI. We report the case of a fatal barotrauma where sectional imaging revealed uncommon findings that were later confirmed at autopsy.