Editorials

Brain damage in divers

Introduction
Diving involves risk of neurological injuries. These may arise from decompression illness (a label which recognises the difficulty in distinguishing clinically decompression sickness due to gas nucleation from gas invasion caused by pulmonary barotrauma), anoxia (caused by near drowning), and the toxic effects of high partial pressures of breathing gases. The possibility that divers and others working in hyperbaric conditions may acquire neuropsychological damage without a clear history of a precipitating event is worrying. Since 1978 five international meetings have discussed this possibility, but no consensus exists whether diving per se causes brain damage.

Much of the evidence of functional abnormalities in divers with no history of decompression illness is anecdotal. Many reports describe findings in mixed groups of divers, some with and some without prior decompression illness.^{1 2} The most quoted study involved a snapshot assessment of intellectual function in Australian abalone divers,³ with no assessment of change over time and no controls. The psychological assessment probably failed to reflect the characteristics of these particular individuals, and their dive practices.

Nevertheless, degeneration and vasculopathy are seen after death in the brains and spinal cords of unaffected divers which resemble the abnormalities found after decompression illness.^{4 5} Retinal fluorescein angiography in divers with no history of decompression illness has demonstrated vasculopathy, which may be a marker for neurovascular injury.⁶ Concern is heightened by evidence of long term injuries to other organs, such as crippling dysbaric osteonecrosis in divers and caisson workers years after hyperbaric exposure.

When neurological damage occurs in divers the prime suspects are gas bubbles. Gas nucleation is generally accepted to be the initiating event in most of the syndromes collectively known as decompression sickness. However, free gas does not invariably lead to decompression sickness. Doppler ultrasound can detect "silent" bubbles in the venous blood of many asymptomatic divers. Most bubbles are filtered out by the pulmonary capillaries. It was once believed that a critical amount of gas nucleation was required before decompression sickness occurred. We now know that this may be true for extreme decompressions in individuals without intracardiac or pulmonary right to left shunts, but in those with a shunt a relatively small bubble load can result in paradoxical gas embolism.^{7 8}

Decompression sickness can affect many systems, but the serious effects are neurological. There is usually abrupt or rapid evolution of a focal central neurological deficit (or deficits). The injury may be mild or severely disabling; it may be permanent or resolve spontaneously or with treatment with oxygen and recompression; episodes may recur. Clinically the spectrum of neurological decompression sickness resembles that of thromboembolic cerebrovascular disease, with one exception: decompression sickness commonly affects the spinal cord. This difference may be explained by the considerable gas load in the cord at the end of many dives compared with the gas content of an equivalent weight of brain tissue. The greater blood flow to the brain means that more gas bubbles embolise the brain, but more dissolved gas is available to amplify embolic bubbles in the cord. Conceivably recurrent subclinical decompression sickness may result in a condition analogous to multi-infarct dementia with gas embolism rather than thromboembolism as the initiator.

There are other neurological insults. During many normal dives neurological effects occur from variations in gas partial pressures. Every depth change of 7 m produces change in ambient pressure equivalent to a trip between sea level and the top of Mount Everest. The narcotic effects of nitrogen at depths of 30 m or less are well described. Narcosis is reversed by ascent but can repeated exposure cause target organ damage like repeated alcohol intoxication? Other breathing gases are also not inert at high partial pressures. Oxygen is neurotoxic. Very deep dives, during which mixtures containing helium are breathed, can result in the high pressure neurological syndrome, which causes excitatory effects including tremor, myoclonus, and convulsions. Repeated insults might produce permanent harm.

Until recently investigational techniques were too insensitive to detect neurological abnormalities in "normal" divers or even in those with clinical effects from decompression illness⁹. Magnetic resonance imaging seems to offer greatest promise. Reul and colleagues found more hyperintense subcortical white matter lesions in the brains of sport divers than in non-diving controls.¹⁰ The difference was due to a subgroup of divers who had multiple brain lesions. In this issue Knauth and colleagues report that multiple brain lesions on magnetic resonance scans in sport divers occur exclusively in those with large right to left shunts (presumed to be patent foramen ovale, though some may be small atrial septal defects or pulmonary arteriovenous shunts) (p 701).¹¹

These observations are consistent with the well documented role of shunts in the pathogenesis of overt decompression illness by means of paradoxical gas embolism but extend this role to subclinical injury. This is plausible. Decompression illness is a spectrum. It may be so mild that divers do not seek treatment.⁸ Divers who have had decompression illness and in whom we find a large shunt often recollect mild neurological symptoms after earlier dives which they did not consider important at the time. The fact that the illness can be mild adds plausibility to studies showing an increased prevalence of subclinical lesions in divers with a large shunt but also cautions against accepting data uncritically from studies in which subjects were self selected.^{10 11}

The results of magnetic resonance scans in others exposed to hyperbaric conditions have not been entirely consistent. Caisson workers also have an increased prevalence of brain lesions.¹² Professional divers do not,¹³ even though necropsy evidence of pathological injury is commoner than in sport divers.⁵ Magnetic resonance imaging does not always reveal abnormalities in cases of clear neurological decompression illness.¹⁴ These apparent contradictions may be due to differences in imaging techniques, methods of subject recruitment, and confounding variables. Interestingly, magnetic resonance findings do not correlate with the results of psychometric tests or electroencephalograms.^{12 13} Further investigation into the possibility that diving per se causes brain damage is required, but we must not forget that evidence of pathological change is not proof of functional deficit.

Peter Wilmshurst, Consultant cardiologist ^a

^a Royal Shrewsbury Hospital, Shrewsbury SY3 8XQ

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