Occup. Med. 1992; 42: 213-214
BALANCE OF OPINION
Does diving damage your brain? I. Calder Wellcome Laboratory for Comparative Neurology, Cambridge, UK
Brain damage as an occupational hazard of professional divers is entirely compatible with the known effects on man to a raised hyperbaric pressure. It is becoming increasingly recognized that the hyperbaric environment results in total body multiple target organ changes1. Peripheral neurological damage has been known for more than a century, but some current concerns are based on the observations that such damage may occur insidiously and without history of an acute incident. An episode of acute decompression illness may cause immediate overt neurological deficits. In contrast to the spinal cord damage, the diver with cerebral artery gas embolism often makes a remarkable recovery with little or no residual signs on neurological examination. This raises the possibility of diffuse type of neurological damage which would not be shown by investigations designed to reveal focal lesions. Unlike the problem posed by dysbaric osteonecrosis when radiology was relatively objective2, no similar test can be applied to the investigation of the central nervous system. Various techniques have been applied in an endeavour to resolve this dilemma. The Technetium-99m labelled hexamethyl propylene amine oxime (HMPAO), in conjunction with single photon emission computerized tomography (SPECT), can provide an estimate of regional cerebral blood flow. Similarly, magnetic resonance imaging (MRI) is in routine neurological examination regarded as a useful technique for identification of lesions. Fluorescin angiography shows retinal vessels to be very sensitive to the effects of diving3. However, all these investigations are too indiscriminating to provide a window on what may or may not be happening in the brain. Long-term neuropsychological changes in divers and other workers in compressed air were first described in 19664, with more supportive evidence being put forward over the next two decades5"8. The described manifestations include memory loss, aggressive or antisocial behaviour, retarded reaction time, tiredness, inability to concentrate or communicate, visual difficulties, loss of interest in personal appearance and low tolerance of alcohol. Criticism of the evidence of such changes has been on the inadequacy of psychological tests, limitation of diagnostic categories and deficiency of statistical analysis9. More recently a study of both saturation and deep air divers has shown an association with neuropsychological impairment. In a series of psychological tests carried out on 282 divers and 243 controls, impairment was found in cognitive ability of Correspondence and reprint requests to: Dr I. Calder, Wellcome Laboratory (or Comparative Neurology, University of Cambridge, Madingley Road, Cambridge CB3 OES, UK.
© 1992 Butterworth-Heinemann for SOM 0962-7480/92/040213-02
the divers10. Where there have been recorded instances of decompression illness, there was a significant decline in the short-term memory component. These results suggest although the damage may be neurologically diffuse, psychologically it appears to be localized. Decompression illness, in all its manifestations, depends fundamentally on the bubble as an initiator. This may be either autochronous (local effervescence of dissolved gas in situ), or embolic. In broad terms, it may be regarded as the initiating point for the cascade of the physiological and pathological effects. The central nervous system is regarded as embracing both brain and spinal cord. Over the years the spinal bends have received much more clinical attention than that of the brain. This has undoubtedly been due to the morefloridclinical and often residual manifestations of spinal damage. In some respects this may be purely quantitative, in that the spinal cord is a small target organ of 40 g compared with a brain of 1200 g; damage to the latter going relatively unrecognized. Until 1981, there was little appreciation of the possible longterm sequelae following recovery from a decompression incident. At that time, a study showed that damage to the posterior and lateral tracts of the cord on histology was much greater than had been identified at a clinical examination a few days before death due to trauma11. Later work on spinal cords of divers, with neither clinical signs nor history of decompression incident, showed evidence of foci of demyelination essentially in the posterior columns12. In 1990, a case of severe atrophy of the caudate nucleus of the brain of a diver was reported, again, with no overt clinical signs13. These appearances show an 'iceberg' phenomenon of hidden damage. Some of these findings may add up to the long-held tenet that even in the best decompression schedules, 'silent' bubbles would evolve14, and thus there is a need for methods of clinically identifying subtle changes. One of the final arbiters in these observations may be found on histology. Current studies have shown definite evidence of damage to small cerebral vessels. The damage/changes in the brain are diffuse, affecting both grey and white matter. The material on which the observations have been made is sparse and valuable and has contributed to the making up of a mosaic of findings15. In acute phases of decompression insult, there may be plasma leakage or vasogenic oedema with focal necrosis in the grey matter, neuronal loss and prominent capillaries indicating early hyperplasia. In the white matter, areas of focal vacuolation of the myelin have been found arranged around small blood vessels, which do not normally show hyalinization.
Occup. Med. 1992, Vol. 42, No 4
The long-term changes found in the brain essentially affect the small arteries with hyalinization of the vessel walls and perivascular lacunae. A lacuna is a small space around a blood vessel in which there is usually an aggregation of proteinaceous debris, lipofuscin containing macrophages and lymphocytes. A complex of these findings was observed in a series of 25 brains studied. These abnormalities were occasionally accompanied by focal damage (infarction) in both white and grey matter. In addition, the changes were selective, in that vessels with a normal wall were present close to those which were hyalinized. These findings lead to proof positive that cerebral vasculopathy develops in divers. The mechanism is still somewhat speculative but it is not systemic on account of the random distribution. The formation of lacunae may be due to gross distension of the vessels by gas and then a slow return to normal size, leaving a surrounding area of degenerated tissue, in which there is residual debris of vasogenic oedema and cellular components. Hyalinization of small arteries is the end result of a pathological process. The mechanism must remain conceptual but with the primary provoking agent being the bubble which results in damage to the blood vessel wall. In simplistic terms, this may be regarded as an expression of Virchof s Triad, in which damage to the blood vessels may be caused by changes in blood components, blood flow or intimal damage; all of which may be part of decompression illness16. The final cause of intimal damage is further supported by the recent concept of hydrophobic and hydrophilic nature of the intima in the stasis of bubbles and the possible medial damage to the vessel walls17. In the final analysis, do the changes to the central nervous system, especially the brain, matter? They certainly do even though changes are subtle and in a relatively large organ. Nevertheless there is significant erosion into the reserves of an organ which is known to undergo a continuous process of degeneration with age18. This emphasizes the need for ongoing research into methods of clinically identifying such changes. Philosophically, the increasing evidence of the subtle changes in all systems of the body, especially the central nervous system, could be regarded as 'knowingly putting health at risk'. Efforts should therefore be targeted towards identifying, quantifying, reducing and finally eliminating such risks.
REFERENCES 1. Palmer AC. Target organs in decompression sickness. Progr Underwater Sci 1990; 15: 15-23. 2. Walder D. Will bone necrosis be a problem? J Soc Underwater Technol 1979; 5: 15. 3. Polkingthorne PJ, Sehmi K, Cross MR, Minassian D, Bird AC. Ocular fundus lesions in divers. Lancet 1988; ii: 1381-82. 4. Rozahegyi I, Roth B. Participation of the central nervous system in decompression. Ind Med Surg 1966;35:101-2. 5. Vaernes RD, Eidsvik S. Central nervous dysfunctions after near miss accidents in diving. Aviat Space Environ Med 1982; S3: 803-7. 6. Badderley A. In: Shields TG, Minsaas B, Elliott DH, McCallum RI (eds), Long term neurological consequences of deep diving. Proceedings of workshop organised by the European Undersea Biomedical Society and Norwegian Petroleum Directorate, Stavanger: Norway, 1983; 165. 7. Smyth E. Deep sea diving may cause loss of memory. New Scientist 1985; No. 1439: 8. 8. Todnem K, Nyland H, Skeidsvoll H, Svihus R, Rinck P, Kambestad BK, Arli JA. Nervous system involvement from occupational diving. An epidemiological study. Undersea Biomed Res 1990; 17: 88-9. 9. Edmonds C, Boughton J. Intellectual deterioration with excessive diving (punch drunk divers). Undersea Biomed Res 1985; 12: 321-6. 10. Morris PE, Leach J, King J, Rawlins J. Psychological and neurological impairment in professional divers. Final report of a pilot study for the Department of Energy (Project Number 2050). Diver Performance Research Unit: University of Leicester, 1991. 11. Palmer AC, Calder IM, McCallum RI, Mastaglia FL. Spinal cord degeneration in a case of 'recovered' spinal decompression sickness. Br Med J 1981; 283: 888. 12. Palmer AC, Calder IM, Hughes JT. Spinal cord degeneration in divers. Lancet 1987; 2: 1365-6. 13. Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in divers. In: Sterk W., Geeraedts L (eds), Conference Papers of the XVI Annual Meeting of the European Undersea Biomedical Society. Foundation of Hyperbaric Medicine: University of Amsterdam, 1990; 137-44. 14. Powell MR, Spencer MP, Von Ramm G. Ultrasonic surveillance of decompression. In: Bennett PB, Elliott DH (eds), The Physiology and Medicine of Diving 3rd edn. London: Balliere Tindall, 1983; 404-34. 15. Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in divers. Neuropathology and Applied Neurobiology 1982; 18: 113-24. 16. Calder IM. Changes found in the central nervous system from autopsies on divers. In: Lin YC, Shida KK, Best (eds), Man in the Sea, Vol. II, 1990; 163-80. 17. Bailey AA. Changes with age in the spinal cord. Arch Neurol 1953; 70: 299-309. 18. Hills BA. A hydrophobic oligolemellar lining to the vascular lumen in some organs. Undersea Biomed Res 1992; 19: 107-20.