Chronic Neurological Adverse Effects of Diving


There is evidence of neuropathological changes in the CNS of some divers who, at the time of death, had had no recorded incidence of decompression illness and who had been considered fit to dive (Mork 1988: Movild and Mork 1994; Palmer et al 1990). There is, however, other than the acute decompression illnesses, no described neurological illness associated with the occupation of diving. (Elliott). Dr. David Elliott has been kind enough to provide us with an update of this field of study. (April 10, 2009)

“Around 2000, separate studies began of two groups of experienced divers who had been working in the North Sea before 1990, one in the Norwegian sector and the other in the UK. After a number of abstracts presented about their progress at UHMS meetings, these two major studies (available for downloading in full from their government websites) were part of a broader review at an international meeting held in Bergen in 2005.”

Hope A, Risberg J (eds) 2006 Long-term health effect of diving. NUI AS: Bergen, Norway. ISBN-13: 978-82-7280-549-3 & ISBN-10: 82-7280-549-9.


This and other related publications deserve careful review. There were some important differences in the protocol between the two studies but nevertheless one conclusion seems to be that similar effects can also be found in non-divers, and that the factors of welding experience, exposure to contaminants and, for some aspects of occupational health, offshore stress factors are relevant. These cross-sectional studies deserve detailed attention, but also continued surveillance is needed in the form of longitudinal studies (as previously recommended by the international Long-Term Health Effects Conference at God√łysund in 1993).”

Neurological Examination

Careful examination of the CNS has to be the basis for any study of long-term effects in divers. Rozsahegyi (1959) reported a possible progressive disseminated encephalopathy among tunnel workers following acute decompression illness, but this has not been confirmed.

Norwegian professional divers have been studied in great detail (Todnem et al, 1990). On hundred fifty six divers were compared with 100 age-matched non-diving controls. If the divers reported fatigue,mood lability, irritability, concentration or memory problems, this was considered evidence of a decompression deficit. Autonomic nervous system symptoms included palpitations, diarrhea and constipation, excessive sweating and sexual dysfunction and each of these was also considered as evidence of decompression illness. The physical examination recorded as positive: increased postural tremor, a modified Romberg and reduced sensation in the feet. No specific syndrome was detected but, when all the isolated symptoms and signs were added numerically, there was a preponderance of abnormal signs in the diving population. As the majority of these divers continued to dive, the clinical significance to the individual of these findings, though statistically significant, has yet to be understood.


Curley (1988) found some transient alterations in 25 Navy divers following saturation but with no evidence of neuropsychological abnormalities. In contrast, Vaernes et al (1989) studied 64 deep saturation divers and 32 experienced divers who were only just commencing saturation diving. The authors found some mild to moderate changes which could be interpreted as random variations but they state that these could also represent some specific abnormalities. They conclude that their findings are broadly in agreement with Curley in that no major deterioration was evident. Nevertheless they suggest that their more meticulous examination might indicate the presence of a mild pathological process which cannot be detected by standard neurological examinations.

A study of 282 commercial divers and 182 non-diving controls (Morris et al, 1991) suggested that there is impairment of cognitive function in apparently healthy divers who have experienced decompression sickness. In those without previous decompression illness there was some evidence of impairment of memory and verbal reasoning but these changes were interpreted as related to age and not to diving. There was no evidenceof clinical personality change associated with diving experience and they conclude that less than 10% of the total decline in divers with no history of DCS is due to their diving.


The use of the spontaneous electroencephalogram and of evoked action potentials has, like other investigations in this field, begun with the study of persons who have suffered acute decompression sickness. To use the encephalogram in a study of apparently healthy divers needs careful definition of procedures and of diagnostic criteria.(Torok 1987). Abnormal signs are at best only a possible indicator of pathology which needs to be supported by other evidence. Nevertheless the finding of some EEG changes in a proportion of symptom-free submarine escape trainees does suggest its potential for the detection of subclinical abnormalities due to embolism (Ingvar et al, 1973). A study of 21 divers with a history of decompression illness and 37 naval diver controls in Finland (Sippinen and Halonen 1987) found that 57% of the dysbaric group had abnormal EEG findings compared with 21% of the control group. In a larger study by Todnem et al (1991) 18% of the divers and 5% of the controls showed abnormal EEGs. The abnormal EEGs were correlated with saturation diving and neurological decompression illness. That saturation divers have more frequently have abnormal EEGs, even in the absence of a history of decompression illness, leads the authors to advocate the use of the EEG in the periodical health examination of deep divers.

A number of studies using evoked responses during and after acute decompression illness have shown that the changes can be significant, but there have been few studies in divers without DCI. The view that the somato-sensory evoked potential (SSEP) is less sensitive than a neurological examination in detecting abnormalities in divers with effects of decompression illness (Overlock et al, 1989) is not necessarily relevant to studies of SSEP in the research laboratory where the technique can be more precisely controlled, particularly when related to the height of an individual. A study sponsored by the UK Health & Safety Executive (Elliott et al, 1995) demonstrated that a proportion of divers who had never reported acute decompression illness did have a statistically significant prolongation of the P40 latency of the posterior tibial SEP but concluded that this phenomenon had no significance in these persons who continue to dive and would not affect their future quality of life.


Ernest S. Campbell, M.D., FACS

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