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Chronic Neurological Adverse
Effects of Diving

POSSIBLE NEUROLOGICAL EFFECTS

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.

Since then the two university groups have also published elsewhere, including

Ross JAS, Macdiarmid JI, Osman LM et al.  Health status of professional divers and offshore oil industry workers.  Occ.Med. 2007; 57: 254-261

Irgens Ǻ, Grønning M, Troland K et al.  Reduced health-related quality of life in former North Sea divers is associated with decompression sickness.  Occ Med 2007; 57: 349-354

Ross JAS, Macdiarmid J, Oman L et al (letter)

and

Irgens Ǻ, Troland K, Sundal E et al. (reply).

Health-related quality of life in former North Sea divers. Occ Med 2007; 57(8): 611-2.

These 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 Godøysund 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.


Neuropsychological

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.


Electrophysiology

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.


 
Brain Damage in Divers
Editorial and Letters in the British Journal of Medicine



Pertinent Abstracts

There have been recent conflicting reports concerning neurological damage from DCS accidents, patent foramen ovale and in sport scuba divers without either DCS or PFO. We present abstracts of these articles in no particular order so that you may read and draw your own conclusions. Our conclusion is that there is not yet enough information to make a value judgement of the possibility that sport scuba diving causes long-term brain damage.



Relation between Directly Detected Patent Foramen Ovale and Ischemic Brain Lesions in Sport Divers

Markus Schwerzmann, MD; Christian Seiler, MD; Ernst Lipp, MD; Raphael Guzman, MD; Karl O. Lövblad, MD; Martin Kraus, MD; and Nils Kucher, MD
Pages 21-24

Background:  In divers, the significance of a patent foramen ovale and its potential relation to paradoxical gas emboli remain uncertain.
Objective:  To assess the prevalence of symptoms of decompression illness and ischemic brain lesions in divers with regard to the presence of a patent foramen ovale.
Design:  Retrospective cohort study.
Setting:  University hospital and three diving clubs in Switzerland.
Participants:  52 sport divers and 52 nondiving controls.
Measurements:  Prevalence of self-reported decompression events, patent foramen ovale on contrast transesophageal echo-cardiography, and ischemic brain lesions on magnetic resonance imaging.
Results:  The risk for decompression illness events was 4.5-fold greater in divers with patent foramen ovale than in divers without patent foramen ovale (risk ratio, 4.5 [95% CI, 1.2 to 18.0]; P = 0.03). Among divers, 1.23  2.0 and 0.64  1.22 ischemic brain lesions per person (mean  SD) were detected in those with and those without patent foramen ovale, respectively. Among controls, 0.22  0.44 and 0.12  0.63 lesion per person were detected (P < 0.001 for all groups).
Conclusions:  Regardless of whether a diver has a patent foramen ovale, diving is associated with ischemic brain lesions.
Ann Intern Med. 2001;134:21-24.


Neurology 2000 Dec 12;55(11):1743-6
Neurologic outcome of controlled compressed-air diving

Cordes P, Keil R, Bartsch T, Tetzlaff K, Reuter M, Hutzelmann A, Friege L, Meyer T, Bettinghausen E, Deuschl G

Departments of Neurology (Drs. Cordes, Keil, Bartsch, Meyer, and Deuschl), Diagnostic Radiology (Drs. Reuter and Hutzelmann), and Psychiatry (L. Friege), Christian-Albrechts University of Kiel.

The authors compared the neurologic, neuropsychological, and neuroradiologic status of military compressed-air divers without a history of neurologic decompression illness and controls. No gross differences in the neuropsychometric test results or abnormal neurologic findings were found. There was no correlation between test results, diving experience, and number and size of cerebral MRI lesions. Prevalence of cerebral lesions was not increased in divers. These results suggest that there are no long-term CNS sequelae in military divers if diving is performed under controlled conditions.


Laryngoscope 2000 Aug;110(8):1358-60
Neurological consequences of scuba diving with chronic sinusitis.

Parell GJ, Becker GD

University of Florida, Department of Otolaryngology, Head and Neck Surgery, Gainesville, USA.

Sinus barotrauma from scuba diving is relatively common, usually self-limiting, and often the result of transient nasal pathology. We describe serious neurological sequelae occurring in two scuba divers who had chronic sinusitis We suggest guidelines for evaluating and treating divers who have chronic sinusitis. Divers with nasal or sinus pathology should be aware of the potentially serious consequences associated with scuba diving even after endoscopic sinus surgery to correct this condition.



Acta Radiol 2000 Jan;41(1):18-21
Does diving damage the brain? MR control study of divers' central nervous system.

Hutzelmann A, Tetzlaff K, Reuter M, Muller-Hulsbeck S, Heller M

Department of Diagnostic Radiology, Christian-Albrechts-University, Kiel, Germany.

PURPOSE: To evaluate the prevalence of cerebral white matter changes on MR imaging in healthy elderly compressed air divers with a long diving history in comparison with control subjects who have never dived. MATERIAL AND METHODS: The investigation employed 59 experienced elderly divers and 48 control subjects matched for age, body mass index, alcohol and smoking history. MR studies included a fluid attenuated inversion recovery sequence and T1- and T2-weighted pre- and postcontrast images in axial orientation of the whole brain to localize white matter changes. RESULTS: MR images did not show any morphologic abnormalities in the brains of divers. Both groups - divers and controls - did not differ significantly with respect to white matter changes of the brain. CONCLUSION: No increased prevalence of cerebral white matter changes in compressed air divers compared with a healthy worker sample of similar age were found. Thus, extensive compressed air diving may not necessarily be related to radiological changes on MR.


J Appl Physiol 1998 May;84(5):1622-6
Patent foramen ovale and decompression sickness in sports divers.
Germonpre P, Dendale P, Unger P, Balestra C
Centre for Hyperbaric Oxygen Therapy, Military Hospital, Brussels, Belgium.
Free Full Text of Article
Patency of the foramen ovale (PFO) may be a cause of unexplained decompression sickness (DCS) in
sports divers. To assess the relationship between PFO and DCS, a case-control study was undertaken in a
population of Belgian sports divers. Thirty-seven divers who suffered from neurological DCS were
compared with matched control divers who never had DCS. All divers were investigated with
transesophageal contrast echocardiography for the presence of PFO. PFO size was semiquantified on the
basis of the amount of contrast passage. Divers with DCS with lesions localized in the high cervical spinal cord, cerebellum, inner ear organs, or cerebrum had a significantly higher prevalence of PFO than divers with DCS localizations in the lower spinal cord. For unexplained DCS (DCS without commission of any diving procedural errors), this difference was significant for large PFOs only. We conclude that PFO plays a significant role in the occurrence of unexplained cerebral DCS, but not of spinal DCS. We further stress the importance of standardization and semiquantification of future PFO studies that use transesophageal contrast echocardiography. In conclusion, we found a significant correlation between the prevalence of PFO and the occurrence of cerebral, but not spinal, DCS. This is in accordance with the pathophysiological model, in which nitrogen bubbles, passing through the PFO into the arterial circulation, migrate preferably into the carotid and/or vertebral arteries.

Because all known possibly confounding factors either have been matched for or have no detected significant difference, these findings support the hypothesis that PFO is a cause of DCS with cerebral localization.

We would therefore recommend that divers with unexplained DCS and symptoms suggesting a cerebral or high-spinal localization of the lesion be investigated for the presence of PFO. If a grade 2 PFO is present, paradoxical nitrogen bubble embolization should be considered likely, and we would advise the diver to follow dive profiles that are very low "bubble-prone" in the future, or to give up diving.

Furthermore, for future PFO studies, we strongly recommend the following: 1) use of a standardized contrast TEE technique, with special attention to the strain and duration of the Valsalva maneuver; 2) semiquantification of the permeability of the foramen ovale; and 3) use of matched divers as control subjects.


BMJ 1997 Mar 8;314(7082):701-5
Free Full Text Article

Cohort study of multiple brain lesions in sport divers: role of a patent foramen ovale.
Knauth M, Ries S, Pohimann S, Kerby T, Forsting M, Daffertshofer M, Hennerici M, Sartor K

Department of Neuroradiology, University of Heidelberg, Klinikum Heidelberg, Germany.

OBJECTIVE: To investigate the role of a patient foramen ovale in the pathogenesis of multiple brain lesions acquired by sport divers in the absence of reported decompression symptoms.
DESIGN: Prospective double blind cohort study. SETTING: Diving clubs around Heidelberg and departments of neuroradiology and neurology. SUBJECTS: 87 sport divers with a minimum of 160 scuba dives (dives with self contained underwater breathing apparatus).
MAIN OUTCOME MEASURES: Presence of multiple brain lesions visualised by cranial magnetic resonance imaging and presence and size of patent foramen ovale as documented by echocontrast transcranial Doppler ultrasonography. RESULTS: 25 subjects were found to have a right-to-left shunt, 13 with a patent foramen ovale of high haemodynamic relevance. A total of 41 brain lesions were detected in 11 divers. There were seven brain lesions in seven divers without a right-to-left shunt and 34 lesions in four divers with a right-to-left shunt. Multiple brain lesions occurred exclusively in three divers with a large patent foramen ovale (P = 0.004).
CONCLUSIONS: Multiple brain lesions in sport divers were associated with presence of a large patent foramen ovale. This association suggests paradoxical gas embolism as the pathological mechanism. A patent foramen ovale of high haemodynamic relevance seems to be an important risk factor for developing multiple brain lesions in sport divers.


Br J Sports Med 1994 Jun;28(2):101-104
Self-reported long-term effects of diving and decompression illness in recreational scuba divers.
McQueen D, Kent G, Murrison A
Department of Psychiatry, University of Sheffield, UK.
The aim of this study was to examine the long-term effects of neurological decompression illness (NDCI) on recreational divers. Thirty-seven divers who had been treated for neurological decompression illness at least 2 years previously, and a control group of 50 divers with no history of decompression illness, responded to a postal questionnaire. Divers in the accident group reported more symptoms of neurological damage, were more likely to believe that diving had a deleterious effect on their health and were more likely to indicate symptoms of psychiatric morbidity. The quantity of diving in the year preceding the survey was associated with reports of neurological damage in both groups and with symptoms of psychiatric morbidity in the accident group. Although requiring confirmation from a longitudinal study, these results suggest that recreational diving can have negative long-term consequences for health, particularly after decompression illness.
 


 
Occup Environ Med 1994 Nov;51(11):730-734
Neurophysiological assessment of divers with medical histories of neurological decompression illness.
Murrison AW, Glasspool E, Pethybridge RJ, Francis TJ, Sedgwick EM
Institute of Naval Medicine, Alverstoke, Gosport, Hampshire.
OBJECTIVE--To examine the possibility that subclinical damage may persist after clinical recovery from neurological decompression illness. METHODS--The neuraxes of 71 divers with medical histories of neurological decompression illness and 37 non-diver controls were examined by recording the somatosensory evoked potentials produced on stimulation of the posterior tibial and median nerves. RESULTS--Although the tests gave some objective support for the presence of "soft" residual neurological symptoms and signs, no evidence was given for the presence of subclinical damage. CONCLUSIONS--The contention that neurological damage persists after full clinical recovery from the neurological decompression illness was not supported.
 


 
Nucl Med Commun 1993 Feb;14(2):117-120
Cerebral perfusion deficits in divers with neurological decompression illness.
Wilmshurst PT, O'Doherty MJ, Nunan TO
Department of Cardiology, St Thomas' Hospital, London, UK.
Cerebral perfusion deficits detected by injection of 99Tcm-hexamethylpropyleneamine oxime (HMPAO) and single photon emission tomography is said to correlate well with clinical findings in divers with neurological decompression illness. We studied 12 divers. Six had residual cerebral signs (group 1) and six had no residual cerebral symptoms or signs (group 2). Perfusion deficits were as common in group 2 as in group 1. The site of the deficit did not correlate well with either the neurological findings at presentation or the residual clinical signs after treatment. The data suggest that claims that HMPAO scanning correlates with clinical findings and can be used for patients management were incorrect.
 


 
Br J Ind Med 1991 Apr;48(4):258-266
Neurological long term consequences of deep diving.
Todnem K, Nyland H, Skeidsvoll H, Svihus R, Rinck P, Kambestad BK, Riise T, Aarli JA
Norwegian Underwater Technology Centre, Bergen.
Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers.
 


 
Br J Ind Med 1990 Oct;47(10):708-714
Influence of occupational diving upon the nervous system: an epidemiological study.
Todnem K, Nyland H, Kambestad BK, Aarli JA
Norwegian Underwater Technology Centre.
Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.
 


 
Acta Neurol Scand 1989 Oct;80(4):333-340
Immediate neurological effects of diving to a depth of 360 metres.
Todnem K, Nyland H, Dick AP, Lind O, Svihus R, Molvaer OI, Aarli JA
Department of Neurology, Haukeland Hospital, University of Bergen, Norway.
Eighteen divers performed a simulated dive to a depth of 360 metres of seawater breathing a mixture of helium and oxygen. Clinical neurological examinations and neurophysiological tests were performed before and after the dives. Two divers had mild ataxic signs and changed electronystagmography after the dive, and one had impaired vibration sense in one lower extremity. Abnormal EEGs with slow waves and sharp potentials, seen primarily in the temporal regions, occurred in 2 divers. No changes were found in the magnetic resonance imaging brain scans. The divers with evidence of previous central nervous system injury, or a history of unconsciousness or previous decompression sickness seemed more likely to develop neurological signs after these deep dives. This study shows that deep diving may induce immediate neurological changes. We recommend that future deep divers have a neurological examination and 2 separate EEGs included in their medical examinations.
 


 
Neurology 1977 Feb;27(2):125-127
Neurologic and psychologic manifestations of decompression illness in divers.
Peters BH, Levin HS, Kelly PJ
It has been widely accepted that the neurologic sequelae of decompression illness are confined to the spinal cord. Of 10 divers who gave a history of an episode of decompression illness involving the central nervous system, we found that eight had unequivocal neurologic deficits implicating multiple supraspinal lesions. Seven of these neurologically impaired divers completed a battery of neuropsychologic tests that revealed severe deficits in all cases. The findings show that diffuse and multiple central nervous system lesions result from decompression illness and demonstrate the importance and close correlation of thorough neurologic and neuropsychologic tests in assessment following diving accidents.
 


 
Paraplegia 1995 Nov;33(11):636-639
Paraplegia and decompression sickness.
Tournebise H, Boucand MH, Landi J, Theobald X
Hopital R. Sabran, Service de Reeducation, Giens, France.
Decompression sickness may include spinal cord damage, which sometimes persists. Casual divers are exposed, as well as professionals. In this study we have reviewed the clinical records of divers admitted with symptoms of spinal cord injuries in our area in the last 6 years. This study is divided into two groups: those who fully recovered (19 divers) and those with neurological sequelae (12 divers).
 


 
Med J Aust 1986 Apr 14;144(8):399-401
Does non-clinical decompression stress lead to brain damage in abalone divers?.
Andrews G, Holt P, Edmonds C, Lowry C, Cistulli P, McKay B, Misra S, Sutton G
Abalone divers are subject to considerable decompression stresses and could be at risk of progressive cognitive impairment. A sample of abalone divers was compared with a sample of fishermen, by means of a battery of neuropsychological tests. No evidence of cognitive impairment was found in the divers, in spite of evidence of their exposure to decompression stress. The implications for other professional divers and for recreational underwater divers who follow standard decompression protocols are reassuring.
 


 
Undersea Biomed Res 1985 Sep;12(3):321-326
Intellectual deterioration with excessive diving (punch drunk divers).
Edmonds C, Boughton J
A survey was performed on a specific occupational group of compressed air divers--the professional abalone divers of New South Wales. One aspect of this survey included the use of psychometric screening tests to elicit evidence of impaired intellectual capacity, which may be related to the compressed air diving. Results of the survey indicate that there is suggestion of intellectual impairment in almost half of this diving population. The fact that this diving group exposed themselves to much greater decompression stress than the more conventional professional diving groups suggests that these results should not be extrapolated to other diving populations. The results are supportive of the anecdotal beliefs that exist regarding this highly selective diving group, i.e., that a syndrome of reduced intellectual capacity (dementia or "punch drunkenness") may be present.
 


 
Occup Environ Med 1997 Apr;54(4):247-253
Correlation between 99Tcm-HMPAO-SPECT brain image and a history of decompression illness or extent of diving experience in commercial divers.
Shields TG, Duff PM, Evans SA, Gemmell HG, Sharp PF, Smith FW, Staff RT, Wilcock SE
Hyperbaric Research Unit, Robert Gordon University, Aberdeen.
OBJECTIVES: To explore the use of 99technetiumm-hexamethyl propylene amine oxime single photon computed tomography (HMPAO-SPECT) of the brain as a means of detecting nervous tissue damage in divers and to determine if there is any correlation between brain image and a diver's history of diving or decompression illness (DCI). METHODS: 28 commercial divers with a history of DCI, 26 divers with no history of DCI, and 19 non-diving controls were examined with brain HMPAO-SPECT. Results were classified by observer assessment as normal (I) or as a pattern variants (II-V). The brain images of a subgroup of these divers (n = 44) and the controls (n = 17) were further analysed with a first order texture analysis technique based on a grey level histogram. RESULTS: 15 of 54 commercial divers (28%) were visually assessed as having HMPAO-SPECT images outside normal limits compared with 15.8% in appropriately identified non-diver control subjects. 18% of divers with a history of DCI were classified as having a pattern different from the normal image compared with 38% with no history of DCI. No association was established between the presence of a pattern variant from the normal image and history of DCI, diving, or other previous possible neurological insult. On texture analysis of the brain images, divers had a significantly lower mean grey level (MGL) than non-divers. Divers with a history of DCI (n = 22) had a significantly lower MGL when compared with divers with no history of DCI (n = 22). Divers with > 14 years professional diving or > 100 decompression days a year had a significantly lower MGL value. CONCLUSIONS: Observer assessment of HMPAO-SPECT brain images can lead to disparity in results. Texture analysis of the brain images supplies both an objective and consistent method of measurement. A significant correlation was found between a low measure of MGL and a history of DCI. There was also an indication that diving itself had an effect on texture measurement, implying that it had caused subclinical nervous tissue damage.
 


 
Undersea Biomed Res 1990 Mar;17(2):95-107
Analysis of neurologic symptoms in deep diving: implications for selection of divers.
Todnem K, Nyland H, Riise T, Kambestad BK, Vaernes R, Hjelle JO, Svihus R, Aarli JA
Department of Neurology, Haukeland Hospital, University of Bergen, Norway.
Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
 


 
Tidsskr Nor Laegeforen 1993 Jan 10;113(1):36-39
Acute and chronic effects of deep diving on the nervous system.
[Article in Norwegian]
Todnem K, Vaernes R
Yrkesmedisinsk avdeling, Haukeland sykehus, Bergen.
Diving deeper than 180 metres of seawater (msw) will impose neurological symptoms in most divers. Atactic signs and abnormal EEGs were found in five of 18 divers immediately after deep diving. Neuropsychological testing before and after deep diving in 64 divers revealed a reduction in autonomic reactivity (48%), increased hand tremor (27%) and impairment of spatial memory and reduced finger coordination (8%) after the dives. These results had not improved one year later. A follow-up study of 40 divers one to seven years after their last deep dive revealed that the divers experienced more problems of concentration and paresthesia in feet and hands than the controls. Two had had seizures, one had suffered episodes of transitory cerebral ischemia and one had experienced transitory global amnesia after the deep dives. In the future, oil installations at depths below 180 msw should be installed and maintained with remote control and robot technology.
 


 
Undersea Hyperb Med 1994 Dec;21(4):391-402
A histopathologic and immunocytochemical study of the spinal cord in amateur and professional divers.
Mork SJ, Morild I, Brubakk AO, Eidsvik S, Nyland H
Department of Pathology, Gade Institute, Haukeland Hospital, University of Bergen, Norway.
To clarify the influence of diving activity on the central nervous system, we studied 10 amateur and 10 professional deceased divers with emphasis on the presence of subacute or chronic pathologic changes in the spinal cord. Of the 10 professional divers (median age 38 yr; range 29-52; median experience in excess of 13 yr), 7 were experienced saturation divers. Five had dived to a maximum depth of 150 meters of seawater, the 2 others to 300 and 500 msw, respectively. Five of the professional divers had experienced decompression sickness. The experience of the amateur divers (median age 29 yr; range 17-51) varied from a few dives to many years of recreational diving. The spinal cords were formalin-fixated and routinely processed for neuropathologic examination, which included light microscopy after immunostaining for glial fibrillary acidic protein and monocyte-macrophage-microglial markers. The microscopic examination did not reveal previous spinal cord damage. Thus, diving activity, saturation diving to extreme depths included, does not in itself seem to lead to necrosis, degeneration, or scar formation in the human spinal cord.
 


 
Undersea Biomed Res 1989 May;16(3):233-251
Neuropsychologic effects of saturation diving.
Vaernes RJ, Klove H, Ellertsen B
Norwegian Underwater Technology Centre (NUTEC) A/S, Bergen.
Neuropsychologic status of saturation divers was assessed before and after 300-500 msw dives (deep saturation diving--DSD group) and before and after 3.5 yr of ordinary saturation diving (saturation diving--SD group). Average baseline results showed the divers to be slightly superior to nondiving controls. Mild-to-moderate neuropsychologic changes (greater than 10% impairment) were found in measures of tremor, spatial memory, vigilance, and automatic reactivity in 20% of the divers after deep dives (DSD group). One year postdive no recovery was observed except for a vigilance test. In the SD group, 20% of the divers showed greater than 10% impairment after 3.5 yr of ordinary saturation diving. Significant reduction in autonomic reactivity was also found and there was a relationship between low autonomic reactivity before saturation diving and number of greater than 10% impairments. For the whole group (DSD + SD divers), negative correlations were found between saturation experience and results on memory and complex visuomotor tests. Years of diving from first to last examination was positively correlated with number of greater than 10% impairments and with reduction in autonomic reactivity. No similar correlations were found to dive variables after about 3 yr of air diving. The mild-to-moderate changes seen in some divers, therefore, seem to be the effects of saturation diving. Since one deep dive may cause an effect similar to the effect of 3.5 yr of ordinary saturation diving, there is reason to believe that repeated deep diving may lead to more pronounced neuropsychologic impairment.


 
J Nucl Med 1996 Jul;37(7):1154-1158
Decompression illness in sports divers detected with technetium-99m-HMPAO SPECT and texture analysis.
Staff RT, Gemmell HG, Duff PM, Sharp PF, Wilcock SE, Shields TG, Smith FW
University of Aberdeen, Department of Bio-Medical Physics and Bio-Engineering, Aberdeen Royal Hospitals, Scotland, United Kingdom.
Diving for sport and recreation has increased in recent years, resulting in more incidences of diving illness. Therefore, we studied potential use of regional cerebral blood flow SPECT imaging with 99mTc-HMPAO in the management of divers who have experienced decompression illness (DCI). METHODS: A group of ten sports divers who had no experience of DCI were compared with ten sports divers who had experienced at least one episode of DCI. Transaxial SPECT images were first compared objectively using a first-order texture measure and then subjectively using a receiver operator characteristic (ROC) experiment. Experienced observers were asked to rate images subjectively in terms of the images' textural appearance. RESULTS: Both these techniques showed that there is a statistically significant difference between the two groups and the images produced by the DCI divers were generally more coarsely patchy when compared to the non DCI divers. The quantitative texture technique proved significantly better in identifying divers with DCI than the visual analysis by observers using ROC curves. CONCLUSION: Differences between the cerebral blood flow patterns of sports divers who have experienced DCI and sports divers who have no experience of DCI can be detected using 99mTc-HMPAO SPECT and a texture analysis technique.


Relation between Directly Detected Patent Foramen Ovale and Ischemic Brain Lesions in Sport Divers

Markus Schwerzmann, MD; Christian Seiler, MD; Ernst Lipp, MD; Raphael Guzman, MD; Karl O. Lövblad, MD; Martin Kraus, MD; and Nils Kucher, MD
Pages 21-24

Background:  In divers, the significance of a patent foramen ovale and its potential relation to paradoxical gas emboli remain uncertain.
Objective:  To assess the prevalence of symptoms of decompression illness and ischemic brain lesions in divers with regard to the presence of a patent foramen ovale.
Design:  Retrospective cohort study.
Setting:  University hospital and three diving clubs in Switzerland.
Participants:  52 sport divers and 52 nondiving controls.
Measurements:  Prevalence of self-reported decompression events, patent foramen ovale on contrast transesophageal echo-cardiography, and ischemic brain lesions on magnetic resonance imaging.
Results:  The risk for decompression illness events was 4.5-fold greater in divers with patent foramen ovale than in divers without patent foramen ovale (risk ratio, 4.5 [95% CI, 1.2 to 18.0]; P = 0.03). Among divers, 1.23  2.0 and 0.64  1.22 ischemic brain lesions per person (mean  SD) were detected in those with and those without patent foramen ovale, respectively. Among controls, 0.22  0.44 and 0.12  0.63 lesion per person were detected (P < 0.001 for all groups).
Conclusions:  Regardless of whether a diver has a patent foramen ovale, diving is associated with ischemic brain lesions.
Ann Intern Med. 2001;134:21-24.

Scuba diving involves a risk for neurologic injuries caused by decompression sickness, arterial gas embolism, anoxia, and the toxic effects of high partial pressure of breathing gases. Most neuroimaging studies for detection of ischemic brain lesions have been performed in divers with acute decompression-related injuries of the central nervous system . However, as a recent study has shown, most divers may be neurologically asymptomatic despite an increased prevalence of brain lesions compared with nondiving controls. Reul and colleagues found 80% of all brain lesions in a subgroup of 27% of divers, possibly those with patent foramen ovale who had paradoxical arterial gas embolism during decompression.  Knauth and coworkers used transcranial Doppler ultrasonography to detect a right-to-left shunt in 87 sport divers; they reported that multiple brain lesions on magnetic resonance imaging (MRI) occurred exclusively in those with a large right-to-left shunt, which was presumed to be a patent foramen ovale. Detection of intravenously injected echocontrast bubbles in the cerebral vasculature is not specific for a patent foramen ovale; moreover, compared with transesophageal echocardiography, detection of these bubbles has been found to be only 68% sensitive in detecting a patent foramen ovale.
We used MRI and transesophageal echocardiography to determine the prevalence of decompression illness symptoms and ischemic brain lesions in relation to a patent foramen ovale in sport divers.


FAQ

Q: I have seen conflicting reports of scuba diving causing long-term damage to the brain. What do you think?

A: There is an enlarging amount of information being reported that purports to show that the brain is indeed endangered by scuba diving. A very direct relationship has been shown in scuba divers who have a patent foramen ovale and who have passage of bubbles across the heart wall into the arterial circulation.

Here is a more reassuring article:

Neurology 2000 Dec 12;55(11):1743-6
Neurologic outcome of controlled compressed-air diving.

Cordes P, Keil R, Bartsch T, Tetzlaff K, Reuter M, Hutzelmann A, Friege L, Meyer T, Bettinghausen E, Deuschl G

Departments of Neurology (Drs. Cordes, Keil, Bartsch, Meyer, and Deuschl), Diagnostic Radiology (Drs. Reuter and Hutzelmann), and Psychiatry (L. Friege), Christian-Albrechts University of Kiel.

The authors compared the neurologic, neuropsychological, and neuroradiologic status of military compressed-air divers without a history of neurologic decompression illness and controls. No gross differences in the neuropsychometric test results or abnormal neurologic findings were found. There was no correlation between test results, diving experience, and number and size of cerebral MRI lesions. Prevalence of cerebral lesions was not increased in divers. These results suggest that there are no long-term CNS sequelae in military divers if diving is performed under controlled conditions.

Finally, here is a disturbing letter in the British Medical Journal by a respected Neuropathologist:
BMJ 1997;314:1761 (14 June)
Brain damage in divers
--------------------------------------------------------------------------------

The risk has been underestimated

Editor–Using magnetic resonance imaging Michael Knauth and colleagues reinforce the message that scuba diving is a dangerous sport1; they show images of some small areas of brain damage found in apparently normal participants. I think that they have greatly underestimated the amount of damage and are wrong to criticise the findings of Reul et al, whose study included greatly enlarged perivascular spaces as lesions.2 Knauth and colleagues cite a paper by Jungreis et al which suggested that such fluid filled spaces may be of no pathological significance3; however, these findings applied to people of stroke age in whom such spaces are indeed significant but should not be confused with lacunar infarcts. Healthy people with a mean age of 35.7 years whom Knauth and colleagues studied do not show large widely scattered perivascular spaces.

In his editorial in the same issue Peter Wilmshurst4 refers to a paper by my colleagues and me, in which we reported the histological study of many small lesions in scuba and young professional divers.5 Distension of the perivascular space was always associated with local destruction of the arterial muscle coat and elastic lamina, leaving a length of vessel of hyaline and collagen. Sometimes the artery or arteriole was itself dilated at that point. Because the lesions appeared abruptly in an otherwise normal length of vessel we presumed that they were the result of acute local luminal hypertension–the effect of a ballooning bubble of gas. I have seen similar lesions in people under 45 in cases of phaeochromocytoma and maternal eclampsia, in which patches of destruction of an arterial wall and microaneurysms occur as a focal response to surges of very high general blood pressure.

The aetiology may be different in these conditions but the pathogenesis of the effect on the mental state is much the same. Apart from direct local damage to brain tissue, it includes permanent interruption of local vasomotor control and inadequate redistribution of blood to areas of the brain associated with thought.

Peter O Yates, Emeritus professor of neuropathology 


Knauth M, Ries S, Pohimann S, Kerby T, Forsting M, Daffertshofer M, et al. Cohort study of multiple brain lesions in sport divers: role of a patent foramen ovale. BMJ 1997;314:701-5. (8 March.) [Abstract/Full Text]

Reul J, Weis J, Jung A, Willmes K, Thron A. Central nervous system lesions and cervical disc herniations in amateur divers. Lancet 1995;345:1403-5. [Medline]

Jungreis CA, Kanal E, Hirsch WL, Martinez AJ, Moossy J. Normal perivascular spaces mimicking lacunar infarction. Radiology 1988;169:101-4. [Abstract]

Wilmshurst P. Brain damage in divers. BMJ 1997;314:689-90. (8 March.) [Full Text]
Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in divers. Neuropathol Appl Neurobiol 1992;18:113-24.

For more information you may want to visit our web page at http://www.scuba-doc.com/LTE.htm  .

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