Posted by Maddiver on December 13, 2001 at 22:53:56:
In Reply to: Re: Subclinical DCS???? posted by Steve on December 13, 2001 at 17:23:54:
Warning this is **very** long and only a subgrouping of the topic...enjoy and as I say below draw your own conclusions....
Posted by Maddiver on December 08, 2001 at 22:16:23:
In Reply to: Diving and memory loss? posted by AADIVER on December 07, 2001 at 07:47:17:
IP:207.218.209.52
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
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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
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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.
Draw your own conclusions......
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.
Posted by maddiver on December 08, 2001 at 22:01:03:
In Reply to: Diving and memory loss? posted by AADIVER on December 07, 2001 at 07:47:17:
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Posted by Maddiver on December 08, 2001 at 22:18:42:
In Reply to: Re: Lesions and memory loss. Re: posted by AADIVER on December 07, 2001 at 10:47:55:
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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.
Further Reading:
Calder I Does diving damage your brain? Occup Med (Oxf) 42 (4): 213-214 (Nov 1992) Todnem et al. Nervous system involvement from occupational diving: an epidemiologic study. Abstract No. 126, Undersea Biomedical Research Supplement to Vol 17, Joint Meeting on Diving and Hyperbaric Medicine, August 1990.
Todnem K, Nyland H, Kambestad BK, Aarli JA Influence of occupational diving upon the nervous system: an epidemiological study. Br J Ind Med 1990 Oct;47(10):708-714
Todnem K, Nyland H, Dick AP, Lind O, Svihus R, Molvaer OI, Aarli JA Immediate neurological effects of diving to a depth of 360 metres. Acta Neurol Scand 1989 Oct;80(4):333-340
Todnem K, Nyland H, Riise T, Kambestad BK, Vaernes R, Hjelle JO, Svihus R, Aarli JA Analysis of neurologic symptoms in deep diving: implications for selection of divers. Undersea Biomed Res 1990 Mar;17(2):95-107
Blood C, Hoiberg A Undersea Biomed Res 12 (3): 351-360 (Sep 1985) Analyses of variables underlying U.S. Navy diving accidents.
Hoiberg A Consequences of U.S. Navy diving mishaps: decompression sickness. Undersea Biomed Res 13 (3): 383-394 (Sep 1986)
Vaernes RJ, Eidsvik S Central nervous dysfunctions after near-miss accidents in diving. Aviat Space Environ Med 53 (8): 803-807 (Aug 1982)
Aarli JA, Vaernes R, Brubakk AO, Nyland H, Skeidsvoll H, Tonjum S Central nervous dysfunction associated with deep-sea diving. Acta Neurol Scand 71 (1): 2-10 (Jan 1985)
Reul J, Weis J, Jung A, Willmes K, Thron A Central nervous system lesions and cervical disc herniations in amateur divers. Lancet 345 (8962): 1403-1405 (Jun 3 1995)
Todnem K, Vaernes R Acute and chronic effects of deep diving on the nervous system. Tidsskr Nor Laegeforen 113 (1): 36-39 (Jan 10 1993) Shields TG Correlation between 99 Tcm-HMPAO-SPECT brain damage and a history of decompression illness or extent of diving experience in commercial divers. Occup Environ Med 54(4), 247-253 1997
Warren LP, Djang WT, Moon RE, et al. Neuroimaging of scuba diving injuries to the CNS. AJR 1988;151:1003-1008
Ahron-Peretz J, Adir Y, Gordon CR, et al. Spinal cord decompression sickness in sport diving. Arch Neurol 1993;50:753-756
Dick APK, Massey EW. Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 1985;35:667-671
Kizer KW. The role of Computed Tomography in the management of dysbaric diving accidents. Radiology 1981;140:705-707
Hallenbeck JM, Bove AA, Elliot DH, et al. Mechanism underlying spinal cord damage in decompression sickness. Neurology 1975;25:308-316
Levin HS, Goldstein FC, Norcross K, et al. Neurobehavioral and Magnetic Resonance Imaging findings in two cases of decompression sickness. Aviat Space Environ Med 1989;60:1204-1210
Hodgson M, Beran RG, Shirtley G. The role of Computed Tomography in the assessment of neurologic sequelae of decompression sickness. Acrh Neurol 1988;45:1033-1035
Calder IM, Palmer AC, Hughes JT. Spinal cord damage found at autopsy in divers. In EUBS 87, diving and hyperbaric medicine. Proceedings of the XIIIth annual meeting of the European Undersea Biomedical Society, Palermo, Italy, September, 1987:310-314