Long Term Effects of Sport Diving

As the popularity of SCUBA diving continues to grow, scientists are better able to determine what the long-term effects, if any, are on the human body. For every overt case of decompression sickness that is treated, there are many divers with covertly occurring intravascular bubbling, whose ramifications we are just beginning to understand. We know that at least one-third of the population has a patent foramen ovale, and those individuals who dive are at increased risk for right-to-left shunting of air bubbles and the possibility of arterial gas embolism.

Another group at high risk for adverse effects is professional divers making repeat deep dives with shortened decompression times. The most well-known adverse injuries of diving are dysbaric osteonecrosis, hearing loss, and permanent neurological deficits, usually the result of a decompression accident; it is speculated, however, that these effects may occur without decompression incident or injury. Reports of cognitive dysfunction and damage to the liver, retina, and heart of the diver with no history of decompression sickness are now emerging. Because these symptoms may occur gradually and away from the dive site, prudent physicians should be aware of the signs and symptoms related to adverse events of diving in order to minimize the morbidity and mortality they can cause.


The combined and equally-distributed gases in the earth’s atmosphere
result in a surrounding ambient pressure that the body acclimates to over time. At sea level, this pressure is described as 1 atmosphere absolute (ATA). Natural gas laws state that when the body is exposed to increased pressure, as in SCUBA diving, gases are forced to go into solution. Upon ascent, these gases can form bubbles which have two consequences: they may block blood vessels or initiate an inflammatory response. Blockage of vessels results in ischemia and infarction of tissues beyond the obstruction, and inflammatory changes can lead to extravasation into the tissues, further compromising the circulation and resulting in edema, scarring, and long-term damage to the spinal cord, brain, and other tissues involved in the process. The most severe manifestations of these physiologic processes are decompression sickness (DCS) and alveolar rupture or cerebral air embolism, secondary to arterial gas embolism (AGE). Because their presentations are similar, these two entities are known as decompression illness (DCI), and are treated in the same manner — with recompression in a chamber using a combination of oxygen and air or helium.

It now appears that subclinical changes can occur without overt manifestations of decompression sickness. This is documented by the increasing frequency of cases of dysbaric osteonecrosis and hearing difficulties diagnosed in commercial divers. Sport scuba divers may be at risk for these other latent symptoms affecting the brain, spinal cord, eyes, and lungs.

SCUBA diving is increasing in popularity. Because the consequences of long-term diving may occur gradually and away from the dive site, it is prudent that physicians are aware of the signs and symptoms related to diving in order to minimize the morbidity and mortality it can cause.

Hyperbaric Terminology and Physics

A basic review of physics and diving terminology will acquaint the physician with some of the important aspects of hyperbaric exposure. At sea level, the body is exposed to 1 ATA of pressure. This is also expressed as 760 millimeters of mercury (mmHg), 33 feet of sea water (FSW), or 14.7 pounds per square inch (psi). The normal atmospheric pressure of 1 ATA is really just a reference point from which we gauge other pressures. When one states that a systolic blood pressure is 120mmHg, we are really saying that it is 120mmHg above that of the surrounding environment, or 880mmHg. This latter pressure is a “gauge” pressure, meaning that the pressure displayed is the actual pressure minus the constant 1 ATA of atmospheric pressure. By the same analogy, the depth gauge of a diver reads “0” on the ocean’s surface or 1 ATA or 33 FSW. At 33 feet under water he will be at 2 ATA, and this is increased by 1 ATA every additional 33 feet he/she descends.

Boyle’s Law Applied to Diving

The response of body organs to changes in ambient pressure depends on whether there is air in the organ and if that air is caught in a closed space within the organ. A fluid-filled space or a solid organ will not change size as the pressure changes because fluids and solids are not compressible. However, a space with elastic walls that is filled with air will change shape according to Boyle’s law, which states that the volume of gas is inversely proportional to the absolute pressure. An example of this is a balloon filled with one cubic foot of air on the surface (1 ATA) which would shrink to a volume of one-half cubic foot if taken to a depth of 33 FSW (2 ATA) and to one-fourth of a cubic foot at 99 FSW (4 ATA).

In most tissues within the body, however, the gas-filled spaces have only a limited capacity to change their volume. The middle ear and the lungs are examples. This volume change does not present a problem as long as the quantity of gas within the space is allowed to change to compensate for changes in pressure. This is the reason for teaching divers to exhale on ascent (the air in the pulmonary alveoli gets bigger as the diver rises in the water) and to clear their ears (add gas to the middle ear) as they descend. If this equalization is not accomplished, tissues are damaged and “barotrauma” – an “ear squeeze” in the case of the ear (Fig. 1) and ruptured alveoli with resultant arterial gas embolism (AGE) in the case of the lung occurs.

Middle ear barotrauma. Reprinted with permission from Best Publishing Co. P.O. Box 30100, Flagstaff, AZ 86003.

Other Laws of Nature

Other important physical principles related to diving are Henry’s law and Dalton’s law. The former states that at a given temperature the amount of gas that will dissolve in a liquid is directly proportional to the partial pressure of the gas; the latter dictates that the pressure in a gas is the sum of the pressures of all the gases present. These are central to understanding decompression sickness.

As a diver descends, the increased pressure causes more nitrogen to enter tissues than was present at the surface. If enough nitrogen enters into solution and the diver then returns to the surface too quickly, the excess gas will not have a chance to be eliminated (“blown off”) gradually through the lungs. The nitrogen will then come out of solution and go into a gas phase (bubbles) which form in the blood and tissues of the body. These bubbles may cause the clinical entity that we call decompression sickness (DCS).

Hyperbaric exposures (situations where there are elevated pressures) may occur in underwater archeology and construction and tunneling projects, hyperbaric oxygen treatment facilities, and in aviation. Pilots are subject to the same problem as divers, except that the situation is reversed: bubbles form on descent, again due to an increase in pressure and nitrogen saturation. Recreational scuba diving is the most common type of hyperbaric exposure, and interest in the sport has risen dramatically in the past decade.

Are There Long-term Effects of Diving?

Workshops have been held to educate the public about the potential risks of diving, in both commercial and recreational settings.[1] Other than osteonecrosis and loss of hearing, there is no consensus about what those risks are, though over the past several years the medical literature and the lay press have suggested that there are potential chronic long-term detrimental effects of diving. These data imply that diving may produce subclinical damage to the brain, spinal cord (Fig. 2, 3), inner ear, retina, and the small airways of the lung. Other studies suggest significant decrement in pulmonary and cognitive functions.

MRI showing spinal cord DCS (cervical and dorsal tract). Reprinted from the Journal of Magnetic Resonance Materials in Physics, Biology and Medicine

Spinal cord DCS (cervical tract). Reprinted from the Journal of Magnetic Resonance Materials in Physics, Biology and Medicine.

One might expect that the dangers of pressure are the same whether one is a commercial, military, or recreational diver and that the differences are of degree rather than kind.

Inherent Problems with Studying Divers

Divers suffering from decompression illness have been studied since the advent of SCUBA diving. However, the scientific methods now being used are more sophisticated, revealing the shortcomings of previous investigations. And the difficulty of studying a specific population over a long period of time is expensive and fraught with problems inherent in certain types of study design.

No Control Group

The use of technetium Tc 99m hexamethyl propylene amine oxime (HMPAO) brain scans in submarine escape trainees with a known episode of cerebral gas embolism was first described by Adkisson and associates[2] in 1989. Since then, 99m HMPAO and simple photon emission-computed tomography (SPECT) have been used to evaluate divers following acute decompression sickness. Their use has been questioned by Hodgeson and colleagues[3], who found no correlation among the four unusual patterns described in divers with decompression history and “no adequate control group to determine baseline function.” Comparison to a control group was not made because the use of the radioactive marker HMPAO in a healthy diving population is expensive, inconvenient, and possibly unethical.

Diagnostic Variability

Another criticism of diving studies is that techniques used to diagnose changes due to decompression illness are not standardized among the different centers where these studies were conducted, preventing any valid comparisons among the results. Individually, however, these studies contribute to the body of knowledge used to investigate the consequences of diving.

Physiologic Consequences of Diving

Patent Foramen Ovale

Bubbles that move from the venous circulation across a patent foramen ovale can cause immediate and acute neurological signs and symptoms from arterial gas embolism.

Patent foramen ovale (PFO) is a persistent opening in the wall of the heart which did not close completely after birth (opening required prenatally for transfer of oxygenated blood via the umbilical cord). This patency can cause a shunt of blood from right to left, but more often there is a movement of blood from the left side of the heart (high pressure) to the right side of the heart (low pressure).

Ordinarily, the left-to-right shunt is not deleterious, but the right-to-left shunt, if large enough, will cause low arterial O2 tension and severely limited exercise capacity. In divers, there exists the risk of paradoxic embolization of gas bubbles which occurs in the venous circulation during decompression.

Intra-atrial shunts can be bi-directional at various phases of the cardiac cycle and some experts feel that a large atrial septal defect is a contraindication to diving. In addition, a Valsalva maneuver, used by most divers to equalize their ears, can increase venous atrial pressure to the point that a right-to-left shunt occurs, thereby transmitting bubbles that have not been filtered out by the lungs.

Dr. Fred Bove, a Temple University cardiologist, conducted a meta-analysis[4] of the adverse effects of diving. His summary analysis of 2.5 million divers (DAN, 1991) revealed only 1400 documented cases of DCS (0.05%), confirming the fact that DCS is a rare event. An analysis of those with patent foramen ovale found that their risk ratio for decompression sickness was increased by a factor of three.

At this time we don’t have enough information to decide whether or not all divers should have an echocardiogram to rule out a patent foramen ovale. If a diver is symptomatic, then a bubble contrast echocardiogram should be done. Bubble contrast echocardiography appears to be the most sensitive method for detecting a shunt, while color flow Doppler appeared to be a poor means of detecting the shunt in a transthoracic echo.

Dysbaric Osteonecrosis

Early in this century thousands of men were employed in the building of tunnels and bridges using compressed air to keep the workplace dry. It is from this population that the first reports of disabling hip and shoulder conditions were verified radiographically as joint degeneration. The insidious nature of this condition can result in considerable bone damage prior to detection. In 1972, Edmonds and Thomas[5] estimated the incidence of dysbaric osteonecrosis was as high as 50% in divers. Ten case studies over the next ten years of divers who sought treatment for persistent joint pain were found to have osteonecrosis. The validity of both the Edmonds and Thomas results and some of the case studies are now being questioned because there was no established standard for radiologic diagnosis of dysbaric osteonecrosis.

Dysbaric osteonecrosis involves infarction of an area of bone due to the obstruction of terminal vessels of the bone’s vascular supply, probably by gas emboli. The condition is thought to be a late manifestation of decompression sickness, frequent exposure to increased pressure, insufficient decompression on ascent, or inadequate treatment of decompression illness. Early diagnosis is by radiographic examination[6], scintography[7], MRI, and more recently ultrasonography.[8]

Osteonecrosis in divers presents in two basic forms: juxta-articular (subchondral), and shaft, which includes the neck and a portion of the long bone. The shaft lesions are predominately saponified fat, are usually asymptomatic, and are seldom of orthopedic significance. The juxta-articular lesions are of greater clinical significance, causing symptoms that are potentially disabling. These lesions show areas of dead bone surrounded by a layer of collagen which forms a fibrous band and new bone. Beyond is an area of creeping substitution and healing trabeculae (Fig. 4).

MRI showing juxta-articular avascular osteonecrosis of the hip. Reprinted with permission from the Virtual Hospital.

Frequently there is pain over the joint which may be aggravated by movement and radiate down the limb, and a slight restriction of movement is common. In the shoulder, the signs mimic rotator cuff lesions, with pain from 60 to 180 degrees abduction and difficulty maintaining abduction against resistance. Following collapse of the cartilage, secondary degenerative arthritis develops with further reduction in joint motion. In caisson work, the femur is affected two to three times more often than the humerus, (Walder, 1969). Just the opposite occurs in diving, the ratio being 1:2 or 1:3 in favor of the humerus being more often affected. (David Elliott, personal communication).


The radiograph is the gold standard for diagnosing dysbaric osteonecrosis but it depends on the quality of the radiograph and the radiologist’s experience. Although only the shoulders and the hips are affected, extensive views of the lower femur and upper tibia are included to identify as many shaft lesions as possible.

The incidence of avascular necrosis in the general population is unknown, so the alternative causes of bone necrosis should be excluded when the condition is found in divers. They include hyperlipidemia, diabetes mellitus, pancreatitis, cirrhosis with chronic alcoholism, long-term steroid therapy, Gaucher’s Disease, and other conditions that may be incompatible with fitness for diving.

Although the diagnostic standard, radiography is not a good tool to demonstrate changes over time. Other techniques are available and have value in screening for the disease. MDP ( 99mTechnetium Methyl-dipolyphosphate) scans are very sensitive to local bone pathology.
A “hot spot” indicates increased perfusion and metabolism and changes are recognized only hours after a dive. A positive scan indicates a need for radiological follow-up and is not diagnostic.

Magnetic resonance imaging (MRI) (Fig. 4) has a remarkable power to detect early lesions but because of expense it is not generally available for routine screening of large populations. It was used in 1981 by the Decompression Sickness Registry, who found that the percentage of bone necrosis, both shaft and juxta-articular, increases in a sample of divers with age and experience. At least one definite lesion was found in 4.2% of a population of 4980 divers. Necrosis was not found in those who had never dived deeper than 30 meters, but was detected in 30 out of 190 men (15.8%) who had dived deeper than 200 meters. It can be argued that screening of deep divers with MRI can detect juxta-articular lesions and prevent joint collapse.[9]

Early recognition is imperative, and can be accomplished by annual long bone radiographic examinations, radiographic investigation of any minor arthralgia or bursitis, and follow-up radiographs two months after a decompression episode. Asymptomatic lesions should restrict diving to shallow depths with proscription of decompression, experimental, and commercial diving. Obviously, juxta-articular lesions preclude any diving whatsoever. Early surgical treatment by decortication of the involved area with prosthesis is recommended.

Otologic Effects

It has been widely theorized that deafness is more prevalent in divers. To prove this hypothesis, Molvaer and Albrektsen[10] and Talmi[11] conducted audiometric examinations in divers and age-matched controls. The divers demonstrated greater hearing loss in both studies compared to controls. Another study by Molvaer[12] found that at most frequencies, divers had higher hearing thresholds (more hearing impaired) than otologically normal subjects of the same age at both the first and final examinations. It appears that in this study, the divers’ hearing deteriorated faster than that of the non-divers. Some of the divers were known to have suffered permanent hearing loss from acute barotrauma. Molvaer concluded that professional diving may cause a more rapid deterioration of high-frequency hearing than that seen in a standard population. He found that smoking potentiates this risk of high-frequency hearing loss. Molvaer[13] has also found that divers are at risk for long-term cochlear-vestibular damage, which is responsible for high-frequency hearing loss.

Slow-onset deafness without an identifiable event is considered a “long-term effect” of diving. However, bombastic noise is the most probable cause of hearing loss in professional divers; the rush of gas entering a chamber during compression, the circulation of gas in diving helmets, the use of noisy underwater tools, and the occasional underwater explosion are typical causes of deafness in divers, though exposure to repetitive episodes of smaller magnitudes may have the same effect.

Pulmonary Function

It was generally thought that divers had larger vital capacities than nondivers, but this theory was rebuked in a study by Thorsem and coworkers.[14] They observed 152 saturation divers and compared them with 106 matched controls, and found differences in lung function variables between the two groups. These changes were consistent with small airways dysfunction and with the transient changes in lung function seen immediately after a single saturation dive. The association found in this study between reduced pulmonary function and previous diving exposure suggests that there are cumulative long-term effects of diving on pulmonary function. Though this change of vital capacity probably has little effect upon the diver’s general health, recent studies, including one by Lehnigk and colleagues[15], have indicated that divers develop some degree of air flow obstruction due to airway narrowing.

Pulmonary diffusion capacity deteriorates with age and this process may be accelerated in divers. Early research has been limited to deep diving, where a diminution of pulmonary diffusion post-dive may not be clinically significant and improves in a few weeks. A change in pulmonary diffusion capacity is also associated with diminution of exercise tolerance but this has functional rather than clinical significance.

Neurologic Effects

Studies[16-21] have shown statistically significant deviations from the norm as indicated by evoked potential, cognition, memory and spinal cord dysfunction, but no association with clinical illness; an example of this would be a delayed P40 response of a posterior tibial sensory-evoked potential in an apparently healthy working diver.

One study using evoked responses[16] during and after acute decompression illness have shown that modifications of evoked responses occur. However, there have been few investigations of divers without a history of DCS.

In a study by Todnem and associates[17], neurologic examinations were performed on 40 air and saturation divers and 100 controls. The divers had significantly more general nervous system complaints and more abnormal neurologic findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long- and short-term memory. The majority of abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurologic symptoms and findings were independently correlated with diving exposure, prevalence of DCS, and age of the diver.

Peters, Levin, and Kelly[18] interviewed 10 divers with a history of decompression illness involving the central nervous system, eight of whom had unequivocal neurologic deficits implicating multiple supraspinal lesions. Seven of these neurologically impaired divers completed a battery of neuropsychologic tests that revealed severe deficits. The findings suggest that diffuse and multiple central nervous system lesions occur secondary to decompression illness and demonstrate the importance of thorough neurologic and neuropsychologic tests to assess the long-term effects of diving accidents.

Work done by Palmer, Calder, and Hughes[19] suggests significant damage occurs at a subclinical level in decompression illness. Spinal cords from 8 professional and 3 amateur divers who died accidentally were examined histopathologically. Degeneration was found in the cords of these divers, affecting the posterior, lateral, and anterior columns. There was also degeneration of afferent fibers in one diver. The recent report by Morild and Mork[20] demonstrating ependymal damage is equally worrisome. Ependymal cells line all the brain cavities and control the production and flow of cerebrospinal fluid. Disruption in this process affects the brain broadly with many dysfunctions of motor, sensory, memory, and cognitive functions. Interference with the dynamics of cerebrospinal fluid may lead to loss of ependymal lining in the ventricles of the brain. The divers these investigators studied were divided into two groups, divers and controls. Mean loss of ependymal cells was compared between the two groups. A statistically significant higher loss of ependyma was found in the total number of divers than in the controls. There was no significant difference between the group of sport divers and the control group. When the divers were divided into sport and professional divers, there was no difference between the sport divers and controls. The largest loss of ependymal cells was found in the professional divers without saturation experience, which was statistically significant when compared to the controls.

Another study by Mork and colleagues[21] found no evidence of degeneration, necrosis, or scar formation changes in the spinal cords of deceased divers studied by histopathological and immunocytochemical methods. Ten amateur and 10 professional divers were studied with emphasis on the presence of subacute or chronic changes in the spinal cord.

Clearly, the risk of long-term diving in the sport community remains to be elucidated. There is evidence that professional divers suffer higher degrees of permanent residua, though these may not be clinically significant. However, as David Elliott points out, ‘in spite of much detailed investigation, none has yet demonstrated a deficit which is of sufficient concern to change current standards of fitness to discontinue diving in healthy divers who have had no decompression incident.'[22]

A careful, standardized, neurologic examination is the foundation for any study of long-term effects in divers. Norwegian professional divers have been studied in great detail. Todnem and associates[23] compared 156 divers with 100 age-matched nondiving controls. Unfortunately the examinations were done after the medical history was taken, creating a bias. In this study, if the divers reported fatigue, mood lability, irritability, difficulty concentrating or memory problems, they were considered to be showing evidence of a decompression deficiency. 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 findings recorded as positive included increased postural tremor, a modified Romberg sign, and reduced sensation in the feet. No specific syndrome was
detected but, when all the symptoms and signs were added numerically, the diving group had higher scores which were statistically significant when compared to the controls.

Todnem and colleagues[17] found that the neurologic exams of commercial saturation divers were correlated with exposure to deep diving, but even more significantly correlated to air and saturation diving and exposure to decompression sickness. This study suggests that deep diving may have long-term effects on the nervous system of the divers.

Todnem and Vaernes[24] retrospectively studied divers with chronic neurologic problems. They found that atactic signs and abnormal EEGs were found in 5 of 18 divers immediately after deep diving. Neuropsychologic 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%) post-dive. 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 with concentration and were more likely to have paresthesia in their feet and hands than were the controls. Two had seizures, one had suffered episodes of transitory cerebral ischemia, and one had experienced
transitory global amnesia after the deep dives.

Neuropsychometric Changes

Edmonds and Hayward[25] administered a battery of neuropsychological tests to a group of abalone divers and a group of fishermen. No evidence of cognitive impairment was found in the divers, despite exposure to decompression stress. However, in another study Edmonds[26] found contradictory results, showing abalone divers develop a syndrome of reduced intellectual capacity (dementia or “punch drunkenness”).

Vaernes and coworkers[27] studied 64 deep saturation divers (DSD group) and 32 experienced divers who were only just commencing saturation diving. The authors found mild-to-moderate neuropsychologic changes (greater than 10% impairment) in measures of tremor, spatial memory, vigilance, and automatic reactivity in 20% of the divers after deep dives (DSD group). One year post-dive no recovery was observed except in the vigilance test. These researchers suggest that their more extensive, neurologic examination might indicate the
presence of a mild pathological process which cannot be detected by standard neurologic examinations.

Other studies[28,29] have 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 attributed to advancing age and not to diving. Thus the evidence relating to neuropsychometric changes in diving is not strong but, once again, there is sufficient concern to justify a properly constructed longitudinal study.

Other Systemic Effects

Investigators such as Polkinhorne[30], Scholz[31], Day[32], Kania[33], and Holden[34] have found ocular changes in divers. Alterations in liver enzymes were documented by Doran[35] and heart and skin effects were found by Maehle and Stuhr[36] and Ahl’en, Iverson, Risberg, Volden, Aarstet and associates[37], respectively.

The effect of diving on the eye has been the subject of considerable attention. Polkinhorn[30] studied the ocular fundi of 84 divers and found that divers had significantly more abnormalities of the retinal pigment epithelium than a comparison group of non-divers. In addition, the prevalence of fundus abnormality was related to the length of diving history. The changes noted were consistent with blockage of retinal and choroidal vessels, either from bubbles during decompression or altered behavior of blood constituents during conditions of increased pressure. Sholz[31], on the other hand, could find no evidence for retinal damage caused by diving in a large study of color vision in divers. In a study of the pupil for neurological defects, Day[32] studied the pupil cycle time in the neurological assessment of divers with equivocal findings. Kania[33] found that professional divers who had never suffered from decompression sickness had fundal changes similar to those divers who had had the disease, leading to the conclusion that diving may cause permanent degenerative changes in the fundus of the eye. Fluorescein angiography was done by Holden[34] on 26 divers who had used safe diving practices for at least 10 years, with 7 controls. There were no significant differences, indicating that the macular abnormalities seen in divers can be controlled by safe diving.

Doran[35] has documented that there are significant alterations in liver enzymes in the saturation diver. Stuhr and Maehle found that in rats, repeated hyperbaric exposures produced decreased cardiac function, mass, and morphology.[36] Chronic skin changes have been noted in a condition called ‘diver’s hand’ seen in occupational saturation diving.[37]

Cellular Changes

Fox[38] studied two diving groups –air divers (n = 77) and helium-oxygen divers (n = 76)– and compared them with two control groups –oil rig workers (n = 75) and non-oil industry subjects (n = 52). Six out of 153 divers (3.9%) had an unusually high number of structural aberrations in a small portion of the dividing lymphocytes. The health risks imposed by these abnormal cells is unknown but the defects they contain are, in most cases, so extreme that the cells are likely to die during mitosis. The aberrations observed were typical of those induced by ionizing radiation and were present in air divers as well as mixed gas divers. None of the affected divers admitted to using gamma-sources for examining welds at depth, whereas some of the divers who had normal chromosomes did use isotopes. Similar damage was not found in the controls.


MRI demonstrating brain infarction and degeneration. Reprinted with Permission from Ray Ballinger, MD, PhD.


Magnetic Resonance Imaging (MRI) has given investigators an additional tool with which to study the central nervous system in divers. With MRI, high signal intensity (bright spots), indicating tissue damage, has been reported in divers and is thought to have great potential for identifying damage done to the CNS. It was first used by the Norwegians (Todnem and associates)[39] to study decompression illness, and they found that up to 33% of all divers had high signal intensity changes. Similar studies by Brubakk[40] and Rinck and coworkers [41] confirmed these findings.


The use of simple photon emission computed tomography (SPECT) and the use of 99m HMPAO in submarine escape trainees with a known episode of cerebral gas embolism was first described by Adkisson and colleagues.[2] This technique has since been used in divers following acute decompression sickness.

The best application of these modalities properly awaits the standardization of techniques and diagnostic criteria between research centers. The use of the radioactive marker 99m HMPAO[42-45] has been curtailed because in apparently healthy individuals it might be deemed unethical.


Spontaneous electroencephalogram[46] and evoked action potentials have been used in persons who suffered acute decompression sickness. Despite careful definition of procedures and diagnostic criteria abnormalities, they are, at best, only possible indicators of pathology.

In a large study by Todnem and researchers[39], abnormal EEGs with focal slow waves mostly in the temporal regions and sharp potentials were found in 18% of the divers and in 5% of the controls (P = 0.003). Abnormal EEGs correlated significantly with the exposure to saturation diving (P = 0.0006) and the prevalence of decompression sickness (P = 0.0102). That saturation divers more frequently have abnormal EEGs, even in the absence of a history of decompression illness, led the research team to advocate the use of the EEG in the periodic health examination of deep divers.

Standardization of Diagnostic Techniques

Lack of diagnostic standardization is the major flaw found in diving-related studies. With agreement on diagnostic techniques and radiologic diagnosis established in the late 1950s and 1960s, investigators have moved away from clinical descriptions of the illness to prevalence surveys of pre-symptomatic lesions in the apparently healthy diving population.[47-51] Further investigations of a prospective nature are required to associate long term diving and adverse effects and determine the circumstances under which these effects occur.


Negative effects of long-term deep diving include dysbaric osteonecrosis, decreased pulmonary function due to airway narrowing, hearing loss, and liver changes. There are studies that suggest neurologic effects of diving, but these studies have been criticized for flaws in design. Damaged cells similar to those found after exposure to ionizing radiation have been observed, but there are no controlled studies to verify that diving caused the cell damage. The severity of the effects and the point at which they manifest themselves in deep divers appears to be established. What remains unknown is the point at which these changes occur in sports divers and at what depths and times. Because no definitive scientific information is available, it can only be speculated that air bubbles will always travel to end organs, affecting them in some manner.

There have been reports of encephalopathy, impairment of cognitive function, and abnormal EEGs using this rationale as an explanation. However, the Divers Alert Network has stated: “The supposition of any damage to the brain rests on the occurrence of so called silent bubbles occurring in the blood or brain and spinal cord. That such bubbles do exist has been well demonstrated by Doppler technology in blood and tissue studies of animals’ spinal cords. Whether or not, however, these silent bubbles are the cause of changes in the brain is unproved…Divers should not be unduly concerned about {the Lancet study}. More research is needed, but the world is filled with many divers who have been diving for over 40 years who show no unusual deterioration in their abilities which would affect their quality of life…Certainly, [the study’s] results should not be discounted. However, in the absence of neurological decompression illness, many other studies in which divers were compared with non-divers, have failed to demonstrate that diving causes long-term neurological impairment or any functional abnormalities.”[52]


1.Hope A, Lund T, Elliott D, et al (eds): Long-term Health Effects of Diving. Flagstaff, Ariz, Best Publishing Company,1994.
2.Adkisson GH, Macleod MA, Hodgson M, et al: Evidence for cerebral perfusion deficits in 28 cases of dysbarism. Lancet 2:119-121, 1989.
3.Hodgson M, Smith DJ, Macleod MA, et al: Case control study of cerebral perfusion deficits in divers using 99Tcm hexamethylpropylene amine oxime. Undersea Biomed Res 18(5-6): 421-431, 1991.
4.Bove AA (ed): Diving Medicine ed 3. p.287. Philadelphia, WB Saunders Co, 1997.
5.Edmonds C and Thomas RL: Medical Aspects of Diving-Part 4. Med Jour 2: 1416, 1972.
6.Harrison JA: Radiological Criteria in Diagnosing Dysbaric Osteonecrosis. pp. 151-9. Dysbarism-related osteonecrosis Washington DC, US Dept. of Health, Education and Welfare, 1974. WE 200 399d 1972, O.
7.Pearson RR: Bone scintigraphy as an investigative aid for dysbaric osteonecrosis in divers. J R Nav Med Serv 68(2):61-68, 1982.
8.Zhang LD: Use of ultrasonography in the diagnosis of dysbaric osteonecrosis. Undersea Biomed Res 17(6):535-541, 1990.
9.Trowbridge WA: An appraisal of the composition data storage project at the Newcastle-upon-Tyne Decompression Sickness Central Registry. Thesis, University of Newcastle-upon-Tyne, England, 1982.
10.Molvaer OI and Albrektsen G: Hearing deterioration in professional divers: An epidemiologic study. Undersea Biomed Res 17(3):231-246, 1990.
11.Talmi YP: Barotrauma-induced hearing loss. Scand Audiol 20(1):1-9, 1991.
12.Molvaer OI and Lehmann EH: Hearing acuity in professional divers. Undersea Biomed Res 12(3): 333-349, 1985.
13.Molvaer OI and Albrektsen G: Alternobaric vertigo in professional divers. Undersea Biomed Res 15(4):271-282, 1988.
14.Thorsen E, Segadal K, Kambestad B, et al: Divers lung function: Small airways disease? Br J Ind Med 47(8):519-523, Aug 1990.
15.Lehnigk B, Jorres RA, Elliott DH, et al: Effects of a single saturation dive on lung function and exercise performance. Int Arch Occup Environ Health, 69(3):201-208, 1997.
16.Murrison AW, Glasspool E, Pethybridge RJ, et al: Neurophysiological assessment of divers with medical histories of neurological decompression illness. Occup Environ Med Nov 51(11):730-734, 1994.
17.Todnem R, Nyland H, Skeidsvoll H, et al: Neurological long term consequences of deep diving. Br J Ind Med 48(4):258-266, 1991.
18.Peters BH, Levin HS, Kelly PJ: Neurologic and psychologic manifestations of decompression illness in divers. Neurology
27(2):125-127, 1977.
19.Palmer AC, Calder IM, Hughes R: Spinal cord degeneration in divers. Lancet 2:1365-1366, 1987.
20.Morild I, Mork SJ : A neuropathologic study of the ependymoventricular surface in diver brains. Undersea and Hyperbaric Medicine 21(1):43-51, 1994.
21.Mork SJ, Morild I, Brubakk AO, et al: A histopathologic and immunocytochemical study of the spinal cord in amateur and professional divers. Undersea and Hyperbaric Medicine 21(4):391-402, 1994.
22.Elliott DH: Long-term sequelae of diving. J R Soc Med 82(2):79-80, 1989.
23.Todnem K, Nyland H, Kambestad BK, et al: Influence of occupational diving upon the nervous system: An epidemiological study. Br J Ind Med 47(10):708-714, 1990.
24.Todnem K, Vaernes R: Acute and chronic effects of deep diving on the nervous system. Tidsskr Nor Laegeforen 113(1), 36-39, 1993.
25.Andrews G, Holt P, Edmonds C, et al: Does non-clinical decompression stress lead to brain damage in abalone divers?. Med J Aust 144(8):399-401, 1986 Apr.
26.Edmonds C and Boughton J: Intellectual deterioration with excessive diving (punch drunk divers). Undersea Biomed Res 12(3):321-326, 1985 Sept.
27.Vaernes RJ, Klove H, Ellertsen B: Neuropsychologic effects of saturation diving. Undersea Biomed Res 16(3):233-251, 1989 May.
28.Vaernes RJ, Klove H, Ellertsen B: Neuropsychological Effects of Saturation Diving. Undersea Biomed Res (3):233-251, 1989, May 16.
29.Reul J, Weis J, Jung A, et al: Central nervous system lesions and cervical disc herniations in amateur divers. Lancet 345(8962):1403-1405, 1995 Jun 3.
30.Polkinghorne PJ, Sehmi K, Cross MR, et al: Ocular fundus lesions in divers. Lancet 2:1381-1382, 1988.
31.Scholz R, Hofmann H, Duncker G: Mass screening of blue color vision in divers with the desaturated Lanthony-15-Hue Test. Fortschr Ophthalmol 88(5):505-508, 1991.
32.Day RT: Pupil cycle time in the long-term neurologic assessment of divers. Undersea Hyperb Med 21(1):31-41, 1994.
33.Kania B and Krzyzak J: Comparative investigations of changes in the ocular fundus of divers. Klin Oczna 92(5-6):92-93, 1990.
34.Holden R, Morsman CD, Lane CM: Ocular fundus lesions in sports divers using safe diving practices. Br J Sports Med 26(2):90-92, 1992.
35.Doran GR, Chaudry L, Brubakk AO, et al: Disturbed liver function in divers – further enzymological evidence. Abstract No. 90, Undersea Biomedical Research Supplement to Vol 17, Joint Meeting on Diving and Hyperbaric Medicine, August 1990.
36.Stuhr LE, Maehle BO: The effect of losartan on cardiac function, mass and morphology in rates after repeated hyperbaric exposures. Scand J Clin Lab Invest 57(3):253-261, 1997, May.
37.Ahl’en C, Iverson OJ, Risberg J, et al: Diver’s hand: A skin disorder common in occupational saturation diving. Occup Environ Med 55(2):141-143 1998, Feb.
38.Fox DP, Robertson FW, Brown T, et al: Chromosome aberrations in divers. Undersea Biomed Res 11(2):193-204, 1984.
39.Todnem K, Skeidsvoll H, Svihus R, et al: Electroencephalography, evoked potentials and MRI brain scans in saturation divers: An epidemiological study. Electroencephalogr Clin Neurophysiol 79(4):322-329, 1991.
40.Brubakk AO: Central nervous system changes in professional divers as evaluated by MRI. Abstract No. 125, Undersea Biomedical Research Supplement to Vol 17, Joint Meeting on Diving and Hyperbaric Medicine, August 1990.
41.Rinck PA, Svihus R, de Francisco P: MR imaging of the central nervous system in divers. J Magn Reson Imaging 1(3):293-299, 1991.
42.Wilmshurst PT, O’Doherty MJ, Nunan TO: Cerebral perfusion deficits in divers with neurological decompression illness. Nucl Med Commun 14(2):117-120, 1993 Feb.
43.Shields TG, Duff PM, Evans SA, et al: Correlation between 99Tcm-HMPAO-SPECT brain image and a history of decompression illness or extent of diving experience in commercial divers. Occup Environ Med 54(4):247-253, 1997 Apr.
44.Broome JR: Brain damage in divers. Br Med J 314(7096):1761, 1997.
45.Staff RT, Gemmell HG, Duff PM, et al: Decompression illness in sports divers detected with technetium-99m-HMPAO SPECT and texture analysis. J Nucl Med 37(7):1154-1158, 1996 Jul.
46.Todnem K and Vaernes R: Acute and chronic effects of deep diving on the nervous system. Tidsskr Nor Laegeforen 113(1):36-39, 1993 Jan.
47.Harrison JA: Early diagnosis and pitfalls in diagnosis of aseptic bone necrosis in divers. Proc R Soc Med 70(7):486-487, 1977.
48.Harrison JA: Aseptic bone necrosis in naval clearance divers: Radiographic findings. Proc R Soc Med 64(12):1276-1278, 1971.
49.Harrison J: Aseptic bone necrosis in divers. Br J Radiol 45(533):393, 1972.
50.Elliott DH: The role of decompression inadequacy in aseptic bone necrosis of naval divers. Proc R Soc Med 64(12):1278-1280, 1971.
51.Elliott DH: Incidence of osteonecrosis in Royal Naval divers. pp. 7-8, in Beckman EL, Elliott DH (eds): Dysbarism-related osteonecrosis, Washington, DC, US Dept, HEW 1974.
52.Divers Alert Network: DAN responds to Lancet article – Long-term consequences of diving. J Underwater Education:27-28, 1996 Fall


Ernest S. Campbell, M.D., FACS

5/5 - (14 votes)

Leave a Reply

Close Menu