‘SAMBAS’, ‘MOOGLIES’ AND OTHER ACUTE EFFECTS OF APNEA
by Lynne Ridgway, PhD cand, Neuroscience in the School of Psychology University of Queensland, Brisbane, Queensland, Australia
Ken McFarland, PhD, Neuroscience in the School of Psychology University of Queensland, Brisbane, Queensland, Australia
Ian B. Stewart, PhD, Institute of Health & Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia
Andrew C. Bulmer, PhD cand, School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia
Having established that there were no detectable long-term or cumulative effects on cognitive functioning in 21 elite apnea divers (3), we embarked on field and laboratory studies to examine the acute effects of apnea diving. Anecdotally, divers report that they occasionally experience a range of cognitive and motor disturbances post apnea including, language production disturbances (‘Mooglie’ – Canadian freedive team 2002), motor control problems (‘sambas’), shallow water blackouts, difficulty with concentration or keeping track of time, feeling “fuzzy in the head” and not being able to recall events immediately prior to the apnea activity. This range of symptoms suggests a global change to neuropsychological functioning similar to that experienced by high altitude mountain climbers, pilots, and patients with clinical hypoxic conditions such as sleep apnea, or chronic obstructive pulmonary disorder (see Virues-Ortega et al.  for a review).
Aims & Hypotheses:
1) Field study: to assess the neuropsychological changes immediately following extended apneas. Based on the literature and anecdotal reports we predicted that divers would show a significant decline in neuropsychological functioning immediately following dynamic and static apnea events compared to baseline.
2) Lab study: to examine the relationship between performance on neuropsychological tasks and levels of hypoxemia attained during apnea. We hypothesized that there would be a strong positive correlation between oxygen desaturation during apnea and neuropsychological functioning immediately following apnea.
Both studies were approved by the University of Queensland Ethics committee, and volunteer participants received information sheets, and signed consent forms. Neuropsychological tests selected were the Symbol Digit Modalities Test (SDMT) (4), a four item explicit memory task, and a computer based simple reaction time task. Each test had multiple equivalent forms to allow for repeated testing. Physiological measures considered for this paper were heart rate, oxygen desaturation, and breath-hold duration. (Note: for full description of additional physiological methods see Stewart et al. ).
Field study: 67 elite divers (m=45, f=22), 31.2±7.2 (mean ± standard deviation) years of age and with 5.9±6.2 years of apnea experience from 22 countries were interviewed, then tested within five minutes post-dynamic and post-static apnea during the 2002 International Pacific Cup.
Laboratory study: Physiological and neuropsychological responses of 10 divers and 10 controls matched for age, education, and anthropomorphic variables, were examined during repeated face immersion apneas.
Field study: During dynamic apnea competition, four of the divers suffered a brief loss of consciousness and two divers suffered a brief loss of motor control ‘samba.’ The ‘sambas’ involved a bilateral motor tremor, eye gaze deviation, and fine head bobbing lasting approximately 10 s, during which time the divers were fully conscious and able to follow commands. Baseline data from a subgroup of 21 divers (3) were used for comparison with 67 divers following dynamic apnea. They dived to 47.4±11.4 m (156±37 ft) depth. The average number of correctly coded symbols in 90 s on SDMT at baseline was 59.5±8.2, whereas the post-dive score was significantly reduced to 54.9±8.5 (p<0.001). No significant differences were evident on the picture memory or reaction time tasks. Data from 58 of the same divers after their static apnea (1-2 days later) resulted in neuropsychological performances not significantly different to baseline, SDMT score of 58.5±7.6. Again, there were no significant differences for the reaction time or the picture memory tasks. Data from three divers who suffered a ‘samba’ during the static apnea revealed SDMT performances that were significantly different to baseline (tdf=2 26.0, p=0.001) with subsequent recovery to baseline performance achieved within 80 min. One diver suffered a temporary blindness (approximately 30 min duration) and unilateral motor weakness following his 4:56 min:s static apnea and was not tested post-apnea.
Laboratory study: Compared to controls, divers had a greater number of previous negative neurological events (NNE; p=0.02), significantly longer maximal apneas (p<0.001), greater heart rate changes (p<0.001), and arterial oxygen desaturation compared to controls (p<0.0001) (Table 1, Figure 1). No group differences were found in peripheral blood flow, hematocrit, lactate, hemoglobin concentrations, or neuropsychological measures. However, divers with largest bradycardia demonstrated slowing of arterial oxygen desaturation two to three times that of other divers (5). There was a significant negative correlation between breath hold duration and arterial oxygen desaturation (r=-0.840, p<0.01).
Figure 1. Minimum arterial oxygen desaturation as a function of maximum breath- hold time in seconds for n= 10 divers and n=10 controls.
These two studies aimed to assess the acute cognitive and behavioral sequelae immediately following extended apneas. The first hypothesis that divers would show a significant decline in cognitive and motor functioning immediately following apnea compared to baseline was supported for the dynamic but not static apnea conditions. Apnea divers, immediately following a competition dive, demonstrated a significant decline in cognitive and motor speed compared to baseline. However, no differences were found on the simple reaction time or picture memory tasks.
These results provide support for the literature that apnea with exercise increases the desaturation effect and lactate accumulation (1) with consequent decline in speed of motor responding (2). An alternative explanation is that anxiety related to the dynamic apnea being on the first day of competition or first exposure to neuropsychological testing may have influenced performance on timed tasks. However, this is unlikely since if anxiety was a factor we would expect performance decrements on the reaction time task as well as the SDMT. A more plausible explanation is that the dynamic apnea despite being of shorter duration placed greater demands on oxygen usage than the longer duration static apnea without any exercise
On the following day, divers’ performances on the same neuropsychological tasks immediately following static apnea were not significantly different to baseline suggesting that a) static apnea does not produce the same neuropsychological difficulties as apnea with exercise, and b) divers had recovered from the neuropsychological decline evident post dynamic apnea. When three divers were examined following a loss of motor control their neuropsychological functioning showed further declines that had resolved within an 80 min time frame.
For the laboratory study, the hypothesis that there would be a strong positive correlation between oxygen desaturation and neuropsychological functioning was not supported, despite the fact that divers did experience a large desaturation effect (SaO2 67±10%) none showed a significant change to neuropsychological functioning on the sensitive tests used.
We conclude that even when apnea is (relatively) brief, if it is accompanied by exercise then neuropsychological and motor functioning is compromised. This effect is exaggerated further if the diver suffers a loss of motor control. However, recovery appears to take place within an 80 min period. Given our preliminary results we would recommend that divers refrain from complex cognitive and motor tasks such as driving a car for at least 90 min following apnea activities. This period is conservative and should be increased if the diver has suffered a NNE such as a loss of consciousness or loss of motor control. Further studies to examine the correlates between neuropsychological functioning and apnea during exercise are warranted.
The authors would like to thank the organizers and participants of the 2002 Pacific Cup of Freediving for their immense support for this research.
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DR. LINDHOLM: One comment. You do get sambas or loss of motor control even from the deep dives. It is just not as common in competition. It seems be, I think, my speculation was when I did the statistics on the competitions is that the divers seem to be able to sense when to come up. That is why so many manage to surface from the static apnea just on the edge of losing consciousness. But when you go for depth, well, you make the decision to surface long before you have any cues of hypoxia. So you can use that. So whether you reach the surface or not, you have to decide a minute or two earlier.
MS. RIDGWAY: I am interested too to know what the oxygen saturation levels are like while you are exercising. Presumably they are lower than when you are just doing a static.
DR. DUEKER: I would hate for people to get the idea that hypoxia from emergent accidents is not a problem and that the only problem in emergent accidents would be if your heart stopped. An awful lot of the data, and I use that in quotations, on emergent accidents are viable is, in a simple word, lousy. It is even worse than lousy.
And I was fascinated that you come from a neuropsych background because in what I consider a rather obscure neuropsych journal there is a marvelous follow-up study on a heroic survival of a near- drowning child. The child was in the water probably 40 min, cold water, full cardiac arrest. He made a perfect recovery. That is what is listed in the literature for 20, 25 years. Someone in neuropsych dug up – well, they did not really dig the patient up because the patient was still alive, but found the patient and ran the patient through a few neuropsych tests. Well, you do not even need to be a neuropsychologist to realize that the child had, no longer a child, had extreme learning disabilities, all kinds of problems. And yet, this child had been held up as a poster child for how good it is to drown in cold water.
So I just do not want people to go home and say, gee, this is fantastic or even more scary, to see it in the printed proceedings and we will end up with an awful lot of problems.
MS. RIDGWAY: I hope that is not what I am suggesting. And I am aware of that study [Hughes et al., 2002], and it is an excellent reminder of why we need follow-up neuropsychological evaluations as this young girl had clear MRI and MEG [magnetoencephalography] scans. She was submerged for 66 min and “recovered completely” but we know that children grow into damaged brains and the problems with frontal lobe executive functions do not appear until the child becomes a teenager and beyond. The longitudinal profile for this girl demonstrated a broad pattern of cognitive difficulties including global memory impairment. For this presentation I highlighted four of the studies of good outcomes that are in the literature on near drowning. There are several others with various outcomes.
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DR. LUNDGREN: Dr. Dueker’s comment is well taken, but we have to be mindful of the fact that we are dealing here with samples where the N is one. There is another example in which a college student who drove through the ice with his car and was clocked as being underwater for 60 min and was then revived. After that he was an A-student. It does not say whether he was a C-student before the accident. But we should not draw conclusions from these isolated examples, as Dr. Dueker admonished.
DR. MULLER: Maybe just echo that a little bit. I would say that 30 min of visual motor symptoms is a relatively significant neuropsych finding. I have had the opportunity to take care of two individuals, closed circuit divers, who have had significant hypoxic events. And 90 min was not enough to let those guys return to work. They had neuropsych findings out at two weeks and 30 days. They were able to recover consciousness fairly quickly, but had persisting neurologic symptoms for two to three hours. So I would agree with that. There is something to hypoxia without ischemia that is causing, if not cell death, some fairly significant impact.
MS. RIDGWAY: It seems there are significant neurotransmitter changes. I wonder if the cognitive changes that I saw correlate with the S100B. I would love to look at such data.
DR. LINDHOLM: I would like to comment on that 30 min case. We know that you can get decompression sickness from breath-hold diving, and the symptoms that you report are with a 30 min span of neurological symptoms sounds very much like a DCI hit. And I think we are going to have a discussion on decompression sickness in breath-hold diving tomorrow by Dr. Wong and Dr. Koshi, and for this, I would just suggest that that symptom is probably not related to the hypoxia. It might be another interesting physiological phenomenon, but another one.
DR. FOTHERGILL: I do not know much about the rules for competition breath-hold diving, but do they provide any 100% oxygen after these hypoxia incidents to alleviate any potential problems.
MR. KRACK: Our standard protocol for loss of motor control or loss of consciousness would be 100% oxygen for five minutes on the surface.
NOTE: To access the entire proceedings of the UHMS DAN 2006 Breath-hold Proceedings, visit Divers Alert Network.
In: Lindholm P, Pollock NW, Lundgren CEG, eds. Breath-hold diving. Proceedings of the Undersea and Hyperbaric Medical Society/Divers Alert Network 2006 June 20-21 Workshop. Durham, NC: Divers Alert Network; 2006.