Decompression illness in Japanese Ama divers
Hideki Tamaki1),2), Kiyotaka Kohshi3), Tatsuya Ishitake1), Robert M Wong4)
1)

Department of Environmental Medicine, Kurume University School of Medicine, Kurume, Japan
2)
Division of Emergency and General Medicine, Tamaki Hospital, Hagi, Japan
3)
Clinical Research Team, The Baromedical Research Foundation, SC, USA
4)
Department of Diving and Hyperbaric Medicine, Fremantle Hospital, Fremantle, Australia

Summary
Decompression illness (DCI) following repetitive
breath-hold (BH) dives has been disputed and debated in the medical fields. We’ve experienced
some professional Japanese breath-hold divers(Ama) with DCI after dives. Their magnetic resonance images of the brain show multiple cerebral
infarcts in border or terminal zone areas, and theselesions are considered to be cerebral gas embolism.
A questionnaire survey conducted in a district revealed that twelve of 185 Ama divers had experienced stroke-like symptoms such as sensory numbness [7], motor weakness [6], speech disturbance[3], and visual deficit [1]. All neurological disorders
were transient and recovered within a month.
However, spinal involvements, which are commonin compressed air diving, have not been seen in
Ama divers. The mechanisms of DCI following BH
diving are not clear. We have hypothesized that venous bubbles formed after repetitive BH dives aretrapped in the small pulmonary arteries and they arecompressed during descending to the bottom andcan pass through the lungs. The arterialized bubbles
expand during ascending to the surface and they
probably induce cerebral gas embolism. However,there are some problems to confirm the hypothesis.
Preface
Although decompression illness (DCI) is wellknown in compressed air diving, the development israre among breath-hold (BH) divers. We have experienced some Japanese professional BH (Ama)divers being afflicted, and their events were mainly
neurological disorders caused by cerebral stroke(1-3). When an interview survey was conducted in avillage, many Ama divers were found to have experienced neurological accidents during BH diving(3). Moreover, several similar cases have been recently reported in professional and amateur BH divers from some areas (4-6). Based on the reported,
clinical symptoms and neuro-radiological findingsof DCI in BH divers, cerebral lesions are particularly prominent. We show the clinical characteristics of DCI in Japanese Ama divers and hypothesize
the mechanisms for DCI following repetitive BHdives.
Japanese Ama divers in Abu-Hagi District
Our interview survey in the village on MishimaIsland showed many Ama divers had experienced
stroke-like neurological accidents during repetitive
BH dives (3). These diving accidents happened
during or after more than three hours of repetitive
dives. All symptoms were neurological disorders,and motor weakness and sensory numbness in one
side were the most common. Others were dysarthria,
visual deficit, convulsive seizure, unconsciousness,and so on. In addition to obvious neurologicalevents, many Ama divers frequently felt dizziness,
nausea and/or euphoria after long-term deep andrepetitive dives. However, there haven’t been any
informations concerning diving accidents in Ama
divers on a large scale.
To estimate diving risks for Ama divers, we’ve
performed a preliminary questionnaire study in
Hagi-Abu district, Yamaguchi Prefecture, Japan.
This area includes 14 diving branches. The association for fishermen and Ama divers controls theirworking schedules as days and periods of time, andhas 381 Ama divers. In 2008 a standard questionnaire was carried out by the support of the association, and we received answers from 185 Ama divers; 28 partially assisted divers and 157 unassisted
divers. They were questioned about their diving

patterns including depth, length of diving shift,diving time and surfacing interval. We obtained ahistory of diving-related physical and neurologicalevents such as skin rash, joint pain, dizziness, vertigo, nausea, euphoria, motor and sensory involvement, unconsciousness and other clinical conditions.
A separate for the divers included questions on thepresence of hypertension, cardiac arrhythmia, diabetic mellitus and cerebrovascular diseases.
Twelve of 185 Ama divers (56 yr: 42 to 71) had
experienced stroke-like neurological disorders during dives; eleven cases were partially assisted divers and one was unassisted (Fig. 1). Partially assisted Ama divers with DCI descended passively
with a 15-20-kg bar weight to the bottom, and thenthey swam to the surface without assistance. Theirdiving depths measured with fish finders were
10-20 msw, and diving time and surface interval
were 30-75 and 10-40 sec, respectively. A
non-assisted Ama diver had motor weakness andparesthesia in one side, and his diving depth was 12msw. The most common symptoms were paresthesia [7] and motor weakness [6] in one side, and dizziness was accompanied with or without neurological disorders. Moreover, limb pain appeared ina partially assisted Ama diver who had also motor
weakness, sensory numbness and speech disturbance. Characteristically, these neurological disorders were transient and resolved completely withina month.
Case Presentation
Case 1: A 33year-old male Ama diver was referredto our hospital due to visual disturbance. He was apartially assisted BH diver who descended to 15-25
msw using a 15-kg weight and then ascended with-out assistance. He repeatedly made 1-1.5 min diveswith 1-min surface interval between dives. He began to dive at 0920 and continued diving until noon,and he started to work after a 20-min lunch break.
He noticed dizziness and blurred vision at around1400. He consulted to a doctor on fourth day, andhis magnetic resonance image (MRI) showed two
cerebral lesions in the left occipital lobe and theright basal ganglia (Fig.2). The right-to-left shunt
could not be detected using the Doppler echocardiography. The size of the lesions regressed for several days, but he had a partial visual deficit fiveyears later.
Case 2: A 43-year-old male Ama diver had a historyof diving accidents at the age of 34 years. His diving patters were similar to those of Case 1. After
deep and repetitive BH dives, he noticed motor
weakness and sensory numbness in his left side.
However, he had a convulsive seizure with unconsciousness three hours after improving of hemiparesis. When he was evaluated nine years after theevent, he had no neurological deficits despite multiple cerebral lesions in the frontal lobes andperiventricular white matter (Fig. 3).
Case 3: A 39-year-old male Ama diver is an acutecase of DCI. His diving patterns were similar orsame as those in above cases. Previously, he hadthree times of diving accident. The first event happened at 17 years old, and the second was 25 yearsof age. Previous diving accident was the left motor
weakness, but at this time he had motor weakness
and sensory numbness in his right side. His brain
MRI on third day showed multiple infractions ofacute and old stages (Fig. 4).
L

Diving accidents in Ama divers


Neurological diving accidents: 12/185 Ama
assisted : 11/28 (39.3%)
nonnon-assisted: 1/157 (0.6%)

Neurologicalsymptoms (12)• paresthesia:
paresthesia: 7• motor weakness: 6• speech: 3• visual: 1

Accompanied
symptoms (10)• dizziness: 8• vertigo: 2• nausea: 2• limb pain: 1

Fig.1 Results of a questionnaire study for Ama divers

4th day

8th day

5 yrs

Fig.2 MRI of the brain in Case 1 with blurred vision

L

Mechanisms of DCI in repetitive
breathbreath-hold divingN
N22 accumulation
accumulationinintissues
tissuesafter
after
repetitive
repetitivedives
dives‘Trapped’‘Trapped’bubbles
bubblesininpulmonary
pulmonaryarteriesarteries

Rt-Lt
Rt-Ltshuntshuntssof
ofthe
theheartheart

Microbubbles
Microbubbles

BubbleBubble formation
formation

9 years after events

ininvenous
venousside
sideofoftissues
tissuesFig.3 MRI of the brain in Case 2 with a history of motor andsensory involvement and convulsive seizure 9 years
earlierL

3rd day

17th dayFig.4 MRI of the brain in Case 3 with acute and chronic
diving accidents

Development Mechanisms
Mechanisms for DCI in BH divers have not been
elucidated (Fig.5). Nitrogen (N2) accumulation in
fatty tissues increases consecutively throughout repetitive BH dives despite quickly reaching a steadystate in the brain (7, 8). From the point of N2 kinetics in BH diving, it is easy to consider that N2 gas
bubbles are formed in the venous side of tissues
rather than the brain. Although the bubble formation following repetitive BH dives is controversial,venous bubbles were recorded in Japanese Ama
divers (9, 10). In addition, some investigators suggest that the bubble formation in venous side is apossible mechanism for cerebral DCI (11-13). After
deep, repetitive BH dives, bubbles may be formed
in venous side and reach to the lungs. Microbubbles
passing through the pulmonary capillaries, are generally harmless to tissues including the brain. Since
an experimental study showed that microbubbles
impair the blood brain barrier transiently (14), we

throughthroughpulmonary
pulmonarycapillaries
capillaries?

‘De‘Denovo’
novo’bubblesbubbles?

Hypoxia
Hypoxia?

ininarteriesarteries

Fig.5 Mechanisms of decompression illness in repetitive
breath-hold dives

once thought the major mechanism of DCI in BH
divers was such microbubbles (2, 3, 11). However,
we do not think microbubbles are the major mechanism of DCI from the MRI findings of Ama divers
with DCI. Because multiple infarcts are located inborder and terminal zones of the cerebral arteries,
we should consider another factor as a majormechanism of DCI in BH divers. Venous bubbles
larger than 21 µm are retained or trapped at small
pulmonary arteries of mammalian lungs (15). When
Ama divers descend to the bottom, such “trapped”
bubbles are compressed and easily pass throughpulmonary capillaries. Such bubbles passing
through the lungs enlarge during ascending to thesurface and the bubbles induce arterial gas embolism. In addition, there is a possibility that
“trapped” bubbles are related to microbubbles.
“Trapped” bubbles and microbubbles are mixed,
and these bubbles probably induce cerebral infarcts.
Moreover, other mechanisms such as cardiac shuntor pulmonary barotrauma should be considered, but
we do not think these are major etiological factorsof DCI caused by repetitive BH dives (16).
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