On January 5, 1996, I published the following essay on the
internet newsgroup Alt.Sex.Bondage (ASB) on the possibility of cumulative brain
damage from repeated episodes on suffocation and/or strangulation.
Cumulative Brain Damage From Breath Control?
Hi Mary, Phillip,
As has been prominently pointed out, in my latest post regarding
the risks of breath control play I mentioned a concern that I had not raised in
my previous posts: That there is hypoxia-induced _cumulative_ brain damage
associated with strangulation and/or suffocation even if no major primary or
secondary complication occurs. Several people, understandably, asked me how I
"really knew" that took place.
Well, truth be told, I didn't, directly,
know that it was true. I *did* have pretty good reason to believe that it was
true. After all, two M.D. Neurologists and a PhD Neurophysiologist had told me
that cumulative damage occurred. Also, another SM friend had told me that he had
been told by an Anesthesiologist that it occurred. So I had been advised, either
directly or indirectly, by no fewer than four people with extensive professional
training in how the nervous system functioned that cumulative damage occurred
secondary to episodes of cerebral hypo-oxygenation.
Additionally, I knew
that brain cells died if (among many other causes) the blood nourishing them got
too low on sugar, or if its pH got too low or too high, or if there was physical
trauma to them. (It's been known for ages that the blows to the head that take
place in boxing, in addition to occasionally causing a fatal intra-cranial
hemorrhage, kill neurons in goodly numbers.)
That was good enough for
me, but was it good enough for a.s.b.? Har!
Still, the requests for
documentation were not unreasonable, and I can see a world-class medical school
from my bedroom window, so I got myself over to its library and spent the better
part of a day searching for verifiable, scientific-quality, information to
support or (God forbid!) refute my claim. It was, after all, possible that all
four of these professionals had been wrong and I would have to issue a craven
apology and retraction.
Well, thanks to a MEDLINE search on the keywords
"cumulative cerebral ischemia," it didn't take me long to get several "hits." I
photocopied the three that seemed the most relevant, and have summarized them
below. Any comments of my own are contained within .
article # 1
"Judo as a possible cause of anoxic brain damage; A
by Owens and Ghandiali
The Journal of
Sports Medicine and Physical Fitness, December 1991
The rules of judo provide for strangulation techniques in which the blood
supply to the brain is blocked by pressure on the carotid arteries; such
techniques produce anoxia and possible unconsciousness if the victim fails to
submit. A case is presented of a patient with signs of anoxic brain damage, with
psychometric investigations showing memory disturbance consistent with a left
temporal lobe lesion. This patient had been frequently strangled during his
career as a judo player; it is suggested that such frequent strangulation was
the cause of the damage. Such an observation indicates the need for caution in
the use of such techniques.
A few quotes from the article:
patient was a 33-year-old male international class judo expert who was admitted
as an emergency following a sudden loss of consciousness followed by definite
left hemiparesis, confusion, and amnesia. Power returned quickly to the left arm
and leg but his memory remained poor; during the six weeks prior to his
admission he had apparently suffered episodes of altered awareness and
occasional loss of consciousness. Skull X-ray was normal and a subsequent CAT
scan revealed no evidence of abnormality. He was discharged with a diagnosis of
suspected anoxic brain damage but following repeated fainting episodes and
persisting difficulties with memory over the following months, he returned for
"It was concluded that anoxia resulting from his
judo experiences had resulted in the lesion and he was discharged with
instructions to cease his participation in the sport."
damage is not a common form of sports injury but the unique characteristics of
judo suggest that under certain circumstances a picture similar to that defined
here may result from participation."
"In addition it should be noted
that judo players are commonly strangled into unconsciousness during teaching
either as an illustration of the effectiveness of the technique or in order to
demonstrate the judo resuscitation procedures ("kuatsu"). Such circumstances do
not, as far as we are aware, occur in any other sport. The present case had
apparently been frequently strangled into unconsciousness during his judo career
and it was surmised that the cumulative effect of such strangulation had been,
at least in part, the cause of the anoxic brain damage. Whilst it is of course
possible that some other factor was responsible, there was nothing in his
detailed case history other than the judo to account for the sustained anoxia,
which is of course rarely seen in a patient of such age. It may be appropriate
therefore to recommend caution to judo players regarding such techniques."
Journal article # 2
"Neuronal damage following
repeated brief ischemia in the gerbil"
by Kato, Kogure, and
Brain Research, 479 (1989)
The effect of repetition of brief ischemia, which causes no morphological
brain damage when given as a single insult, was studied. Two-minute forebrain
ischemia was induced in gerbils singly and three or five times at 60-minute
intervals. Although [a single incident of] two-minute ischemia induced no
neuronal damage, three or five repeated ischemic insults caused neuronal damage
in the selectively vulnerable regions, the severity being dependent on the
number of episodes.
A few quotes from the article:
subjected to a single two-minute ischemia (n=5) revealed no abnormal calcium
accumulation throughout the brain. In all animals subjected to three two-minute
ischemic insults (n=5), abnormal calcium accumulation was shown in the CA1
sector of the hippocampus and the thalamus; there was also such abnormal calcium
accumulation in the dorsolateral part of the striatum and the substantia nigra
in 8 of 10 hemispheres, and in the inferior colliculus in 2 of 10 hemispheres.
Gerbils subjected to five two-minute ischemic insults (n=4) revealed most severe
calcium accumulation in the brain."
"Abnormal calcium accumulation shown
by 45Ca-autoradiography has been reported to be equivalent to the sites of
neuronal damage and is a useful tool for mapping the distribution."
"Gerbils subjected to a single two-minute ischemia (n=5) showed no
neuronal damage throughout the brain. In animals killed four days after three
2-minute occlusions (n=4) the CA1 neurons had disappeared in all animals.
Various degrees of neuronal injury were seen in the striatum and thalamus. In
animals subjected to five 2-minute occlusions, the changes were generally more
pronounced than in animals subjected to three 2-minute occlusions."
present study indicates that repeated ischemia causes brain injury depending on
the number of episodes, even though no morphological brain damage results when
the ischemia is induced as a single insult."
Journal article # 3
"Neuronal damage and calcium accumulation following repeated brief
cerebral ischemia in the gerbil"
by Araki, Kato, and Kogure
Brain Research (528) 1990
Abstract: (Note: The
abstract was presented as a single very long paragraph. I've broken it into
several shorter paragraphs to improve readability.) We investigated the
distribution of neuronal damage following brief cerebral transient ischemia and
repeated ischemia at one-hour intervals in the gerbil, using light microscopy
and 45Ca-autoradiography as a marker for detection of ischemic damage. The
animals were allowed to survive for seven days after ischemia induced by
bilateral carotid artery occlusion.
Following [a single instance of]
two-minute ischemia, neuronal damage determined by abnormal calcium accumulation
was not observed in the forebrain regions. Following [a single instance of]
three-minute ischemia, however, abnormal calcium accumulation was recognized
only in the hippocampal CA1 sector and part of the striatum.
2-minute ischemic insults caused extensive abnormal calcium accumulation in the
dorsolateral part of the striatum, the hippocampal CA1 sector, the thalamus, the
substantia nigra, and the inferior colliculus. The ischemic results were more
severe than that of a single three-minute ischemia. However, three 1-minute
ischemic insults caused abnormal calcium accumulation only in the striatum. On
the other hand, three 2-minute ischemic insults caused severe abnormal calcium
accumulation in the brain. The abnormal accumulation was found in the
dorsolateral part of the striatum, the hippocampal CA1 sector, the thalamus, the
medial geniculate body, the substantia nigra, and the inferior colliculus.
Gerbils subjected to three 3-minute ischemic insults revealed the most severe
abnormal calcium accumulation.
Marked calcium accumulation was seen not
only in the above sites, but also spread in the neocortex, the septum, and the
hippocampal CA3 sector. Morphological study after transient or repeated ischemia
indicated that the distribution and frequency of the neuronal damage was found
in sites corresponding to most of the regions of abnormal calcium accumulation.
The abnormal calcium accumulation, however, was not only found in the regions
such as the neocortex and the hippocampal CA3 sector where the neuronal damage
The present study demonstrates that repeated ischemic insults
at one-hour intervals can produce severe neuronal damage not only in the basal
ganglia and the limbic system, but also in the brainstem. Furthermore, they
suggest that the cumulative effects after repeated ischemic insults are related
to the time of the ischemia or the number of episodes.
A few quotes from
"The present study has demonstrated that brief but repeated
forebrain ischemia in the gerbil can cause severe neuronal damage not only in
the basal ganglia and the limbic system, but also in the brainstem."
is well known that certain regions such as the neocortex, hippocampus, striatum,
thalamus, and cerebellum are selectively vulnerable. The present study also
suggests that repeated ischemic insults can produce severe neuronal damage in
selectively vulnerable regions when it is induced repeatedly at one-hour
intervals. These patterns of neuronal damage after repeated ischemia are
essentially the same as those following a single 10-15 minute ischemia in the
gerbil, and the mechanisms of ischemic neuronal damage in repeated ischemia are
partly the same as those in transient ischemia."
"The neuronal injury of
the brainstem, therefore, may be due to excessive lactic acid accumulation."
"In conclusion, the present study indicates that repeated brief ischemic
insults can cause severe neuronal damage not only in the basal ganglia and the
limbic system but also in the brainstem. Furthermore, they suggest that the
cumulative effect after repeated ischemic insults is related to the time of the
ischemia and the number of episodes."
xxxxxxxxxx End of journal material
Please, folks, no gerbil jokes.