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?

by Jay Wiseman

Hi Mary, Phillip, et al.,

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 [ ].

Journal article # 1
"Judo as a possible cause of anoxic brain damage; A case report"
by Owens and Ghandiali
The Journal of Sports Medicine and Physical Fitness, December 1991
Abstract: 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:
"The 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 further assessment."

"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."

"Anoxic brain 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 Nakano
Brain Research, 479 (1989)
Abstract: 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:
"Gerbils 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."

"The 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.

Two 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 was seen.

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 article:
"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."

"It 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."

End of journal material

Please, folks, no gerbil jokes.

Regards,
Jay Wiseman