Cummulative brain damage from breath control jay wiseman anoxia cerebral

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.Anoxia cerebral 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

anoxia cerebral

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

anoxia cerebral

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.Anoxia cerebral

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.Anoxia cerebral

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

anoxia cerebral

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

anoxia cerebral

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

anoxia cerebral

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.Anoxia cerebral 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

anoxia 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,

anoxia cerebral

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

anoxia cerebral

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

anoxia cerebral

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

anoxia cerebral

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.

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End of journal material xxxxxxxxxx

Please,

Folks, no gerbil jokes.

Regards,

Jay