Acute traumatic brain injury (ATBI) represents the neurologic consequence of concussive and subconcussive blows to the head. Evidence suggests that ATBI may be associated with boxing and collision sports such as American football and soccer, thus potentially exposing millions of athletes annually. Of all sports, boxing is associated with a large number of deaths relative to the number of participants and ATBI, because the objective of a boxing match is to make one’s opponent unable to fight.

Whereas much of the rest of a pugilist’s body is protected by bone, fat, skin and well developed muscle, the brain is encased only by the skin-covered skull and attached to its interior by fine filaments of blood and nerve networks. (One of the most useful models to describe the brain is that of a sack of jelly, the size of two fists suspended in a box by threads on all sides).

When a boxer sustains a direct blow to the head – which has been likened to the effect of being hit by a 12lb padded, wooden mallet traveling at 20mph – the head rotates sharply and then returns to its normal position at a much slower speed.

Consequently, the different densities of the different parts of the brain also move at different rates and the overall result is the creation of a “swirling” effect inside the brain. Resulting damage: surface damage from brain hitting against inner surface of skull; tears to nerve networks; tension between brain tissue and blood vessels may cause lesions and bleeding; pressure waves created causing differences in blood pressure to various parts of the brain; (rarely) large intra-cerebral clots.

The above scenario has also been termed a contra-coup injury . A brain bruise is also extremly common a well. This usually happens to the front and sides of our brain known a frontal and temporal lobes, respectivly.

The effect on the boxer is grogginess, weakness, paralysis, weakening of limbs, inability to focus, possible loss of consciousness, i.e. the “knock-out”. Long-term effects are cumulative ( a.k.a. Cummulative Traumatic Brain Injury CTBI) and may not show immediately after a boxing match. Most signs of damage are more likely to appear towards the end of a boxer’s career or even after retirement. (See article: “Boxing & Parkinson’s”)

The amount of ATBI seems to also bee direclty to the onset of CTBI. Stretched fibers may recover after many weeks but cut nerve fibers do not repair. Ex-boxers are less able to sustain natural ageing of brain or diseases of brain and may be more likely to suffer diseases such as Alzheimer’s and Parkinson’s. Boxers’ brains are smaller; surface grey matter is thinner, fluid-containing ventricles enlarged because of the decrease in white matter.

Letter from Wendy Gunther, M.D.

A Couple of years ago I read in the medical literature a report from a bunch of scientific wackos who hooked up a judoka to heart monitors and EEG equipment, then had them choked out by their sempai. The monitors showed that blood flow to the brain is indeed momentarily interrupted (surprise, surprise) and that there are temporary EEG abnormalities while unconscious, but that full recovery occurred after each choke.

One fellow was willing to be choked out five times for Science and each time he had the same level of function that he had before (of course, you gotta wonder what’s the baseline for a person who is willing to be repeatedly choked unconscious for Science?).

The forensic literature says that if you are going to kill a person by interrupting blood flow to their brain, you need to hold pressure for minimum two minutes. How they got this information I do not know. People have been convicted of murder based on it, because having to hold pressure for two solid minutes is good evidence of intent.

Reversing this, it would suggest that if your friend chokes you out and lets go as you hit the mat, you ought to recover fully just as the judoka in the experiment recovered fully. However, interrupting blood flow to the brain is not the only way to cause death. There are two other methods with which you should be concerned. One is bradycardia and arrhythmia based on carotid sinus stimulation, and the other is positional asphyxia.

The bradycardia one means that if you’re choking just the right spot very high and fairly lateral on the neck, up behind the sternocleidomastoid muscle and only an inch lower than the jawbone, you may accidentally put your thumb on the sensor located in the wall of the carotid where it divides into internal and external branches.

That sensor is there to tell the heart to slow down if the blood pressure going into the brain is too high. If you push hard enough on the vessel and up the pressure in it, the sensor tells the heart, “Whoa! We gotta surge of 80 mm Hg in here! Back it off!” And the heart obediently slows down to nothing, at which point it can start to fibrillate and you die. The reason this is rare is dual.

Number one, the sensor is small and hard to get to, so it’s chance if you happen to be over it. Number two, young people with resilient arteries are almost all resistant to this reaction to carotid compression. Old people with hardened arteries are much more susceptible.

However, this has been thought to be the genesis of death in cases in which the perpetrator confessed, “I was mad at her, yeah, and I took her throat in my hands, but honest to God I didn’t do anything! She just went limp the instant I touched her!” and the autopsy is negative.

So this is always something to bear in the back of your mind when practicing chokes: if your partner is the one in a thousand whose arteries aren’t resistant to this, and if you hit exactly the right spot, they could go limp in your hands and die without your even achieving a good choke. Scary Huh.

Positional asphyxia is likelier because one tries to get it in judo. If you’re on his diaphragm so he can’t breathe and you choke him, and you hold it too long, he might die. Again, if your choke lasts only a second or three, this is unlikely. It is much likelier if he is hog-tied or even merely face down. I would never practice chokes with a face-down opponent.

Tracheal compression is less worrisome to me, even though an element of it is present in most judo chokes (correct me if I mean strangles — I’m not a judoka), simply because it takes so much effort to do it enough to flatten the C-shaped trachea. And you’d have to really flatten the trachea to prevent any air at all from going back and forth.

I have been told it can be done easily from behind with a nightstick, but I have never seen it done from the front or back with hands alone; if you get your hands, or his collar, into good tracheal compression position, you’re probably pressing on his jugulars and carotids too, and he’ll go out from those long before you significantly flatten his airway. A good thing — the vessels recover completely from being pressed flat; the airway gets damaged, and it can swell up and choke off air flow minutes to hours later.

If any of you has access to Spitz and Fisher ed.iii (the $190 volume that’s the bible of the forensic pathologist), on p. 447 Spitz says: “It is said that five pounds of pressure per square inch suffice to occlude the carotid arteries and jugular veins. Thirty-two pounds are required to block the airway.”

And later, on p. 448 he goes on: “Actual compression of the airway by the noose in hanging cases is not as common as is generally believed. Supportive evidence for this includes the finding of vomitus in the airway of numerous hanging victims. Suicidal hanging by persons with an artificial opening into their airway (tracheostomy) below the level of the noose also illustrates this point.

Such individuals continue to breathe while dying” (presumably, of jugular/carotid compression). “Obstruction of the airway usually elicits a struggle, a dramatic condition known as air hunger. … Judging from the circumstances in which [jugular/carotid compressed] individuals are found, there is certainly no indication that this is an unpleasant mode of death.” (Emphasis his.)

So if you’re gonna choke ‘em out, and you wanna be nice, or you don’t want to elicit struggle, seems like you would go for the five-pound vessels rather than the thirty-two-pound airway. Unless you’re old-style LAPD.

He also quotes Reay and Eisele’s fascinating 1983 article in the American Journal of Forensic Pathology, “Death from law enforcement neck holds,” to say that in the judo-derived police carotid sleeper hold, “blood flow to the head is reduced by an average of 85% in approximately six seconds… Despite the apparent harmlessness of the carotid sleeper hold, occasional deaths do occur… Movement during a struggle may turn a sleeper hold into a choke hold with serious, even fatal, consequences”.

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