Perhaps the most intriguing aspect of dim-mak is the pressure point knockout. Those who have witnessed such a feat are usually amazed at how easily a person is knocked unconscious as well as how little force is used.
This form of knockout is unique to dim-mak and is quite different from the classic boxing knockout, where one is struck in the head causing a concussion. The pressure point knockout has more in common with fainting than boxing. In fact, when a person faints at the sight of blood or upon hearing bad news, the body undergoes almost the same changes in blood pressure and heart rate as it does
during a pressure point knockout. The mechanism of the pressure point knockout involves changes in the autonomic nervous system that cause a sudden drop in blood pressure leading to a loss of consciousness.
Vasovagal faint (syncope) is the medical term for a loss of consciousness due to a sudden drop in blood pressure. A vasovagal reaction is defined as a drop in blood pressure with lightheadedness, nausea, and vomiting but no loss of consciousness.
It has been found that during a vasovagal faint there is a sudden dilation of the blood vessels in combination with a decrease in heart rate. This causes an acute drop in blood pressure leading to decreased blood perfusion of the brain. In response to this, the blood vessels in the brain constrict, leading to a further decrease in blood perfusion.1 This dramatic decrease in blood perfusion
causes the brain to be deprived of oxygen and leads to a loss of consciousness.
The manner in which the autonomic nervous system induces a sudden drop in blood pressure is quite complex.
Normally there is a partial constriction of the peripheral blood vessels due to a constant signal from the sympathetic nervous system. When the body needs to increase blood pressure, it increases the stimulation of the sympathetic nervous system. This causes the heart rate to increase and the blood vessels to constrict, leading to an increase in blood pressure. During a vasovagal faint, the parasympathetic nervous system slows or stops the heart and interrupts the sympathetic signal to the major blood vessels, causing them to open wider. The combined effect of the dilated blood vessels and the decreased heart rate is a drastic reduction in blood pressure.
The reason there is a drop in blood pressure when the blood vessels dilate is because there is a larger tube for the blood to flow through. One can think of the comparison between water flowing out of a squeeze bottle with the squirt top on and then suddenly without any top. The pressure coming out would decrease unless one squeezed the bottle harder. In the body, when the blood vessels dilate, the heart normally pumps faster and harder to keep the blood pressure up. During a vasovagal faint, the blood vessels dilate, but the heart rate slows down, which causes the blood pressure to drop.
There are many different methods of inducing a vasovagal faint. The exact mechanism of how this occurs is complicated, but the basic neurologic connections will be outlined here. Try not to become overwhelmed with the neuroscience involved; the important
concept is that there are neurological connections between the dim-mak points and the area of the brain that can cause a vasovagal faint.
All of the dim-mak methods that cause a knockout stimulate an area of the brain called the nucleus tractus solitarii. Medical research has found that excessive neural traffic in this area can cause a vasovagal faint.2 The nucleus tractus solitarii is responsible for the increased activity of the parasympathetic nervous system and the withdrawal of the sympathetic signal to the blood vessels. This occurs through a number of mechanisms. One involves the inhibition of areas in the vasomotor center of the brain. There are two areas called the reticularis gigantocellularis and the reticularis parvicellularis that have been found to cause high blood pressure when stimulated.3 Normally the nucleus
tractus solitarii inhibits these areas and maintains the blood pressure in a normal range.4 When the nucleus tractus solitarii is stimulated, there is excessive inhibition of these areas, which causes an interruption of the sympathetic signal supplying the blood vessels. The result is an increase in the diameter of the blood vessels and a decrease in blood pressure. At the same time, the nucleus tractus solitarii stimulates the motor nucleus of the vagus nerve, leading to an increase in the parasympathetic effects on the heart. This causes the simultaneous decrease in the heart rate.
The nucleus tractus solitarii can be stimulated in three different ways in order to induce a vasovagal faint.
Applying the concept of aberrant reference, it can be stimulated indirectly by using dim-mak point combinations to simulate pain in some of the internal organs. Another option
involves causing pain in the type C nerves, which stimulates the nucleus tractus solitarii indirectly through the hypothalamus. The type C nerves can be attacked through most of the dim-mak points, but extreme force is required to do so. Finally, attacking points on the carotid sinus, trigeminal nerve, facial nerve, glossopharnygeal nerve, vagus nerve, optic nerve, and the occipital nerves can stimulate the nucleus tractus solitarii directly. Each of these methods will be discussed separately.
First, the phenomenon of aberrant reference can be used to cause pain in the heart, lungs, digestive tract, bladder, or genitals. For example, if
reference combination will have this effect whenever it causes simulated pain in one of the organs mentioned. In addition, because a vasovagal faint is associated with increased parasympathetic effects on the heart, any combination of points that causes a vasovagal faint will also cause an increase in the parasympathetic effects on the heart.
The concept of convergence can be used to achieve the same effect. Very strong stimulation of a peripheral nerve can cause the brain to think the pain is coming from the internal organ that the nerve was connected to by convergence. If the pain is in one of the organs mentioned, the result could be a vasovagal faint. For example, if one stimulated the ulnar nerve, the brain might perceive the pain as coming from the heart because the ulnar nerve and the heart are both connected to the spinal cord at T1 (see fig. 15). It
should be noted that convergence and aberrant reference are synergistic when used together; however, the resultant enhanced parasympathetic effects on the heart could lead to cardiac arrest.
The easiest method of causing a vasovagal faint involves stimulating points on nerves that can directly stimulate the nucleus tractus solitarii.
All of these nerves can cause a vasovagal faint as well as a very strong increase in parasympathetic nervous system activity that can lead to very serious parasympathetic mediated effects such as heart block and cardiac arrest. It all depends on how strongly the nerves are stimulated. When such nerves are set up or used in combination, they are much more likely to cause a vasovagal faint or cardiac arrest. The points located on the following nerves can all be attacked to cause a vasovagal faint directly. They
include cranial nerves 2, 5, 7, 9, and 10; the greater and lesser occipital nerves; and the carotid sinus. (See Figures 9 and 17.)