Physical Pain
What good is ‘controlled pain’ if you don’t know what it is you’re controlling?
How can you measure?
What do you avoid?
When does trauma become damaging and to what extents?
Not even beginning to delve into the extremely important psycho emotional issues, what are the physical mechanisms?
I see differentiation in pain types and sensory stimuli, as well as the term ‘endorphins’ flung about in here to describe any of a number of [for some, it seems] otherwise indescribable body and head rushes. Just for information’s sake – a primer on what’s going on…
The sense of pain is complex because it involves not only sensation but feelings and emotions as well. For this reason, the neurophysiology of pain involves structures not normally considered as part of the sensory nervous system.
Furthermore, classically, the ascending sensory (excitatory) aspects of pain signals have been emphasized. The intrinsic capacity of CNS structures to suppress pain signals has recently become the focus of much attention and research.
PAIN RECEPTION
The sense of pain is served by free nerve endings located in the skin and certain visceral tissues. Pain can be caused by stimuli of different natures. For example, strong mechanical stimuli (intense pressure), very hot and very cold thermal stimuli, and certain chemical stimuli such as acidic substances can all cause pain.
It is important to note that the pain receptors generally have a high threshold of stimulation, so they are usually activated when stimulus strength is very high.
Because such strong stimuli are usually noxious, pain sensation is also called ‘nociception’, and the pain receptors activated by nociceptive stimuli are called ‘nociceptors’.
All nociceptive stimuli cause tissue damage, the extent of which may vary from the slight effects of a simple pinch to the severe consequences of burns.
Tissue damage results in the local release of certain internal nociceptive substances such as serotonin, histamine, and kinin peptides (bradykinin, etc.) in the injured tissue. These substances then act on the free nerve endings, activating pain signals.
TWO PAIN SYSTEMS
There are two systems of pain transmission to the CNS, which are associated with two different types of pain experience. When one steps on a thumbtack, one feels a =sharp= sensation, followed a while later by a more =dull= sensation.
In addition to arriving earlier, the sharp and prickling sensation is short-lasting, and its source can be accurately localized.
The dull sensation is long-lasting and diffuse; it hurts and aches, but the ache source cannot be pinpointed and generally is ascribed to a larger body part.
The sharp pain is conveyed by thin but myelinated, relatively fast, nerve fibres (Type A-delta), and the dull, aching, hurting pain by unmyelinated slow conducting Type C fibres.
Conduction velocity in the A-delta fibres is about 10 times faster than in the C fibres (10m/sec vs. 1m/sec).
Both types of fibres terminate in the dorsal horn and ascend by the spinothalamic pathway. Whereas the slow/aching pain signals make a major input to the brain stem ‘reticular formation’ and essentially terminate in the thalamus, the sharp/fast pain signals ascend more directly to the thalamus and up to the sensory cortex.
The cortical component gives the fine localization capacity to the sharp/fast pain system, whereas the heavy subcortical projection of the dull/slow pain system to the reticular formation and the structures of the limbic system is associated with the aching/hurting component.
Patients with damage to the sensory cortex can still feel pain and are hurt by it, but they are unable to accurately localize the source.
It is often described in asb that there is a difference between thud and sting – the above is critical information if thud is either a product or objective of intense activity: thud type pain indicates a more significant nociceptous result, and if thud without sting is achieved and administered – damage can occur and be unsensed by the sub, unreacted to in a readily ascertainable fashion, and measuring a sub’s level of damage by their reaction or apparent surface damage can be misleadingly inaccurate. Not knowing this can result in serious damage.
CENTRAL DESCENDING PAIN INHIBITION
Electrical stimulation of certain neuronal groups in the brain stem reticular formation makes the conscious animal completely oblivious to pain stimuli.
From the reticular formation, descending control fibres project to the dorsal horn of the spinal cord, where they =suppress= the relay of pain signals to the brain.
This system is what helps animals and humans cope with the debilitating hurtful consequences of pain arising during physical stress and fighting.
THINK SHOCK
Although CDPI cannot be directly stimulated, it can be induced with severe overload to the A-delta system – (emotional shock is unrelated to CDPI and has no immediate neurochemical manifestations affecting sensory systems).
Some refer to CDPI as adrenaline shock � adrenaline is not a factor, and vasodilators given on misdiagnoses have resulted in neurological damage.
(Avoid substances with vasodilating properties [certain decongestants, etc.] when the subjects condition has gone to CDPI – continuing play under such circumstances would be excessively dangerous and could result in substantial damage due to loss of pain sensation.)
This is the most dramatic and most frequent form of conscious pain inhibition due to physical trauma. In dolorimetry and chemical monitoring, there is found very little to no neurological deviation between thresholds in individuals for each of the different inhibition vehicles. (i.e. It’s not ‘individual’ as far as physical effect goes.) If you’re ‘not feeling any pain anymore’ but you still retain most other sensation, you’ve achieved central descending pain inhibition. (The theory is that the yogis of India have so practiced extreme pain that they can force themselves into neural shock, and that CDPI provides athletes and soldiers their ability to continue struggling in the face of bodily hurts and trauma.)
ENDORPHINS
One mechanism by which higher reticular centres inhibit pain is when descending fibres activate certain inhibitory interneuron’s in the dorsal horn, which release a peptide neurotransmitter known as ‘enkephalin’.
Enkephalin suppresses the transmission of pain signals by binding with particular receptor molecules (sometimes referred to as opiate receptors) present in the synapses of cells in the dorsal horn.
The binding either decreases the amount of neurotransmitter ‘substance-P’ released from the type C pain afferents or induces post-synaptic inhibition of the relay cells.
Morphine and other opiate analgesics act in the same way to relieve pain. If you still feel intense A-delta pain but no C pain, that is an ‘endorphin high’. It’s less like ‘feeling no pain’ and more akin to ‘severe pain but y’know, man, I feel goooood’.
It’s still there, it’s not anaesthetized; the best analogy I can come up with is ‘it’s there, but you just Don’t care.’ This one is most dangerous of all, because type A pain is intense but gives little to no sense of internal damage, and because type C pain is blocked, cumulative damage can go utterly undetected.
There is no ‘induction method’ for this kind of inhibition, it most often occurs as a product of repetitive trauma and nociceptous stimulation to visceral organs and prolonged body-wide dermal irritation (that’s why long-distance runners get it, they’re abusing themselves).
AFFERENT PAIN INHIBITION
The interneurons of the dorsal horn are also involved in a different type of pain inhibition. It has long been known that skin rubbing relieves the dull hurtful pain sensation originating from that or a nearby area.
Theories have abounded about circulation and chi and other systemically centered reasons, but in fact, rubbing activates the large fast-conducting tactile fibres (type A-alpha) while pain is conveyed by the C fibres.
In the dorsal horn, branches of touch fibres activate inhibitory interneurons, which in turn inhibit the synaptic transmission of pain signals.
THINK GATE
The more powerful tactile signals limit the transmission gates in the dorsal horn to their own, suppressing and excluding access for the weaker pain signal.
Acupuncture analgesia, although imprecise and wrapped in mysticism is functionally possible (with a great deal of experimentation) due to afferent PI as well as components of CDPI and postsynaptic inhibition.
Rubbing is not a vehicle to restoring circulation, but to blocking pain signals – it doesn’t stick, so as soon as you stop, the pain is given free travel again.
OTOH, if restriction or elevation is maintained and circulation is restricted but not cut off, circulation need not be enhanced to provide relief of pain by rubbing. Do not expect rubbing to restore circulation, that’s not its function in relief of pain.
REFLEXIVE CONTRACTION
Prolonged reflexive involuntary contractions (tickling reaction, laughter, twitching)[not involuntary reflexes like shivering, etc.] are linked to serotonin stimulation which improves mood without substantially altering physical sensation.
There is a clear threshold at which such contractions shut-off. The danger in pushing this limit is that the threshold is rather high, and in the event of oxygen deprivation or fluid build-up to certain muscle groups due to restraints or position or pre-existing medical conditions, spasm can set in.
Diaphragm spasm can cause hyperventilation or even asphyxia, other spasms can cause severe cramps and even the tearing of muscle tissue.
There are no sure-fire non-drug methods for inducing inhibitory neurotransmitter activity beyond different types of applied trauma – study the types, and the trauma that has been shown to induce them, and don’t experiment blindly with physical extremes using a slave as a guinea pig – that slave has entrusted you with their safety; honour it by understanding their body, by mastering the necessary procedures and by maintaining competence in the means of emergency treatment for any troubles.
As with any play, know the possible complications (=learn= them: take an extension course in anatomy, then physiology, read a few texts, keep up to date on pain physiology), anticipate them sufficiently that you are prepared to deal with them (advanced first-aid is a must), and accept responsibility for what you do to another when they have surrendered their body to you.’, ”Feelings’ and ‘apparent look’ are well and fine, but alone are not accurate indicators of safety, as hopefully this li’l ditty has explained.