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Pain is a complicated sensation in that it has physical, emotional and rational components. The physical aspect is a function of an individual's responsiveness to
nociceptive input, while the emotional component deals with the limbic system and the rational component deals with cortically formulated responses and expectations. Because of this complexity, different people react differently to similar pain inputs.

While most of us have a similar threshold, a set point at which we begin to become aware of pain, people have a wide range of pain tolerance. The tolerance is how much pain it takes before it becomes too much pain. Probably the largest contributing factor to these differences is the individual limbic reaction to pain. Also mood has an effect, as do the various distractions of circumstance.

Pain is sometimes the result of some strictly mental or psychological predisposition, and sometimes the result of damage to the central or peripheral nervous system
(neuropathic pain). However most often it is a response to some real trauma, or a perceived threat of trauma (nociceptive pain).

The key players in nociception are as follows:

The peripheral sensory receptors (found in skin, tendon, ligament & muscle)
Afferent (ascending) nerve fibres associated with these receptors
The dorsal horns of the spinal segments
Ascending spinal cord tracts (laminae)
Descending spinal cord tracts (laminae)
The reticular formation of the medulla & midbrain
The thalamus
The limbic system
The corticothalamic network
The cortex

Myelinated Nociceptors

Noxious stimulus activates both myelinated sensory receptors (nociceptors) and unmediated nociceptors. Nerve fibres that are coated in myeline are known as A-DELTA nerve fibres. These generally have a thickness in the range of 1-5 micrometers. The conduction of impulses is more efficient and faster than the unmediated fibres, in the range of 5-15 meters per second.

Some of these nociceptors respond exclusively to sharp pressure (high threshold receptors) and some also respond to heat greater than 45 degrees C. The A-DELTA receptors are in the skin and are the receptors primarily involved in acupuncture stimulation. A certain number of these receptors may be found in the supervening fascia that encases muscles as well.

The A-DELTA nociceptors are quickly adapting in that the resulting pain upon stimulation is sharp and passes rapidly. These impulses give rise to reflex withdrawal of the offended area.

Unmyelinated Nociceptors

Nerve fibres that are not coated in myeline are known as A-DELTA nerve fibres. The thickness of these is less, in the range of .25-1.5 micrometers. The conduction velocity is also less, about .5-2 meters per second. The unmediated fibres are also called C-fibres, or polymodal C-fibres. The term polymodal refers to the fact that heat, pressure or chemical stimulation produces a response in these fibres, although the response actually comes in all cases from the chemicals associated with trauma.

The C-fibres that lead to nociceptors located deep in muscle tissue are also called Group IV fibres. Also present are fibres connected to muscle spindles called Group I fibres (proprioceptive) that respond to being stretched, A-BETA fibres called Group II, and A-DELTA or 'fast pain' fibres called Group III.

The A-BETA fibres pass directly through the dorsal horns and up to the Gracile and Cuneate nuclei of the Medulla, where they act through the medial lemniscuses on axons originating in the ventrobasal thalamus. These axons target the periaqueductal grey area in the midbrain at the head of the descending inhibitory system using serotonin and modulated by opioid peptide. This means that the
A-BETA myelinated low threshold mechanoreceptor system acts to inhibit pain at the injury site through the periaqueductal grey area, effectively blocking the C-fibber
transmission. Also, upon entering the dorsal horn, these A-BETA fibres act on local circuit interneurons that use Gamma Amino Butyric Acid as a neurotransmitter and are
therefore suppressive in their nature. These interneurons further suppress C-fibber impulses after the initial signals arrive at the spine.

Generally upon initial stimulation a sharp pain is felt as a result of the initial triggering of A-DELTA fibres, and this is followed after a second or two by a dull and deep
pain that is a result of subsequent activation of the C-fibres around the injury site. While the A-DELTA nociceptors respond directly to the trauma, the C-fibres
respond to chemicals released in the surrounding tissue, which takes a bit more time.

Effects of A-DELTA stimulation are immediate, often resulting in the involuntary withdrawal of the offended area; in more extreme stimulations a crossed extension
reflex is triggered at the spinal level by reflex arcs found in the portion of the spinal column known as spinal Lamina II, or alternatively the Substantia Geletinosa. In
such a response muscles are operated by the spinal reflex circuit such that the offended area is withdrawn while the contra lateral body moves forward. This causes an equal and opposite reaction, facilitating the withdrawal of the founded area with a twisting motion. In most extreme stimulations the whole body flexes in an involuntary spasm, which some call the Launch Reflex.

Effects of C-Fibber secondary stimulation are ill-defined deep pain, tenderness, dull aching, and sometimes muscle spasm, cramp and rigidity.

Trauma Induced Nociception

Various substances are released in the vicinity of an injury that synergistically stimulate both the Group III (A-DELTA, 'fast pain') and Group IV (C-fibber, 'slow pain')
nociceptors. Bradykinin is released into the tissue, as well as Histamine, Leukotrienes and Prostaglandins. Also Serotonin is released, which acts to increase the effect of the Bradykinin. This action chemically activates the C-fibres, which triggers the release of Substance P, which causes fluids to be retained in the tissue as well as causing vasodilation. Substance P also causes more Histamine to be released from mast cells in the area and further triggers serotonin to be released from platelet cells.

Besides this immediate effect on nearby tissue, there is also an inflammatory response triggered by reflex actions taking place in the spinal Lamina II. Signals are fed back to the site of the injury and surrounding tissues that further increase pain and inflammation.

Pain Gate Theory

The Pain Gate theory started as a simple idea that there exist in each dorsal horn of the spine a switch whereby afferent impulses might be either facilitated or switched
off. The A-BETA large diameter myelinated axons tend to close the gate while the smaller A-DELTA myelinated and C-fibber unmediated nerves tend to open it. Also the condition of the pain gate is influenced by the brain's descending inhibitory system.

The larger diameter nerve cells act to excite suppressive interneurons that presynaptically inhibit pain pathways, while the smaller diameter nerve cells act to suppress the suppressive interferon themselves, effectively enhancing pain. It has more recently been determined that there are also excitatory interneurons present in the Substantia Geletinosa and post synaptic connections that play a role in the pain gate process. Further, it has been revealed that not one but many descending regulatory projections act synergistically to modulate pain gating, with the exact
origin and chemical nature of many of them being as yet undetermined.

Although both larger and smaller diameter nerves are involved in the gating or facilitation of pain transmissions through the Substantia Geletinosa, the impulses that are themselves gated are the smaller unmediated C-fibres that normally transmit the 'slow pain'.
Pain Pathways

There are two main ascending nerve paths by which pain and other sensory modalities make their way from the body to the brain, one of which is phylogenetically much older than the other. In the development of animals, the first pathway to materialize was the Paleo-Spino-Reticulo-Diencephalic pathway. Later with the
evolution of more complex animal forms was added the Neo-Spino-Thalamic path.

The Neospinothalamic path

The Neospinothalamic path is used to transmit the A-DELTA fast pain signals through spinal lamina I and II, across to ascending columns on the contra lateral side of the spinal cord and up through the Ventrobasal nucleus of the thalamus and on to the somatosensory cortex in the post central gyrus. This information is used to determine when a stimulus reaches the threshold of pain, and also which impulses are relevant to ongoing contextual processes. This leads to the suppression of irrelevant signals and optimization of those signals that are salient.

The Paleospinoreticulodiencephalic Path

This much older pathway deals with the transmission of the C-fibber slow pain signals to the Reticular Formation and subsequently through the thalamic intralaminar nuclei and to the cortex. Upon their initial entry into the dorsal horn of the spine, the fibres must cross from Lamina I & II through many intervening relays on the way to Laminae V, VI & VII. It is through these many switches that the circuitry of pain gating is thought to exert its effect on these signals, after which they may pass into the Anterolateral spinal tract and on up to the reticular tissue. The reticular tissue projects with axons that bifurcate, targeting both the spinal gate circuits and also
the thalamus. Also the hypothalamus, limbic system and frontal cortex are projected to. Thus the emotional response to pain and also autonomic effects are initiated.

Pain Referral

Impulses from internal organs enter the ventral horn of the spine along with the projections from supervening body areas that are often distant, and these both target the same dorsal horn transmission cells. Since much of our focus is on dealing with the more copious input from these supervening areas, there is sometimes some contextual confusion, and visceral pain becomes referred erroneously to some body area. Also sometimes there is a summation of some visceral pain with some simultaneous cutaneous pain that happens to target these same cells. The results can be as simple as a phantom pain, or as draconian as an improper control signal being sent to some vital organ via synergistic sympathetic/parasympathetic modulation, causing organ malfunction.

 

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