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Types of Nociceptive Pain

Discuss about the Pain and Nociception for Neurophysical Underpinning.

Signaling of threats and tissue injury occurrence is the most vital function of the central nervous system. This feature is performed by afferents (nociceptors) which are specialized, and they are responsive to noxious and injury stimuli. However, there is need to elude the differences between nociception and pain since they have always been underpinned on the anatomy associated with the central nervous system as well as that of peripheral. Also, it is important to consider the roles that nociceptors play in pain perception. Nociception is said to be the processing of information by the peripheral and the central nervous system (commonly referred to as CNS).This information is related to inner or outer body environment.

Nociceptors have the ability to give a response to noxious stimuli, including cold, heat, mechanical, and chemical mediators. Because nociceptors are capable of responding to stimuli of heterogeneous nature, they are primarily denoted to as polymodal receptors. However, not all of the nociceptors respond to every noxious stimulus. The detectors of noxious stimuli are nerve endings which are found all over the body, and their origin is from PSNs. PSNs are the first element in the polyneuronal chain that leads to pain perception. Noxious stimuli activate the nociceptors and send information to the trigeminal homologue or spinal cord dorsal horn (Ferrini, Russo, & Salio, 2014). The information is then forwarded to the stem of the brain and to the cerebral cortex where pain perception occurs (Rouwette et al., 2012). There are two types of nociceptive pain such as somatic pain that can be traced easily within the body and originates from the skin surface as well as deeper tissues including muscles and joints. The second type is visceral pain that is not well localized and originates from organs that are inside the body.

On the other hand, pain can be described as an unpleasant sensation of the nervous system which is triggered by noxious stimuli applied to the body which may include squeezing, high heat intensity, rotating a joint or even skin fold. These provide the body with actual or potential damage. Consequently, this gives a quick alerting signal to the nervous system for the creation of a motor response that will reduce anything related to physical harm (Magee, & Elwood, 2013). Although it is always rare to experience congenital insensitivity, people with the condition can go through great health problems including auto-amputation, corneal scarring, and self-mutilation. As such, it is practically essential to discuss the origin as well as the source of the word “pain,” which came from a Greek word ‘poine’ that stands for a penalty. Usually, pain accompanies nociception. There are three pain experiences, and the first one is sensory, and it is experienced when discriminative system enhances the processing of information concerning the strength, quality, temporal, intensity, and the three-dimensional facets of pain. Naturally, the second experience is known to be motivational since the system is effective and defines the individual´s behaviors. Subsequently, the third experience is cognitive in nature as the system evaluates whether the people understood the response concerning the pain experience (Cheng & Flamenbaum, 2016).

Types of Pain Based on Pathogenesis

Evidently, three types of pain can be derived according to their pathogenesis. The first one is acute physiological nociceptive pain which is produced especially the minute a sharp noxious stimulus is physiologically pricked to healthy vertebrate tissue (Messlinger & Handwerker, 2015). This elicits withdrawal hence preventing the tissue from further damage. Next is pathophysiological nociceptive pain which is felt when there is an inflammation or damage to the tissue (Zhang et al., 2012). It may appear spontaneously without stimulation, or as allodynia- pain stimulation below pain threshold, or as hyperalgesia- extreme noxious stimulated pain. The third type is neuropathic pain which occurs after an injury or a disease to CNS or the peripheral. Mainly, it may often give abnormal feeling because of lack of a given signal to noxious tissue. In essence, persistent and short timed sensation of burning or even electrical is often elicited (Xia, Mørch, & Andersen, 2016).

Any of the followings can cause neuropathic pain, which are metabolic diseases such as diabetes mellitus, axotomy, plexus damage, and herpes rapturing. In case the central neurons are damaged, a pain that can occur is referred to as central neuropathic pain (Zhang et al., 2012). When a patient has pain for more than six months, it is described to be "chronic" and may be as a result of chronic diseases or continuous nociceptive process. In assumption, different tissue nociceptors share much of their general characteristics. However, there is evidence to prove precisely that the dorsal root ganglion (DRG) neurons that supply fibre to various body tissues are different by how they pass electrophysiological properties.

There are also many Aδ and C fibers presents and acts as specified nociceptors that detect potential damaging stimuli. A part of Aδ and C fibers consists of cold and warmth sensory nerves that record innocuous cold and warm stimuli and not noxious cold and heat. These fibers are also present in the joints, skin and the visceral nerves and are referred to as mechano- insensitive nociceptors which are alerted during inflammation and give a response to mechanical and also to thermal stimuli (Djouhri, 2016). A typical sensory nerve fiber generates their action potentials in the sensory endings when the receptive field is stimulated. Often, damaged nerve fibers produce pathological discharges that are fundamentally generated at the surface where the nerve is damaged or within the body cell at DRG (Djouhri, 2016). Ectopic discharges are released in thick myelinated Aβ fibers, Aδ, and C fibers, and hence when a nerve injury occurs, these two are involved in pain generation.

Characteristics of Nociceptors

While viewing the ontogeny of pain, it is always crucial to note in a considerate way that there are possibilities of pinpointing the smaller groups of sensory neurons. These include nociceptors in early stages before they proceed to cause an impact to central and peripheral systems. Neurogenesis as well as the synaptogenesis of these neurons is biologically produced in two waves. Giving the example of a rat, the development of what is scientifically known as myelinated Aβ fibers originating from the neuraxis occur before development of unmyelinated C-fibers (Djouhri, 2016). Neonates of many species show exaggeration in reflex responses to a stimulus that are noxious mediated spinally, as compared to the adult vertebrates.

In vertebrates and some invertebrates, there is a common framework of sensory transmission for varying senses. Their neural cells have functional parts where the receptor molecule of the sensors detects the stimuli, and hence the receptor molecule undergoes a conformal change that brings about transduction process (Pogorzala, Mishra, & Hoon, 2013). This triggers the receptor cell membrane potential to change, which is referred to as the receptor potential. Under normal circumstances, sensory neuron- site of sensory transduction is always overly far from the synaptic terminal, and as a result, receptor potential should be transformed to a chain of the action potential that carries the pain through axon to the synapse.

Being one of the stimuli, hypersensitivity is an increased response to painful stimuli occurring in the following manner where tissues have been damaged due to a significant noxious stimulus. This leads to excessive sensitivity to pain. It is evidenced that primary and secondary hypersensitivity can be present in the body tissues. In contrast, the primary can be described as high sensitivity around the area an injury has occurred and is due to sensitization of the periphery nociceptors, whereas secondary occurs in the surroundings of the injured part and is due to central nociceptors sensitization (Hsieh et al., 2012). An excellent example is an inflammation caused by a sore throat which can be intense such that the swallowing exercise becomes a major problem due to pain. Pain hypersensitivity can last long after the disappearance of the primary cause, and this is now a disease and not a symptom anymore when it reaches that stage. According to pain scientists, two pain aspects are usually derived as an adaptation of injured tissue for their protection during healing period (Mettam, McCrohan, & Sneddon, 2012). These are allodynia that is often said to be a pain as a result of actual innocuous stimuli and hyperalgesia which is response triggered by normally painful stimuli.

Ontogeny of Pain

Fig 1: Shows nociceptive stimulus-response characteristics where hyperalgesia is shown by the high response to noxious stimuli without a change in nociceptors threshold while Allodynia is shown by nociceptors threshold to give a response (Mettam, McCrohan, & Sneddon, 2012).

It is imperative for one to bear in mind that not all of the nociceptors bring about sensitization. Another group of sensory receptors may desensitize when after exposure to great stimuli compared to nociceptors which sensitize on exposure to high noxious stimuli. Desensitization may occur when the photoreceptors in the eyes of humans are in exposure to bright light and later face a room which is not well lit, where one feels blind and as time goes by one can see what was not visible before inside the chamber. This is described to be a light adaptation.

In conclusion, on exposure to noxious stimuli, an animal’s brain perceives the pain experience leading to discomfort in or outside the body. Pain caused by the accidental hitting of individual’s elbow or head can be minimized by rubbing the area to assist in providing some relief. Studies on animals bearing transections of the neuraxis show those compound responses to stimuli can undergo elicitation in the absence of pain. Behavior index and extrapolation in human and other vertebrates are the current measures of pain. After nerve injury, innocuous stimuli may be a source of pain while repeated noxious stimuli exposure leads to hypersensitivity and create responses to this stimulus which are noxious and innocuous. The neural system may suffer a long-term damage caused by an injury and hence interference with the processing of nociceptive information. Also, physiological factors may encourage the onset of the pain felt during and up to when an injury to the tissue occurs. Finally, pain as opposed to nociception is not purely the acknowledgement of the setting, existence, and scale of nociceptive input. Instead, it is multifaceted event with a significant emotional as well as touching component.

References

Cheng, M.K. and Flamenbaum, R., 2016. Cognitive Behavioral Therapy Formulation With Chronic Pain. Journal of Cognitive Psychotherapy, 30(1), pp.3-15.

Djouhri, L., 2016. Aδ-fiber low threshold mechanoreceptors innervating mammalian hairy skin: A review of their receptive, electrophysiological and cytochemical properties in relation to Aδ-fiber high threshold mechanoreceptors. Neuroscience & Biobehavioral Reviews, 61, pp.225-238.

Ferrini, F., Russo, A. and Salio, C., 2014. Fos and pERK immunoreactivity in spinal cord slices: comparative analysis of in vitro models for testing putative antinociceptive molecules. Annals of Anatomy-Anatomischer Anzeiger, 196(4), pp.217-223.

Hsieh, Y.L., Chiang, H., Lue, J.H. and Hsieh, S.T., 2012. P2X3-mediated peripheral sensitization of neuropathic pain in resiniferatoxin-induced neuropathy. Experimental neurology, 235(1), pp.316-325.

Magee, B. and Elwood, R.W., 2013. Shock avoidance by discrimination learning in the shore crab (Carcinus maenas) is consistent with a key criterion for pain. Journal of Experimental Biology, 216(3), pp.353-358.

Messlinger, K. and Handwerker, H.O., 2015. Physiology of pain. Schmerz (Berlin, Germany), 29(5), pp.522-530.

Mettam, J.J., McCrohan, C.R. and Sneddon, L.U., 2012. Characterisation of chemosensory trigeminal receptors in the rainbow trout, Oncorhynchus mykiss: responses to chemical irritants and carbon dioxide. Journal of Experimental Biology, 215(4), pp.685-693.

Pogorzala, L.A., Mishra, S.K. and Hoon, M.A., 2013. The cellular code for mammalian thermosensation. Journal of Neuroscience, 33(13), pp.5533-5541.

Rouwette, T., Vanelderen, P., Reus, M.D., Loohuis, N.O., Giele, J., Egmond, J.V., Scheenen, W., Scheffer, G.J., Roubos, E., Vissers, K. and Kozicz, T., 2012. Experimental neuropathy increases limbic forebrain CRF. European Journal of Pain, 16(1), pp.61-71.

Xia, W., Mørch, C.D. and Andersen, O.K., 2016. Test-retest reliability of 10 Hz conditioning electrical stimulation inducing long-term potentiation (LTP)-like pain amplification in humans. PloS one, 11(8), p.e0161117.

Zhang, X.L., Mok, L.P., Lee, K.Y., Charbonnet, M. and Gold, M.S., 2012. Inflammation-induced changes in BK Ca currents in cutaneous dorsal root ganglion neurons from the adult rat. Molecular pain, 8(1), p.37.

Zhang, Z.J., Dong, Y.L., Lu, Y., Cao, S., Zhao, Z.Q. and Gao, Y.J., 2012. Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain. Journal of neuroinflammation, 9(1), p.136.

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