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pain perception
pain perception
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Pain is a sensation felt by all. Whether it is due to an injury or illness, falling down or emotionally scarred inside, majority of humans feel pain. The somatic sensation pain is derived from nociceptors (Bear, Connors & Paradiso, 2007). Nociceptors are liberated unmyelinated nerve endings that acts as an indicator of injury or risk of injury to the body tissue (Bear, Connor & Paradiso, 2007). Selective activation of nociceptors can elicit the conscious occurrence of pain (Bear, Connors & Paradiso, 2007). The underlying questions remains, how is pain processed in the brain. Do we all process pain the same? What factors are responsible for contributing to the processing of pain?
Damage to human tissue that would generate pain can be caused by numerous stimuli. Some of the stimuli include but is not limited to, tough mechanical stimulation, excessiveness in temperature, oxygen dispossession, and contact with chemicals (Bear, Connors & Paradiso, 2007). All of the above factors have potential to cause tissue damage thus activating nociceptors (Bear, Connors & Paradiso, 2007). Activating of the nociceptors generate action potentials. At the location of the injury, the damaged cells cause a discharge of numerous substances that stimulates ion channels on nociceptor membranes to open (Bear, Connors & Paradiso, 2007). The opening of the nociceptor membranes generates a pain sensation.
The fact that the perception of pain varies is well recognized. Depending on the synchronized intensity of nonpainful sensory contribution and the behavioral perspective, the same intensity of nociceptor activity can generate additional or fewer pain (Bear, Connors & Paradiso, 2007). Pain induced by action in nociceptors can additionally...
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...ors & Paradiso, 2007). Studies propose numerous brain areas can be attributed to pain suppression (Bear, Connors & Paradiso, 2007). One particular area is a sector of neurons in the midbrain called periventicular and periaqueductal gray matter (Bear, Connors & Paradiso, 2007). In general, the PAG obtains contributions from an array of brain structures (Bear, Connors & Paradiso, 2007). Most of these structures are responsible for the transmission of signals correlated to emotional status (Bear, Connors & Paradiso, 2007). Neurons in the PAG bear the responsibility to transmit descending axons into a variety of midline areas of the medulla (Bear, Connors & Paradiso, 2007). In turn the medullary neurons task axons along to the dorsal horns of the spinal cord, in efforts to successfully depress the activity of nociceptive neurons (Bear, Connors & Paradiso, 2007).
It has been shown that intrathecal administriton of GABA receptor antagonists cause hyperalgesia and allodynia. Constitutive, the increase in the endogenous GABA activity in the spinal cord alleviate pain resulting from noxious and innoxious mechanical and thermal stimuli. Different GABA receptors have different roles in alleviating thermal and mechanical pain in different animal pain models. There is no study to date that has examined the involvement of GABA A and GABA B in sensory dimension of neuropathic pain resulting from compression of spinal cord. The current study tests the hypothesis that GABA A or GABA B receptors contributes to the allodynia and hyperalgesia observed after spinal cord injury. The results showed that the effect of GABA A and GABA B receptors on mechanical hyperalgesia is similar but these receptors have different effects on thermal hyperalgesia. While using baclofen as GABA B receptor agonist does not affect the thermal pain, thermal hyperalgesia resulting from spinal cord injury was greatly alleviated by different doses of GABA A agonist, muscimol. Both Baclofen and muscimol are able to reduce the mechanical and cold allodynia has been seen after spinal cord injury but the effect of baclofen is dose dependent with no effect in higher doses used in this study. While almost all doses of muscimol were used in this study reduce the amount of cold and mechanical allodynia. The other result obtained in this study is the short term effect of GABA agonist. The anitinociceptive effect of Baclofen and muscimol appear to be maxium at 15 min after injection and gradually diminished by time and their analgesic effect disappeared 3 hours after injection.
Peripheral and central mechanisms involving nerve lesions and their input are substantial when perceiving phantom pain. Due to the impairment of peripheral nerves in the process of amputation, regenerative sprouting of damaged axons occurs and the activity rate of inflamed C-fibres and demyelinated A-fibres spontaneously increases (Flor, 2002). As a consequence of this nerve injury, a neuroma, which is a mass of pruned and tangled axons, may form in the residual limb producing abnormal (ectopic) activity (Katz, 1992). Flor, Nikolajsen and Jenson (2006) proposed that ectopic discharge from a neuroma in the stump illustrates abnormal afferent input to the spinal cord, which is a possible mechanism for unpro...
Each person will respond differently to the pain experience. Therefore, the individual’s attitudes, personal experiences and knowledge are also antecedents to the concept of pain. For instance, a person that has been exposed to severe pain knows the
The most common and well described pain transmission is “gate control theory of pain”. This theory was first proposed by Melzack and Wall in 1965 whereby they used the analogy of gate to explain the inhibition of pain which exists within the dorsal horn of the spinal cord. For instance, when tissue damage occurs, substances such as prostaglandin, serotonin, histamine and bradykinin are released from the injured cell. Individual usually consume or apply pain medications such as NSAIDs whereby these medications will cause electrical nerve impulse at the end of the sensory nerve fiber via nociceptor. Nociceptor is a pain receptor that is commonly found in the skin, cornea of eye and organ of motion such as muscles and ligaments. These nerve impulses
Have you ever wondered why when you stub your toe on the chair in the living room, it helps tremendously to yell out an expletive or two and vigorously rub the area? I may not be able to discuss the basis for such language in this paper, but we will explore the analgesic response to rubbing that toe, in addition to the mechanism of pain and alternative treatments such as acupuncture and transcutaneous electrical nerve stimulation.
These include the specificity theory which maintains that specific fibers and pain receptors are activated by injury after which the pain signals are projected via the spinal pathway to an area in the brain that interprets the pain. In this regard, the specificity theory virtually equates the peripheral injury with the psychological experience caused by the pain (Anderson, 2004, p. 355). However, this theory has been found to harbor several limitations as research about pain has intensified with time. In light of this, the gate theory that was proposed by Melzack and Wall has had a major contribution to the understanding of pain transmission and perception (Pain Game Part 2, 2011). Research has demonstrated that pain is affected by psychological and physiological factors which helps to explain the mechanism underlying inhibition and/or facilitaion of pai...
Spinothalamic system- sends pain from our bodies to our brains in order for it to register
Some cells cause inflammation of the tissue, which raises the temperature of the injured area and is adaptive because it prevents pathogens from entering and spreading into the host. The area of injured tissue also remains very sensitive to pain in order to avoid any type of stimuli
Nociception is the term commonly used to refer to the perception of pain. The receptors involved in pain detection are aptly enough referred to as nociceptors - receptors for noxious stimuli. (1) These nociceptors are free nerve endings that terminate just below the skin as to detect cutaneous pain. Nociceptors are also located in tendons and joints, for detection of somatic pain and in body organs to detect visceral pain. Pain receptors are very numerous in then skin, hence pain detection here is well defined and the source of pain can be easily localized. In tendons, joints, and body organs the pain receptors are fewer. The source of pain therefore is not readily localized. Apparently, the number of nociceptors also influences the duration of the pain felt. Cutaneous pain typically is of short duration, but may be reactivated upon new impacts, while somatic and visceral pain is of longer duration. (2) It is important to note that almost all body tissue is equipped with nociceptors. (1, 2) As explained above, this is an important fact, as pain has primary warning functions. If we did not feel pain and if pain did not impinge on our well-being, we would not seek help when our body aches. Hence, it makes evolutionary sense for the body to be so well equipped with nociceptors in almost all locations. The most notable exception to this logic is the brain. The brain itself has no nociceptors and therefore is pain insensitive. Why is this all-important structure not equipped with and therefore indirectly protected by nociceptors?
Most of the time, we react to someone else's physiological pain automatically. For instance, when we are watching a soccer match on the TV and a player distained the knee, we suddenly react with a grimace of pain. Indeed, studies indicate that people who see or imagine others in pain tend to empathically share what others feel at both behavioural and neural levels (Lamm et al., 2011). Empathy implies that we deal with the complex processes that make possible the extraction of sensory and emotional qualities of vicarious pain and map them onto the same neural substrates engaged in the first-hand experience of the same pain. Although studies originally suggested that empathy for pain involves only the anterior cingulate cortex and the anterior insula, i.e., the two main affective nodes of the pain matrix (Singer et al, 2004), subsequent evidence demonstrated that also the regions that are part of the sensory node of the pain matrix, such as the primary somatosensory and motor cortices, play an important role in the basic form of empathy for pain called sensorimotor contagion (Avenanti et al., 2005; Avenanti, Minio Paluello et al., 2006; Lamm & Decety, 2007; Singer et al., 2006, Betti and Aglioti, 2016). Painful stimuli could induce a
Staats, P.S., Hekmat, H., & Staats, A.W. (2004). The psychological behaviorism theory of pain and the
Somatic pain is that in which nociceptors in the cutaneous or deep tissues are activated by noxious stimuli. This is usually characterized by dull, aching pain which is well localized. This type of pain may be commonly experienced by individuals with metastatic bone pain or those who h...
While pain has always been present in humans' lives, Loeser and Melzack (1999) report that it is in only the past 30 years that pain research has made advances in both the treatment and the understanding of pain. There are three basic categories of pain: transient, acute, and chronic.
college of obstetricans in 2010, they state that the cortex is needed in order to feel pain. Another
Hemmings H.C.and Hopkins P.M., (2006) Foundations of Anesthesia 2sd ed. Elsevier. Hudspith M.J., Siddall P.J. and Munglani R. Physiology of Pain.