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Acute Pain Physiology

Pain is often classified by its pathophysiology into 2 major types: nociceptive and neuropathic. Nociceptive pain involves the normal neural processing of pain that occurs when không lấy phí nerve endings are activated by tissue damage or inflammation.[10] Neuropathic pain involves the abnormal processing of stimuli from the peripheral or central nervous systems and is thought to serve no useful purpose.[10] Nociception involves the 4 processes of transduction, transmission, perception, and modulation.[10,22] These processes are highly complex, but a simple summary can aid understanding of pain mechanisms and pain interventions. First, tissue damage releases chemical mediators, such as prostaglandins, bradykinin, serotonin, substance P, and histamine. These substances then activate nociceptors, resulting in transduction, or the generation of an action potential (an electrical impulse). In the second process -- transmission -- the action potential moves from the site of injury along afferent nerve fibers to nociceptors the spinal cord. Release of substance P and other neurotransmitters carry the action potential across the cleft to the dorsal horn of the spinal cord, from where it ascends the spinothalamic tract to the thalamus and the midbrain. Finally, from the thalamus, fibers send the nociceptive message to the somatosensory cortex, parietal lobe, frontal lobe, and the limbic system, where the third nociceptive process -- perception -- occurs.[11]

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Acute Pain Physiology Authors and DisclosuresCognitive impairment, pain, and analgesiaBiology of painPain transmission and peripheral group III metabotropic glutamate receptors (mGluRs)Pain control during prostate biopsy and evolution of local anesthesia techniquesTranscutaneous electrical nerve stimulation (TENS)Pain genetics Concluding remarksElectroencephalography-Based MonitorsThe Gamma-Band Oscillation PowerCognitive-affective modulation of pain: The placebo and nocebo phenomena and their impact on pain treatment☆Mini-dictionary of termsLinking the heart and pain: Physiological and psychophysiological mechanismsSummary pointsIntroductionPublisher SummaryPharmacogenomicsCatechol-O-Methyltransferase (COMT)Molecular aspects of neuroinflammation: Contribution of eicosanoids, cytokines, and chemokinesChronic neuroinflammationWhat are the four stages of pain transmission?What pathway is responsible for the emotional response to pain?What is the transmission of pain?What are the 4 processes of nociception?

Perception, the conscious experience of pain, involves both the sensory and affective components of pain. Clinical research in recent years has yielded greater understanding of the limbic system the area of the anterior cingulated gyrus and its role in the emotional response to pain.[23] The final nociceptive process -- modulation -- results from activation of the midbrain. Multiple types of neurons from this area that have a variety of neurotransmitters, including endorphins, enkephalins, serotonin (5-HT), and dynorphin, descend to lower areas in the central nervous system; these neurons stimulate the release of additional neurotransmitters, which ultimately trigger the release of endogenous opioids and inhibit transmission of the pain impulse the dorsal horn. Improved understanding of nociception has promoted the development of new treatment options and enabled the use of various medications and interventions to target nociceptive processes.[11,22]

Cite this: Elsa Wuhrman, Maureen F. Cooney. Acute Pain: Assessment and Treatment - Medscape - Jan 03, 2011.

Acute Pain OverviewAcute Pain PhysiologyAssessment of Acute PainTreatment of Acute Pain: OverviewReferences

Authors and Disclosures

Author(s)

Elsa Wuhrman, MS, FNP

Assistant Clinical Professor, School of Nursing, Columbia University Medical Center, Tp New York, NY; Nurse Practitioner, Acute Pain Services, Department of Anesthesiology, New York Presbyterian Hospital, Tp New York, NY

Disclosure: Elsa Wuhrman, MS, FNP, served as a participant in an APN Leadership Summit for PriCara.

Elsa Wuhrman, MS, FNP, has also disclosed that she intends to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

Maureen F. Cooney, DNP, FNP

Instructor of Anesthesiology, Tp New York Medical College, Valhalla, Tp New York; Adjunct Professor, Pace University Lienhard School of Nursing, Pleasantville, Tp New York; Nurse Practitioner, Pain Medicine, Westchester Medical Center, Valhalla, Tp New York

Disclosure: Maureen F. Cooney, DNP, FNP, has disclosed the following relevant financial relationships:
Served as a thành viên of a speakers bureau for: Cephalon, Inc.; GlaxoSmithKline. Served as a participant in an APN Leadership Summit for PriCara.

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Cognitive impairment, pain, and analgesia

Vanesa Cantón-HabasJosé Manuel Martínez-MartosManuel Rich-RuizMaría Jesús Ramirez-ÉxpositoMaría del Pilar Carrera-González, in Features and Assessments of Pain, Anaesthesia, and Analgesia, 2022

Biology of pain

Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, whereas nociception is the neural process of encoding noxious stimuli (IASP, 2022). The human body toàn thân is equipped with different types of sensory neurons and nociceptors, which form the primary unit of pain, which are able to detect stimuli that have the potential to cause damage. When a noxious stimulus activates an ion channel on a nociceptor, it produces a depolarization of the nociceptor, generating an electric potential. If the receptor’s potential is of sufficient magnitude to reach the activation threshold for voltage-dependent channels, it will trigger an action potential generation and the transmission of a pain signal to the spinal cord (Dubin & Patapoutian, 2010; Reichling, Green, & Levine, 2013).

Pain perception

Pain perception begins in the periphery, and then ascends in several tracts, relaying different levels. Pain signals arrive in the thalamus and midbrain structures that form the pain neuromatrix, a constantly shifting set of networks and connections that determine conscious perception. Several cortical regions become active simultaneously during pain perception; activity in the cortical pain matrix evolves over time to produce a complex pain perception network. Dysfunction any level has the potential to produce an unregulated, persistent pain (Fenton, Shih, & Zolton, 2015). Understanding pain is fundamental to improve the evaluation, treatment, and innovation in the management of acute and persistent pain syndromes.

However, it is well-known that the perception of clinical pain per se seems to vary greatly from person to person in the general population. Nevertheless, intraindividual differences also exist. In fact, several factors, such as spontaneous neuronal fluctuations, attention, expectation of pain, cognitive and emotional states, sleep habits and stress, may influence pain perception (Kröger, Menz, & May, 2022).

Pain in aging

Throughout life, age-related changes occur in relation to pain sensitivity. As a matter of fact, this suggests that pain perception diminishes in old age (El Tumi, Johnson, Dantas, Maynard, & Tashani, 2022). Authors as Dubin and Patapoutian (2010) state that pain perception is correlated with the activation of some but not all subtypes of heat and mechanic nociceptors. Moreover, judgments of pain threshold are also influenced by differences in central nervous system processing of noxious peripheral input from superficial and deep tissue and differences in pain modulator processes. However, pain perception is also influenced by biopsychosocial and age-related environmental factors changes; therefore, pain perception is likely to be a complex phenomenon.

In this context, it has been proposed that sex differences in pain perception are greater during reproductive years in women since pain sensitivity is believed to decline postmenopause (LeResche, Mancl, Drangsholt, Saunders, & Korff, 2005). Authors as Lautenbacher, Peters, Heesen, Scheel, and Kunz (2022) describe that aging decreases sensitivity for pain of low intensity, being the reduced sensitivity especially apparent for heat pain and for pain applied in the head. In contrast, the aging does not seem to have a strong effect on pain tolerance.

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URL: https://www.sciencedirect.com/science/article/pii/B9780128189887000042

Pain transmission and peripheral group III metabotropic glutamate receptors (mGluRs)

Eui Ho Park, Hee Chul Han, in The Neurobiology, Physiology, and Psychology of Pain, 2022

Abstract

Pain perception serves to protect living organism against an actual or potential tissue damage. Glutamatergic signaling of nervous system plays a crucial role in initiating and maintaining pain. It is important to note that the glutamatergic signaling in peripheral nervous system (PNS) is responsible for the first phase of pain processing. Recent animal studies support that some types of glutamate receptors such as NMDA receptor and group I metabotropic glutamate receptors (mGluRs) in cell bodies and primary afferent fibers of PNS can potentiate the nociceptive processing. However, much interest was less present in the role of peripheral group III mGluRs for regulating pain. Therefore, the present review will focus on peripheral group III mGluRs of PNS that can offer a better understanding of inhibitory role and therapeutic potential in pain processing.

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URL: https://www.sciencedirect.com/science/article/pii/B978012820589100021X

Pain control during prostate biopsy and evolution of local anesthesia techniques

Mustafa Suat Bolat, ... Recep Büyükalpelli, in Features and Assessments of Pain, Anaesthesia, and Analgesia, 2022

Transcutaneous electrical nerve stimulation (TENS)

Pain perception is transferred to the brain through the dorsal horn of the medulla spinalis. Pain sensation is mainly mediated by small nerve fibers (C-fibers), whereas touch and pressure sensations are transferred by large nerve fibers (A-beta fibers). Some conditions may affect this transmission according to the gate-control theory, described by Melzack and Wall in the mid-1960s (Melzack & Wall, 1965). Transmission cells and inhibitory interneurons control this transmission traffic together. Increased stimulation of the large fibers compared to small fibers causes inhibitory neuron stimulation, resulting in less sensation of pain.

Roughly, when a painful stimulus is given, small nerve fibers are activated, transmission cells are stimulated, and the pain sensation is transferred to the upper centers. At that time, stimulation of large nerve fibers, for example, by massaging the trauma site activates the inhibitory interneurons and pain ceases. Gate control theory does not explain the pain control homogeneously in all patients. Psychological factors and the past experiences of pain may affect the sense of pain perception. As a noninvasive technique, TENS is based on the principle of interfering with neural traffic. Stimulation of the thoracal 11–12 skin dermatomes by a TENS device activates A-beta fibers. Thus, C-fibers transmitting the pain sensation to the upper center are inhibited. In a recent study, the INFLATE technique has been described and presented to the literature with satisfactory pain control (Fig. 3A–C). Following the application of IRLA, a two-electrode two-channel TENS device is attached to the anterior suprapubic, and posterior presacral skin surfaces using adhesive electrodes correspond to bilateral T11–12 dermatomes. Following adjustment of the frequency and energy level, 3–6 min of stimulation is provided, and then the biopsy is started. The advantage of this technique is that it does not require penetrating local anesthetic agent applications (Bolat, Cinar, Asci, & Buyukalpelli, 2022).

Fig. 3. Transcutaneous electrical nerve stimulation (TENS) according to INFLATE (Infiltration-không lấy phí local anesthesia technique). Electrode attachment sites are shown on the abdominal wall (A) and posterior surface (B). The TENS device with electrode connections (C). T11–12 shows the thoracal 11–12 dermatome lines both on anterior and posterior surfaces. Symp, symphysis pubis.

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URL: https://www.sciencedirect.com/science/article/pii/B9780128189887000248

Pain genetics

William Renthal, in Rosenberg's Molecular and Genetic Basis of Neurological and Psychiatric Disease (Sixth Edition), 2022

Concluding remarks

Disorders in pain perception can occur any step along the signaling pathway. Without the membrane-bound nociceptors that initially detect noxious stimuli, no pain signal is generated. Without the structural proteins, ion channels, and neurotransmitters involved in transducing pain signals to the brain, the signal is not delivered. And finally, without multiple CNS networks functioning together, pain perception either does not occur or does not result in the appropriate behavioral response. As would be expected, we know the most about heritable phenotypes for which the sequencing of multiple affected family members was the easiest. These human mutations along with rodent pain models and newly emerging genetics tools have yielded numerous breakthroughs in our understanding of pain physiology and promise many more to come.

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URL: https://www.sciencedirect.com/science/article/pii/B9780128138663000230

Electroencephalography-Based Monitors

Gabriel Tran, ... Vincent Bonhomme, in Neuromonitoring Techniques, 2022

The Gamma-Band Oscillation Power

GBOp has limitations in assessing pain perception. First, nonnociceptive stimuli may trigger a significant GBO component.44 GBOp still needs to be evaluated in large cohorts of patients, as well as in patients receiving longer lasting stimuli than the transient nociceptive laser ones. At present, these techniques remain within the fields of research, requiring careful experimental protocols, sophisticated extraction process, and high computational complexity.132 However, GBOp remains promising as a tool to unravel residual pain perception in noncommunicative patients with disorders of consciousness and to monitor pain-treatment efficacy in those patients.

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URL: https://www.sciencedirect.com/science/article/pii/B9780128099155000048

Cognitive-affective modulation of pain: The placebo and nocebo phenomena and their impact on pain treatment☆

Sergiu Albu, ... Mary W. Meagher, in The Neurobiology, Physiology, and Psychology of Pain, 2022

Mini-dictionary of terms

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Placebo hypoalgesia refers to decreased pain perception that appears in the context of pain treatment but is unrelated to the pharmacological effects of the drug.

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Nocebo hyperalgesia represents an increase in pain sensitivity, a nonspecific effect observed in the context of pain treatment/interventions.

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Expectation (or expectancy) represents specific conscious reasoning about the likelihood of future events (or the effects of interventions), which is based on instructions, previous experiences, and social observation.

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Anticipatory anxiety is a physiological and affective response to an uncertain threatening context or an emotionally aversive future sự kiện.

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Instructional learning is a form of learning the effects and responses to interventions through explicit verbal or written suggestions.

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Social learning is a form of knowledge acquisition that occurs through observation of the effects of intervention in others.

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Conditioned analgesia/hyperalgesia represents learning-based response of pain modulation induced by repeated pairing of an initially neutral stimulus (inert substance/intervention) with an active drug/intervention, which then leads to analgesic/hyperalgesic response when the inert substance/intervention is administered.

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Endogenous pain modulatory systems encompass brain and spinal cord structures that provide facilitation or inhibition of nociceptive inputs.

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Pain catastrophizing is characterized by negative thoughts and feelings (rumination, magnification, and helplessness) that may enhance pain experiences and increase the risk of developing chronic pain.

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Open-hidden paradigm represents drug administration when the patient is given information about the medication being administered compared to a drug administration by an automated system when the patient is unaware of a drug being given.

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Cognitive behavioral therapy is a form of psychotherapy that modifies maladaptive cognitions (thoughts and beliefs) and behaviors, improving emotion regulation and pain.

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Mindfulness practices and acceptance and commitment therapy promote awareness and acceptance of one’s experiences and coping strategies, with a shift from passive to active coping with pain and related distress.

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URL: https://www.sciencedirect.com/science/article/pii/B9780128205891000336

Linking the heart and pain: Physiological and psychophysiological mechanisms

Dmitry M. Davydov, in Features and Assessments of Pain, Anaesthesia, and Analgesia, 2022

Summary points

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The cardiovascular system and systems regulating pain perception are closely interrelated.

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Acute and persistent noxious stimuli and pain-related feelings and thoughts moderate mechanisms regulating cardiovascular activity (e.g., increase in essential hypertension incidence).

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Individual responses to noxious stimuli are modified (diminished or augmented) by mechanisms regulating cardiovascular activity (e.g., by increased or decreased gain in bradycardic baro-responses to blood pressure increases).

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Hypertension associated with only a systolic blood pressure increase determines higher pain severity through several pronociceptive mechanisms.

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Hypertension with both systolic and diastolic blood pressure elevation is associated with a decrease of pain intensity and severity through an antinociceptive mechanism.

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Antihypertensive drugs can increase chronic pain severity as well as the probability of new cases of chronic pain, and thus can be disadvantageous for pain control by pain-killing drugs.

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Pain can be controlled by antihypotension drugs and nondrug treatments.

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Pain control effectiveness can be predicted and monitored by specific cardiovascular measures.

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An individual level of suffering from pain in its different nociceptive, affective, and cognitive domains can be assessed by various indicators of affected regulation of blood pressure.

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Pain-o-meter technology can be developed using indicators of common mechanisms regulating cardiovascular and pain systems.

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URL: https://www.sciencedirect.com/science/article/pii/B978012818988700011X

Introduction

H.L. Fields, in Pain Syndromes in Neurology, 1990

Publisher Summary

This chapter reviews neural mechanisms relevant to pain perception and also reviews neuropathic pain. The treatment and analysis of pain requires an understanding and appreciation of the mechanisms thorough which the sensations of pain is transmitted to the receptors and thereafter to the brain where the sensation is interpreted as pain; along with this, an appreciation of the systems that the body toàn thân employs in dealing with pain. In the somatosensory system, the transduction process normally occurs in the peripheral terminals of dorsal root ganglion cells—primary afferents. Primary afferents fall into distinct classes determined by the specific types of stimuli they respond to and the conduction velocity of their axons. Those that respond with increased discharge to stimuli that are tissue damaging or potentially tissue damaging are termed primary afferent nociceptors (PANs). The peripheral terminals of PANs are sensitive to one or more of the following types of stimulus: thermal, mechanical, or chemical. Clinical pains are accompanied by tenderness and, often hypersensitivity. In part these two reflect the sensitization of PANs. PANs enter the spinal cord via the dorsal root, and synapse with second-order neurons, some of which project to supraspinal nuclei implicated in pain sensation, such as the ventrobasal nucleus of the thalamus. The major ascending pathway for pain transmission lies in the antero-lateral white matter of the spinal cord. The pain-modulating system consists of a network of neurons running from the cortex and hypothalamus via the mid-brain periaqueductal gray, and rostral medulla to the dorsal horn.

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URL: https://www.sciencedirect.com/science/article/pii/B9780407011243500071

Pharmacogenomics

Y.N. Martin, W.T. Nicholson, in Essentials of Neuroanesthesia, 2022

Catechol-O-Methyltransferase (COMT)

Indirect pathways can also impact opioid effectiveness. Pain perception and even efficacy of opioid analgesia can be influenced by catecholamines.63 Catecholamines are inactivated by the enzyme COMT. A known common polymorphism G1947A leads to reduction in COMT enzyme activity64 and subsequent lower catecholamine levels.65 The largest reduction in enzyme activity is seen with the C158M polymorphism.66,67 Those with the G1947A variant allele have been shown to have decreased tolerance to experimental pain.67 Conflicting studies in cancer pain show the wild-type allele to have increased morphine requirements.68

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URL: https://www.sciencedirect.com/science/article/pii/B9780128052990000580

Molecular aspects of neuroinflammation: Contribution of eicosanoids, cytokines, and chemokines

Akhlaq A. Farooqui, in Neuroinflammation, Resolution, and Neuroprotection in the Brain, 2022

Chronic neuroinflammation

Chronic inflammation develops slowly below the threshold of pain perception. As a result, the immune system continues to attack brain tissue the cellular level. Chronic inflammation lingers for years causing continued insult to the brain tissue reaching the threshold of detection (Wood, 1998) and initiating the pathogenesis of chronic diseases such as Alzheimer's disease (AD). A characteristic feature of chronically inflamed brain is the presence of an increased number of monocytes, microglia cells, and astrocytes in the central nervous system (Akiyama et al., 2000). Chronic inflammation disrupts hormonal signaling networks in the brain. In the brain, chronic neuroinflammation is supported by long-term activation of microglia and astrocytes along with sustained release of low levels of inflammatory mediators leading to an increase in oxidative and nitrosative stress (Tansey et al., 2007). The sustained release of inflammatory mediators (PGs, LTs, TXs, cytokines, and chemokines, monocyte chemoattractant proteins, complement factors, proteases, protease inhibitors, pentraxins) not only alters the inflammatory cycle and activates additional microglial cells, but also promotes proliferation, leading to further release of inflammatory factors. In nonneural tissues, sustained inflammation due to persistent activation of inflammatory cells or defects in the resolution program results in a fibrogenic response, which involves the overall remodeling of tissue structure and eventual organ failure. Fibrogenic response is supported not only by sustained inflammation and cell proliferation, but also by growth factor responses. Owing to the chronic and sustained nature of the inflammation, there is often compromise of the BBB, which increases infiltration of peripheral macrophages into the brain parenchyma to further perpetuate the inflammation (Rivest, 2015). Chronic inflammation induces deficits in long-term potentiation (LTP), the major neuronal substrate for learning and memory, in middle-aged but not in young rats (Liu et al., 2012). Rather than serving a protective role as in acute neuroinflammation, chronic neuroinflammation is most often detrimental and damaging to the brain tissue. It is not known, whether neuroinflammation has beneficial or harmful outcomes in the brain. It may depend critically on the duration of the inflammatory response. Prolonged chronic inflammatory state has detrimental health effects and predisposes to a wide variety of chronic diseases, especially those that are more prevalent with advanced age, such as cardiovascular diseases, diabetes, and neurodegenerative diseases (Farooqui et al., 2007). Chronic inflammation is also a strong predictor of both disability and mortality in the elderly—even in the absence of clinical disease (Penninx et al., 2004; Farooqui, 2013). Significant information is available on the generation of proinflammatory mediators such as proinflammatory eicosanoids and cytokines. However, little is known about internal and external factors that modulate the dynamic aspects of acute and chronic neuroinflammation. Depending on its timing and magnitude in the brain tissue, neuroinflammation serves multiple purposes. As stated above, neuroinflammation is not only involved in the protection of uninjured neurons and removal of degenerating neuronal debris, but also contributes in assisting repair and recovery processes (Farooqui, 2010, 2011). In AD, it is proposed that the intractable nature of the Aβ plaques and tangles contributes to a chronic inflammatory reaction to clear this debris (Cai et al., 2014). Thus, senile plaques contain dystrophic neurites, activated microglia, and reactive astrocytes (Akiyama et al., 2000). Aggregated amyloid fibrils and inflammatory mediators secreted by microglial and astrocytic cells contribute to neuronal dystrophy (Findeis, 2007). Chronically activated glia can mediate neurodegeneration in adjacent neurons by releasing highly toxic products such as reactive oxygen species (ROS), nitric oxide (NO), glutamate, proteolytic enzymes, and complementary factors (Halliday et al., 2000). Generation of above mediators is aided by inflammatory enzyme systems such as the inducible nitric oxide synthase (iNOS) and the cyclooxygenase enzyme (COX)-2. Thus, converging evidence suggests that all these factors can contribute to neuronal dysfunction and cell death, either alone or in concert. It is not yet known whether the above events precede disease states or are a direct consequence of the damage that occurs in pathology of neurodegenerative diseases. For example, Aβ plaques have been shown to induce proinflammatory effects in animal models of AD (Tuppo and Arias, 2005), supporting the view that neuroinflammatory events initiate or even aid in the progression of AD (Heneka and O’Banion, 2007; Bales et al., 2000).

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What are the four stages of pain transmission?

There are four major processes: transduction, transmission, modulation, and perception. Transduction refers to the processes by which tissue-damaging stimuli activate nerve endings.

What pathway is responsible for the emotional response to pain?

The intralaminar nuclei also projects to the frontal cortex, which in turn projects to the limbic structures where the emotional response to pain is mediated. The archispinothalamic tract is a multisynaptic diffuse tract or pathway and is phylogenetically the oldest tract that carries noxious information.

What is the transmission of pain?

Acute (normal) pain transmission is part of a survival response to prevent tissue damage and attend to and protect damaged tissue. A cycle of afferent transmission, response to stimuli, followed by temporary hypersensitivity, then attenuation and resolution occurs.

What are the 4 processes of nociception?

Nociception involves the 4 processes of transduction, transmission, perception, and modulation. These processes are highly complex, but a simple summary can aid understanding of pain mechanisms and pain interventions. Tải thêm tài liệu liên quan đến nội dung bài viết Which process of pain transmission is associated with an emotional response to pain