Pain

Jun Chen; Ji Sheng Han; Zhi Qi Zhao; Feng Wei; Jen Chuen Hsieh; Lan Bao; Andrew C.N. Chen; Yi Dai; Bi Fa Fan; Jian Guo Gu; Shuang Lin Hao; San Jue Hu; Yong Hua Ji; Yong Jie Li; Yun Qing Li; Qing Lin; Xian Guo Liu; Yan Qing Liu; Yan Lu; Fei Luo; Chao Ma; Yun Hai Qiu; Zhi Ren Rao; Lin Shi; Bai Chuang Shyu; Xue Jun Song; Jing Shi Tang; Yuan Xiang Tao; You Wan; Jia Shuang Wang; Ke Wei Wang; Yun Wang; Guang Yin Xu; Tian Le Xu; Hao Jun You; Long Chuan Yu; Sheng Yuan Yu; Da Ying Zhang; De Ren Zhang; Jun Ming Zhang; Xu Zhang; Yu Qiu Zhang; Min Zhuo

doi:10.1007/978-1-4939-3474-4_32

Pain

Jun Chen^*, Ji Sheng Han, Zhi Qi Zhao, Feng Wei, Jen Chuen Hsieh, Lan Bao, Andrew C.N. Chen, Yi Dai, Bi Fa Fan, Jian Guo Gu, Shuang Lin Hao, San Jue Hu, Yong Hua Ji, Yong Jie Li, Yun Qing Li, Qing Lin, Xian Guo Liu, Yan Qing Liu, Yan Lu, Fei LuoChao Ma, Yun Hai Qiu, Zhi Ren Rao, Lin Shi, Bai Chuang Shyu, Xue Jun Song, Jing Shi Tang, Yuan Xiang Tao, You Wan, Jia Shuang Wang, Ke Wei Wang, Yun Wang, Guang Yin Xu, Tian Le Xu, Hao Jun You, Long Chuan Yu, Sheng Yuan Yu, Da Ying Zhang, De Ren Zhang, Jun Ming Zhang, Xu Zhang, Yu Qiu Zhang, Min Zhuo

^*Corresponding author for this work

Institute of Brain Science

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Pain is one of the most common causes of suffering. The physiological function of pain is to alert the body of potentially noxious conditions encountered from the external or internal environment. Pain can be differentiated into acute pain and chronic pain according to its duration, with 3 months as a tentative defining point in humans. Acute pain is good for protection from dangerous health issues and relatively easy to control. Chronic pain, on the other hand, is absolutely annoying and notoriously difficult to manage. Chronic pain can be induced by various causes, such as inflammatory or metabolic disorders of the peripheral tissue, musculoskeletal strain, peripheral or central nervous lesion and diseases, etc., yet their common mechanism is hypersensitivity of the pain transmission and perception systems, which may result in a structural disorganization. The suffering from chronic pain has been a powerful driving force for pain research both in academic institutions and in the industry. This chapter focuses on the system of noxious signal transmission, from the ion channel and nociceptor to the psychological reaction, from the ascending pain perception pathways to the descending pain modulatory pathways, being facilitatory or inhibitory. Principles of biomedical interventions on acute and chronic pain are also outlined.

Original language	English
Title of host publication	Neuroscience in the 21st Century
Subtitle of host publication	From Basic to Clinical, Second Edition
Publisher	Springer New York
Pages	1091-1149
Number of pages	59
ISBN (Electronic)	9781493934744
ISBN (Print)	9781493934737
DOIs	https://doi.org/10.1007/978-1-4939-3474-4_32
State	Published - 1 Jan 2016

Keywords

Acupuncture modulation
Acupuncture modulation of pain
Amygdala
Axonal reflex
Behavioral pain hypersensitivity
Bell-magendie law
Biochemical neuroimaging
Brain matrix
Brain mechanisms
Cerebellum
Cortical and subcortical processing
Disinhibition
Drug modulation
Functional neuroimaging
Gabapentin
Gatecontrol theory of pain
Gene therapy and stem cell treatment
Glial cells
Hyperalgesia
Hypothalamus
Insula
K2P
Nerve injury-induced neural plasticity
Neurochemical markers
Neurogenic inflammation
Neuromodulation
Neuromodulation
Neuropathic
Nociception
Nociceptive flexion reflex (NFR)
Nociceptive specific (NS) neurons
Nonsteroidal anti-inflammatory drugs (NSAIDs)
P2X3 receptor
P2Y receptors
Pain
Pain
Pain
Pain
Pain
Pain
Pain matrix
Peptidergic population of c nociceptors
Periaqueductal gray (PAG)
Peripheral mechanisms
Peripheral nociceptors
Placebo modulation
Placebo modulation
Primary afferent depolarization (PAD)
Pro-inflammatory cytokines
Psychological modulation
Rostral ventromedial medulla (RVM)
Specificity theory
Spinal cord dorsal horn
Spinal pain sensory neurons
Structural neuroimaging
Tanezumab
Thalamic pain syndrome
Transient receptor potential vanilloid receptor 1 (TRPV1)
Tripartite synaptic model
Vanilloid receptor-like protein 1 (VRL1)
Ventrolateral orbital cortex (VLO)
Voltage-gated potassium channels (VGPCs)
Voxel-based morphometry
Windup phenomenon

Access to Document

10.1007/978-1-4939-3474-4_32

Cite this

Chen, J., Han, J. S., Zhao, Z. Q., Wei, F., Hsieh, J. C., Bao, L., Chen, A. C. N., Dai, Y., Fan, B. F., Gu, J. G., Hao, S. L., Hu, S. J., Ji, Y. H., Li, Y. J., Li, Y. Q., Lin, Q., Liu, X. G., Liu, Y. Q., Lu, Y., ... Zhuo, M. (2016). Pain. In Neuroscience in the 21st Century: From Basic to Clinical, Second Edition (pp. 1091-1149). Springer New York. https://doi.org/10.1007/978-1-4939-3474-4_32

@inbook{ba3b0d9af18341c882adc5cb92757e15,

title = "Pain",

abstract = "Pain is one of the most common causes of suffering. The physiological function of pain is to alert the body of potentially noxious conditions encountered from the external or internal environment. Pain can be differentiated into acute pain and chronic pain according to its duration, with 3 months as a tentative defining point in humans. Acute pain is good for protection from dangerous health issues and relatively easy to control. Chronic pain, on the other hand, is absolutely annoying and notoriously difficult to manage. Chronic pain can be induced by various causes, such as inflammatory or metabolic disorders of the peripheral tissue, musculoskeletal strain, peripheral or central nervous lesion and diseases, etc., yet their common mechanism is hypersensitivity of the pain transmission and perception systems, which may result in a structural disorganization. The suffering from chronic pain has been a powerful driving force for pain research both in academic institutions and in the industry. This chapter focuses on the system of noxious signal transmission, from the ion channel and nociceptor to the psychological reaction, from the ascending pain perception pathways to the descending pain modulatory pathways, being facilitatory or inhibitory. Principles of biomedical interventions on acute and chronic pain are also outlined.",

keywords = "Acupuncture modulation, Acupuncture modulation of pain, Amygdala, Axonal reflex, Behavioral pain hypersensitivity, Bell-magendie law, Biochemical neuroimaging, Brain matrix, Brain mechanisms, Cerebellum, Cortical and subcortical processing, Disinhibition, Drug modulation, Functional neuroimaging, Gabapentin, Gatecontrol theory of pain, Gene therapy and stem cell treatment, Glial cells, Hyperalgesia, Hypothalamus, Insula, K2P, Nerve injury-induced neural plasticity, Neurochemical markers, Neurogenic inflammation, Neuromodulation, Neuromodulation, Neuropathic, Nociception, Nociceptive flexion reflex (NFR), Nociceptive specific (NS) neurons, Nonsteroidal anti-inflammatory drugs (NSAIDs), P2X3 receptor, P2Y receptors, Pain, Pain, Pain, Pain, Pain, Pain, Pain matrix, Peptidergic population of c nociceptors, Periaqueductal gray (PAG), Peripheral mechanisms, Peripheral nociceptors, Placebo modulation, Placebo modulation, Primary afferent depolarization (PAD), Pro-inflammatory cytokines, Psychological modulation, Rostral ventromedial medulla (RVM), Specificity theory, Spinal cord dorsal horn, Spinal pain sensory neurons, Structural neuroimaging, Tanezumab, Thalamic pain syndrome, Transient receptor potential vanilloid receptor 1 (TRPV1), Tripartite synaptic model, Vanilloid receptor-like protein 1 (VRL1), Ventrolateral orbital cortex (VLO), Voltage-gated potassium channels (VGPCs), Voxel-based morphometry, Windup phenomenon",

author = "Jun Chen and Han, {Ji Sheng} and Zhao, {Zhi Qi} and Feng Wei and Hsieh, {Jen Chuen} and Lan Bao and Chen, {Andrew C.N.} and Yi Dai and Fan, {Bi Fa} and Gu, {Jian Guo} and Hao, {Shuang Lin} and Hu, {San Jue} and Ji, {Yong Hua} and Li, {Yong Jie} and Li, {Yun Qing} and Qing Lin and Liu, {Xian Guo} and Liu, {Yan Qing} and Yan Lu and Fei Luo and Chao Ma and Qiu, {Yun Hai} and Rao, {Zhi Ren} and Lin Shi and Shyu, {Bai Chuang} and Song, {Xue Jun} and Tang, {Jing Shi} and Tao, {Yuan Xiang} and You Wan and Wang, {Jia Shuang} and Wang, {Ke Wei} and Yun Wang and Xu, {Guang Yin} and Xu, {Tian Le} and You, {Hao Jun} and Yu, {Long Chuan} and Yu, {Sheng Yuan} and Zhang, {Da Ying} and Zhang, {De Ren} and Zhang, {Jun Ming} and Xu Zhang and Zhang, {Yu Qiu} and Min Zhuo",

note = "Publisher Copyright: {\textcopyright} Springer Science+Business Media, LLC 2013 and Springer Science+Business Media New York 2016.",

year = "2016",

month = jan,

day = "1",

doi = "10.1007/978-1-4939-3474-4_32",

language = "English",

isbn = "9781493934737",

pages = "1091--1149",

booktitle = "Neuroscience in the 21st Century",

publisher = "Springer New York",

address = "United States",

}

Chen, J, Han, JS, Zhao, ZQ, Wei, F, Hsieh, JC, Bao, L, Chen, ACN, Dai, Y, Fan, BF, Gu, JG, Hao, SL, Hu, SJ, Ji, YH, Li, YJ, Li, YQ, Lin, Q, Liu, XG, Liu, YQ, Lu, Y, Luo, F, Ma, C, Qiu, YH, Rao, ZR, Shi, L, Shyu, BC, Song, XJ, Tang, JS, Tao, YX, Wan, Y, Wang, JS, Wang, KW, Wang, Y, Xu, GY, Xu, TL, You, HJ, Yu, LC, Yu, SY, Zhang, DY, Zhang, DR, Zhang, JM, Zhang, X, Zhang, YQ & Zhuo, M 2016, Pain. in Neuroscience in the 21st Century: From Basic to Clinical, Second Edition. Springer New York, pp. 1091-1149. https://doi.org/10.1007/978-1-4939-3474-4_32

TY - CHAP

T1 - Pain

AU - Chen, Jun

AU - Han, Ji Sheng

AU - Zhao, Zhi Qi

AU - Wei, Feng

AU - Hsieh, Jen Chuen

AU - Bao, Lan

AU - Chen, Andrew C.N.

AU - Dai, Yi

AU - Fan, Bi Fa

AU - Gu, Jian Guo

AU - Hao, Shuang Lin

AU - Hu, San Jue

AU - Ji, Yong Hua

AU - Li, Yong Jie

AU - Li, Yun Qing

AU - Lin, Qing

AU - Liu, Xian Guo

AU - Liu, Yan Qing

AU - Lu, Yan

AU - Luo, Fei

AU - Ma, Chao

AU - Qiu, Yun Hai

AU - Rao, Zhi Ren

AU - Shi, Lin

AU - Shyu, Bai Chuang

AU - Song, Xue Jun

AU - Tang, Jing Shi

AU - Tao, Yuan Xiang

AU - Wan, You

AU - Wang, Jia Shuang

AU - Wang, Ke Wei

AU - Wang, Yun

AU - Xu, Guang Yin

AU - Xu, Tian Le

AU - You, Hao Jun

AU - Yu, Long Chuan

AU - Yu, Sheng Yuan

AU - Zhang, Da Ying

AU - Zhang, De Ren

AU - Zhang, Jun Ming

AU - Zhang, Xu

AU - Zhang, Yu Qiu

AU - Zhuo, Min

N1 - Publisher Copyright: © Springer Science+Business Media, LLC 2013 and Springer Science+Business Media New York 2016.

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Pain is one of the most common causes of suffering. The physiological function of pain is to alert the body of potentially noxious conditions encountered from the external or internal environment. Pain can be differentiated into acute pain and chronic pain according to its duration, with 3 months as a tentative defining point in humans. Acute pain is good for protection from dangerous health issues and relatively easy to control. Chronic pain, on the other hand, is absolutely annoying and notoriously difficult to manage. Chronic pain can be induced by various causes, such as inflammatory or metabolic disorders of the peripheral tissue, musculoskeletal strain, peripheral or central nervous lesion and diseases, etc., yet their common mechanism is hypersensitivity of the pain transmission and perception systems, which may result in a structural disorganization. The suffering from chronic pain has been a powerful driving force for pain research both in academic institutions and in the industry. This chapter focuses on the system of noxious signal transmission, from the ion channel and nociceptor to the psychological reaction, from the ascending pain perception pathways to the descending pain modulatory pathways, being facilitatory or inhibitory. Principles of biomedical interventions on acute and chronic pain are also outlined.

AB - Pain is one of the most common causes of suffering. The physiological function of pain is to alert the body of potentially noxious conditions encountered from the external or internal environment. Pain can be differentiated into acute pain and chronic pain according to its duration, with 3 months as a tentative defining point in humans. Acute pain is good for protection from dangerous health issues and relatively easy to control. Chronic pain, on the other hand, is absolutely annoying and notoriously difficult to manage. Chronic pain can be induced by various causes, such as inflammatory or metabolic disorders of the peripheral tissue, musculoskeletal strain, peripheral or central nervous lesion and diseases, etc., yet their common mechanism is hypersensitivity of the pain transmission and perception systems, which may result in a structural disorganization. The suffering from chronic pain has been a powerful driving force for pain research both in academic institutions and in the industry. This chapter focuses on the system of noxious signal transmission, from the ion channel and nociceptor to the psychological reaction, from the ascending pain perception pathways to the descending pain modulatory pathways, being facilitatory or inhibitory. Principles of biomedical interventions on acute and chronic pain are also outlined.

KW - Acupuncture modulation

KW - Acupuncture modulation of pain

KW - Amygdala

KW - Axonal reflex

KW - Behavioral pain hypersensitivity

KW - Bell-magendie law

KW - Biochemical neuroimaging

KW - Brain matrix

KW - Brain mechanisms

KW - Cerebellum

KW - Cortical and subcortical processing

KW - Disinhibition

KW - Drug modulation

KW - Functional neuroimaging

KW - Gabapentin

KW - Gatecontrol theory of pain

KW - Gene therapy and stem cell treatment

KW - Glial cells

KW - Hyperalgesia

KW - Hypothalamus

KW - Insula

KW - K2P

KW - Nerve injury-induced neural plasticity

KW - Neurochemical markers

KW - Neurogenic inflammation

KW - Neuromodulation

KW - Neuropathic

KW - Nociception

KW - Nociceptive flexion reflex (NFR)

KW - Nociceptive specific (NS) neurons

KW - Nonsteroidal anti-inflammatory drugs (NSAIDs)

KW - P2X3 receptor

KW - P2Y receptors

KW - Pain

KW - Pain matrix

KW - Peptidergic population of c nociceptors

KW - Periaqueductal gray (PAG)

KW - Peripheral mechanisms

KW - Peripheral nociceptors

KW - Placebo modulation

KW - Primary afferent depolarization (PAD)

KW - Pro-inflammatory cytokines

KW - Psychological modulation

KW - Rostral ventromedial medulla (RVM)

KW - Specificity theory

KW - Spinal cord dorsal horn

KW - Spinal pain sensory neurons

KW - Structural neuroimaging

KW - Tanezumab

KW - Thalamic pain syndrome

KW - Transient receptor potential vanilloid receptor 1 (TRPV1)

KW - Tripartite synaptic model

KW - Vanilloid receptor-like protein 1 (VRL1)

KW - Ventrolateral orbital cortex (VLO)

KW - Voltage-gated potassium channels (VGPCs)

KW - Voxel-based morphometry

KW - Windup phenomenon

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U2 - 10.1007/978-1-4939-3474-4_32

DO - 10.1007/978-1-4939-3474-4_32

M3 - Chapter

AN - SCOPUS:85018934714

SN - 9781493934737

SP - 1091

EP - 1149

BT - Neuroscience in the 21st Century

PB - Springer New York

ER -

Pain

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