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The physiology and pathophysiology of pain
/content/chapter/10.22233/9781910443231.chap8
The physiology and pathophysiology of pain
- Authors: Mary P. Klinck and Eric Troncy
- From: BSAVA Manual of Canine and Feline Anaesthesia and Analgesia
- Item: Chapter 8, pp 97 - 112
- DOI: 10.22233/9781910443231.8
- Copyright: © 2016 British Small Animal Veterinary Association
- Publication Date: April 2016
Abstract
Pain management in animals has improved over the past 2-3 decades. Previously, there was a tendency both to under-recognize and to under-treat animal pain. Vertebrate animals share a common anatomy and physiology involved in pain processing, therefore, injuries, diseases and procedures that are painful in humans are likely to be painful in animals. This chapter looks at definitions for types of pain, processing nociceptive information, altered pain states, sensitization, inflammatory pain, neuropathic pain , therapeutic targets in the pathophysiology of pain and physiological considerations in pain assessment.
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Figures
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8.1
Diagram illustrating the ascending and descending nociceptive pathways with connections within the spinal cord to the autonomic nervous system and skeletal muscle. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.1
Diagram illustrating the ascending and descending nociceptive pathways with connections within the spinal cord to the autonomic nervous system and skeletal muscle. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.2
Diagram of (a) a nociceptive first-order neuron and (b) a prototypical neuron, illustrating structural differences. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.2
Diagram of (a) a nociceptive first-order neuron and (b) a prototypical neuron, illustrating structural differences. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.3
Diagram of a nociceptor terminal illustrating various transducers sensitive to noxious stimuli and ion channels. Influx of calcium and sodium ions in sufficient concentration will cause an action potential along the nerve axon. Potassium ions are usually inhibitory. ASIC = acid-sensing ion channels; TRP = transient receptor potential. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.3
Diagram of a nociceptor terminal illustrating various transducers sensitive to noxious stimuli and ion channels. Influx of calcium and sodium ions in sufficient concentration will cause an action potential along the nerve axon. Potassium ions are usually inhibitory. ASIC = acid-sensing ion channels; TRP = transient receptor potential. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.4
Diagram of a transverse section of the spinal cord, illustrating the central terminals of the first-order Aβ (green), Aδ (orange) and C (red) neurons within the dorsal horn of the grey matter. The Roman numerals represent the position of the terminals in Rexed’s laminae of the spinal cord. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.4
Diagram of a transverse section of the spinal cord, illustrating the central terminals of the first-order Aβ (green), Aδ (orange) and C (red) neurons within the dorsal horn of the grey matter. The Roman numerals represent the position of the terminals in Rexed’s laminae of the spinal cord. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.5
Diagram of a synapse between first- and second-order nociceptive neurons. Receptors for AMPA and NMDA are ionotropic for glutamate (as is the kainate receptor, not shown on the diagram). The glutamate receptor is metabotropic for glutamate. The metabotropic receptors NK1 and CGRP are for substance P and calcitonin gene-related peptide (CGRP), respectively. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.5
Diagram of a synapse between first- and second-order nociceptive neurons. Receptors for AMPA and NMDA are ionotropic for glutamate (as is the kainate receptor, not shown on the diagram). The glutamate receptor is metabotropic for glutamate. The metabotropic receptors NK1 and CGRP are for substance P and calcitonin gene-related peptide (CGRP), respectively. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.6
Diagram showing details of the inhibitory effects between the terminals of first- and second-order neurons within the dorsal horn of the spinal cord. Alpha-2 adrenergic, GABA and mu opioid receptor stimulation decreases the chance of an action potential developing in the second-order neuron. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.6
Diagram showing details of the inhibitory effects between the terminals of first- and second-order neurons within the dorsal horn of the spinal cord. Alpha-2 adrenergic, GABA and mu opioid receptor stimulation decreases the chance of an action potential developing in the second-order neuron. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.7
(a) Increased brain metabolism in the SII cortex as well as the thalamus and PAG of osteoarthritic cats is illustrated in transverse sections of the brain during positron emission tomography/magnetic resonance imaging techniques (
Guillot et al., 2015
). (b) Four transversal slices of: (A) an osteoarthritic cat brain imaged with [18F]-fluorodeoxyglucose using a small animal positron emission tomography (PET) scanner; (B) brain regions of interest (ROI) segmented from magnetic resonance (MR) images; (C) PET signal co-registered with MR images. ROI identification from left to right: Slice 1: salmon, prefrontal cortex; aqua, motor cortex; purple, primary somatosensory cortex; yellow, anterior cingulate cortex. Slice 2: purple, primary somatosensory cortex; yellow, anterior cingulate cortex; dark blue, insula; dark red, secondary somatosensory (SII) cortex. Slice 3: blue, thalamus; dark yellow, visual cortex. Slice 4: dark yellow, visual cortex; green, periaqueductal gray (PAG) matter; orange, mesencephalon; light red, superior temporal cortex. © 2016 British Small Animal Veterinary Association
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8.7
(a) Increased brain metabolism in the SII cortex as well as the thalamus and PAG of osteoarthritic cats is illustrated in transverse sections of the brain during positron emission tomography/magnetic resonance imaging techniques (
Guillot et al., 2015
). (b) Four transversal slices of: (A) an osteoarthritic cat brain imaged with [18F]-fluorodeoxyglucose using a small animal positron emission tomography (PET) scanner; (B) brain regions of interest (ROI) segmented from magnetic resonance (MR) images; (C) PET signal co-registered with MR images. ROI identification from left to right: Slice 1: salmon, prefrontal cortex; aqua, motor cortex; purple, primary somatosensory cortex; yellow, anterior cingulate cortex. Slice 2: purple, primary somatosensory cortex; yellow, anterior cingulate cortex; dark blue, insula; dark red, secondary somatosensory (SII) cortex. Slice 3: blue, thalamus; dark yellow, visual cortex. Slice 4: dark yellow, visual cortex; green, periaqueductal gray (PAG) matter; orange, mesencephalon; light red, superior temporal cortex.
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8.8
Graph illustrating various pain states. See text for further details. © 2016 British Small Animal Veterinary Association
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8.8
Graph illustrating various pain states. See text for further details.
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8.9
Diagram illustrating the changes that cause allodynia, hyperalgesia and spontaneous pain. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.9
Diagram illustrating the changes that cause allodynia, hyperalgesia and spontaneous pain. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.10
Diagram showing the action of inflammatory mediators on nociceptors and peripheral sensitization. ATP = adenosine triphosphate; CGRP = calcitonin gene-related peptide; IL = interleukin; TNF = tumour necrosis factor. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.10
Diagram showing the action of inflammatory mediators on nociceptors and peripheral sensitization. ATP = adenosine triphosphate; CGRP = calcitonin gene-related peptide; IL = interleukin; TNF = tumour necrosis factor. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.11
Central sensitization produces changes within the terminals of the neurons to ensure that nociceptive transmission occurs. See text for further details. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.11
Central sensitization produces changes within the terminals of the neurons to ensure that nociceptive transmission occurs. See text for further details. AMPA = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NK1 = neurokinin-1; NMDA = N-methyl-d-aspartate. (© Juliane Deubner, University of Saskatchewan, Canada)
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8.12
Neuropathic pain originates from nerve damage and local changes such as increased sympathetic activity and input from Aβ fibres. There is less descending inhibition of nociceptive transmission. Aδ fibres are not shown for clarity. (© Juliane Deubner, University of Saskatchewan, Canada) © 2016 British Small Animal Veterinary Association
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8.12
Neuropathic pain originates from nerve damage and local changes such as increased sympathetic activity and input from Aβ fibres. There is less descending inhibition of nociceptive transmission. Aδ fibres are not shown for clarity. (© Juliane Deubner, University of Saskatchewan, Canada)