Pain - PDF
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Benha University
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Summary
This document defines pain as an unpleasant sensory and emotional experience. It details pain receptors, pain thresholds, and pain responses, covering acute and chronic pain. Different types of pain are discussed, such as cutaneous, deep, visceral, and neuropathic pain.
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# Pain ## Definition: - Unpleasant sensation caused by tissue damage (1979). - It is a protective sensation as the subject reacts to remove pain stimulus and seek medical advice. - The International Association for the Study of Pain (IASP)(2020): An unpleasant sensory and emotional experience asso...
# Pain ## Definition: - Unpleasant sensation caused by tissue damage (1979). - It is a protective sensation as the subject reacts to remove pain stimulus and seek medical advice. - The International Association for the Study of Pain (IASP)(2020): An unpleasant sensory and emotional experience associated with, actual or potential tissue damage. This new definition includes those unable to articulate their pain verbally, such as infants and the elderly. ## Pain Receptors (Free Nerve Ending) - Slowly or non-adaptive receptors ### According to Mechanism of Tissue Damage * **Mechanical pain receptors** stimulated by mechanical injurious stimuli. * **Thermal pain receptors:** stimulated by extreme temperatures. * **Chemical pain receptors:** stimulated by chemical injurious stimuli. * **Polymodal:** respond to all types of stimulation. ## The Threshold of Pain - The same for all people but Reaction to pain differs from one person to another. - Through their pathways, pain fibers give branches to: - **Reticular formation** for Cortical arousal reactions. - **Limbic system** for emotional reactions, anxiety and restlessness. - **Anterior horn cells of the spinal cord** for motor reactions, flexion withdrawal reflex. - **Hypothalamus** for autonomic reactions. ### Pain Responses * **Acute pain:** sympathetic stimulation, ↑↑HR ↑↑RR and ABP ,profuse sweating. - **Saver pain:** parasympathetic, hypotension, bradycardia, GI disturbance. - **Hyperalgesia** ## Hyperalgesia (Subject Response) vs. Sensitization (Fiber Response) | Hyperalgesia (Subject Response) | Sensitization (Fiber Response) | |---|---| | Decreased pain threshold | Decreased threshold for response| | Increased pain in response to suprathreshold stimuli | Increased response to suprathreshold stimuli | | Spontaneous pain | Spontaneous activity | - **Hyperalgesia:** Pain sensation from the skin is abnormally exaggerated. Non-painful stimuli become painful in healthy skin surrounding the site of injury. ## Mechanism of Stimulation - Damaged tissues release chemical mediators of pain, including histamine, bradykinins, K⁺ and prostaglandins. ## Tissue Damage - Tissue damage creates an "inflammatory soup." - Substance P, released from nerve endings, increases capillary permeability and contributes to inflammation. - Substance P causes mast cells to release histamine, which in turn activates nociceptor endings. ## Receptors on Nociceptive Unmyelinated Nerve Terminals in the Skin * Nociceptive stimuli, such as heat, can activate some receptors directly due to transduction of the stimulus energy by receptors, for example the transient receptor potential (TRP) channel TRPV1. * This can also occur indirectly by activation of TRP channels on keratinocytes, for example TRPV3. * Nociceptors, such as mechanoreceptors, can also be activated by the release of intermediate molecules, such as ATP, ASIC, acid-sensitive ion channel, P2X, ionotropic purinoceptor, P2Y, G-protein-coupled purinergic receptor. ## Tissue Injury and Inflammation - Tissue injury and inflammation lead to the release of numerous chemicals from non-neuronal and neuronal cells, such as mast cells, macrophages, platelets, immune and endothelial cells, Schwann cells, keratinocytes, fibroblasts, and peripheral nociceptor terminals. - These mediators include protons (H+), purines (adenosine, adenosine triphosphate), nerve growth factor (NGF), cytokines such as tumor necrosis factor (TNF-a) and interleukins (IL-1ß, IL-6), leukemia inhibitory factor (LIF), prostaglandin E 2 (PGE 2), bradykinin, histamine, serotonin (5-HT), platelet activating factor (PAF), and endothelin. ## Peptidergic Neurons - Peptidergic neurons contain peptides, such as substance P [SP], calcitonin gene–related peptide [CGRP], and somatostatin [SST]. - The cell bodies of nociceptive somatic and visceral afferents are located in DRGs. - Slowly conducting Ad and C fibers, including nociceptors, have small cell bodies. ## Somatosensory Pathways ### Dorsal Column System (A) - Fine touch, pressure, proprioception. - Receptor - First-order neuron - Second-order neuron - Third-order neuron - Somatosensory cortex - Thalamus - Brain Stem - Spinal Cord - Nucleus gracilis = lower body - Nucleus cuneatus = upper body ### Anterolateral System (B) - Pain, temperature, light touch. - Receptor - First-order neuron - Second-order neuron - Third-order neuron - Somatosensory cortex - Thalamus - Brain stem - Spinal Cord ## **Diagram** - A diagram is included showing a simplified representation of the dorsal column and anterolateral somatosensory pathways. ## Ascending Sensory Tracts - **Ventral spinothalamic tract** - Crude touch - Crude pressure - Tickling & itching sensation - **Lateral spinothalamic tracts** - Pain - Temperature - **Dorsal column** - Fine touch - Tactile localization - Tactile discrimination - Stereognosis - Texture of material - Fine pressure - Vibration sense - Proprioception ## Physiological Classification of Somatic Sensation | Mechanoreceptive Sensation | Thermal Sensation | Pain Sensation | |---|---|---| | (A) Tactile Sensation | Warm | Cutaneous | | - Crude touch | Cold | Deep | | - Tickling & itching | | Visceral | | - Fine touch | | Neuropathic | | - Pressure | | | | - Vibration | | | | (B) Position Senses | | | | - Static | | | | - Kinetic | | | ## Neospinothalamic vs Paleospinothalamic Pathways | Neospinothalamic | Paleospinothalamic | |---|---| | Pathway of fast pain (Aδ) | Pathway of slow pain (C) | | Type of Afferent Nerve Fiber | | | First Order Neuron | Dorsal Root Ganglia (DRG) its axons enter the spinal cord via posterior root and end on posterior horn cells | | | Second Order Neuron | Lamina marginals (I) Cells of dorsal horn | SGR Lamina II, III | | Third Order Neuron | Axons cross to opposite side in front of central canal and ascend in lateral spinothalamic tract to brain stem | | | | Ventrobasal thalamic nuclei then to somatosensory cortex | 90% of fiber to reticular formation of brain stem to activate the whole cortex. | | | | 10% to Ventrobasal thalamic nuclei then to somatosensory cortex | ## Types of Pain Sensation <start_of_image> - **According to site of pain sensation:** - Cutaneous - Deep - Visceral - Neuropathic - **According to quality of pain sensation:** - Fast (sharp pain, pricking pain, acute pain, and electric pain). - Slow (slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain). - **According to type of pain sensation:** - Somatic pain (musculoskeletal): from skin, muscle, soft tissue. - Spasm-ischemia- intermittent claudication, trauma or injury to deep structure e.g., fracture bone - Visceral ## 1- Fast and Slow Cutaneous Pain | Fast Pain | Slow Pain | |---|---| | Felt within 0.1 sec after pain stimulus | After 1 sec | | Receptor: mechanical &thermal | All types of pain receptors | | Afferent: Aδ → glutamate | C→supstance P | | Short duration | Prolonged & increase with time | | Pathway: neospinothalamic tract | Paleospinothalamic tract | | Well localized | Poorly localized | | Occurs in skin, may in pleura, peritoneum & pericardium | Occurs in skin, deep tissues, viscera | ## 2- Deep Pain - Pain results from injury muscles and tendons, joint, ligaments and joints and it is conducted along C fibers. - **Causes:** - Ischemic pain caused by decrease blood supply to muscle due to narrowing of the vessel wall, compression on vessel wall & intravascular thrombosis. - For example: - Cardiac muscle ischemia → anginal pain. - Skeletal muscle ischemia → intermittent claudication. ## 3- Visceral Pain - Pain from internal viscera of the abdomen and pelvis. - **Causes:** - Overdistention of a hollow viscus. - Spasm of a hollow viscus, pain here due to obliteration of blood vessels or mechanical stimulation of mechanical pain receptors. - Chemical irritation by HCL in peptic ulcer. - Ischemia leads to accumulation of pain metabolites. - Inflammation of the viscera. appendicitis. - Ischemia leads to accumulation of pain metabolites. ## Characters of Visceral Pain - **Diffuse, poorly localized** due poor cortical representation of viscera and low-density innervation, rhythmic cramps (colic) due to rhythmic contraction of smooth muscles, each time a peristaltic wave travels along an overly excitable spastic organ → cramp occur. - **Referred to surface structures.** - **Associated with autonomic changes** (hypotension, bradycardia, nausea, vomiting, sweating). - **Guarding phenomenon.** ## 4- Referred Pain - **Definition:** Pain felt on a surface area originating from the same dermatome as the diseased viscus (skin area supplied by the same posterior root as the diseased viscus). - **Examples:** - Cardiac pain is felt retrosternal, epigastrium, root of the neck &inner part of left arm. - Appendix pain is felt around Umbilicus. - Gall bladder pain is felt in epigastrium & tip of right scapula. - Renal pain is felt in back, inguinal region. & testicles. ## Mechanism of Referred Pain: - **Convergence-Projection Theory:** Afferent pain fiber the skin & diseased viscus converge on the same cells of Subsantia Gelatinosa of Rolandi (SCR) which will finally activate the same cortical neuron. Whatever the source of pain, the cortex will project it to the skin as it is the commonest source of pain due to it has a large number of pain receptors and it is more exposed to the stimulation. Also, the skin is represented in the cortex while viscera are not represented. ## 5- Neuropathic Pain - **Chronic type of pain** caused by damage or pathological changes in nerve fibers in the peripheral or central nervous system. It is characterized by occurring in bouts or paroxysms. - It is described as electric, burning & shooting pain. - **Examples:** - Trigeminal neuralgia, Herpes zoster, diabetic neuropathy & phantom limb pain. ## Diagram - A diagram is used to show a simplified representation of the convergence-projection theory of referred pain. - The page contains additional diagrams/illustrations that were not converted into markdown.