Objectives 1. Recognize the pain pathways from peripheral stimulus to supraspinal processing. NURSE ANESTHESIOLOGY PROGRAM FLORIDA INTERNATIONAL UNIVERSITY 2. Understand the differences between pain fibers. LINDA WUNDER, CRNA MSN 3. Discuss pain modulation from supraspinal processing to substantia gelantinosa. 4. Explain the physiology of nociception. Pain is conducted along three neuron pathways PAIN PATHWAYS (first, second and third order neurons) that transmit noxious stimuli from the periphery to 1. Peripheral stimulus the cerebral cortex. 2. Receptor (transduction) Primary afferent neurons are located in the dorsal root ganglion which lie in the vertebral 3. Peripheral transmission foramina at each spinal cord level. Each neuron 4. Spinal transmission has a single axon that bifurcates, sending one 5. Ascending tracts end to the peripheral tissues it innervates and 6. Supraspinal processing the other into the dorsal horn of the spinal cord. PAIN PATHWAYS PAIN PATHWAYS First order neurons Second order neurons The majority, enter the dorsal spinal root at each Spinal cord gray matter is divided by Rexed cervical, thoracic, lumbar, and sacral level into 10 lamina Pain fibers originating in the head are carried by First six makeup the dorsal horn, receive all the trigeminal (V), facial (VII), glossopharyngeal afferent neural activity, represent the (IX), and vagal (X) principle site for modulation of pain Each have specific ganglion which hold cell Second order neurons are either nociceptive- bodies of these nerves. The first order neurons in the ganglia (head) reach the brainstem and specific or wide dynamic range (WDR) synapse with the second order neuron PAIN PATHWAYS PAIN PATHWAYS Lamina I responds to nociceptive stimuli from cutaneous Spinothalamic tract and deep somatic tissues Cross the midline to the level of origin to the Lamina II (substancia gelatinosa), contains many contralateral side of the spinal cord interneurons responsible for processing and modulating nociceptive input from cutaneous tissue. Major site of Divided into lateral and medial action for opoids Lateral spinothalmic tract projects— Lamina VII contains preganglionic sympathetic neurons location,density,duration of pain in the ventral Lamina V and I contains visceral afferents posteriorlateral nucleus of the thalamus Lamina V responds to both noxious and non noxious Medial spinothalamic tract projects—unpleasant stimuli and receives both somatic and visceral inputs emotional perception of pain in the medial Thus referred pain thalamus PAIN PATHWAYS PAIN PATHWAYS Spinalreticular pain pathway- arousal and THIRD ORDER NEURONS autonomic responses to pain Located in the thalamus Spinalmesencephalic--anti-nociceptive Send fibers to the somatosensory areas I and descending pathways because of its II in the post central gyrus of the parietal projections in the periductal gray area cortex and superior wall of the sylvian fissure AFFERENT NERVE FIBERS A and B fibers are mylinated Fiber Group Innervation Mean Mean A delta fibers are fast, sharp well-localized Diameter Velocity µm m/sec sensation A A are further defined as alpha, beta, gamma, and alpha Muscle spindle motor to skeletal 15 100 Beta Touch & pressure afferents 8 50 delta gamma Motor to muscle spindle 6 20 C fibers are nonmylinated delta Mechanoreceptors, nociceptors <3 15 B Sympathetic preganglionic 3 7 C fibers slow poorly localized C Mechanoreceptors, nociceptors, 1 1 The classification of these fibers are based on sympathetic post ganglionic diameter and velocity of conduction Each innervation provides a specific function PHYSIOLOGY OF NOCICEPTION Free nerve endings sense heat, mechanical, and chemical damage Mechanonociceptors– respond to pinch and pinprick Silent nociceptors—respond to inflammation Ploymodal mechoheat nociceptors—respond to heat and pressure PHYSIOLOGY OF NOCICEPTION PHYSIOLOGY OF NOCICEPTION ALOGENS—include bradykinin, Visceral organs—silent nociceptors histamine,serontonin,5-HT,histmine, Nociceptive C fibers travel from the serontonin, H+, K+, some prostaglandins, and esophagus, larynx, and trachea with the possibly ATP vagus nerve to enter the nucleus solitarius in Somatic nociceptors included muscle tendon, the brainstem fascia, bone Cornea and tooth pulp and innervated by A delta and C fibers CHEMICAL MEDIATORS OF PAIN PERIPHERAL MODULATION OF PAIN 1.Substance P—released by first order neurons Release of alogens from damage tissues both peripherally and in the dorsal horn Facilitates transmission in pain pathways via NK- Histamine from mast cells, basophils,platlets 1 receptor activation Serontonin from mast cells, platlets Sends collaterals to blood vessels, sweat glands, hair, mast cells in the dermis Factor XII allows the release of bradykinin Degranulates histamine and serotonin from Phospholiase A2 on phospholipids produce platelets, is a vasodilator,chemoreactor for prostaglandins and form arachidonic acid and leukocytes the cascade begins Innervates the viscera—post ganglionic sympathetic discharge PERIPHERAL MODUL ATION OF PAIN Cyclooxygenase coverts arachidonic acid to prostacyclin and PGE2 This potentiates the edema from bradykinin Lipoxygenase pathway converts AA into leukotrienes ASA and NSAID inhibit cyclooxygenase Corticosteriods inhibit prostaglandin production through blockage of phospholipase A2 activation CENTRAL MODULATION NEUROCHEMICAL MEDIATORS 1. Wind up and sensitization of second order sP, CGRP,cholecystokinin, angiotensin, neurons—increase frequency of repetitive galanin, L-glutamate, L-aspirate: interact prolong discharge even after C fibers input with G protein-coupled membrane receptors has stopped on neurons. 2. Receptor field expansion—Dorsal horn This starts the process that increases neurons increase their receptive fields to become more responsive to stimuli (noxious intracellular calcium or not) 3. Hyperexcitability of flexion reflexes. NEUROCHEMICAL MEDIATORS MODULATION OF PAIN Impulses arising in the periventricular/periaquaiductal gray matter of Glutamine and asparate wind-up activation of the brainstem are transmitted through the raphe magnus to the NMDA and non-NMDA receptors—this substantia gelatinosa by way of the descending dorsolateral funiculus. increases intracellular calcium in spinal Action potentials arriving at the substantia gelantinosa activate neurons and activates phospholiapaseA2 enkephalin neurons. The release of enkephalin decreases the release of substance P, thereby reducing the number of pain impulses Then to arachidonic acid and the cascade ascending in the lateral spinothalamic tract. Also, action potentials descending in the dorsolateral funiculus hyperpolarize cell bodies of begins the second neurons in the pain pathway, thereby decreasing the number of action potentials in the ascending lateral spinothalamic tract. The descending dorsolateral modulates pain. MODULATION OF PAIN MODULATION OF PAIN Intravenous opioids produce analgesia in part by initiating action potentials in the descending dorsolateral funiculus. Spinal analgesia, mediated by mu-2 receptors, occurs when the number of pain impulses passing through the substantia gelantinosa is decreased. Intravenous opioids act in other sites in the brain(limbic system,hypothalamus,and thalamus) produce supra spinal analgesia is mediated primarily by mu-1 receptors Opioids act in a complex fashion to decrease the perception of pain and decrease the response to pain MODULATION OF PAIN MODULATION OF PAIN PREEMPTIVE ANALGESIA ACUTE PAIN Induces an effective analgesic state prior to Defined as that which is caused by noxious surgical trauma stimulation due to injury, a disease process, By: infiltration of site with local anesthetic, or abnormal function of muscle or viscera. It central neural blockade, administration of is nearly always nociceptive. effective opioids, NSAIDs, or ketamine Two types of acute pain: somatic and visceral This attenuates peripheral and central sensitization to pain The use of preemptive analgesia may reduce the postoperative analgesic requirements ACUTE PAIN: SOMATIC ACUTE PAIN: VISCERAL Disease process or abnormal function of an internal organ or its Superficial somatic -skin, subcutaneous, covering (eg, parietal pleura, pericardium, or peritoneum). mucous membranes Four types: true localized visceral, true localized parietal, referred visceral, referred parietal Well localized-sharp, pricking, throbbing, True visceral is dull, diffuse, midline and is associated with abnormal burning sympathetic or parasympathetic activity (N/V, sweating, changes in B/P and HR ) True parietal is sharp and localized Referred-disease process involving the peritoneum or pleura over Deep somatic – muscles, tendons, joints, the central diaphragm is referred to the neck and shoulder whereas bones disease affecting the parietal surfaces of the peripheral diaphragm is referred to the chest or upper abdominal wall Less well localized, dull, aching ACUTE PAIN: SYSTEMIC ACUTE PAIN: SYSTEMIC RESPONSE RESPONSE Sympathetic activation increases efferent CARDIOVASCULAR: hypertension, sympathetic tone to all viscera and releases tachycardia, enhanced myocardial irritability, catecholamines from the adrenal medulla. increased SVR The hormonal response results from Increased CO, may be decrease with increased sympathetic tone and patients who have compromised ventricular hypothalamically mediated reflexes function Increased myocardial oxygen demand, therefore, pain