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 pathways PAIN PATHWAYS (first, second and third order ) 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 which lie in the vertebral  3. Peripheral transmission foramina at each spinal cord level. Each neuron  4. Spinal transmission has a single 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 . The first order neurons in the ganglia (head) reach the brainstem and specific or wide dynamic range (WDR) 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 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 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 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, <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 can aggravate or precipitate myocardial ischemia

ACUTE PAIN: SYSTEMIC RESONSE ACUTE PAIN: SYSTEMIC RESPONSE  GASTROINTESTINAL & URINARY:  Enhanced sympathetic tone increases  RESPIRATORY: Increase in total body O2 sphincter tone and decreases intestinal and consumption and CO2 production increases urinary motility, promoting ileus and urinary minute ventilation retention  Hyper-secretion of gastric acid promotes stress ulceration, together with deceased motility, predisposes the patients to severe aspiration pneumonitis ACUTE PAIN: SYSTEMIC ACUTE PAIN: SYSTEMIC RESPONSE RESPONSE  Endocrine: increase in catabolic hormones  IMMUNE : Produces leukocytosis with (catecholamines, cortisol, and glucagon) and lymphopenia, predisposes patients to decrease in anabolic hormones (insulin and infection testosterone)  HEMATOLOGIC: Increases in platelet  Develops a negative nitrogen balance, adhesiveness, reduced fibrinolysis, and carbohydrate intolerance and increased lipolysis hypercoagulability  Increase in cortisol with increase in  PERCEPTION: Anxiety, sleep disturbance—if renin,aldosterone,angiotensin, and duration of pain is prolonged depression and antidiuretic hormone results in NA retention anger and water retention

ACUTE PAIN: SYSTEMIC RESPONSE  MODERATE TO SEVERE ACUTE PAIN, REGARDLESS OF SITE, CAN AFFECT NEARLY EVERY ORGAN FUNCTION AND MAY ADVERSLY INFLUENCE POSTOPRATIVE MORBIDITY AND MORTALITY

CHRONIC PAIN CHRONIC PAIN

 Chronic pain is defined as that which persists  Patients with chronic pain often have an beyond the usual course of an acute disease attenuated or absent neuroendocrine or after a reasonable time for healing to response occur.  Psychological mechanisms, sleep and  This period varies between 1-6 months affective disturbances  Chronic pain may be nociceptive,  Neuropathic pain classically spontaneous, has neuropathic, or a combination of both a burning sensation, and is associated with hyperpathia CHRONIC PAIN CHRONIC PAIN

 COMMON FORMS: Musculoskeletal  Peripheral-central and central mechanisms for chronic disorders, chronic visceral disorders, lesions pain of the peripheral nerves, nerve roots, dorsal  1. Spontaneous self-sustaining neuronal activity in the primary afferent neuron (neuroma) root ganglia , phantom limb pain, lesions of  2. Marked mechanosensitivity associated with chronic the central (stroke, spinal nerve compression cord injury, multiple sclerosis) and cancers 3. Short circuits between pain fibers, following invading the nervous system demyelination, activating nociceptors by nonnoxious stimuli  4. Reorganization of receptor fields in the dorsal horn neurons

CHRONIC PAIN CHRONIC PAIN

 5. Spontaneous electrical activity in the  Treatment includes a wide variety of blocks, dorsal horn cells or thalamic nuclei COX inhibitors, opioids, antidepressants,  6. Release of segmental inhibition in the neuroleptic agents, anticonvulsants, spinal cord corticosteroids and systemic local anesthetics  7. Loss of descending inhibitory influences that are dependent on normal sensory input  8. Lesions of the thalamus or other supraspinal structures References

 http://www.youtube.com/watch?v=n2Jzt3zd8  http://www.youtube.com/watch?v=n2Jzt3zd8 vQ vQ  Nagelhout, J., & Plaus, K. (2010) Nurse anesthesia (4 th ed.). St. Louis: Elsevier. Stoelting, R., & Miller, R. (2007). Basics of anesthesia (5 th ed.). Philadelphia: Elsevier.