NRAN 80526 Pain.pptx

Pain NRAN 80526 Casey Crow DNP, CRNA Objectives Define pain Nociceptive vs non-nociceptive Define chronic pain Describe pain physiology: transduction, transmission, perception, modulation Describe pain pathophysiology Define types of chronic pain: psychopathic, nociceptive...

Pain NRAN 80526 Casey Crow DNP, CRNA Objectives Define pain Nociceptive vs non-nociceptive Define chronic pain Describe pain physiology: transduction, transmission, perception, modulation Describe pain pathophysiology Define types of chronic pain: psychopathic, nociceptive, neuropathic, post surgical pain syndrome, wind-up Distinguish types of neuropathic pain, specifically CRPS Type I and Type II Objectives Distinguish neuropathic pain from nociceptive pain Describe pharmacology for the patient with chronic pain Describe anesthetic management of a patient with chronic pain: perioperatively Describe multimodal analgesia Describe the CRNAs role in advanced pain management Some questions How can inadequate postop pain affect patients? What is peripheral and central sensitization? How can preventive analgesia be successful? How can the risk of opioid-related respiratory depression be decreased? Which drugs inhibit COX 1 and 2? What is the mechanism of action? What are considerations for the opioid-dependent patient? Some more questions Which fibers transmit nociceptive information to the spinal cord from their free nerve endings? What are non-opioid drugs used for neuropathic pain syndromes? What are the 2 types of CRPS? What are the differences? What are the types of nociceptive pain? What is nonnociceptive pain? What is the process of pain physiology? What is wind-up? Pain Stats Estimated 50 million adults suffer from chronic pain 19.6 million of those: high-impact chronic pain Limits quality of life and work activities Opioid crisis Challenge: alleviating pain, reducing opioid misuse/abuse CRNAs: experts in area of pain management “Fifth vital sign” 1990s Why is pain management important? High pain levels Chronic pain patients Delirium Opioid tolerance Chronic pain Opioid induced syndrome hyperalgesia Increased hospital Central sensitization stay Psychiatric conditions Low patient Implants/devices satisfaction Increased opioid use Pain Physiologic “an unpleasant Emotional sensory and Behavioral emotional Acute vs Chronic experience Based on longevity associated with Nociceptive or non-nociceptiveactual or potential tissue Underlying pathophysiology damage or described in Nociceptive vs Nonnociceptive Nociceptive: stimulation of specific nociceptors Somatic: identifiable locus as a result of tissue damage Releases of chemicals from injured cells that mediate pain Well localized, sharp, hurts at point of stimulus Visceral: diffuses, referred to another area Vague: dull, cramping, squeezing Associated with distension of organ or obstruction Accompanied with autonomic reflexes: nausea, vomiting, diarrhea Nociceptive vs Nonnociceptive Nonnociceptive: neuropathic Damage to peripheral or central neural structures Abnormal processing of painful stimuli Dysfunction of the CNS: spontaneous excitation Burning, tingling, shock-like Inflammatory pain: sensitization of the nociceptive pathway from multiple mediators being released at the site of tissue inflammation without neural injury Neuropathic Pain v Nociceptive Pain 3 differences Neuropathic Pain Nociceptive Pain Pain persistent Pain improves Inflammation continues Inflammation resolves even with evidence of wound healing Allodynia No allodynia NSAIDs inadequate NSAIDS effective Chronic Pain Persistent pain Damage nervous system Decreased productivity Physical and psychological disabilities Definition: persistent pain, associated with a distinct period of uninterrupted pain of 3 months or more, that includes a negative sensory and emotional experience Time frame: usually 2-6 months Complex phenomenon Inflammatory, neuropathic, psychogenic Pain Stimulation 3 subdivisions Painful stimulation without tissue damage Elicits withdrawal from the stimulation, then terminated Tissue damage without nerve damage Pain persists after removal of the stimulus Sensation spread to local area of injury Protect the body and promotes healing Body’s physiologic response: release K, RBC, WBC, CF< PGs, inflammatory substances Nerve damage Disease state that invades damaged nerves Trauma to tissue involving nerve fibers Unintentional transection of a nerve Demyelinating or axonal injury Pain Stimulation Pain Pain elicits a normal response to withdrawal Purpose: activation of neurotransmission: recognizes injury, limits further damage Transmission of sensory impulses through afferent peripheral nervous system to the spinal nervous system, to the perceptive centers of the brain A delta and C nociceptive fibers Produce action potentials Mediated by release of substance P and excitatory amino acids Afferent nervous system to dorsal horn of the spinal cord Inhibitory mechanism: modulates sensation and response If simulation is sufficient to overcome the inhibitory mechanism, the sensory information proceeds to the pain perception centers in the brain Information elicits a motor response to pain Additionally: experience, expectation and mood Purpose of Pain Chronic pain: trigger inappropriate activation of neuropeptides in the spinal nerve pathways creating negative consequences NMDA → Normal conditions: inactive due to magnesium stability Pathologic chronic pain: displacement of magnesium, NMDA receptor activation and exaggerated release of Sub P and excitatory amino acids Pain Physiology 4 processes Transduction Transmission Perception Modulation Transmission AP transmitted from periphery to the CNS 2 primary afferent nerves A delta fibers C fibers Impulse travels along afferent peripheral nerve fibers to the dorsal horn of the spinal cord Synapse with 2nd order neurons Cross the spinal cord Ascent to the thalamus and brainstem Relayed to other areas of the brain Transmission A delta fibers C fibers Fast Slow Myelinated Unmyelinated Thin A beta fibers Heavily myelinated Large diameter Innocuous or low-threshold mechanical stimulation Transduction Transformation of a noxious stimuli into an AP Nociceptors detect noxious stimuli Peripheral nociceptors conduct noxious stimuli to dorsal horn of spinal cord A delta: myelinated, primary afferent neurons, fast-sharp pain Alert of tissue damage C fibers: smaller, nonmyelinated, mechanical, thermal, chemical injuries, polymodal fibers Transduction Release of chemical mediators from inflammatory response Release of neurotransmitters from nociceptive nerve endings Sub P, glutamate, bradykinin, histamine, serotonin, prostaglandins, cytokines, calcitonin gene-related peptide Causes depolarization and repolarization, action potential results, pain impulse is generated Transduction Noxious stimuli is converted into an electrical impulse: action potential (AP) Occurs at nociceptors: pain nerves Release of neurochemicals activate or sensitize nearby nociceptors Primary treatment of pain Reduce transduction through inhibition of chemicals released during painful Perception Potential or actual tissue trauma is recognized as pain by a conscious person Type, intensity, bodily local discriminated by the brain Emotional component influences future behavioral response Modulation Input from brainstem influences central transmission in spinal cord Inhibition of painful perception Release of neurotransmitters: serotonin, norepinephrine, endogenous opioids Pain Pathophysiology Pain is not localized to 1 region 3 anatomic regions: peripheral, spinal, and cerebral Extended period of time can lead to dysfunctional changes in these areas May become irreversible Basis for chronic pain Dysfunction in any of these areas Removal of stimuli is insufficient Inhibitory mechanism are ineffective Perceptive function is altered Must address all areas of pain physiology Pain Pathophysiology Addressing and removing the cause of pain Assist the peripheral system with blockade of noxious stimulation Facilitate a return to balance in spinal ascending inhibitory system Normalize the forebrain’s perception of stimulation Pain Pathophysiology Effect on all systems in the body Pain causes/contributes to other disease processes CV: tachycardia, HTN Pulm: respiratory depression Renal failure Obesity Liver failure Thrombosis: DVT, PEs Types of Chronic Pain Psychogenic: pain without identified physical cause All pain has a psychological component Nociceptive: inflammatory Neuropathic: caused by a disease, lesion, or damage to somatosensory nervous system Chronic Postsurgical Pain: persistent post- surgical pain Wind-Up: evolution of chronic pain Types of Chronic Pain Nociceptive Peripheral and CNS: local and systemic Protective mechanism Begins a sensory response through the peripheral and CNS to create perception of pain and trigger further protective mechanisms Localized response: inflammatory mediators, capillary vasodilation, smooth muscle contraction, synaptic transmission of pain impulse to CNS Histamine, bradykinin, substance P Neural process that translates and processes injurious stimuli to something the brain can understand  Inflammation and peripheral nociception Figure 56.1 Types of Chronic Pain Neuropathic Caused by a disease, lesion, or damage to somatosensory nervous system Innervation of the skin, muscles, joints and tissue facias Perception of touch, temperature, pan, pressure, movement, position, vibration Sensory receptors: chemo-, mechanico-, nocio-, thermo- Send signals to spinal cord and then to brain for sensory processing Radiate within the somatosensory nervous system Abnormal sensations: dysesthesia, allodynia Allodynia: triggering of pain response from stimuli that do not normally provoke pain Burning sensation with small changes in temp or light touch Neuropathic Changes in Na and Ca channel subunit expression Functional changes Redistribution and alteration of subunit compositions of Na and Ca channels Spontaneous firing at ectopic sites along the sensory pathway Neuropathic Less responsive to analgesics than somatic or visceral pain No single disease process explanation No single site of damage, injury, dysfunction Aberrant somatosensory processing Abnormal neural activity in peripheral nerves and/or CNS Neuropathic Pain Syndromes Herpes Zoster and Postherpetic Neuralgia Diabetic Painful Neuropathy Complex Regional Pain Syndrome HIV neuropathy Phantom Pain Amputation Pain Radiculopathies Alcoholism Injury/degeneration: MS, neuromas Neuropathic Pain Syndromes Complex Regional Pain Syndrome (CRPS) 2 Types: I and II I: reflex sympathetic dystrophy (RSD) II: causalgia Risk factors: previous trauma, nerve injury (causalgia), previous surgery, work-related injuries, females S/S: spontaneous pain, hyperalgesia, allodynia, trophic, sudomotor, vasomotor abnormalities, active and passive movement disorders Preceding nerve injury in CRPS II CRPS Pathophysiology CRPS: increased proinflammatory cytokines Release of inflammatory mediators: pain and allodynia Central sensitization: questionable Increased activity in nociceptive afferents due to peripheral noxious stimuli, tissue damage, or nerve injury Increased synaptic transmission of somatosensory neurons in dorsal horn of spinal cord SNS overactivity Catecholamine hypersensitivity, formation of reflex arc Arc follows SNS modulated by cortical centers producing peripheral vascular disturbances CRPS CRPS Diagnosis 2 of 4 categories Sensory: evidence to hyperalgesia or allodynia Vasomotor: evidence of temperature asymmetry (>1 degree C) and or skin color changes and or asymmetry Sudomotor/edema: evidence of edema or sweating changes and or sweating asymmetry Motor/trophic: evidence of decreased range of motion and or motor dysfunction and or trophic changes Motor: weakness, tremor, dystonia Trophic: hair, skin, nails Autonomic and trophic changes CRPS Treatment Corticosteroids Sympathetic nerve blocks PT CRPS that does not respond to nerve Gabapentin blocks, PT, and or NMDA antagonist pharmacologic IM/SC calcitonin management, may TCAs respond to spinal Beta blockers cord stimulator Clonidine Spinal cord stimulator Types of Chronic Pain Chronic Postsurgical Pain (CPSP) Reasons for CPSP nonconclusive Long term synaptic plasticity with the brain “persistent pain state that is apparent more than 2 months postoperatively that cannot be explained by other causes such as recurrence of disease, apparent inflammation, or others” Neuropathic in nature, not always associated with an identifiable nerve injury 1 in 4 surgical patients receive adequate relief of acute pain CPSP Predictors: Type of surgeries Thoracotomy, thoracic penetration: mastectomy, thoracotomy, cholecystectomy, nephrectomy, sternotomy, chest and upper abdominal procedures Amputation and inguinal surgical procedures Preop pain Others: thyroid function, occult wound infection, psychological, young age, immunosuppressant therapy Prevention: regional anesthesia, preop anti- inflammatories, anti hyperalgesia meds, antidepressants, short term opioid use, anticonvulsants, NMDA antagonists Types of Chronic Pain Wind-up Evolution of chronic pain Repetitive stimulation from chronic inflammation or nerve damage Dorsal horn neurons progressively transmitting increasing number of pain impulses Prevention is critical Address patient symptoms and focus on treatment of underlying cause of pain False labels: drug seeker, chronic complainer, crazy Not a psychological condition, can lead to psychological dysfunction Wind-Up Chronic repetitive stimulation Increased Hyperalgesi cellular a calcium Overwhelmed inhibitory neuropathways from Increased chronic discharge of Release of neurologic pathway neurons inflammator y substances excitability Synthesis of prostaglandi Cyclooxygen ns Reduction ase in production neuropathw ay inhibition Wind-Up Neuronal plasticity transforms The capacity of neurons to change their function, chemical profile or structure at the level of the receptors, spinal cord and brain Leads to changes in somatosensory system Loss of GABA and glycine inhibition Glutamate releases- activation of NMDA receptors Wind-Up Glutamate: neurotransmitter Activates AMPA/kinate receptors NMDA receptors Accumulates Displaces Mg, with Sub P Mg normally blocks NMDA receptor Without Mg, NMDA not blocked Wind-Up Goals: Remove primary stimulus: periphery Improve the function of inhibitory mechanisms: central spinal area Manage psychological impact of pain: prefrontal cerebral area Address each area of pain physiology Wind-Up New Receptor Upregulation of pain receptors Irreversible Treatment of Chronic Pain Local anesthetics, Block Na channels, inhibit production antiepileptics of AP Bind presynaptically in dorsal horn, Opioids decrease NT release, glutamate Peripheral and spinal Interfere propagation of AP to CNS nerve blocks Epidural and intrathecal Pre and post synaptic inhibition at analgesics dorsal horn neurons Cognitive-behavioral Distraction, relaxation techniques Antidepressants, SC stimulation, epidural Modulation of pain perception intrathecal drug delivery systems Pharmacology NSAIDS Acetaminophen Opioids Antidepressants Anticonvulsants NMDA receptor agonists Others NSAIDS Anti-inflammatory and analgesic COX inhibitors: prevent synthesis of prostaglandins from arachidonic acid Arachidonic Acid: present in cellular tissue and released when injured Prostaglandins: vasodilation, erythema, edema, fever, nociceptor sensitization Long term effects: nephrotoxicity, thrombotic events, peptic ulceration, bleeding COX1 and COX2: nonselective vs selective Cyclooxygenase Activity, Table 57.1 COX-1 Activity COX-2 Activity Hemostasis Inflammatory response Fever Pain sensation Anticoagulation Modulation of cell proliferation COX-1 Benefits COX-2 Benefits Possible reduced neuroinflammation targeted Reduced inflammation at microglia Reduced fever Cardioprotective anticoagulation Reduced pain sensation Possible cancer progression reduction COX-1 Inhibition Risks COX-2 Inhibition Risks Bleeding Increased risk of thrombotic Increased risk of gastric irritation and ulcers activity Acetaminophen Not an NSAID: lacks anti-inflammatory properties Inhibit COX activity centrally, not peripherally Reduction of nociceptor activity centrally Safe for patients with hematologic or cardiovascular problems Caution: liver failure Used in many combo-drugs Opioids CNS, not peripherally acting Short term relief of operative and traumatic injury Bind to opioid receptors in CNS that inhibit nociception Mu, Kappa, Delta Inadequate long term solution for chronic pain Does not treat the source of pain Substantial negative side effects Addictive and dependent Dosing strategies: nonopioid drugs to address side effects, rotation of opioids Antidepressants Pain perception: chemically mediated event Improve mood, increase treatment compliance, reduce opioid use Block neuronal reuptake of serotonin and NE in CNS SNRI: seem to be the most advantageous Less side effects, effective in treatment of chronic pain Rejected by patients: label pain as psychological Antidepressants Anesthetic considerations Cause sedation Enzyme induction: anticipate increased anesthetic needs Heart block: hypotensive effects, prolonged PR, widened QRS Bleeding risk: reduced serotonin can cause decreased platelet aggregation Anticholinergic effects Do not need to be discontinued prior to surgery Anticonvulsants Block Na channels GABA agonist, glutamate antagonist Block Ca channels Sedation, anxiolysis, muscle relaxation More efficacious for specific neuropathic pain than chronic nociceptive pain Gabapentin, pregabalin Diabetic neuropathic pain, fibromyalgia, postherpetic neuralgia, trigeminal neuralgia Take as close to schedule as possible If abruptly stopped, can seize even if they have never had a seizure Additional Options Muscle relaxants: short term symptomatic relief of muscle spasms Topical anesthetics: NSAIDs and anesthetics May help restore normal peripheral nociceptive inhibitory systems Local anesthetics: depresses action potential and stabilizes membrane GABA agonists: sedation, anxiolysis, anticonvulsant, muscle relaxation Benzodiazepines: anxiolysis, sedation and skeletal muscle relaxation Additional Options Sleep aids: cellular regulation and regeneration Cannabinoids: conflicting data, may be effective for chronic pain patients who are opioid tolerant Buprenorphine-naloxone: more effective for patients without opioid dependence or addiction Buprenorphine Therapy Partial mu receptor agonist Kappa and delta receptor antagonist Ceiling effect on respiratory depression Respiratory depression can still occur: reduced respiratory reserve, benzos, CNS depressants No ceiling for analgesia High receptor affinity, slow dissociation Buprenorphine-naloxone combo Uncontrolled postop pain Displaces opioid agonist from receptor Long half life Buprenorphine Therapy Treatment plan: 2 options Discontinue prior to surgery Delay surgery to allow for adequate taper, opioid abuse relapse, overdose Continue prior to surgery Majority recommendation Higher doses of short acting opioids may be required Multimodal analgesia, regional anesthesia, nonpharmacologic interventions Buprenorphine Therapy  Multimodal Treatment Options for Chronic Pain Table 57.5 Management Modalities Types Medications Anti-inflammatory NSAIDS Muscle relaxants Opioids Neuropathic Anticonvulsants, TCA, SSRI SNRI NMDA antagonist Alpha 2 agonist Topical Rehabilitation Physical therapy Occupational therapy TENS Bracing Interventional Epidural injections Facet joint injections Peripheral nerve blocks Major joint/bursa injection Implantable Spinal cord stimulator Targeted Pain Management Interventional treatments: special techniques, equipment, implanted devices and injections to diagnosis and treat pain- related disorders Treat inflammatory process: injection of anti- inflammatories and analgesics Goals: improve sensory and motor function, promote healing, reset inhibitory pathways and processes that were damaged by chronic pain dysfunction Targeted Pain Management Injections Nerve blocks Radiofrequency and cryoablation Sympathetic blocks Implantable devices: spinal cord stimulator TENS: nonpainful stimulation that competes with nociceptor fibers in dorsal horn, inhibition of painful sensory perceptions Intrathecal drug delivery systems Anesthesia for Chronic Pain Preop Is the patient opioid-dependent? Current opioid use: dose and type Continue preoperatively Is the patient managed by a pain-management team? Consult if indicated Current medications? Multimodal approach Discuss with patient pain management goals and plan Anesthesia for Chronic Pain Preop Opioids: adequate doses need to be maintained to avoid withdrawal symptoms Continuation of opioid on day of surgery Opioid-dependent: increased opioid requirement to be 30-100% greater than opioid-naïve patient Methadone: continue baseline dose throughout perioperative course >200 mg/day: prolongation of QT interval Baseline EKG, risk of Torsades de pointe Opioid agonist/antagonist: continue, may need increased dose Avoid partial agonist/antagonist and full antagonist if opioid dependent patient: withdrawal Preventive Analgesia Method to prevent or attenuate sensitization of nerve fibers and inflammation Various analgesics given before surgery Consider the entire perioperative period Preventive Analgesia Sample Considerations Tylenol: 1000 mg Patient OxyContin: 10 mg Home meds Lyrica: 75-150 mg Surgery Celebrex: 200-400 Timing mg Flexeril: 10mg Level of Scopolamine patch consciousness Valium: 5-10 mg Anesthesia for Chronic Pain Intraoperative Continuation of baseline opioid Increase intraop opioid due to tolerance Titration of opioids HR BP Pupillary size Respiratory rate and depth Consider alternative opioid Multimodal analgesia Anesthesia for Chronic Pain Postoperative Multimodal continuation Regional anesthesia PCA Monitor and assess pain/analgesia Nonpharmacologic comfort measures Multimodal Analgesia Ketamine Magnesium Lidocaine Dexmedetomidin Opioid Sparing e Techniques Additional drugs: Does not mean Acetaminophen opioids are not Ketorolac administered Methocarbamol McLott Mix Ketamine NMDA receptors: involved in wind-up and development of chronic pain NMDA receptors support synaptic plasticity, CNS pain processing, and modulation of central pain sensitization induced by incision and tissue damage Ketamine Reverses central sensitization and enhances descending modulatory pathways Indications: chronic postsurgical pain, OIH, opioid tolerant, sleep apnea Contraindications: pregnancy, active psychosis, poorly controlled CV disease, severe liver disease Ketamine: NMDA receptor antagonist Low dose (0.1-0.5 mg/kg) adjunct to general anesthesia Reduction in postoperative opioid requirements Reduction in nausea, postop analgesia Hallucinations and vivid dreams not reported Ketamine Magnesium Blocking calcium channels: regulation of calcium influx into the cell Antagonism of NMDA receptors in CNS Binds to different receptor than ketamine Super additive effect: used together to enhance analgesic effect Modulates pian and inflammatory responses Reduces central sensitization to peripheral injury Prevents development of hyperalgesia Reduction in pain scores Reduction in analgesic consumption Magnesium Bolus: 30-50 mg/kg 10- 15 prior or shortly after induction Infusion: 6-25 mg/kg/hr Magnesium Side effects/toxicity Lidocaine Na channel blockade Benefits: reduction in pain, nausea, ileus duration, opioid requirement, length of hospital stay Exceeds half life by more than 5 times, 8-24 hours Secondary to a modulation of inflammatory signals Inhibits NMDA receptors and calcium channels Inhibits polymorphonuclear granulocytes: release of proinflammatory cytokines and reactive oxygen species Suppression of wide dynamic range neurons, inhibition of C fibers Avoid toxic levels Visual disturbances, dizziness, cardiac dysrhythmias, neurologic changes Lidocaine 2 mg/kg/hour Dexmedetomidine Alpha 2 adrenergic receptor agonists High affinity, high selectivity Centrally acting Sedative, anxiolytic, analgesic properties Blunts central sympathetic response Additional benefits Lessens postoperative shivering Minimal respiratory depression Hemodynamic stability Short duration of action Sedation: procedures, mechanical ventilation, general anesthesia adjunct Additional Meds Acetaminophen: 15 mg/kg or 1 g IVPB over 15 min Opioid sparing effect Decreases postop nausea and vomiting Caution: liver failure Ketorolac: 15-30 mg IV Ask surgeon, bleeding risk Caution: renal dysfunction, geriatrics, received PO NSAID or COX2 inhibitor preop Report to PACU Methocarbamol: 50-1000 mg IV CNS depressant with sedative and skeletal muscle relaxant effects Caution: seizure disorders, geriatrics, renal dysfunction McLott Mix Opioid-free anesthesia: the next fr ontier in surgical patient safety - P MC (nih.gov) McLott Mix CRNA roles in Nonsurgical Pain Management Advanced Pain Management Fellowship at TCU Director: Jackie Rowles, DNP, MBA, MA, CRNA, ANP-BC, NSPM-C, FNP, FAANA, FAAN Subspecialty, separate distinction from anesthesia Physical assessment, diagnosis, treatment plan development, consultation CRNA roles in Nonsurgical Pain Management Conditions Treated Spinal mediated pain Joint pain Myofascial pain Malignancy Post-traumatic pain Bone pain Nerve pain Headaches Treatment goals: reduction, relief, healing References Clinical Anesthesia 8th Edition – Barash Nurse Anesthesia 7th Edition – Nagelhout Anesthesia and Co-Existing Disease 8th Edition - Stoelting Perioperative Magnesium for Postoperative Analgesia: An Umbrella R eview of Systematic Reviews and Updated Meta-Analysis of Randomi zed Controlled Trials - PMC (nih.gov) “Oh Mg!” Magnesium: A Powerful Tool in the Perioperative Setting (a sra.com) Opioid-free anesthesia: the next frontier in surgical patient safety - P MC (nih.gov) McLott Mix - McLott Mix Some answers Inadequate pain relief has adverse physiologic effects and can contribute to morbidity and mortality as well as delay of recovery and return to daily activities. Neuroplastic changes in the nervous system occur due to tissue injury and leads to sensitization. The analgesic depth, technique and duration of analgesia must be extensive and include both surgical and postsurgical periods. Respiratory depression can be decreased by using opioid-sparing multimodal pharmacotherapy, regional anesthesia, and continuous monitoring of the patient with pulse ox and capnography. NSAIDS inhibit COX 1 and 2 which converts arachidonic acid to prostaglandins. Opioid dependent patients require a multimodal approach, regional anesthesia, nonopioid analgesics and opioid analgesics. An adequate dose of opioid needs to be maintained to avoid precipitating withdrawal symptoms. Some more answers A delta and C fibers are nociceptor pain transmitters. A beta fibers normally transmit non-noxious information but also participate in nociceptive transmission. Antidepressants and anticonvulsants are effective for the treatment of neuropathic pain syndromes. Anticonvulsants are first line treatment due to their favorable side-effect profile and speed of therapeutic effect. Regional sympathetic dystrophy (I) and causalgia (II) are the 2 types of CRPS. Type I is more difficult to diagnose as there is no evidence of peripheral nerve injury. There is preceding nerve injury in CRPS II. Somatic and visceral pain are forms of nociceptive pain due to stimulation of specific nociceptors. Neuropathic pain is nonnociceptive pain due to peripheral or central neural structures. Transduction, transmission, perception and modulation describes pain physiology. Wind up results from chronic pain and is due to repetitive stimulation from chronic inflammation or nerve damage.