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Course 1 acute versus chronic pain


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This chapter describes the neurological and neurosynaptic pathways for both acute and chronic pain. It also delineates the psychological differences between acute and chronic pain. Finally, it introduces the concept of the specific type of pain associated with a specific tissue type, which is useful in the diagnosis of pain problems. This chapter is the foundation for understanding all subsequent chapters on pain.

Published in: Health & Medicine

Course 1 acute versus chronic pain

  1. 1. Acute versus Chronic PainNelson Hendler, MD, MSFormer Assistant Professor of NeurosurgeryJohns Hopkins University School of MedicinePast president-American Academy of Pain Managementwww.MarylandClinicalDiagnostics.comLecture 1
  2. 2. Anatomy of a Nerve- I• Everything in the body works due to nerve input• Nerves are the signal system of the body• Think of a nerve as an electrical telephone wirewhich transmits information from one place toanother, via electrical impulses• Just like an electrical wire, nerves have insulation,called myelin, which can be very thick, or thin.• The myelin is made by a special cell called aSchwann cell.• The myelin wraps around the nerve in layers
  3. 3. Anatomy of a Nerve - II• A nerve has a cell body, which provides themetabolic energy for the nerve, and receivesinformation from other nerves.• The fiber extending from the cell body is an axon• The axon ends in a “button termineaux” orterminal button or swelling, where the chemicalscalled neurosynaptic transmitters are made• These neurosynaptic transmitters are whatcreate the specificity of nerve transmission• Nerve activity can be modified at the cellmembrane electrically & the synapse chemically
  4. 4. Anatomy of a Nerve III• The center of a axon is called axoplasm, whichtransports nutrients to the entire nerve• The cell wall of the nerve is a lipo-proteinmembrane with channels through it, modified bysodium (Na+), potasium (K+) calcium (Ca++),magnesium (Mg++) and other cations• When a nerve discharges, due to stimulation ofthe cell body, the channels change, and allowNa+ into the axon, and K+ goes out• Then a pump in the axon (Na+/K+ ATPase) movesthe cations back to original position
  5. 5. Anatomy of a Nerve IV• The transient flow of Na+ into the axon, and K+ outof the axon creates a electron flow along the axon• This flow moves a signal electrically along the nerve• This electrical signal reach the end of the nerve andcauses the release of the chemicals- theneurosynaptic transmitters• So a sensory nerve receives stimulation, eithermechanical or chemical, and transmits thisinformation electrically, along the axon, until itreaches the end where it then converts it to achemical message again.
  6. 6. Anatomy-Peripheral Receptors• Meissners corpuscles are mechanoreceptor, inthe skin, which senses vibration, and light touch• Pacinian corpuscles in the skin sense pressure• Free Nerve endings have no myelin-so sensitive• Afferent Nervous System-carries sensorymessages to the brain- pain is one of these• There are three major types of pain nerves• A beta fibers have a moderate amount of myelin• A delta fibers have some myelin• C fibers – have no myelin or very little myelin
  7. 7. Electrical vs chemical transmission• Once a peripheral pain receptor is stimulated,this starts a series of events which allow themessage of pain to reach the cortex of the brain• This transmission is electrical along the axon andchemical at the end of the nerve with theneurosynaptic transmitters• Without pain information reaching the cortex ofthe brain, there is no perception of pain• Pain relief is directed to preventing the messageof pain from reaching the cortex of the brain
  8. 8. Blocking the Pain Message• Modify the electrical transmission in the axonusing anti-convulsants to stabilize the membrane,by hyper-polarizing the membrane, or put incations, like lithium (Li+), which interfere withnormal cation activity of Na+, K+, Mg++ and Ca++• Modify the release of neurosynaptic transmitters,by enhancing those which produce pain relief,and blocking those which transmit the messageof pain• Stop cortical reception by electrical stimulation ofthe sensory cortex or cutting out the cortex
  9. 9. Electrical & Chemical Transmission• Acute pain is a fast transmission process, i.e. thetime from stimulation ‘til the message reachesthe brain is short• Chemical transmission of a message at thesynapse is much slower than the electricaltransmission along the axon• Acute pain is a fast pain pathway, with only 2synapses. You want fast transmission when yourhand is In a fire. Pain tells you something is wrong• Chronic pain is a slow pain pathway with manysynapses. It tells you something is still wrong
  10. 10. The Value of Spinal Synapses• Pain information from sensory nerves enterslamina III and V of the posterior horn of thespinal cord, and synapse there.• Wide dynamic range neurons modify thisinformation, regulating intensity• Neuronal plasticity allow pain to continue toexist at a spinal level, even after the source ofthe original source of the pain is removed• Crossing pain fibers in the spinal cord helplocalize the location of the pain
  11. 11. Neurochemical and Anatomical Pathway ForAcute Pain-Fast Transmission(2 synapses)• Neo-Spino-Thalamic Tract (Acute Pain)BRAINSpinal Cord sends message to the brainPeripheral Sensory Nerve(A beta, A delta, C fibers)carries the message to thespinal cordMechano orpressure receptor(Meisner orPachiniancorpusule) orchemoreceptor (Cfiber) in a fingerSynapses (Chemically mediated)ThalamusSomato-SensoryCortex(Pain)Chemical synapses lends specificity, and a site to manipulate pain perception
  12. 12. Neurochemical and Anatomical Pathway For Chronic Pain(Many areas of the brain are involved and multiplesynapses- so this is slower transmission)• Palleo-Spino-Thalamic Tract (Chronic Pain)-SlowBRAINSpinal Cord sends message to the brainPeripheral Sensory Nerve(A beta, A delta, C fibers)carries the message to thespinal cordMechano orpressure receptor(Meisner orPachiniancorpusule) orchemoreceptor (Cfiber)Synapses (Chemically mediated)ReticularActivatingSystemThalamusHypothalamusLimbicSystemSomato-SensoryCortex (Pain)Chemical transmission is slower than electrical transmission
  13. 13. Other Neurosynaptic transmitters inthe Brain• Biogenic Amines: dopa, dopamine, nor-epinephrine, epinephrine, serotonin.• 35% of neurosynaptic transmitters-GABA• 10% of neurosynaptic transmitters-Ach• 2%-5% of all neurosynaptic transmitters in thebrain use biogenic amines• 95% of biogenic amines transmitters are in thehypothalamus and limbic system.• 90% of encephalins are in limbic system
  14. 14. Neurochemical and AnatomicalPathway For Chronic Pain• Palleo-Spino-Thalamic Tract (Chronic Pain)-slowBRAINSpinal CordPeripheral Sensory Nerve(A beta, A delta, C fibers)Mechano orpressure receptor(Meisner orPachiniancorpusule) orchemoreceptor (Cfiber)Sleep caused by serotoninReticularActivatingSystemThalamusHypothalamusLimbicSystemSomato-SensoryCortex (Pain)Encephalin, and 95% of biogenic amines exist in thesame area
  15. 15. The Synapse and Neuro-SynapticTransmitters (NST)• Pre-synaptic Synapse Post-synaptic• MAO and COMT break down NST• 1)Transmitters are released from nerve A, 2) bind to the receptors, on nerve B, causing nerveB to fire, and 3) then reuptake occurs to stop the action of the NST.Post-SynapticReceptor SitesNerve transmissionof informationNerve transmissionof informationNeuro-synaptictransmitter (NST)1231COMTMAOBA
  16. 16. How medications works on the synapse• Pre-synaptic Synapse Post-synaptic• Increase activity by1)Cause Release 2) Stop Reuptake 3)Mimic NSTPost-SynapticReceptor SitesNerve transmissionof informationNerve transmissionof informationNeuro-synaptictransmitter231I
  17. 17. How medications works on the synapse• Pre-synaptic Synapse Post-synaptic• Decrease activity by1) Stop Release 2) Increase Breakdown 3)Block NSTPost-SynapticReceptor SitesNerve transmissionof informationNerve transmissionof informationNeuro-synaptictransmitter31COMT22
  18. 18. The Axon and Cell Body• Transmission along a nerve, causing Na+ influxK+Na+AxoplasmExtracellular fluidNa+/K+ channelK+ comes out,Na+ goes inPumps Na+ out,and K+ back inThis entire process generates a current (90uV) across cell membrane
  19. 19. Mechanism of Action of Various Drugs• Medication can work at the synapse, which is veryspecific (as an example, there are 20 subtypes ofserotonin receptors)• Medication can work on the nerve membrane(more non-specific).• Medication can inhibit natural transmitters byblocking release of transmitters or blockingreceptor sites,• Medication can release transmitters, or blockreuptake pre-synaptically, so the transmitterremains on a receptor longer
  20. 20. Psychological FactorsAcute Pain- impacted by psychological statesAcute Pain –is reduced by enkephlins, ACTH, andendorphins released at time of stress.Chronic Pain- less influenced by psychologicalstates, but causes depression and anxietyChronic Pain goes through 4 stagesNo psychological change-expecting to get wellSomatic concern and anxiety when not getting wellDepression when realizing that pain is chronicAdjustment to the deficit
  21. 21. Other Factors Influencing Acute Pain• Pain tells a person “something is wrong with yourbody”• If the cause of pain is obvious, like your finger in afire, you know to withdraw your finger from a fire• But when a blister forms, this can not onlyproduce pain, but also fear of the unknown• Will the skin fall off? How long will the pain last?• Will the pain spread to my hand? Will this getinfected? Will I lose sensation in the finger?• Fear of the unknown produces anxiety
  22. 22. Psychological Issues of Acute Pain• The “psychological state” of anxiety worsens theperception of pain• When someone is in an accident, with a seriousinjury, the anxiety over the loss of the use of anarm or leg is overwhelming.• Education about the body, and reducing the“anxiety about the unknown” can be reduced byeducation of the injured person• Convert “anxiety” into a realistic “fear” byeducation about the body,• Tell the truth. Avoid phony reassurances
  23. 23. Modification of Acute Pain• Assess the type of pain which is present• See the next slide for an overview method• The next slide has only suggestions. It is not asubstitute for clinical judgment on the scene• Tell the patient what you are finding, and whatyou think the source of the pain might be• Educate the patient, with drawings of the body• Give the patient odds about outcome—”Themedical literature says about 90% of patientshave no residual problems” etc.
  24. 24. Mechanism of Pain• Pain occurs when tissue damage occurs, due toexcessive heat, cold, stretching, pressure, celldisruption from a cut, or chemical irritation• Different types of pain are caused by damage tothe bone, blood vessels, skin, muscle or nerve• Cellular damage causes the release of a series ofinflammatory chemicals• The chemical irritation creates an electricaldischarge from the sensory nerves which thenleads to a series of neuronal transmissions to thebrain
  25. 25. Damage to Different Tissue Feels Differently• NOTE: Damage to different tissue feels differently• Pain can be constant or intermittent• Damage to nerves feels like a burning pain, orpins and needles• Damage to bone feels like a deep achy pain• Damage to muscles feels like a cramp or spasm• Damage to blood vessels feels like a throbbing,pounding pain• Damage to skin feels like a burning, sharp pain• Each type of pain responds to best a differenttype of medication
  26. 26. Methods to Assess PainBurning Throbbing Sharp Dull Aching SpasmConstant Thissuggestnerveirritation –chemical,metabolic,or viralThis suggestvascularcompression-look for thesource ofthecompressionThissuggestsentrap-ment ofsensorynerves inskinSuggest acompres-sion,tumor,deepbruise, orinfection-get bonescanDeep achypainsuggestsbonebruise orfractureget bonescanThis suggestnerveentrapment,orcompressionlook for thesource ofcompressionIntermittent This wouldbeassociatedwith spasmof muscleor bloodvessel-treat thosesourcesThis suggestvascularspasm- usemedicationswhichreducespasm likeImitrexSeen invisceralspasm,such asCrohn’sdisease-use anti-spasmoticPain onlywith use-sprain orstrain duetodamageto tendonorligamentThissuggestsinflama-toryprocess-use non-steroidalanti-inflama-tory drugsThissuggestsmusclespasm-usemusclerelaxants
  27. 27. Overview of the Nervous SystemOrganizationEfferent -motor autonomicAfferent –sensoryBrainSpinal CordSympathetic ParasympatheticAlpha Beta Muscaric NicotinicAlpha 1 Alpha 2 Beta 1 Beta 2MusclesSkin
  28. 28. Systems Associated with Pain• Motor Nerves leave the brain to the spinal cord• They emerge from the spinal cord as nerve roots• The nerve roots then mix in either the brachial orlumbar plexus, and emerge as mixed motorsensory nerve, with specific names such as theulnar nerve or sciatic nerve• As an example, the sciatic nerve has contributionsfrom the L1-L2, L2-L3, L3-L4,L4-L5, and L5-S1 nerveroots, which mix in the lumbar plexus, and createthe sciatic nerve, a mixed motor-sensory nerve• These mixed nerves have motor and sensory fibers
  29. 29. Mixed Motor-Sensory Nerve in Cross-sectionThe motor fibers comefrom the brain to themuscle. The sensorynerves come from the skin,muscle and bone, and goto the brain. The sensoryfibers are the A beta, Adelta and C fibers. Themixed motor-sensory nervearises after the lumbar orbrachial plexus, and is anamed nerve, like the ulnarnerve, sciatic nerve or tibialnerve. The sensory nervefibers carry messages tothe brain, and the motornerve carries messagefrom the brain to themuscle.Motor nerves have thick myelin, and sensory nerve have less myelin. Both types ofnerves are wrapped together in a bundle, which is a mixed motor-sensory nerve. .
  30. 30. Types of Sensory Nerve Fibers• The sensory fibers are sparsely myelinated, orunmyelinated• The sensory fibers are the A beta, A delta andC fibers• C fibers are unmyelinated unlike mostother fibers in the nervous system.[1]This lackof myelination is the cause of theirslow conduction velocity, which is on theorder of no more than 2 m/s.[1]C fibers are onaverage 0.2-1.5 μm in diameter.[1]Purves, Dale; (2004). Neuroscience. Massachusetts: Sinauer Associates, Inc
  31. 31. C Fiber Activity• C fibers are considered polymodal becausethey can react to various stimuli. They react tostimuli that are thermal, or mechanical, orchemical in nature. C fibers respond to allkinds of physiological changes in the body. Forexample, they can respond to hypoxia,hypoglycemia, hypo-osmolarity, the presenceof muscle metabolic products, and even lightor sensitive touch. C fiber receptors includethe following functionsPurves, Dale; (2004). Neuroscience. Massachusetts: Sinauer Associates, Inc
  32. 32. Functions of C-Fibers• C fiber nociceptors– responsible for the second, burning pain• C fiber warming specific receptors– responsible for warmth• ultra-slow histamine-selective C fibers– responsible for itch• tactile C fibers– sensual touch• C mechano- and metabo- receptors in muscles or joints– responsible for muscle exercise, burn and cramps
  33. 33. A -delta Fiber Activity• Because of their higher conduction velocity,Aδ fibers are responsible for the sensation ofa quick shallow pain that is specific on onearea, termed as first pain. They respond to aweaker intensity of stimulus. C fibers respondto stimuli which have stronger intensities andare the ones to account for the slow, butdeeper pain, and spread out over anunspecific areaPurves, Dale; (2004). Neuroscience. Massachusetts: Sinauer Associates, Inc
  34. 34. Spinal Connections• C fibers synapse to “second-orderprojection neurons” in the spinal cord atthe upper laminae of the dorsal horn inthe substantia gelatinosa. The second-order projection neurons are of the widedynamic range (WDR) type, whichreceive input from both nociceptiveterminals as well as myelinated A-typefibers.• Baron, Ralph (2006). "Mechanisms of Disease: neuropathic pain—a clinicalperspective". Nature Clinical Practice Neurology 2.
  35. 35. Spinal Synapses• After repeated stimulation, WDR (widedynamic range) neurons, in the substaniagelatenosa, experience a general increase inexcitability• C fibers cause central sensitization of thedorsal horn in the spinal cord in response totheir hyperactivity.• Sensitized C fibers release glutamate• Glutamate interacts with thepostsynaptic NMDA receptors, which createsthe sensitization of the dorsal horn.
  36. 36. Various lamina of the dorsal hornI-V are sensory laminae.Synapses occur here.Various nuclei, which are acollection of cell bodies,which give rise to axons
  37. 37. Pain Connections After the Spine• The second-order neurons ascend tothe brain stem and thalamus inthe ventrolateral, or anterolateral, quadrantof the contralateral half of the spinal cord,forming the spinothalamic tract. Thespinothalamic tract is the main pathwayassociated with pain and temperatureperception, which immediately crosses thespinal cord laterally. This crossover feature isclinically important because it allows foridentification of the location of injury.• Purves, Dale; (2004). Neuroscience. Massachusetts: Sinauer Associates, Inc
  38. 38. Pathway of chronic pain-Spine to Brain• Central sensitization of the dorsal horn neurons that isevoked from C fiber activity is responsible for temporalsummation of “second pain” (TSSP). This event is called‘windup.’Windup is associated with chronic pain andcentral sensitization. Functional MRIs show common areasactivated by the TSSP responses which includecontralateral thalamus, anterior and posterior insula, mid-anterior cingulate cortex, and supplemental motorareas. TSSP events are also associated with other regions ofthe brain that process functions such as somatosensoryprocessing, pain perception and modulation, cognition, andpre-motor activity in the cortex.(1)Staud,Roland;"BrainactivityrelatedtotemporalsummationofC-fiberevokedpain".Pain(1-2ed.)129(1–2):130–142.
  39. 39. Activity in the Brain• Pain transmission reaches a variety of cells ofthe lamina 1 of the cortex of the brain• There are different cell types in this layer• These varying neurons are responsible for thedifferent feelings we perceive in our body• They can be classified by their responses toranges of stimuli• The brain uses the integration of these signalsto maintain regulation of the body, by positiveor negative feedback, like a thermostat