2 PainOf all the components of the injury response, none is less consistent or less understood than an individuals response to painThe sensation of pain is a diffuse entity inherent to the nervous system and basic to all peopleIt is a personal experience that all humans endureAcute pain is the primary reason why people seek medical attention and the major complaint that they describe on initial evaluation.
3 Chronic pain may be more debilitating than the trauma itself and, in many instances, is so emotionally and physically debilitating that it is a leading cause of suicide.Pain serves as one of the body’s defense mechanisms by warning the brain that its tissues may be in jeopardy, yet pain may be triggered without any physical damage to tissues.The pain response itself is a complex phenomenon involving sensory, behavioral (motor), emotional, and cultural components.
4 What are the nerve fibers that stimulate pain? Once the painful impulse has been initiated and received by the brain, the interpretation of pain itself is based on interrelated biological, psychological, and social factors.What are the nerve fibers that stimulate pain?Nociceptors.Once these are stimulated, “pain” impulses are sent to the brain as a warning that the body’s integrity is at risk.The emotional response may be expressed by screaming, crying, fainting, or just thinking that hurts!”
5 When the pain is intense or unexpected, an immediate reflex loop activates the behavioral response by sending instructions to motor nerves to remove the body part from the stimulus.Sticking your finger with a needlePlacing your hand on a hot stoveThese stimuli’s activate specialized nerve fibers to send signals through a peripheral nerve networkRouting the impulses up the spinal cord to the brain
6 When the afferent impulse reach the spinal cord, a reflex loop is formed within the tract to activate the muscles necessary to remove your hand or finger from the stimulus.The remaining impulses of the reflex continue on to the brain, where they are translated as pain, and you respond by saying “ouch!” or other choice words.If an individual has knowledge about a potentially painful stimulus, such as receiving an injection, cognitive mechanisms can inhibit the reflex loop and block portions of the behavioral response.As a the painful stimulus increases, so does the conscious effort required to keep from trying to escape from the stimulus.
7 The cultural components of pain are almost too complex to define. The emotional component may still be in place as you grimace, make a fist, or think “what is this jerk doing to me.”The cultural components of pain are almost too complex to define.However, pain perception has been linked to ethnicity and socioeconomic status.ExampleItalian patents are less inhibited in the expression of pain than are the Irish or Anglo-Saxon patientsUltimately, cultural components can be viewed as any variable that relates to the environment in which a person was raised and how that environment deals with pain and responses to pain.
8 Pain ProcessNoxious input or nociceptive stimulus causes the activation of pain fibers.The painful impulse is triggered by the initial mechanical force of the injury (whether sudden or gradual onset) and is continued by chemical irritation resulting from the inflammatory processIn subacute and chronic conditions, pain may be continued by reflex muscle spasm in a positive feedback loop or through the continued presence of chemical irritation
9 The pain response is initiated by stimulation of nociceptors Nociceptors- specialized nerve endings that respond to painful stimuliMechanical stress or damage to the tissues excite mechanosensitive nociceptorsChemosensitive nociceptors are excited by various chemical substances released during the inflammatory responseChemical irritation of nerve endings may produce a severe pain response without true tissue distruction
10 Unlike other types of nerve receptors, nociceptors display a sensitization to repeated or prolonged stimulationDuring the inflammatory process, the threshold required to initiate an action potential is lowered, and the continued stimulation of the chemosensitve receptors perpetuates the cycle
11 All noxious impulses are transmitted afferently to the thalmus To understand the complexity of pain, comprehension of the various neurophysiological pathways involved in transmission, perception, and inhibition of pain is critical.The nervous systemForms a complex network of afferent and efferent pathways.Transmitting and reacting to impulses that the brain perceives as being painfulAll noxious impulses are transmitted afferently to the thalmusThis produces the “painful” stimulus which triggers the physiological and psychological process described earlier
12 Modulation of Pain Acute pain response begins with a noxious stimulus. IE. A burn or cut externally or internally a muscle strain or ligament sprainAfter trauma chemicals are released in and around the surrounding tissues.Immediately after the trauma, primary hyperalgesia occursLowers the nerve’s threshold to noxious stimuli and magnifying the pain response
13 Within hours, secondary hyperalgesia occurs ↑ the size of the painful area as the chemicals diffuse into the surrounding tissuesCauses hypersensitivityThe initiation of the pain process always begins with a chemical stimulus.Review chemical precursorsDuring acute traumaCell walls become damagedCauses dopamine and norepinephrine (NE) to be released from precursors in the cell membraneCauses the activation of phospholipasAllowing the cell membrane to release arachidonic acidWhen released in the presence of cyclooxygenase, it converts to prostaglandin
14 Prostaglandins have many roles in inflammation, but they also sensitize the nerve endings to other chemicalsIE bradykininWhich in turn initiate nociceptionBradykinin, found in plasma and released during coagulation that follows injury, are direct activators of nociception.Powerful vasodilators, ↑ vascular permeability during the inflammatory responseNSAID’s play and important role in the tx of acute pain in that they block the formation cyclooxygenase and prevent the synthesis of prostaglandins.Therefore, NSAID’s are important as an early mediator for the interruption of the pain and inflammation cycle
15 Pain fibersA-delta fibers- a type of nerve that transmits painful information that is often interpreted by the brain as burning or stinging painC-fibers- a type of nerve that transmits painful information that is often interpreted by the brain as throbbing or aching
16 After an injury, A-delta and C fibers carry noxious stimuli from the periphery (using which pathway?) to the dorsal horn of the spinal cord.The noxious stimuli activates 10-20% of the A-delta fibers and 50-80% of the C-fibers.Triggered by strong mechanical pressure or intense heat, A-delta fibers produce a fast, bright, localized pain sensation.C-fibers are triggered by thermal, mechanical, and chemical stimuli and generate a more diffuse, nagging sensation
17 After an injury, such as a sprained ankle, you athlete feels Sharp, well-localized, stinging or burning sensation coming from which fibers??A-delta fibersThis initial reaction allows an indiviual to realized that trauma has occurred and to recognize the response as painVery quickly, the stinging or burning sensation becomes an aching or throbbing sensation, which indicates activation of which fiberC-fibersA third type of peripheral afferent nerve fiber warrants mention. A-beta fibers, respond to light touch and low intensity mechanical information.Rubbing and injured areaThese interrupt nociception to the dorsal horn
18 Ascending PathwaysFirst-order neurons- A-beta, A-delta, and C nerve fibers.Because they all originate in the periphery and terminate in different areas of the dorsal hornThe gray matter of the spinal cord is divided into 10 layers of cell bodies called LaminaeBefore synapsing in the laminae the peripheral afferent nerves course into the tract of LissauerWhere A-delta and C fibers divide and send impulses up and down one to two segments of the spinal column.Once in the dorsal horn of the spinal cord, the small A-delta and C fibers synapse with neurons and terminate in the various laminae
19 Lamina I contains several types of neurons The 2 of interest to us areWide-dynamic-range (WDR) neuronsNociceptive-specific (NS) neuronsWDR- respond to both noxious and non-noxious stimuliNS- respond only to noxious stimuliThese neurons in lamina I are part of the cells that make up the Long spinothalamic tract (STT)
20 The Substantia Gelatinosa (SG), found partially within lamina II, contain small internuncial neurons These neurons can excite (stalked cells) or inhibit (islet cells) the transmission of noxious stimuliThese neurons in the SG send axons to lamina I and release enkephalin and gamma-aminobutyric acid.Both which inhibit the transmission of noxious stimuliEnkephalin- a substance released by the body that reduces the perception of pain by bonding to pain receptors sites
21 WDR cells from laminae I & 5 make up the majority of fiber in the STT. Lamina III and IV- composed of WDR neuron cells and low-threshold mechanoreceptors.The mechanoreceptors play a limited role in the modulation and transmission of painLamina V- is a major synapse of A-delta and C fibers in the dorsal horn.It also has a large # of WDR cells that respond to a spectrum of stimuli from light touch to mechanical pressure and heatWDR cells from laminae I & 5 make up the majority of fiber in the STT.Where first order neurons terminate and second order neurons originateSecond order- A nerve that has its body located in the spinal cord. It connects second and third order neuronsThird order- a nerve that has its body in the thalamus and extending into the cerebral cortex
22 1st order neurons course from the periphery to synapse in the dorsal root ganglion and the laminae before crossing the spinal cord to the STTOnce in the STT, noxious stimulus is then transmitted to the brain via 2 different portions of the STTThe neospinothalamic (lateral) tract (NSTT)Paleospinothalamic (ventral) tract (PSTT)This dual-tract system of afferent pain pathways enables the body to have immediate warning of the presence, location, and intensity of an injury as well as the slow, aching reminder that tissue damage has occurred.
23 NSTT receives input from A-delta fibers that synapse with the nociceptive-specific neurons and the WDR neurons in Laminae I & V.These neurons of the NSTT immediately cross the ventral white column of the spinal cord to the opposite antrolateral white column.Once in the ant horn, the fibers of the NSTT and a portion of STT synapse with motor units or stimulate preganglionic neurons of the sympathetic or parasympathetic system and then communicate with the thalamus.This transmission is responsible for the motor and autonomic response associated with tissue damage and info pertinent to the siteIntensityAnd duration of the painful stimulus
24 The NSTT has been described as the sensory discriminative pathway of pain. The PSTT is located more medially, but still is in the anterolateral portion of the white matter of the spinal cord.The PSTT receives input predominately from the C fibers.These synapse with the nociceptive-specific neurons and the WDR neurons in Laminae I & V2nd order neurons of Laminae I & V cross over the spinal cord and project to the reticular formation (RF)A diffuse network of cells and fibers located in the brain stem. Influences alertness, waking, sleeping, and certain reflexes.The RF is located in the central portion of the brain stem, medulla oblongata, hypothalamus, thalamus, limbic system, and periaqueductal gray (PAG).
25 The RF is responsible for evoking motor, sensory, and autonomic responses to noxious stimuli. This allows the injured person to respond rapidly to the stimuli.The PSTT has multiple synapses with other areas of the central brain responsible for poorly localized, dull, aching pain as well as for the behavioral, emotional, and affective aspects of pain.
26 AKA: motivational-affective system. The brains limbic system aids in integrating higher brain function with motivational and emotional reactions.Contains afferent nerves from the hypothalamus and the brain stem.Receives descending influence from the cortex.This communication is responsible for the emotional response to painful experiences.When an injury occurs, the neural communication between the limbic system, thalamus, RF, and cortex produces reactions such as fear, anxiety, or crying.In short , the limbic system is responsible for the body’s affective qualities of reward, punishment, aversive drives, and fear reactions to painAKA: motivational-affective system.
27 Because of the proliferation of nerve cells and the cortex’s functions The integration of the cortex is an important component in both the ascending and descending aspects of pain modulation.Via axons, ascending pain stimuli are transmitted from the thalamus to the central sulcus in the parietal lobe (somatosensory cortex), where the pain is discriminated and localized.Because of the proliferation of nerve cells and the cortex’s functionsConsciousnessSpeechHearingMemoryThoughtIt is unlikely that the afferent synapses that occur during noxious stimulation affect only one efferent neuron.Thus, many areas of the cortex can be stimulated during a painful experience.
28 Descending PathwaysThe descending pain modulation mechanisms could influence both the input and the mediation of the noxious stimuliOne of the descending mechanisms originates in the cortex’s corticospinal tract.The corticospinal tract descends from the cortex to the medulla, where fibers cross over to the opposite side of the medulla and to lower levels of the spinal cord, where it terminates in laminae I-VII and transends through the dorsolateral funiculus (large fiber tract)This tract could act to exert postsynaptic (descending) control over the afferent transmission of thermal, mechanical, and C fiber input at laminae I & II
29 The hypothalamus sends ß-endorphins via neurons to the PAG A second structure exerting descending control of noxious stimuli is the PAGPAG receives input from the cortex, limbic system, hypothalamus, and PSTT.The hypothalamus sends ß-endorphins via neurons to the PAGHere they are routed to the nucleusmagnocellularies of the rostral medulla that descends laterally to the dorsal horn.Another descending control system arises form the nucleus raphae magnus in the upper medullaDescending axons from this region of the brain track down to the lower medulla and the spinal cord, where they release serotonin at their terminal end, producing analgesia at laminae I, II, and V.
30 The notion of central control and descending inhibition of pain is based on the body’s ability to use and produce various forms of endogenous opiates.Each having a distinct function and a specific receptor affinity.The enkephalins are found throughout the central nervous system, but particularly in the dorsal horn.Thus, the aggregation of noxious stimuli may cause both presynaptic and postsynaptic control of nociception in the dorsal horn via enkephalin release
31 Dynorphins are primarily located in laminae I & 5, making it feasible for them to inhibit pain. Levels of dynorphin ↑ in laminae I & 5 during periods of hyperstimulation.However, their rapid degradation limits their role in long-term pain reduction.During periods of intense noxious input, ß-endorphins are released and provide temporary inhibition to noxious stimulation.This concept is based on their location in the PAG and the idea that their release would block interneuron interaction.
32 Review of the process of Pain Transmission Much decision making in the tx of pain can be based on the understanding of the physiological and chemical interaction that occurs after trauma.In simple terms, pain transmission appears to be fairly straightforward.The acute pain response is initiated when substances are released form injured tissues, causing a noxious stimulus to be transmitted via A-delta and C fiber to the dorsal horn
33 Once in the dorsal horn, the stimulus is transmitted to the higher brain centers via the STT, which bifurcates into 2 tracts.The impulse is propagated via the NSTT to the thalamus and then to the cortex, where discrimination and location of the stimulus are assessed.At the same time, noxious stimulation is projected upward toward the RF, the PAG matter, the hypothalamus, and the thalamus via the PSTTNeurons in the thalamus send axon projections to the limbic system and the cortex.Once the noxious stimuli have reached the higher centers of the brain, the descending control mechanisms are activated, the incoming noxious stimuli can be inhibited at various levels, and endogenous opiates can be released.
34 Pain Theory: Historical Perspectives Theories regarding the cause, nature, and purpose of pain have been debated since the dawn of humankind.Most early theories were based on the assumptions that pain was related to a form of punishment.The word “pain” is derived from the Latin word “poena” meaning fine, penalty, or punishment.
35 The ancient Greek believed that pain was associated with pleasure because the relief of pain was both pleasurable and emotional.Aristotle reassessed the theory of pain and declared that the soul was the center of the sensory processes and that the pain system was located in the heart
36 The Romans, coming closer to contemporary thought, viewed pain as something that accompanied inflammation.In the 2nd century, Galen offered the Romans his works on the concepts of the nervous system.However, the views of Aristotle weathered the winds of time.In the 4th century, successors of Aristotle discovered anatomic proof that the brain was connected to nervous systemDespite this, Aristotle’s belief prevailed until the 19th century, when German scientist provided irrefutable evidence that the brain is involved with sensory and motor function
37 Specificity Theory of Pain Modulation Modern concepts of pain theory continue to advance from the ideas of Aristotle.However, controversy still exists as to which theories are correct.The theories accepted at the turn of the century were the specificity theory and the pattern theory, two completely different and seemingly contradictory views
38 The specificity theory suggests that there is a direct pathway from peripheral pain receptors to the brain.The pain receptors are located in the skin and are purported to carry pain impulses via a continuous fiber directly to the brain’s pain centerThe pathway includes the peripheral nerves, the lateral STT in the spinal cord and the hypothalamus (the brain’s pain center)This theory was examined and refuted using clinical, psychological, and physiological evidence by Melzack and Wall in 1965.They discussed clinical evidence describing pain sensations in severe burn patients, amputee patients, and patients with degenerative nerve disease.
39 These syndromes do not occur in a fixed, direct linear system Rather in the quality and quantity of the perceived pain are directly related to a psychological variable and sensory input.This theory had been previously addressed by Pavlov, who inflicted dogs with a painful stimulus, then immediately gave them food.The dogs eventually responded to the stimulus as a signal for food and showed no responses to the pain
40 The psychological aspect of pain perception was later addressed by Beecher, who studied 215 soldiers seriously wounded in the Battle of Anzio, finding that only 27% requested pain-relieving medication (Morphine).When the soldiers were asked if they were experiencing pain, almost 60% indicated that they suffered no pain or only slight pain, and only 24% rated the pain as bad.This was most surprising because 48% of the soldiers had received penetrating abdominal wounds.Beecher also noted that none of the men were suffering from shock or were insensitive to pain because inept intravenous insertions resulted in complaints of acute pain.
41 The conclusion was drawn that the pain experienced by these men was blocked by emotional factors. The physical injuries that these men had received was an escape from the life-threatening environment of battle to the safety of a hospital, or even release form the war.This relationship suggests that it is possible for the central nervous system to intervene between the stimulus and the sensation in the presence of certain psychological variables.No physiological evidence has been found to suggest that certain nerve cells are more important for pain perception and response than others; therefore, the specificity theory can be discounted.
42 Contemporary Pain Control Theories Although both the specificity and pattern theories of pain transmission were eventually refuted, they did provide some lasting principles that are still present in contemporary pain modulation theoriesThe strengths of these 2 theories, plus findings obtained through additional research, were factored together to for the basis of the current perspective regarding pain transmission and pain modulation.Still, there is much to be learned and studied before the exact mechanisms of pain transmission and perception are understood.
43 Next time Gate control theory Levels Theory of pain control Assessment of painVisual analogue scaleMcGill pain questionaireSubmaximal effort tourniquet testPlacebo effectReferred painChronic PainPain management techniquesChapter 3: Development and delivery of treatment protocol
44 Pattern Theory of PainStates that there are no specialized receptors in the skin.Rather, a single “generic” nerve responds differently to each type of sensation by creating a uniquely coded impulse formed by a spatiotemporal pattern involving the frequency and pattern of nerve transmission.
45 An analysis of the word’s elements “Spatio”- the distance between the nerves impluses“temporal”- the frequency of the transmissionAn example of this type of coding can be found with most institutional phone systems.A call from inside a university has a different ring from an outside call.Although this theory was closer to being neurological correct there were still shortcomingsMelzack and Wall refuted this theory as well, based on the physical evidence of physiological specialization of receptor-fiber units.Plus this theory failed to account for the brains role in pain perception.
46 Gate Control TheoryImplies a non-painful stimulus can block the transmission of a noxious stimulus.Is based on the premise that the SG, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses.This then influences the first central transmission (T) cells, which corresponds with the NSTT or the PSTT and activate a central control triggering the mechanisms responsible for the response and perception of pain.
47 The SG acts as a modulating gate or a control system between the peripheral nerve fibers and central cells that permits only one type of never impulse (pain or no pain) to pass through.Serving in a capacity similar to that of a “switch operator” in a railroad yard, the SG monitors the amount of activity occuring on both incoming tracts in a convergent systemOpening and closing the gate to allow the appropriate information to be passed along to the T cell.Impulses traveling on the fast, nonpain fibers ↑ activity in the SG.Impulses on the slower pain fibers exert an inhibitory influence.When the SG is active, the gate is in its “closed” position and a nonpainful stimulus is allowed to pass on to the T cell.
48 Example: Bumping the head The initial trauma activates the A-delta and, eventually, C fibersRubbing the traumatized area stimulates the A-beta fibers, which activate the SG to close the spinal gateThus inhibiting transmission of the painful stimulus
49 Assessment of pain Visual analogue scale McGill pain questionnaire PictureMcGill pain questionnairePart I: is used to localize the pain and identify whether the perceived source of the pain is superficial (external), internal, or both.Part II: incorporates the VAS that was described in the visual analogue scale.Part III: is the pain rating index, a collection of 76 words grouped into 20 categories. Patients are to underline or circle the words in each group that describes the sensation of pain being experienced.Groups 1-10= somatic in natureGroups 11-15= affectiveGroup 16= evaluativeGroup 17-20= miscellaneous words that are used on in the scoring process.
50 ScoringAdd up the total number of words chosen, up to the maximum of 20 words (one for each category)The level of intensity of pain is determined by the value assigned to each word.1st word = 1 point2nd word = 2 pointAnd so onPt could have a high score of 20, but have a low-intensity score by selecting the 1st word in each category.
51 Submaximal Effort Tourniquet Test In 1966, Smith et al described a method of matching a patients pain using a SETT.The SETT is performed by inflating a BP cuff to above systolic pressure on the pt elevated arm.Once the cuff is inflated, the pt is instructed to open and close the hand or fist rhythmically.A handgrip dynamometer and a metronome can be used for standardization.The pt should continue opening and closing the hand or fist until the cramping sensation that he or she feels “matches” the pain from the “original” pathology.The amount of time that elapses form onset to fruition of matched pain is the recorded objective measure.The SETT can be repeated at every tx session to gauge tx progress and is effective in matching all types of pain
52 Placebo Effect Placebo stems from the Latin word for “I shall please” Used to describe pain reduction obtained from a mechanism other than those related to the physiological effects of the tx.Linked to psychological mechanismsAll TM have some degree of placebo effectMost studies involving TM involving the use of a sham TM (ultrasound set at the intensity of 0) and an actual treatment have shown ↓ levels of pain in each group.
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