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PAIN & PAIN CONTROL THEORIES

PAIN & PAIN CONTROL THEORIES. Managing Pain. What is Pain?. “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain Subjective sensation

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PAIN & PAIN CONTROL THEORIES

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  1. PAIN & PAIN CONTROL THEORIES Managing Pain

  2. What is Pain? • “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain • Subjective sensation • Pain Perceptions – based on expectations, past experience, anxiety, suggestions • Affective – one’s emotional factors that can affect pain experience • Behavioral – how one expresses or controls pain • Cognitive – one’s beliefs (attitudes) about pain • Physiological response produced by activation of specific types of nerve fibers • Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy. • Composed of a variety of discomforts • One of the body’s defense mechanism (warns the brain that tissues may be in jeopardy) • Acute vs. Chronic – • The total person must be considered. It may be worse at night when the person is alone. They are more aware of the pain because of no external diversions.

  3. Where Does Pain Come From? • Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset • Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vessels • Visceral Pain – originates from internal organs; diffused @ 1st & later may be localized (i.e. appendicitis) • Psychogenic Pain – individual feels pain but cause is emotional rather than physical

  4. Pain Sources • Fast vs. Slow Pain – • Fast – localized; carried through A-delta axons in skin • Slow – aching, throbbing, burning; carried by C fibers • Nociceptive neuron transmits pain info to spinal cord via unmyelinated C fibers & myelinated A-delta fibers. • The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec. • The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec. • Acute vs. Chronic

  5. What is Referred Pain? • Occurs away from pain site • Example: Kerr’s sign • Types of referred pain: • Myofascial Pain – trigger points, small hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain • Active – hyperirritable; causes obvious complaint • Latent – dormant; produces no pain except loss of ROM • Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury • Sclerotome: area of bone/fascia that is supplied by a single n. root • Myotome: m. supplied by a single n. root • Dermatome: area of skin supplied by a single n. root

  6. Noxious – harmful, injurious Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals) Nociceptor – nerve receptors that transmits pain impulses Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue Pain Tolerance – amount of pain a person is willing or able to tolerate Accommodation phenomenon – adaptation by the sensory receptors to various stimuli over an extended period of time (e.g. superficial hot & cold agents). Less sensitive to stimuli. Hyperesthesia – abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli Paresthesia – abnormal sensation, such as burning, pricking, tingling Inhibition – depression or arrest of a function Inhibitor – an agent that restrains/retards physiologic, chemical, or enzymatic action Analgesic – a neurologic or pharmacologic state in which painful stimuli are no longer painful Terminology

  7. P-Q-R-S-T format Provocation – How the injury occurred & what activities   the pain Quality - characteristics of pain – Aching (impingement), Burning (n. irritation), Sharp (acute injury), Radiating within dermatome (pressure on n.)? Referral/Radiation – Referred – site distant to damaged tissue that does not follow the course of a peripheral n. Radiating – follows peripheral n.; diffuse Severity – How bad is it? Pain scale Timing – When does it occur? p.m., a.m., before, during, after activity, all the time Pattern: onset & duration Area: location Intensity: level Nature: description Questions to Ask about Pain

  8. Pain Assessment Scales • Visual & Numeric Analog Scales • None Severe 0 10 • Locate area of pain on a pictures • McGill pain questionnaire • Evaluate sensory, evaluative, & affective components of pain • 20 subcategories, 78 words

  9. McGill Pain Questionnaire • 78 words that describe pain are grouped into 20 sets and divided into 4 categories representing dimensions of the pain experience • Completion may take 20 minutes • Administered every 2-4 weeks

  10. Goals In Managing Pain • To control acute pain and protect patient from further injury while encouraging progressive exercise in a supervised environment. • Reducing pain is an essential part of treatment

  11. Goals In Managing Pain • Encourage body to heal through exercise designed to progressively increase functional capacity and to return the patient to work, recreational and other activities as swiftly and safely as possible

  12. Transmission of Pain • Types of Nerves • Neurotransmitters

  13. Types of Nerves • Afferent (Ascending) – transmit impulses from the periphery to the brain • First Order neuron • Second Order neuron • Third Order neuron • Efferent (Descending) – transmit impulses from the brain to the periphery

  14. First Order Neurons • Stimulated by sensory receptors • End in the dorsal horn of the spinal cord • Types • A-alpha – non-pain impulses • A-beta – non-pain impulses • Large, myelinated • Low threshold mechanoreceptor; respond to light touch & low-intensity mechanical info • A-delta – pain impulses due to mechanical pressure • Large diameter, thinly myelinated • Short duration, sharp, fast, bright, localized sensation (prickling, stinging, burning) • C – pain impulses due to chemicals or mechanical • Small diameter, unmyelinated • Delayed onset, diffuse nagging sensation (aching, throbbing)

  15. Neural Transmission (First Order Neurons) • First order or primary afferents transmit impulses from the sensory receptor to the dorsal horn of the spinal cord

  16. Afferent First Order Neurons

  17. Second Order Neurons • Receive impulses from the FON in the dorsal horn • Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve • T Cells (transmission cells): transmission cell that connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain • Travel along the spinothalmic tract • Pass through Reticular Formation • Types • Wide range specific • Receive impulses from A-beta, A-delta, & C • Nociceptive specific • Receive impulses from A-delta & C • Ends in thalamus

  18. Neural Transmission (Second Order Neurons) • Second order afferent fibers carry sensory messages from the dorsal horn to the brain • Second order afferent fibers are categorized as wide dynamic range or nociceptive specific

  19. Neural Transmission(Second Order Neurons) • Wide dynamic range second order afferents receive input from A, A and C fibers. • Second order afferents serve relatively large, overlapping receptor fields • Nociceptive specific second order afferents respond exclusively to noxious stimulation • Receive input only from A and C fibers

  20. Third Order Neurons • Begins in thalamus • Ends in specific brain centers (cerebral cortex) • Perceive location, quality, intensity • Allows to feel pain, integrate past experiences & emotions and determine reaction to stimulus

  21. Neural Transmission(Third Order Neurons) • All of these neurons synapse with third order neurons which carry information to various brain centers where the input in integrated, interpreted and acted upon

  22. Descending Neurons • Descending Pain Modulation (Descending Pain Control Mechanism) • Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina) • Periaquaductal Gray Area (PGA) – release enkephalins • Nucleus Raphe Magnus (NRM) – release serotonin • The release of these neurotransmitters inhibit ascending neurons • Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes analgesia. • Endogenous opioid peptides - endorphins & enkephalins

  23. Neurotransmitters • Chemical substances that allow nerve impulses to move from one neuron to another • Found in synapses • Substance P - thought to be responsible for the transmission of pain-producing impulses • Acetylcholine – responsible for transmitting motor nerve impulses • Enkephalins – reduces pain perception by bonding to pain receptor sites • Norepinephrine – causes vasoconstriction • 2 types of chemical neurotransmitters that mediate pain • Endorphins - morphine-like neurohormone; thought to  pain threshold by binding to receptor sites • Serotonin - substance that causes local vasodilation &  permeability of capillaries • Both are generated by noxious stimuli, which activate the inhibition of pain transmission • Can be either excitatory or inhibitory

  24. Sensory Receptors • Mechanoreceptors – touch, light or deep pressure • Meissner’s corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkel’s corpuscles (deep pressure) • Thermoreceptors - heat, cold • Krause’s end bulbs ( temp & touch), Ruffini corpuscles (in the skin) – touch, tension, heat; (in joint capsules & ligaments – change of position) • Proprioceptors – change in length or tension • Muscle Spindles, Golgi Tendon Organs • Nociceptors – painful stimuli • mechanosensitive • chemosensitive

  25. Sensory Receptors

  26. Nerve Endings • “A nerve ending is the termination of a nerve fiber in a peripheral structure.” (Prentice, p. 37) • Nerve endings may be sensory (receptor) or motor (effector). • Nerve endings may be: • Respond to phasic activity - produce an impulse when the stimulus is  or , but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles) • Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs) • Superficial – Merkel’s corpuscles/disks, Meissner’s corpuscles • Deep – Pacinian corpuscles,

  27. Merkel’s corpuscles/disks - Sensitive to touch & vibration Slow adapting Superficial location Most sensitive Meissner’s corpuscles – Sensitive to light touch & vibrations Rapid adapting Superficial location Pacinian corpuscles - Sensitive to deep pressure & vibrations Rapid adapting Deep subcutaneous tissue location Krause’s end bulbs – Thermoreceptor Ruffini corpuscles/endings Thermoreceptor Sensitive to touch & tension Slow adapting Free nerve endings - Afferent Detects pain, touch, temperature, mechanical stimuli Nerve Endings

  28. Nociceptors • Sensitive to repeated or prolonged stimulation • Mechanosensitive – excited by stress & tissue damage • Chemosensitive – excited by the release of chemical mediators • Bradykinin, Histamine, Prostaglandins, Arachadonic Acid • Primary Hyperalgesia – due to injury • Secondary Hyperalgesia – due to spreading of chemical mediators

  29. Pain Control Theories • Gate Control Theory • Central Biasing Theory • Endogenous Opiates Theory

  30. Gate Control Theory • Melzack & Wall, 1965 • Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SON • Transmission Cell (T-cell) – distal end of the Second or neurons (SON) • If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neurons • If A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons

  31. Gate Control Theory • Gate - located in the dorsal horn of the spinal cord • Smaller, slower n. carry pain impulses • Larger, faster n. fibers carry other sensations • Impulses from faster fibers arriving @ gate 1st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation). Brain Pain Gate (T cells/ SG) Heat, Cold, Mechanical

  32. Gate Control Theory • Sensory information coming from A fibers is transmitted to higher centers in brain • “Pain message" carried along A & C fibers is not transmitted to second-order neurons and never reaches sensory centers

  33. Central Biasing Theory • Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectations • Cause release of enkephalins (PAG) and serotonin (NRM) • Enkephalin interneuron in area of the SG blocks A-delta & C neurons

  34. Endogenous Opiates Theory • Least understood of all the theories • Stimulation of A-delta & C fibers causes release of B-endorphins from the PAG & NRM Or • ACTH/B-lipotropin is released from the anterior pituitary in response to pain – broken down into B-endorphins and corticosteroids • Mechanism of action – similar to enkephalins to block ascending nerve impulses • Examples: TENS (low freq. & long pulse duration)

  35. Mechanisms of Pain Control • The theories presented are only models • Pain control is the result of overlapping mechanisms • Useful in conceptualizing the perception of pain and pain relief

  36. Pain Management • Therapeutic modalities can be used to • Stimulate large-diameter afferent fibers( TENS, massage, analgesic balms) • Decrease pain fiber transmission velocity (cold, ultrasound) • Stimulate small-diameter afferent fibers and descending pain control mechanisms (accupressure, deep massage, TENS)

  37. Pain Management • Therapeutic modalities can be used to • Stimulate release of endogenous opioids through prolonged small diameter fiber stimulation with TENS

  38. Goals in Managing Pain • Reduce pain! • Control acute pain! • Protect the patient from further injury while encouraging progressive exercise

  39. Other ways to control pain • Encourage central biasing – motivation, relaxation, positive thinking • Minimize tissue damage • Maintain communication w/ the athlete • If possible, allow exercise • Medications

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