pain control theories
TRANSCRIPT
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PAIN & PAIN CONTROL THEORIES
Managing Pain
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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 sensationPain Perceptions – based on expectations, past experience, anxiety, suggestions
Affective – one’s emotional factors that can affect pain experienceBehavioral – how one expresses or controls painCognitive – one’s beliefs (attitudes) about pain
Physiological response produced by activation of specific types of nerve fibersExperienced 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.
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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
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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
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What is Referred Pain?Occurs away from pain site
Examples: McBurney’s point, 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
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TerminologyNoxious – harmful, injurious
Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)
Nociceptor – nerve receptors that transmits pain impulsesPain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissuePain 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
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Questions to Ask about Pain
P-Q-R-S-T formatProvocation – How the injury occurred & what activities the painQuality - 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 scaleTiming – When does it occur? p.m., a.m., before, during, after activity, all the time
Pattern: onset & duration
Area: location
Intensity: level
Nature: description
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Pain Assessment ScalesVisual & Numeric Analog Scales None Severe
0 10Locate area of pain on a picturesMcGill pain questionnaire
Evaluate sensory, evaluative, & affective components of pain
• 20 subcategories, 78 words
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Transmission of Pain
Types of Nerves
Neurotransmitters
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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
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First Order NeuronsStimulated by sensory receptorsEnd in the dorsal horn of the spinal cordTypes
A-alpha – non-pain impulsesA-beta – non-pain impulses
• Large, myelinated• Low threshold mechanoreceptor; respond to light touch & low-
intensity mechanical infoA-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)
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Second Order NeuronsReceive 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
TypesWide range specific
• Receive impulses from A-beta, A-delta, & C
Nociceptive specific• Receive impulses from A-delta & C
Ends in thalamus
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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
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Descending NeuronsDescending 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 enkephalinsNucleus 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
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NeurotransmittersChemical substances that allow nerve impulses to move from one neuron to anotherFound in synapses
Substance P - thought to be responsible for the transmission of pain-producing impulsesAcetylcholine – responsible for transmitting motor nerve impulsesEnkephalins – reduces pain perception by bonding to pain receptor sitesNorepinephrine – 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
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Sensory ReceptorsMechanoreceptors – touch, light or deep pressure
Meissner’s corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkel’s corpuscles (deep pressure)
Thermoreceptors - heat, coldKrause’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 tensionMuscle Spindles, Golgi Tendon Organs
Nociceptors – painful stimuli mechanosensitivechemosensitive
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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 corpusclesDeep – Pacinian corpuscles,
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Nerve EndingsMerkel’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/endingsThermoreceptor
Sensitive to touch & tension
Slow adapting
Free nerve endings -Afferent
Detects pain, touch, temperature, mechanical stimuli
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NociceptorsSensitive to repeated or prolonged stimulationMechanosensitive – excited by stress & tissue damageChemosensitive – excited by the release of chemical mediators
Bradykinin, Histamine, Prostaglandins, Arachadonic Acid
Primary Hyperalgesia – due to injurySecondary Hyperalgesia – due to spreading of chemical mediators
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Pain Control TheoriesGate Control Theory
Central Biasing Theory
Endogenous Opiates Theory
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Gate Control TheoryMelzack & Wall, 1965Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SONTransmission Cell (T-cell) – distal end of the SON
If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neuronsIf A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons
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Gate Control TheoryGate - 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
Heat, Cold, Mechanical
Gate (T cells/ SG)
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Central Biasing Theory
Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectationsCause release of enkephalins (PAG) and serotonin (NRM)Enkephalin interneuron in area of the SG blocks A-delta & C neurons
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Endogenous Opiates TheoryLeast understood of all the theoriesStimulation 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)
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Goals in Managing Pain
Reduce pain!
Control acute pain!
Protect the patient from further injury while encouraging progressive exercise
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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