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  1. list 3 reasons why we study pain:
    • many of the modalities used in AT reduce pain associated with an injury
    • learn how to apply knowledge of rehab and desired outcomes to newly developed modalities
    • indication of pathology
  2. what is pain:
    • noxious (damaging & uncomfortable) stimulus that is associated with actual or potential tissue damage
    • a stimulus of sufficient intensity that triggers a sense organ to fire
    • nerves (are the sense organ) fire as all or none - little pain vs. a lot of pain depends on how many nerves are fired
  3. can you have nociception without pain?

    can you have pain without nociception?
    • nociception without pain: "feels like there will be a reinjury"
    • pain without nociception: amputation, phantom pain
  4. list 4 objectives of understanding pain:
    • pain is a subjective sensation
    • perception of pain can be subjectively modified by past experiences and expectations
    • much of what we do to treat pain is to change perception of pain
    • control of pain is an essential aspect of caring for the injured pt.
  5. list and describe the 3 dimensions of pain:
    • sensory: discriminative (what you feel... sharp, dull, where)
    • cognitive: evaluative (interpret with higher brain, quantify pain)
    • affective: motivational (how does it change things)
  6. list 3 positive effects of pain:
    • warns us that something is wrong
    • invokes a spasm to protect the injured area (primary for back pain)
    • provides a stimulus for the withdrawal reflex
  7. list 7 negative effects of pain:
    • enhances disability (unable to do normal)
    • can cause prolonged spasm
    • decrease in circulation (no new oxygen, secondary death)
    • muscle atrophy (no muscle contraction)
    • develop disuse habits (limping, trundelenburg gait)
    • conscious or unconscious guarding
    • loss of athletic ability
  8. list 7 social and cultural influences on pain:
    • cognitive-evaluative (impact of injury, past experiences)
    • gender
    • personality type
    • presence of peers
    • ethnicity
    • type of sport
    • overriding events
  9. list the 3 types of pain:
    • acute
    • chronic
    • referred
  10. immediate, sudden onset of pain; a signal that something is wrong is called:
    acute pain

    • usually resolves in < 6 months (the whole healing process)
    • potential protection from injury
    • underlying pathology
    • results in muscle spasm, guarding, etc.
    • corresponds to evens of acute inflammatory response
  11. pain lasting beyond usefulness (usually >6 months), with no identifiable or treatable cause is called:
    chronic pain

    • leads to medication abuse
    • difficulty sleeping
    • depression
  12. list 7 types of chronic pain that is a disease entity unto itself:
    • reflex sympathetic dystrophy (RDS) - advanced
    • CRPS - Complex regional pain syndrome
    • rheumatic disease - arthritis
    • intractable back pain
    • intractable phantom limb pain
    • neuropathy
    • myofascial pain syndrome
  13. a pathology that is one area and the pain is perceived in another area is called:

    list 4 reasons why this pain may outlast the effects of the injury:
    referred pain

    • may outlast the effects of the injury
    • it alters the reflex pattern of the nerves
    • of continued mechanical stress on msucles
    • learned habits of guarding
    • long-term established trigger points (TPs are localized, deep tenderness in a firm band of muscle)
  14. pain caused by irritating nerve roots and extending distally is called:
    • radiating pain
    • -or-
    • radicular
    • -or-
    • radiculopathy
  15. pain from an amputated limb is called:

    what is this the result of:
    • phantom pain
    • result of: activiation of nerves at the surface of the stump (theory)
  16. the level of noxious stimulus required to alert the individual to a potential threat to tissue is called:
    pain threshold
  17. a measure of how much pain a person can or will withstand is called:
    pain tolerance
  18. compare nociceptive pain vs. ischemic pain..

    • nociceptive pain (inflammation)
    • cardinal signs - redness, edema, heat
    • tissue damage
    • close relationship between stimulus and pain
    • beneficial effects of NSAIDS

    • ischemic pain
    • symptoms after prolonged postures
    • rapid ease of symptoms after posture changes
    • symptoms toward end of day
    • poor response to NSAIDS
    • often no history of trauma
  19. the reduction in impulse frequency that occurs with a prolonged, constant stimulus or frequently repeated stimuli si called:
    • accommodation
    • -or-
    • adaption
    • ex: carrying a back pack
  20. list in order from the most to least sensitive tissue to pain (5):
    • joint capsule: has the most nerves (proprioceptors)
    • periosteum: covering around the bone (stress fx's)
    • subchondral bone, tendon, and ligaments
    • muscle and coritcal bone (less dense part of the bone)
    • synovium and articular cartilage (not high healing potential; pain is usually associated with another injrury)
  21. list the following of mechanoreceptors..

    general term:
    specific nature:
    general term: pressure

    • specific nature
    • movement of hair in a hair follicle
    • light pressure
    • deep pressure
    • touch

    • term
    • afferent nerve fiber
    • meissner's corpuscle
    • pacinian corpuscle
    • merkels touch corpuscle

    • location
    • base of hair follicles
    • skin
  22. list the following of nociceptors:

    general term:
    specific nature:
    • general term: pain
    • specific nature: distension (stretch)
    • term: free nerve endings
    • location: wall of gastrointestinal tract, pharynx, skin
  23. list the following of proprioceptors:

    general term:
    specific nature:
    general term: tension

    • specific nature
    • distension
    • length changes
    • tension changes

    • term
    • corpuscles of ruffini
    • muscles spindles
    • golgi tendon organs

    • locations
    • skin and capsules in joints and ligaments
    • skeletal muscles (spindles)
    • between muscles and tendons (golgi tendons)
  24. list the following of thermoreceptors:

    general term:
    specific nature:
    • general term: temperature changes
    • specific nature: cold, heat
    • term: krause's end bulbs, corpuscles of ruffini
    • location: skin, skin and capusles in joints and ligaments
  25. transmission of information...

    • neurons: classified using various categories
    • axons: can either be myelinated or unmyelinated
    • neurotransmitters: a substance that passes impulses between neurons
    •   - acetylcholine, substance P
  26. transmission of information..

    afferent nerve fibers:
    efferent nerve fibers:
    • nocioceptors: (pain receptors) respond to noxious (damaging) stimuli 
    •   -chemoreceptive
    •   -mechanoreceptive
    •   -thermoreceptive
    • afferent nerve fibers: carry impulses to sense organs to the spinal cord
    • efferent nerve fibers: carry impulses from the brain the to muscles or the periphery
  27. define hyperesthesia (allodynia) of transmission of pain:

    primary hyperesthesia:
    secondary hyperesthesia:
    • hyperesthesia (allodynia): a normal non painful stimulus becomes painful
    • primary hyperesthesia: occurs  immediately after an injury, lowering of nerve's threshold (sensitization) to noxious stimuli
    • secondary hyperesthesia: increase in size of the painful area, due to the diffusion of chemicals into the surrounding area
  28. non-noxious afferents... axon class 1a:

    conduction velocity:
    specialized endings:
    receptor location: 
    • myelin: yes
    • conduction velocity: 70-120 m/s
    • specialized endings: muscle spindle
    • receptor location: muscle
    • sensation: proprioception
  29. non-noxious afferents... axon class 1b:

    conduction velocity:
    specialized endings:
    receptor location:
    • myelin: yes
    • conduction velocity: 70-120
    • specialized endings: golgi tendon organ
    • receptor location: tendon
    • sensation: muscle stretch, compression
  30. non-noxious afferents... axon class A(beta):

    conduction velocity:
    specialized endings:
    receptor location: 
    • myelin: yes
    • conduction velocity: 25-70 m/s
    • specialized endings: meissner corpusle, Ruffini endings, hair follicle, paciniform endings, muscle spindle
    • receptor location: skin, joint, muscle
    • sensations: touch, pressure, vibration, position sense, stretch of muscle
  31. list the 3 non-noxious afferents:
    • 1a
    • 1b
    • A(beta)
  32. list the 2 noxious afferents:
    • A(delta)
    • C
  33. noxious afferents... axon class A(delta):

    conduction velocity:
    specialized endings:
    receptor location: 
    • myelin: yes (thinly)
    • conduction velocity: 2-25 m/s
    • specialized endings: free nerve endings
    • receptor locations: skin, muscle, joint, tendons, disc, bone, periosteum, fascia
    • sensation: noxious stimuli
  34. non-noxious afferents... axon class C:

    conduction velocity:
    specialized endings:
    receptor location: 
    • myelin: no
    • conduction velocity: <2 m/s
    • specialized endings: free nerve endings
    • receptors locations: skin, muscle, joint, tendons, disc, bone, periosteum, fascia
    • sensation: noxious stimuli
  35. list the following of internal sources of the transmission of pain...

    substance P:
    prostaglandin, histamine:
    • fxn: chemcial mediators of inflammation process sensitize
    • bradykinin: direct stimulation of nerve fibers (vasodilation)
    • substance P: neurotransmitter released centrally to produce (sensitize) pain from peripheral (lowers threshold for pain fibers)
    • prostaglandin, Histamine: sensitization of nerve fibers so that other meidators can inititate nociception
    • transduction: converts original stimuli to action potential
    • propagates along afferant fibers to Spinal cord
    • histamine: vasodilate, directly stimulates nociceptors
  36. peripheral pathways of transmission of pain....

    which fibers are 1st order afferants:
    • first order afferants: A(delta) and C fibers
    • ~50% of sensory endings are nociceptors
    •   -80% are C fibers (more likely to feel dull, achy pain, slow, so no new stimulus - C fibers... new stimulus the A(delta))
    •   - 20% A delta
  37. A-deltas and C fibers transmit sensations of:
    A-delta neurons originate from:
    A deltas transmit:
    C neurons originate from:
    C neurons transmit:
    • A-deltas and C fibers transmit sensations of:pain and temperature (A-delta fibers are larger)
    •  A-delta neurons originate from:receptors located in skin
    •  A deltas transmit: "fast pain"
    • C neurons originate from:both superficial tissue (skin) and deep tissue (ligaments and muscle)
    •  C neurons transmit: "slow pain"
  38. noxious (pain) fibers:

    large, thinly myelinated (local, sharp, stinging, and burning sensations):
    small unmyelinated (diffuse aching, throbbing, and nagging sensation)
    located in the dorsal root ganglia:
    • large, thinly myelinated (local, sharp, stinging, and burning sensations): A delta
    • small unmyelinated (diffuse aching, throbbing, and nagging sensation): C fibers
    • located in the dorsal root ganglia: cell bodies
  39. facilitators and inhibitors of synaptic transmission...

    biogenic amine transmitters:

    blocks noxious stimuli through descending neruons that block ascending pain sensations:
  40. facilitators and inhibitors of synaptic transmission...

    biogenic amine transmitters:

    inhibits pain tranmission between 1st and 2nd order neurons:
    • norepinephrine
    • also released in inflammation: vasoconstriction
  41. facilitators and inhibitors of synaptic transmission..

    neuroactive peptides:

    peptide belived to be a NTM of small diameter primary afferents that is released between 1& 2 order neurons
    • substance P
    •   - hyperalgesia: normally not painfull, but release of NTs makes it painful
  42. facilitators and inhibitors of synaptic transmission..

    neuroactive peptides:

    opiod that inhibits the release of substance P - some descending neurons release it to block ascending signals:
  43. facilitators and inhibitors of synaptic transmission..

    neuroactive peptides:

    an opiod endogenous to the CNS:
    beta endorphins
  44. peripheral pathways of the transmission of pain..

    a nociceptive neuron is on that transmits pain signals...

    the 1st pain, or initial rxn, activation of the A delta fibers is called:
  45. peripheral pathways of the transmission of pain..

    a nociceptive neuron is on that transmits pain signals...

    second pain, activation of C fibers is called:
  46. the mechanism of pain, central pathways...

    1st order neurons synapse:

    2nd order neurons known as:
    • 1st order neurons synapse: directly or with interneuron... with 2nd order in dorsal horn of gray matter (substantia gelatinosa)
    • 2nd order neurons known as: transmission or T cells
  47. list and describe the 5 steps in the pain spasm pain cycle:
    • T cell activation can also increase muscle spasm via spinal reflex
    • synapse with motor efferent in anterior horn
    • activates
    • gives reflexive muscle contraction
    • subsequent mechanical and chemical stimuli with further activates hypersensitive nociceptors
    • correct physical agents may....
    • slow cycle/break cycle: ice, elevation, activates A betas... massage, rubbing, compression, stim (electricity)
  48. mechanism of pain, central pathways..

    2nd order neurons carry stimuli in the:
    contralateral anterolateral section of the spinal cord
  49. the mechanism of pain, central pathways...

    which of the spinothalamic tracts projects to the thalamus, transmits sensory and noxious stimuli, and transmits sharp, more localized pain:
    • lateral spinothalamic tract
    • *project to thalamus (changes in BP, HR)
  50. of the mechanism of pain, central pathways.. the anterospinothalamic tract....

    what does it separate:
    synapses with interneurons in which 3 structures:
    projects to the:
    also relays to which structure that has a high concentration of opiate receptors:
    what type of pain does it transmit:
    • separates: from lateral tract in the brainstem
    • synapse with interneurons in: reticular formation, hypothalamic, and limbic systems (emotions, crying, anger)
    • projects to:the thalamus
    • also relays to: periaqueductal gray matter where there is high concentration of opiate receptors (natural endorphins, NT that helps inhibit pain)
    • pain transmitted: prolonged, aching pain with stronger association to emotional disturbances (chronic pain)
    • more likely to be on pain killers
  51. mechanisms of pain control...

    pain modulated at Spinal cord level:
    gate theory (ascending pathway)
  52. mechanisms of pain control...

    pain modulated at peripheral, spinal cord, and cortical levels is called:
    endogenous opiate system (descending)
  53. mechanisms of pain control...

    descending pathway based on cognitive assessment (prepared for pain, body releases endorphins) is called:
    central biasing
  54. define the gate control theory of pain modulation:
    • severity of pain dictated by balance of excitatory and inhibitory inputs to T cells in spinal cord
    • inhibitory..
    • excitatory: A beta's
    • many physical agents thought to control pain by activating nonnoxious sensory receptors
  55. explain why the gate control theory (melzack and Wall) supports that nonpainful stimulus can block the transmission of noxious stimulus:
    never fibers

    • C fibers and A delta (pain impulses)
    • small diameter
    • unmyelinated
    • slow

    • A beta (non pain fibers)
    • large diameter
    • myelinated
    • fast
  56. explain how the gate control theory "works" when the fibers are approaching the substantia gelatinosa of the dorsal horn ) (6):
    • information from ascending A-beta afferents and (pain messages) carried along A-deltas and C fibers enter the dorsal horn
    • impulses stimulate the substantia gelatinosa at the dorsal horn of the spinal cord inhibiting synaptic transmission in A-delta and C fibers afferent pathways
    • non-noxious will block noxious
    • noxious will get thru eventually
    •   -pain stimulus remains present or increases
    •   - non-noxious is removed or accommodation occurs
    • sensory information coming from A-beta fibers is transmitted to higher centers in brain
    • "pain message" carried along A-delta and C Fibers is not transmitted to 2nd order neurons and never reaches sensory centers
  57. endogenous opiate system, pain modulation...

    endorphins or opiopeptin:
    controls pain by:
    confirmed through:
    high concentrations in which 2 structures:
    • endorphins or opiopeptin: endogenous opiate like peptide shown to modulate pain
    • control pain by: binding to opiate receptors (thoughout peripheral and central nervous system) like morphine
    • confirmed thru: use of naloxone (opiate antagonist) - suboxone
    • high concentration in: PAGM and Raphe nnucleus in brain (stimulation gives analgesia (relives pain))
    • also found in nerve endings and superficial layer of dorsal horn in Spinal cord
  58. list and describe the 3 mechanisms of pain modulation by the endogenous opiate system:
    • opiate receptors binding thought to inhibit release of Substance P (sensitize) at peripheral level
    • Opioids have a synaptic inhibitory action (presynaptic and post synaptic inhibition)
    • indirectly inhibit pain by inhibiting release of GABA (gamma- aminobutyric acid) (inhibits acitivity of A-beta's, non noxcious pain) in PAGM  - GABA inhibits activity of A-betas, PAGM, and raphe nucleus thus increasing pain
  59. describe how stressful situations (noxious, uncomfortable) (physical, emotional) are also shown to cause release of endogenous opiates:
    • explanation of noxious estim and acupuncture to relieve chronic pain (longer results than gate theory)
    • can get ready for pain
    • placebo effect also partially explained by opiate theory (confirmed thru use of naloxone (opiate antagonist))
    • long lasting pain relief
  60. theories presented are only models
    pain control is the result of overlapping mechanisms
    • useful in conceptualizing the perception of pain and pain relief
    • odalities are used with specific tx parameters to open or close the gate to elicit desired tx responses
  61. list and describe the 3 pain management techniques:

    behavioral and congnitive:
    • physical
    • using therapeutic modalities
    • immobilization, ect
    • modalities address the symptoms
    • do not rely solely on the use of therapeutic modalities

    • behavioral and cognitive
    • decrease anxiety
    • educate about pain and injury
    • use focus, relaxation, diversion, motivational, and positive thinking techniques

    pharmacological: use of chemical to alter pain

    all of these techniques should be part of a pain management program
  62. list 3 modifications or alterations that pharmacologic pain management provides:
    • modifies inflammatory mediators (prostaglandins)
    • alters transmission from periphery to cortex (opiates)
    • alters central perception of pain
    • selection based on: cause, length, and side effects
Card Set:
2014-02-16 03:22:15
physiology psychology pain

physiology and psychology of pain
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