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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
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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
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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
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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.
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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)
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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
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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
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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
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list the 3 types of pain:
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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
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pain lasting beyond usefulness (usually >6 months), with no identifiable or treatable cause is called:
chronic pain
- leads to medication abuse
- difficulty sleeping
- depression
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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
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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 injuryit 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)
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pain caused by irritating nerve roots and extending distally is called:
- radiating pain
- -or-
- radicular
- -or-
- radiculopathy
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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)
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the level of noxious stimulus required to alert the individual to a potential threat to tissue is called:
pain threshold
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a measure of how much pain a person can or will withstand is called:
pain tolerance
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compare nociceptive pain vs. ischemic pain..
symptoms:
nsaids:
- nociceptive pain (inflammation)cardinal signs - redness, edema, heat
- tissue damage
- close relationship between stimulus and pain
- beneficial effects of NSAIDS
- ischemic painsymptoms after prolonged postures
- rapid ease of symptoms after posture changes
- symptoms toward end of day
- poor response to NSAIDS
- often no history of trauma
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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
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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)
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list the following of mechanoreceptors..
general term:
specific nature:
term:
location:
general term: pressure
- specific naturemovement of hair in a hair follicle
- light pressure
- deep pressure
- touch
- termafferent nerve fiber
- meissner's corpuscle
- pacinian corpuscle
- merkels touch corpuscle
- locationbase of hair follicles
- skin
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list the following of nociceptors:
general term:
specific nature:
term:
location:
- general term: pain
- specific nature: distension (stretch)
- term: free nerve endings
- location: wall of gastrointestinal tract, pharynx, skin
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list the following of proprioceptors:
general term:
specific nature:
term:
location:
general term: tension
- specific naturedistension
- length changes
- tension changes
- termcorpuscles of ruffini
- muscles spindles
- golgi tendon organs
- locationsskin and capsules in joints and ligaments
- skeletal muscles (spindles)
- between muscles and tendons (golgi tendons)
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list the following of thermoreceptors:
general term:
specific nature:
term:
location:
- 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
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transmission of information...
neurons:
axons:
neurotransmitters:
- neurons: classified using various categories
- axons: can either be myelinated or unmyelinated
- neurotransmitters: a substance that passes impulses between neurons
- - acetylcholine, substance P
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transmission of information..
nocioceptors:
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
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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
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non-noxious afferents... axon class 1a:
myelin:
conduction velocity:
specialized endings:
receptor location:
sensation:
- myelin: yes
- conduction velocity: 70-120 m/s
- specialized endings: muscle spindle
- receptor location: muscle
- sensation: proprioception
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non-noxious afferents... axon class 1b:
myelin:
conduction velocity:
specialized endings:
receptor location:
sensation:
- myelin: yes
- conduction velocity: 70-120
- specialized endings: golgi tendon organ
- receptor location: tendon
- sensation: muscle stretch, compression
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non-noxious afferents... axon class A(beta):
myelin:
conduction velocity:
specialized endings:
receptor location:
sensation:
- 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
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list the 3 non-noxious afferents:
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list the 2 noxious afferents:
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noxious afferents... axon class A(delta):
myelin:
conduction velocity:
specialized endings:
receptor location:
sensation:
- 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
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non-noxious afferents... axon class C:
myelin:
conduction velocity:
specialized endings:
receptor location:
sensation:
- 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
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list the following of internal sources of the transmission of pain...
fxn:
bradykinin:
substance P:
prostaglandin, histamine:
transduction:
- 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
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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
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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"
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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
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facilitators and inhibitors of synaptic transmission...
biogenic amine transmitters:
blocks noxious stimuli through descending neruons that block ascending pain sensations:
serotonin
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facilitators and inhibitors of synaptic transmission...
biogenic amine transmitters:
inhibits pain tranmission between 1st and 2nd order neurons:
- norepinephrine
- also released in inflammation: vasoconstriction
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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
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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:
enkephalin
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facilitators and inhibitors of synaptic transmission..
neuroactive peptides:
an opiod endogenous to the CNS:
beta endorphins
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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:
epicriptic
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peripheral pathways of the transmission of pain..
a nociceptive neuron is on that transmits pain signals...
second pain, activation of C fibers is called:
protopathic
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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
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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)
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mechanism of pain, central pathways..
2nd order neurons carry stimuli in the:
contralateral anterolateral section of the spinal cord
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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)
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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
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mechanisms of pain control...
pain modulated at Spinal cord level:
gate theory (ascending pathway)
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mechanisms of pain control...
pain modulated at peripheral, spinal cord, and cortical levels is called:
endogenous opiate system (descending)
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mechanisms of pain control...
descending pathway based on cognitive assessment (prepared for pain, body releases endorphins) is called:
central biasing
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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
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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
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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
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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
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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
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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
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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
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list and describe the 3 pain management techniques:
physical:
behavioral and congnitive:
pharmacologic:
- physicalusing therapeutic modalities
- immobilization, ect
- modalities address the symptoms
- do not rely solely on the use of therapeutic modalities
- behavioral and cognitivedecrease 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
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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
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