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Physical Agents > Pain modulation > Flashcards

Pain modulation Flashcards

1
Q

Duality of pain

A
  • Physiological experience

- Psychological experience

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2
Q

Function of pain

A
  • warning for withdrawl
  • alerts that something is wrong
  • protective function ( spasm)
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3
Q

Goals of pain treatment

A
  • To resolve the underlying pathology causing pain
  • to modify the patient’s perception of pain so as to allow them to participate in other PT interventions
  • to allow the pt to maximize their functional abilities
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4
Q

categories of pain nociceptive: Somatic

A

Activation of nociceptors found in most body tissue

  • respond to mechanical and chemical stimuli
  • found in integument, arthromusculoskeltal systems
  • caused by injury, disease, or surgical intervention
  • often referred to as normal pain
  • often treated with EPAs
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5
Q

categories of pain nociceptive: Visceral

A

Activation of nociceptors found in viscera

  • Referred
  • diffuse and poorly localized
  • specificity: not all visera are sensitive to pain
  • EPAs not effective
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6
Q

categories of pain neuropathic: Peripheral pain

A

disease associated with peripheral nerves

-often treated with EPAs

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7
Q

categories of pain neuropathic: Central pain

A

due to pathological functioning of the CNS

  • often delayed as in stroke, MS, Parkinson’s
  • Seldom treated with EPAs
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8
Q

categories of pain psychogenic

A
  • originates from nonorganic sources
  • associated with emotional, cognitive, and behavioral responses
  • Not treated with EPAs
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9
Q

categories of pain carcinogenic

A
  • Caused by cancerous pathology
  • severe
  • EPAs not effective
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10
Q

Types of pain

A
  • Acute
  • Chronic
  • Referred
  • Radicular
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11
Q

Acute pain

A
  • time limited
  • mediated through rapidly conducting pathways
  • associated with increased sympathetic nervous system activity
  • intensity: related to extent of tissue damage
  • location- well localized and defined
  • duration- as long as noxious stimulus persists
  • serves as protective function
  • may impair function
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12
Q

Acute pain treatment aimed to:

A
  • Facilitate resolution of underlying disorder
  • reduce inflammation
  • modify the transmission of pain from periphery to CNS
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13
Q

Chronic pain

A
  • duration: several months to years
  • symptoms: similar to original symptoms
  • history of many treatment failures
  • history of many medications tried
  • continued use of analgesics and tranquilizers despite no long term effects
  • intensity: unbearable or incapacitating
  • often seeking the “right treatment” to cure pain
  • result
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14
Q

Chronic pain psychosocial changes

A
  • Depression
  • Disturbed sleep
  • Altered moods
  • weight changes
  • decreased energy
  • decreased physical, social, and recreational activities
  • increased family stresses
  • increased economic difficulties
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15
Q

Chronic pain psychosocial results from

A

changes in sympathetic NS, adrenal activity, reduced production of endogenous opioids, or sensitization of primary afferents

  • increased sensitivity to both noxious (hyperalgesia) and non-noxious (allodynia) stimuli
  • wind-up or central hypersensitization
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16
Q

Referred pain

A

Pain felt at a location distant from its source
-from a nerve to its area of innervation
- from one area to another derived from the same dermatome
- from one area to another derived from the same embrionic segment
Peripheral nerve pathways from different areas converge on the same area of the spinal cord
-synapse with the same second order neurons to ascent to the cerebral cortex

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17
Q

Referred Pain example

A

Pain is referred from the diaphragm to the tip of the shoulder-both areas initially develop in the neck region during embyological development

  • both have efferent innervation from phrenic nerve
  • both have afferent innervation to the second & fourth level of C-spine
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18
Q

Pain of visceral or musculoskeletal origin converging on sam neuron in spinal cord

A
  • usually interpreted as musculoskeletal
  • musculoskeletal more common thus brain learns that stimulus along this pathway is more likely to be musculoskeletal and distributed to musculoskeletal area
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19
Q

Radicular pain

A
  • Originating from an irritated nerve root

- follows dermatomal reference

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20
Q

Danger alarm system

A
  • Transduction-Danger receptors
  • peripheral transmission
  • modulation
  • central transmission
  • perception
  • pain control theories
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21
Q

Transduction

A

Sensors-danger receptors

  • in walls and at ends of neurons
  • convey info to spinal cord
  • can be specialized
    • mechanical
    • chemical
    • temperature
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22
Q

Superficial peripheral sensory receptors

A
  • Mechano
  • Thermo
  • Noci
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23
Q

Mechano receptors

A
  • Meissner’s corpuscles-Pressure and touch
  • Pacinian corpuscles- Pressure and touch
  • merkle cells- skin, stretch, & pressure
  • Ruffini endings- skin, stretch, & pressure
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24
Q

Thermoreceptors

A
  • Cold receptors
  • Hot receptors
  • **Temperature and temperature change
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25
Q

Nociceptors

A

Free nerve endings- Pain

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26
Q

Deep peripheral sensory receptors

A
  • Proprio

- Noci

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27
Q

Proprioceptors

A
  • Golgi tendon organ: change in muscle length & muscle spindle tension
  • Pacinian corpuscle: change in jt position & vibration
  • Ruffini endings: jt end range/?heat
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28
Q

The danger alarm system transduction: Sensors (danger receptors)

A

Respond by opening
- allow + charged particles into neuron
- sets off AP
Can be opened or shut by chemicals
- pain meds closes sensor thus it cannot transmit impulses to spinal cord
- bee sting opens sensors thus floods spinal cord with impulses
-life of sensor is short (days)
- number and type of sensor is under direction of neuronal DNA in dorsal horn nuclei
- rate of production generally stable
- can change sensitivity of neuron if change rate of sensor production

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29
Q

The danger alarm system transduction: Nociceptor “danger receptor”

A
  • free nerve endings involved in danger detection
  • skin-cutaneous danger
  • tendons & jts- somatic danger
  • body organs- somatic danger
  • Responds to all manner of stimuli
  • if enough sensors are opened a danger message is sent to spinal cord
  • high activation threshold
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30
Q

The danger alarm system: Peripheral transmission afferent nerve pathway

A

Part of neuron with cell body outside spinal column in dorsal root ganglion

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31
Q

The danger alarm system: peripheral transmission peripheral nerve afferent fibers

A
  • beta fibers: 6-12 um diameter myelinated transmit impulses at >30 m/sec
  • delta fibers- 1-6 um diameter myelinated, transmit impules @ up to 30 m/sec
  • C fibers- 1 mm thick unmyelinated transmit impulses @ 1-4 m/sec
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32
Q

A-beta fibers

A
  • first order afferents, myelinated
  • large, myelinated, fast conducting
  • low stimulation threshold
  • location: skin
  • info transmitted: touch, vibration, hair deflection
  • originates in hair follicles, Meissner’s corpuscles, pacinian corpuscles, merkle cell endings, ruffini endings
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33
Q

A-delta fibers

A
  • first order afferent, myelinated
  • originate from warm/cold receptors, few hair follicles, and free nerve endings
  • group III afferents
  • noxious mechanical stimulus (pinch, prick,crushing)
  • may transmit non noxious stimulus also
  • large, myelinated, slower than A-beta
  • quick onset, short duration
  • well localized to area of injury
  • not involved in emotional response
  • not blocked by opiates
  • info transmitted: touch, temp, pressure, pain
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34
Q

C-fibers

A
  • first order afferent, unmyelinated
  • 80% of afferent danger-transmitting fibers
  • AKA: group IV afferents
  • small, unmyelinated, transmit AP slowly
  • respond to noxious levels of mechanical, thermal, and chemical stimulation
  • result in sensation felt as dull, throbbing, burning, aching, tingling, tapping
  • slow onset after initial stimulus
  • long lasting emotionally difficult to tolerate
  • diffuse locally
  • can be accompanied by autonomic responses such as sweating, increase HR, BP, or nausea
  • reduced by opiates, blocked by opiate antagonist naloxone
  • location: muscle, skin
  • info transmitted: pain, touch, temp, pressure, pain
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35
Q

Danger alarm system peripheral transmission: mechanical trauma

A

Activates both A-delta and C-fibers
Drop brick on foot
-immediate sharp sensation ( A-delta)
- produced by high intensity mechanical stimulus
-deep ache may develop that lasts hours (c-fibers)
-produced by chemical mediators of inflammation process

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36
Q

Danger alarm system central transmission: A delta fibers

A

Ascend in lateral spinothalamic tract and synapse with 3rd order neurons in thalamus, relay info to somatosensory cortex in postcentral gyrus

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37
Q

Danger alarm system central transmission: C-fibers

A

Ascend in anterior spinal thalamic tract and synapse in reticular formation and intralaminar nuclei of thalamus, relay info to association cortex

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38
Q

First pain pathway

A
  • Frontal lobe>
  • medial lemiscus in midbrain>
  • Spinal nucleus of CN V>
  • Dorsal column second order nueron
  • lateral spinothalamic tract>
  • 1st order neuron
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39
Q

Second pain pathway

A
  • Dorsal root ganglion in spinal column>
  • up paleospinothalamic, spinomesencephalic, and spinoreticular tracts (multisynaptic afferent systems)
  • CNs V, IX, X>
  • periaqueductal grey>
  • frontal lobe
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40
Q

Danger alarm system central transmission: neurons that transmit pain

A
  • NS: nociceptive specific

- WRD: wide range dynamic

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41
Q

Danger alarm system central transmission: spinothalamic tract

A

primary nociceptive pathway

- transmits type/location of pain

42
Q

Danger alarm system central transmission: spinoreticular tract

A

Motivational, emotional, unpleasant aspect of pain

43
Q

Danger alarm system central transmission: spinomesencephalic tract

A

Sensorimotor integration of pain

44
Q

Danger alarm system central transmission: spinohypothalamic tract

A

Lymbic tract: autonomic responses associated with pain

45
Q

Danger alarm system central transmission: sub-cortical centers

A
  • reticular formation
  • periaqueductual gray
  • hypothalamus
  • pitutiary
  • thalamus
  • limbic system
46
Q

reticular formation

A

meidates autonomic and sensory functions

47
Q

periaqueductual gray

A

directs descending inhibition

48
Q

hypothalamus:

A

controls endocrine functions and vegetative state

49
Q

pitutiary

A

master gland for endocrine system

50
Q

thalamus

A

final gateway and relay center

51
Q

limbic system

A

involved in emotional, motivational, and affective behavior

52
Q

Danger alarm system central transmission: Somatosensory cortex

A
  • Area of brain that identifies location of pain
  • central processing center
  • location and extent of danger associated with activation of somatosensory cortex
53
Q

Danger alarm system central transmission: association cortex

A
  • Responsible for affect that is associated with danger signals
  • appraise the danger associated with the situation
  • results in pain tolerance
54
Q

Specificity theory

A
  • Pain modulation theory
  • sensation of pain depends on stim of specific nerve endings that are specialized for that sensation
  • specific pain fibers are responsible for transmission of pain
  • will always transmit the same sensation
  • Von frey identified free nerve endings in skin that caused pain when stimulated
  • However…
  • sensation of pain does NOT have precise one to one relationship with type of receptor stimulated
  • many types of stimuli can be perceived as painful
  • pain can be modulated by input from the spinal cord or brain
55
Q

Pattern theory

A
  • pain mod theory
  • senstation of pain results from appropriate intensity/frequency of stim of receptors that also respond to other stimuli like touch, pressure, temp
  • temporal and spatial summation of impulses from periphery to cerebral levels determines perception of pain
  • accounts for wide variety of stimuli can cause sensation of pain
  • central influence of pain perception
  • BUT:
  • fails to consider role of specific identified receptors
  • fails to account for affective or central pain mod
56
Q

Peripheral pain modulation theory

A
  • Desensitize peripheral receptors activated during inflammatory process
  • bradykini, prostaglandin E2 and serotonin facilitate nociceptor sensitivity
  • stein identified opioid receptors at peripheral nerve terminals
  • effects most pronounced during inflammatory conditions
  • non thermal US reduces pain during inflammatory stage
  • MENS microcurrent electrical nerve stimulation desensitizes peripheral receptors
57
Q

Gate control theory

A
  • Melzak and wall 1965
  • nerve impulses evoked by injury are influenced in the spinal cord by other nerve cells that act like gates
  • pain sensation> balance of excitation & inhibition input on T-cells
  • increased activity of nonnociceptor sensory afferents> presynaptic inhibition of T cells
  • closes spinal “gate” to higher cerebral cortex centers> decreased sensation to pain
  • enkephalin interneuron inhibits pain transmission in dorsal horn
58
Q

Gate control theory mechanism

A
  • IA, IIA, A-beta fibers stimulate T cells which cause second order wide dynamic range afferent. they also stimulate the spinal gate which releases enkephalon interneuron that stimulates T cells to release enkephalon to cause second order nociceptive afferent
  • A-delta fibers and C-fiber nociceptors also stimulate T cell to release Enkephalon
59
Q

Gate control theory influenced by phys agents

A
  • electrical stimulation, massage, traction, compression> activate nonnociceptor sensory afferents ( low-threshold, large diameter, nonnociceptor sensory nerves)
  • inhibits T cell activation in spinal cord
  • Does NOT account for desending controls from higher brain centers
60
Q

Supraspinal and Descending pain modulation

A
  • uses feedback loops to inhibit pain transmission at dorsal horn
  • results in release of endogenous opioids
  • involves numerous nuclei in brainstem reticular formation including PAG and raphe nucleus
61
Q

Endogenous opioid system

A
  • 1973 disovered separate opiate binding sites in the CNS
  • 1975 two peptides (met-enkephalin and luenkephlin) produced physiological effects similar to morphine
  • bind specifically with opiate antagonist
  • other similar peptides identified
  • beta-endorphin, dynorphin A and B
62
Q

Endogenous opioid system: opiopeptins

A

Control pain by binding with specific opiate receptors in the NS

  • localized in many peripheral nerve endings
  • identified in PAGM, raphe nucleus in brain stem> structures that induce analgesia
  • inhibit release of substance P from C fiber terminals
  • always have inhibitory effect
  • presynaptic inhibition- suppress influx of calcium
  • post synaptic inhibition-activate outflow of K+ current
  • indirectly inhibit pain transmission by inhibiting release of GABA in PAGM and raphe nucleus
63
Q

Motor pain modulation

A
  • Used to enhance the production of endogenous endorphins in anterior pituitary
  • low frequency (2-7 cps) high intensity stimulation of peripheral nn stimulates pituitary
  • has stimulating effect on raphe nucleus and PAG region of midbrain
  • end result: stimulation of descending pain control system in dorsal horn
64
Q

Noxious pain modulation

A
  • Stimulation of C-fibers activates PAG region
  • second system activates the Pons
  • end result is stimulation of descending inhibition system in dorsal horn
  • long phase duration E-stim an dice can be used to activate this system
65
Q

Neuromatrix theory

A
  • Pain is multidimentional experience
  • produced by characteristic patterns of nerve impulses generated by widely distributed nerve network in the brain
  • determined by heredity
  • included psychosocial factors, prior pain experience, cognitive and emotional experiences, general life stress
66
Q

Nerve block pain modulation

A
  • After nerve depolarization there is a refractory period where cell membrane cant depolarize
  • application of medium frequency electrical current hyperpolarizes membrane further and blocks AP
  • area between electrodes becomes temporarily anesthetized
67
Q

Pain relies on context

A
  • Splinter in finger
  • ignition cues
  • sensory cues that help start painful experience
  • social consequences of being in pain
68
Q

Altered danger alarms

A

Spinal cord

  • adaptation begins within few secs
  • danger messenger neurons increase sensitivity to incoming excitatory chemicals
  • results in:
    • hyperalgesia: that which hurts now, hurts more
    • allodynia: that which did not hurt, now does
69
Q

Pain assessment techniques

A
  • VAS
  • Pain charts
  • McGill pain Questionnaire
  • Activity pattern indicators profile
  • numeric pain scales
  • pressure algometry
70
Q

Mcgill pain questionnaire (MPQ)

A

includes descriptors of sensory, affective, and evaluative aspects of pts pain

  • sensory: temporal, spatial, pressure, thermal
  • affective: fear, anxiety, tension
  • evaluative: congnitive experience of pain in past and learned behaviors
  • circles one word that best describes their pain
  • sensitive to clinical changes
71
Q

semantic differential scales

A
  • word lists and categories that represent various aspects of pain experience
  • Pt selects words that best describe pain experiences
  • provide quantifiable data for intra and intersubject comparisions
72
Q

Pressure algometry

A

-determines a pt’s force to pain onset

73
Q

Pain management approaches: pharmacological

A
  • modify inflammatory mediators peripherally
  • alter pain transmission from periphery to cortex
  • alter central perception of pain
  • agent choosen depends on:
  • cause of pain
  • length of time meds will be needed
  • side effects of meds
74
Q

Systemic analgesics

A
  • easy to administer
  • inexpensive
  • include NSAIDS, acetaminophen, opiates, and opiods, and antidepressants
75
Q

NSAIDS

A
  • have analgesic, anti-inflammatory, antipyretic, anticoagulant and possibly anticancerous effects
  • can relieve mod severe pain of musculo origin especially if associated with inflammation
  • inhibit conversations of arachidonic acid to cyclooxygenase and prostaglandins
  • requires small dose to control pain vs inflammation
  • reduce activity in C and A-delta fibers in acute and chronic jt inflammation
76
Q

NSAID side effects

A
  • GI irritation and bleeding
  • dec platelet aggregation
  • kidney damage
  • bone marrow supression
  • rashes and anorexia
77
Q

NSAID drugs (types)

A
  • Aspirin: 1st NSAID
  • ibuprofin (motrin)
  • naproxen sodium ( naprosyn, aleve)
  • piroxicam ( feldene)
  • celecoxib (celebrex) and rofecoxib (vioxx) cyclooxygenase type 2 inhibitors
78
Q

NSAID how they work

A
  • Original NSAIDS inhibited both cyclooxygenase subtype 1 and 2
  • type 1> synthesized PGs that protect cells, maintain fx
  • type 2> synthesized in response to cell injury, mediate pain, inflammation
  • Cox 2 select drugs> inhibit synthesis of PGs in pain and inflammation
79
Q

Acetaminophen

A

Tylenol

  • effective for mild to mod severe pain
  • has no significant antiinflammatory or anticoagulant effect
  • can cause liver damage with prolonged usage
80
Q

Opiates

A
  • narcotics that contain opium or derivatives
81
Q

types of opiates

A
  • strong agonist (morphine)
  • moderate agonist ( codeine)
  • antagonists ( naloxone)
  • mixed agonist/ antagonist ( butophanol)
82
Q

how opiates work

A
  • bind to opiate receptors
  • blocked by naloxone
  • mimic effects of endorphins and bind to opiate specific receptor sites in CNS
  • may block pain by inhibiting release of presynaptic neurotransmitters and inhibiting interneuron activity early in nociceptive pathway
83
Q

opiates adverse effects

A
  • sedation
  • mood changes
  • confusion
  • respiratory depression
  • postural hypotension
  • constipation
  • nausea and vomiting
  • tolerance and dependence
84
Q

Antidepressants

A
  • used in treatment of chronic pain
  • amitryptiline (elavil) effects on sleep, nerve function, and mood
  • pts with chronic pain and depression report higher levels of pain and pain related behaviors
85
Q

Spinal analgeisa

A

Epidural or subarachnoid space

  • opiates, local anesthetics, corticosterioids
  • provides analgeisa to area innervated by segments of cord
  • most effective if pain has a spinal distribution
  • by-passes blood brain barrier increasing effectiveness and lessening side effects
86
Q

spinal analgesia: Opiates

A
  • Stimulate opiate receptors in dorsal horn of spinal cord
  • fat soluble: rapid onset short duration
  • water soluble: slow onset prolonged duration
87
Q

Spinal analgesia: local anesthetics

A
  • completely block nociceptive transmission

- increased concentrations can cause numbness and weakness

88
Q

spinal analgesia: catabolic corticosteroids

A
  • relieve pain due to inflammation of spinal nerve roots or surrounding structures
  • prolonged use- osteoporosis, fat, muscle wasting
89
Q

Local injections

A
  • Relieving pain from local inflammation
  • not after acute truama due to effect on healing by reducing inflammatory response
  • prolonged use can cause tissue breakdown and deterioration
90
Q

Phys agents directly:

A
  • moderate release of inflammatory mediators
  • modulate pain at spinal cord level
  • altering nerve conduction
  • increase endorphin levels
91
Q

phys agents indirectly

A 
Decrease sensitivity of muscle spindle system
- reducing muscle spasm
Vascularity (reduce edema and ischemia)
- modify vascular flow
- modify blood flow
Help resolve underlying cause of pain
92
Q

Moderate release of inflammatory mediators: cryotherapy

A
  • reduces metabolic rate

- reduces production of serotonin, histamine, bradykinin, substance P, and prostaglandins

93
Q

Moderate release of inflammatory mediators: sub thermal ultrasound

A
  • alters cellular formation and release of inflammatory mediators
94
Q

Modulate pain a Spinal cord level: stimulate large diameter afferent fibers

A
  • TENS
  • superficial massage
  • analgesic balms
95
Q

Modulate pain a Spinal cord level: decrease pain fiber transmission

A
  • Cryotherapy
  • ultrasound
  • iontophoresis
  • phonophoreis
96
Q

Modulate pain a Spinal cord level: stimulate small diameter afferent fibers and descending pain control mechanisms

A
  • Deep massage

- TENS (acupuncture like)

97
Q

Modulate pain a Spinal cord level: stimulate release of beta endorphins through prolonged small diameter fiber stimulation

A
  • TENS

- E-stim

98
Q

Altering nerve conduction

A
  • decreased nerve conduction is proportional to decrease in temp and duration of temp change
  • 5 mins of cooling> reverses within 15 mins
  • 20 mins cooling> needs greater than 30 mins to reverse
  • cryotherapy
  • ice pack, ice massage
99
Q

increasing endorphin levels

A

E-stim

  • certain parameters can control pain by stimulating release of opiopeptides at the spinal cord and higher centers
  • pain relief reversed by naloxone
100
Q

advantages to phys agents

A
  • fewer and generally less severe side effects than meds
  • pts do not develop dependency
  • do not cause sedation
  • many able to be applied independently
  • may help remediate the underlying cause of pain

Physical Agents (21 decks)

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