Pain Models, Modulation, And Assessment Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is pain a physical or emotional experience?

A

Both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The perception of pain is influenced by what factors?

A

Culture, motivation, emotional state, and physical experiences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is pain always associated with tissue damage or a detectable underlying cause?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What results in pain?

A

Structural change in the NS and possibly psychological changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/f: pain is SUBJECTIVE and if described by the patient, REAL

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T/f: pain is critical to survival and a warning sign to limit movt

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is one of the cardinal signs of inflammation?

A

Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the number one reason for injured or uninjured persons to seek medical care?

A

Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T/f: pain can limit athletic and functional performance

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T/f: pain guides medical, PT, AT, diagnoses

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between peripheral and central sensitization?

A

Peripheral sensitization is increased responsiveness and reduced threshold of nociceptors to stimulation of their receptive fields (outside of the CNS)

Central sensitization is also an increased responsiveness of nociceptors but within the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are nociceptors?

A

Sensory receptors capable of tranducing/encoding actual or potentially tissue damaging stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do nociceptors carry signals?

A

They convert mechanical/thermal/chemical energy into electrical signals that are carried up to the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where are peripheral terminals of nociceptors/free nerve endings found?

A

In/around the skin, muscle, tendons, joint structures, periosteum, IVD, and peripheral nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Are cutaneous receptors deep or superficial?

A

Superficial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the types of cutaneous receptors.

A

Mechanoreceptors
Thermoreceptors
Nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are mechanoreceptors?

A

Cutaneous receptors that respond to stroking, touch, skin stretch, and pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are thermoreceptors?

A

Cutaneous receptors that respond to temp and temp changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What kind of cutaneous receptors do A-delta and C fiber have?

A

Nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are polymodal nociceptors?

A

Nociceptors that respond to multiple noxious stimuli (mechanical, thermal, chemical)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are silent nociceptors?

A

Mechanically insensitive nociceptors that become activated by inflammatory mediators (prostaglandins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are deep tissue receptors located?

A

In the muscles, joints, tendons, and connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What can PTs do to stimulate deep tissue receptors?

A

Deep tissue massage
Friction massage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are proprioceptors?

A

Deep tissue receptors that respond to joint position changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

T/f: stretching jt tissues to end range or putting direct pressure over the capsule can stimulate nociceptors

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Muscle nociceptors can be activated by what things?

A

Pressure and ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Silent nociceptors make up what portion of joint receptors?

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What deep tissue receptors become activated after tissue injury and respond to noxious stimuli?

A

Silent nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/f: after inflammation, silent nociceptors fire spontaneously and respond to noxious joint movt

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is peripheral sensitization?

A

Increased responsiveness and reduced threshold of nociceptors to stimulation after tissue injury and/or imflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

When there is a reduced threshold, is there increased or decreased perception of pain?

A

Increased perception of pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What three things does peripheral sensitization result in physiologically?

A

Increased spontaneous activity
Decrease in threshold of response to noxious stimuli
Increase in receptor field size (larger area become sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

T/f: silent nociceptors can begin to respond to both noxious and innocuous jt pressure and movt

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why does hyperalgesia result from peripheral sensitization?

A

Bc there is an increase in input to the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the primary afferent substances/NTs?

A

Neuropeotides
Glutamate
Opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the primary afferent neuropeptides?

A

Substance P and calcitonin gene related peptide (CGRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where are the afferent neuropeptides sub p and CGRP located?

A

In small diameter afferents (A-delta and C fibers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

T/f: primary afferent neuropeptides sub p and CGRP can be released from peripheral terminals of primary afferent fibers to produce an inflammatory response in the periphery

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is neurogenic inflammation?

A

An inflammatory response resulting from the release of primary afferent neuropeptides in the periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does the CNS component (dorsal root reflexes) create an inflammatory response?

A

APs are generated in the SC, transmitted to the periphery, and releases neuropeptides from the peripheral terminal, enhancing an inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Is glutamate an excitatory or inhibitory NT?

A

Excitatory NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Where is glutamate found?

A

In primary afferents and peripheral terminals of nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does injection of glutamate peripherally result in?

A

Hyperalgesia and sensitization of primary afferent fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When is glutamate unregulated in jt afferents?

A

After inflammation, it increases in the inflamed tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

T/f: clinically, with knee inflammation in RA/OA, there’s an expression of opioid peptides in immune cells

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

T/f: there is a peripheral endogenous mechanism to reduce pain in inflamed tissues

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where are the first order nerve fibers located?

A

In the CNS with cell bodies in the DRG, synapse in the SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where are A-beta fibers located?

A

On skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What info do the A-beta fibers transmit?

A

Touch, vibration, and hair deflection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Are A-beta fibers large or small diameter fibers? Myelinated or unmyelinated? Fast or slow conducting?

A

A-beta fibers are large diameter, myelinated, and fast conducting fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

T/f: A-beta fibers are easily stimulated

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the first fibers to fire and the first to go in neuropathies?

A

a-beta fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where are A-delta fibers located?

A

On skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What info do A-delta fibers transmit?

A

Nociceptive info from warm/cold receptors, touch, chemical and noxious mechanical stimulation (pinching, prickling, crushing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Are A-delta fibers large or small diameter? Myelinated or unmyelinated, fast or slow conducting?

A

A-delta fibers are small diameter, myelinated, slower conducting fibers with a higher threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where are C fibers located?

A

On muscles and skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What fibers are chronic pain fibers that create a bruning and aching sensation?

A

C fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What info do C fibers transmit?

A

Nociception from muscles

Touch, pressure, temp from skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Are C fibers large or small diameter, myelinated or unmyelinated, fast or slow conducting?

A

C fibers are small diameter, unmyelinated, slowest conducting sensory fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What fibers require a greater stimulation than other fibers to elicits a response?

62
Q

What longer lasting pain sensations do C fibers carry?

A

Dull, aching, burning pain

63
Q

Pain transmission involves a __ neuron pathway from the periphery to the cortex

64
Q

What are the spinal tracts involved in pain transmission?

A

Spinothalamic, thalmocortical, and central nociceptive pathways

65
Q

Where does the descending pathway flow?

A

From the cortex to the periphery

66
Q

T/f: the descending pathway is activity that occurs AFTER the cortex has received input

67
Q

What structures have the potential to affect pain through a descending mechanism?

A

The PAG, reticular formation, rostral ventromedial medulla (RVM), and raphe nucleus

68
Q

Normally, there is a balance bw facilitation and inhibition from descending modulation, when should this shift?

A

After tissue injury

69
Q

Using _____ modulation is the goal of pain management, modalities, meds, and stress relief

A

Descending

70
Q

How does descending facilitation of pain occur?

A

Supraspinal centers can enhance nociception, resulting in referred pain, secondary hyperalgesia, and mirror image or CL hyperalgesia

71
Q

What brain structure is involved in the emotion component of pain (fear and emotion)?

A

The amygdala

72
Q

How does the descending inhibition of pain work?

A

ES of the PAG, RVM produces analgesia and inhibits spinal neurons that respond to noxious stim

Other structures of the brain inhibit pain when activated (somatosensory cortex, thalamus, hypothalamus, reticulospinal tract, rubrospinal tract)

73
Q

What areas of the brain in the descending pathway can inhibit pain when activated?

A

The PAG, RVM, somatosensory cortex, thalamus, hypothalamus, reticulospinal tract, and rubrospinal tract

74
Q

Most sites that inhibit pain relay either directly or indirectly through what structure?

75
Q

What structure serves as the final common pathway to the SC?

76
Q

Where are endogenous opioids and their receptors located?

A

Everywhere in the body

77
Q

T/f: endogenous opioids bind to the same sites as opiate drugs and inhibit transmission of pain impulses

78
Q

What are beta endorphins?

A

Large peptide chain endogenous opioids found in distinct areas of the CNS

79
Q

What is the half life of beta endorphins?

80
Q

Does beta endorphins provide long lasting or short lasting pain modulation

A

Long lasting pain modulation

81
Q

What are enkephalins and dynorphins?

A

Small amino acid chain endogenous opioids

82
Q

What is half life of enkephalins and dynorphins?

A

45sec to 20 min

83
Q

What do enkephalins do?

A

They counteract sub p to block or modulate pain signals

84
Q

Are enkephalins and dynorphins long or short acting endogenous opioids?

A

Short acting

85
Q

T/f: when using enkephalins and dynorphins as a nerve block, it only provides pain relief when on bc it is short acting

86
Q

What opioid receptors does beta-endorphin activate?

A

Mu receptors

87
Q

What opioid receptors do enkephalins activate?

A

Delta receptors

88
Q

What opioid receptors do dynorphins activate?

A

Kappa receptors

89
Q

What opioid receptors do clinical opioids activate?

A

Mu receptors

90
Q

What are the descending NTs?

A

NE
Serotonin
Substance P
CGRP
adenosine
GABA
caffeine

91
Q

Where are NE terminals located in the body?

92
Q

What does NE do as a descending NT?

A

Inhibits/facilitates the DH depending on the receptor is activated

93
Q

Where is serotonin found in the body?

A

In the PAG, RVM with projections to the SC

94
Q

Application of serotonin to the SC ____ activity of DH neurons and provides analgesia

95
Q

What meds are commonly used for chronic pain bc they decrease the reuptake of NE and serotonin so that they are more available to inhibit nociceptive info?

96
Q

What are the excitatory NTs in the descending pain pathway?

A

Substance P and CGRP

97
Q

What do excitatory NTs substance P and CGRP do?

A

Increase activity and responsiveness of DH neurons

98
Q

What are the inhibitory NTs in the descending pain pathway?

A

Adenosine, GABA, NE, and serotonin

99
Q

What do the inhibitory NTs do?

A

Decrease pain

100
Q

What substance is a competitive adenosine receptor antagonist that MAY interfere with TENS effectiveness?

101
Q

What does adenosine do?

A

Reduces neuropathic pain

102
Q

What does GABA do?

A

Reduces hyperalgesia and causes analgesia

103
Q

What is the most common use of TM?

A

For treatment of MSK injuries to relieve pain

104
Q

What can be used to modulate pain, allow controlled exercise, provide pain relief, and restoration of fxn?

A

Therapeutic modalities

105
Q

What is the goal of using TM?

A

To decrease pain so therapeutic exercise and fxnal activities can be performed and FXN CAN BE RESTORED

106
Q

What pain modulation is trying to get rid of pain right at the painful area?

A

Modulation of peripheral pain

107
Q

What is modulation of peripheral pain?

A

Targeting desensitization of peripheral nociceptors

108
Q

If a receptor has a higher threshold or is more difficult to stimulate, are more or less impulses sent to the SC?

109
Q

T/f: modulation of peripheral pain attempts to counteract the effects of acute inflammation and mechanical stimuli

110
Q

When immune cells are in inflamed areas, they secrete what to create an analgesic effect?

A

Endogenous opioids

111
Q

What modalities are proposed to modulate pain at the peripheral level?

A

Microcurrent ES
non thermal US
Laser

112
Q

What mode of pain modulation aims to block pain before it gets to the brain?

A

Spinal level pain modulation

113
Q

What is gait control theory?

A

The ascending influence of pain modulation where areas of the DH act as pre-synaptic inhibitors by stimulating the inhibitory interneuron to stop pain signals

114
Q

How does spinal level pain modulation work?

A

A-beta afferent activity stimulates enkephalin interneurons, release of enkephalin at the terminus of interneurons blocks the transmitter substance used to depolarize the second order afferent nerves that transmit pain signals to the brain so that pain is not perceived

115
Q

How can ESTIM be used for spinal level pain modulation?

A

It can be applied to activate A-beta afferent nerves to activate inhibitory enkephalin interneurons of the DH and block pain transmission

116
Q

How does supraspinal/descending pain modulation work?

A

It causes inhibitory signals at the SC

117
Q

The feedback loops from what three brain structures is important in controlling pain?

A

PAG
Raphe nucleus
Pons

118
Q

How is the PAG involved in supraspinal/descending pain modulation?

A

PAG contains enkephalin-rich neurons that excite the raphe nucleus which projects down to the SC to block pain transmission by the DH

119
Q

Where are the serotonin-containing neurons located?

A

In the raphe nucleus of the medulla

120
Q

Stimulation of the raphe nucleus produces what?

A

Powerful analgesia

121
Q

Serotonin released by the stimulation of the raphe nucleus is thought to activate what?

A

Inhibitory interneurons

122
Q

How may serotonin inhibit pain pre-synaptically?

A

By blocking C fiber terminals for sub P and glutamate

123
Q

T/f: the hypothalamus and pituitary gland are stimulated by pain impulses

124
Q

T/f: the pituitary can release precursors to powerful analgesic and antiinflammatory agents

125
Q

Does supraspinal activity of the hypothalamus and pituitary gland suppress or enhance pain transmission and perception?

A

Suppresses pain transmission and perception

126
Q

Any ESTIM techniques that can elicit _____ activity can be used to modulate pain by utilizing supraspinal/descending pain modulation

127
Q

What is diffuse noxious inhibitory control (DNIC)?

A

The use of pain fiber stimulation to elicit pain relief

128
Q

What is rhythmic pain modulation?

A

Rhythmic stimulation that has powerful analgesic properties through A-beta fiber activation (PNF?)

129
Q

T/f: rhythmic pain modulation endures the production of endorphins and descending pain modulation

130
Q

Endogenous opioid production is believed to be enhanced by ESTIM set with what parameters?

A

Low frequency, high intensity stimulation of peripheral nerve fibers for muscle contraction

2-7 cycles

131
Q

How does nerve block pain modulation work?

A

Creation of action potential failure

132
Q

What is action potential failure?

A

When a nerve is stimulated so much it shuts down

When a nerve depolarizes it produces a refractory period during which the nerve’s threshold increases

133
Q

What kind of nerve stimulation hyperpolarizes the membrane creating an inhibitory effects for a nerve block?

A

Comtinued stim of a nerve at a fast pace of >1000 pps

134
Q

What is wedenskis inhibition?

A

When the membrane is unable to keep up with stimulation and the AP fails

135
Q

What is the most valid and reliable measure for DPTs to diagnose MSK problems and for directing, progressing, and assessing the efficacy of treatment?

136
Q

Pain is a _____ complaint that must be _____ measured

A

Subjective, objectively

137
Q

What characteristics of pain do we want to include in a pain assessment?

A

The location, description/quality, frequency, provocation

138
Q

What form can be used to assess the location, description, and quality of pain?

A

The brief pain inventory short form

139
Q

If pain is constant, is the pain number ever zero?

140
Q

If pain is present for a % of the day, what kind of pain is it?

A

Intermittent pain

141
Q

When pain is present <20% of the day, what kind of pain is it and how should we document that?

A

It is episodic pain

We should document the number of episodes per day and how long the episodes last

142
Q

What do we want to know about pain provocation?

A

What makes it better or worse

If it is sudden or gradual onset

The effects of WB

Sitting vs standing in the spine

If there is pain at night

143
Q

What is fear avoidance?

A

The description of how people with chronic pain believe increased activity, movt, or exercise will not only increase pain but further damage tissues

144
Q

What questionnaire can be used to quantify fear avoidance?

A

Fear avoidance beliefs questionnaire

145
Q

With increased fear avoidance, there is ____ physical activity, ____ participation in rehab and ____ outcomes and chronic conditions

A

Decreased, decreased, poor

146
Q

What is pain catastrophizing?

A

Negative cognitive effective response to actual or potential pain

147
Q

What are the three main categories seen in pain catastrophizing?

A

Magnification, rumination, feeling of helplessness

148
Q

Hat should we look for if a pain can’t communicate that they are in pain?

A

Look at their facial expressions, VSs, and signs of muscle guarding

149
Q

What technique in our toolbox can we use to help calm pts with high fear avoidance?

150
Q

What is pain catastrophizing associated with?

A

Pt reported higher pain severity

Greater disability

Greater illness behavior

Higher chronic pain after injury

Higher opioid use

151
Q

What questionnaire can we use to help chronic pain pts understand how to overcome pain?

A

Self efficacy questionnaire

152
Q

What is covered in the self efficacy questionnaire?

A

Pain management

Physical fxns coping