Pain Models, Modulation, And Assessment Flashcards
(152 cards)
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
2
Q
Is pain a physical or emotional experience?
A
Both
3
Q
The perception of pain is influenced by what factors?
A
Culture, motivation, emotional state, and physical experiences
4
Q
Is pain always associated with tissue damage or a detectable underlying cause?
A
Nope
5
Q
What results in pain?
A
Structural change in the NS and possibly psychological changes
6
Q
T/f: pain is SUBJECTIVE and if described by the patient, REAL
A
True
7
Q
T/f: pain is critical to survival and a warning sign to limit movt
A
True
8
Q
What is one of the cardinal signs of inflammation?
A
Pain
9
Q
What is the number one reason for injured or uninjured persons to seek medical care?
A
Pain
10
Q
T/f: pain can limit athletic and functional performance
A
True
11
Q
T/f: pain guides medical, PT, AT, diagnoses
A
True
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
13
Q
What are nociceptors?
A
Sensory receptors capable of tranducing/encoding actual or potentially tissue damaging stimuli
14
Q
How do nociceptors carry signals?
A
They convert mechanical/thermal/chemical energy into electrical signals that are carried up to the CNS
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
16
Q
Are cutaneous receptors deep or superficial?
A
Superficial
17
Q
What are the types of cutaneous receptors.
A
Mechanoreceptors
Thermoreceptors
Nociceptors
18
Q
What are mechanoreceptors?
A
Cutaneous receptors that respond to stroking, touch, skin stretch, and pressure
19
Q
What are thermoreceptors?
A
Cutaneous receptors that respond to temp and temp changes
20
Q
What kind of cutaneous receptors do A-delta and C fiber have?
A
Nociceptors
21
Q
What are polymodal nociceptors?
A
Nociceptors that respond to multiple noxious stimuli (mechanical, thermal, chemical)
22
Q
What are silent nociceptors?
A
Mechanically insensitive nociceptors that become activated by inflammatory mediators (prostaglandins)
23
Q
Where are deep tissue receptors located?
A
In the muscles, joints, tendons, and connective tissue
24
Q
What can PTs do to stimulate deep tissue receptors?
A
Deep tissue massage
Friction massage
25
What are proprioceptors?
Deep tissue receptors that respond to joint position changes
26
T/f: stretching jt tissues to end range or putting direct pressure over the capsule can stimulate nociceptors
True
27
Muscle nociceptors can be activated by what things?
Pressure and ischemia
28
Silent nociceptors make up what portion of joint receptors?
1/3
29
What deep tissue receptors become activated after tissue injury and respond to noxious stimuli?
Silent nociceptors
30
T/f: after inflammation, silent nociceptors fire spontaneously and respond to noxious joint movt
True
31
What is peripheral sensitization?
Increased responsiveness and reduced threshold of nociceptors to stimulation after tissue injury and/or imflammation
32
When there is a reduced threshold, is there increased or decreased perception of pain?
Increased perception of pain
33
What three things does peripheral sensitization result in physiologically?
Increased spontaneous activity
Decrease in threshold of response to noxious stimuli
Increase in receptor field size (larger area become sensitive
34
T/f: silent nociceptors can begin to respond to both noxious and innocuous jt pressure and movt
True
35
Why does hyperalgesia result from peripheral sensitization?
Bc there is an increase in input to the CNS
36
What are the primary afferent substances/NTs?
Neuropeotides
Glutamate
Opioids
37
What are the primary afferent neuropeptides?
Substance P and calcitonin gene related peptide (CGRP)
38
Where are the afferent neuropeptides sub p and CGRP located?
In small diameter afferents (A-delta and C fibers)
39
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
True
40
What is neurogenic inflammation?
An inflammatory response resulting from the release of primary afferent neuropeptides in the periphery
41
How does the CNS component (dorsal root reflexes) create an inflammatory response?
APs are generated in the SC, transmitted to the periphery, and releases neuropeptides from the peripheral terminal, enhancing an inflammatory response
42
Is glutamate an excitatory or inhibitory NT?
Excitatory NT
43
Where is glutamate found?
In primary afferents and peripheral terminals of nociceptors
44
What does injection of glutamate peripherally result in?
Hyperalgesia and sensitization of primary afferent fibers
45
When is glutamate unregulated in jt afferents?
After inflammation, it increases in the inflamed tissues
46
T/f: clinically, with knee inflammation in RA/OA, there’s an expression of opioid peptides in immune cells
True
47
T/f: there is a peripheral endogenous mechanism to reduce pain in inflamed tissues
True
48
Where are the first order nerve fibers located?
In the CNS with cell bodies in the DRG, synapse in the SC
49
Where are A-beta fibers located?
On skin
50
What info do the A-beta fibers transmit?
Touch, vibration, and hair deflection
51
Are A-beta fibers large or small diameter fibers? Myelinated or unmyelinated? Fast or slow conducting?
A-beta fibers are large diameter, myelinated, and fast conducting fibers
52
T/f: A-beta fibers are easily stimulated
True
53
What are the first fibers to fire and the first to go in neuropathies?
a-beta fibers
54
Where are A-delta fibers located?
On skin
55
What info do A-delta fibers transmit?
Nociceptive info from warm/cold receptors, touch, chemical and noxious mechanical stimulation (pinching, prickling, crushing)
56
Are A-delta fibers large or small diameter? Myelinated or unmyelinated, fast or slow conducting?
A-delta fibers are small diameter, myelinated, slower conducting fibers with a higher threshold
57
Where are C fibers located?
On muscles and skin
58
What fibers are chronic pain fibers that create a bruning and aching sensation?
C fibers
59
What info do C fibers transmit?
Nociception from muscles
Touch, pressure, temp from skin
60
Are C fibers large or small diameter, myelinated or unmyelinated, fast or slow conducting?
C fibers are small diameter, unmyelinated, slowest conducting sensory fibers
61
What fibers require a greater stimulation than other fibers to elicits a response?
C fibers
62
What longer lasting pain sensations do C fibers carry?
Dull, aching, burning pain
63
Pain transmission involves a __ neuron pathway from the periphery to the cortex
3
64
What are the spinal tracts involved in pain transmission?
Spinothalamic, thalmocortical, and central nociceptive pathways
65
Where does the descending pathway flow?
From the cortex to the periphery
66
T/f: the descending pathway is activity that occurs AFTER the cortex has received input
True
67
What structures have the potential to affect pain through a descending mechanism?
The PAG, reticular formation, rostral ventromedial medulla (RVM), and raphe nucleus
68
Normally, there is a balance bw facilitation and inhibition from descending modulation, when should this shift?
After tissue injury
69
Using _____ modulation is the goal of pain management, modalities, meds, and stress relief
Descending
70
How does descending facilitation of pain occur?
Supraspinal centers can enhance nociception, resulting in referred pain, secondary hyperalgesia, and mirror image or CL hyperalgesia
71
What brain structure is involved in the emotion component of pain (fear and emotion)?
The amygdala
72
How does the descending inhibition of pain work?
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
What areas of the brain in the descending pathway can inhibit pain when activated?
The PAG, RVM, somatosensory cortex, thalamus, hypothalamus, reticulospinal tract, and rubrospinal tract
74
Most sites that inhibit pain relay either directly or indirectly through what structure?
The RVM
75
What structure serves as the final common pathway to the SC?
The RVM
76
Where are endogenous opioids and their receptors located?
Everywhere in the body
77
T/f: endogenous opioids bind to the same sites as opiate drugs and inhibit transmission of pain impulses
True
78
What are beta endorphins?
Large peptide chain endogenous opioids found in distinct areas of the CNS
79
What is the half life of beta endorphins?
4 hours
80
Does beta endorphins provide long lasting or short lasting pain modulation
Long lasting pain modulation
81
What are enkephalins and dynorphins?
Small amino acid chain endogenous opioids
82
What is half life of enkephalins and dynorphins?
45sec to 20 min
83
What do enkephalins do?
They counteract sub p to block or modulate pain signals
84
Are enkephalins and dynorphins long or short acting endogenous opioids?
Short acting
85
T/f: when using enkephalins and dynorphins as a nerve block, it only provides pain relief when on bc it is short acting
True
86
What opioid receptors does beta-endorphin activate?
Mu receptors
87
What opioid receptors do enkephalins activate?
Delta receptors
88
What opioid receptors do dynorphins activate?
Kappa receptors
89
What opioid receptors do clinical opioids activate?
Mu receptors
90
What are the descending NTs?
NE
Serotonin
Substance P
CGRP
adenosine
GABA
caffeine
91
Where are NE terminals located in the body?
The SC
92
What does NE do as a descending NT?
Inhibits/facilitates the DH depending on the receptor is activated
93
Where is serotonin found in the body?
In the PAG, RVM with projections to the SC
94
Application of serotonin to the SC ____ activity of DH neurons and provides analgesia
Decreases
95
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?
SSRIs
96
What are the excitatory NTs in the descending pain pathway?
Substance P and CGRP
97
What do excitatory NTs substance P and CGRP do?
Increase activity and responsiveness of DH neurons
98
What are the inhibitory NTs in the descending pain pathway?
Adenosine, GABA, NE, and serotonin
99
What do the inhibitory NTs do?
Decrease pain
100
What substance is a competitive adenosine receptor antagonist that MAY interfere with TENS effectiveness?
Caffeine
101
What does adenosine do?
Reduces neuropathic pain
102
What does GABA do?
Reduces hyperalgesia and causes analgesia
103
What is the most common use of TM?
For treatment of MSK injuries to relieve pain
104
What can be used to modulate pain, allow controlled exercise, provide pain relief, and restoration of fxn?
Therapeutic modalities
105
What is the goal of using TM?
To decrease pain so therapeutic exercise and fxnal activities can be performed and FXN CAN BE RESTORED
106
What pain modulation is trying to get rid of pain right at the painful area?
Modulation of peripheral pain
107
What is modulation of peripheral pain?
Targeting desensitization of peripheral nociceptors
108
If a receptor has a higher threshold or is more difficult to stimulate, are more or less impulses sent to the SC?
Less
109
T/f: modulation of peripheral pain attempts to counteract the effects of acute inflammation and mechanical stimuli
True
110
When immune cells are in inflamed areas, they secrete what to create an analgesic effect?
Endogenous opioids
111
What modalities are proposed to modulate pain at the peripheral level?
Microcurrent ES
non thermal US
Laser
112
What mode of pain modulation aims to block pain before it gets to the brain?
Spinal level pain modulation
113
What is gait control theory?
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
How does spinal level pain modulation work?
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
How can ESTIM be used for spinal level pain modulation?
It can be applied to activate A-beta afferent nerves to activate inhibitory enkephalin interneurons of the DH and block pain transmission
116
How does supraspinal/descending pain modulation work?
It causes inhibitory signals at the SC
117
The feedback loops from what three brain structures is important in controlling pain?
PAG
Raphe nucleus
Pons
118
How is the PAG involved in supraspinal/descending pain modulation?
PAG contains enkephalin-rich neurons that excite the raphe nucleus which projects down to the SC to block pain transmission by the DH
119
Where are the serotonin-containing neurons located?
In the raphe nucleus of the medulla
120
Stimulation of the raphe nucleus produces what?
Powerful analgesia
121
Serotonin released by the stimulation of the raphe nucleus is thought to activate what?
Inhibitory interneurons
122
How may serotonin inhibit pain pre-synaptically?
By blocking C fiber terminals for sub P and glutamate
123
T/f: the hypothalamus and pituitary gland are stimulated by pain impulses
True
124
T/f: the pituitary can release precursors to powerful analgesic and antiinflammatory agents
True
125
Does supraspinal activity of the hypothalamus and pituitary gland suppress or enhance pain transmission and perception?
Suppresses pain transmission and perception
126
Any ESTIM techniques that can elicit _____ activity can be used to modulate pain by utilizing supraspinal/descending pain modulation
C fiber
127
What is diffuse noxious inhibitory control (DNIC)?
The use of pain fiber stimulation to elicit pain relief
128
What is rhythmic pain modulation?
Rhythmic stimulation that has powerful analgesic properties through A-beta fiber activation (PNF?)
129
T/f: rhythmic pain modulation endures the production of endorphins and descending pain modulation
True
130
Endogenous opioid production is believed to be enhanced by ESTIM set with what parameters?
Low frequency, high intensity stimulation of peripheral nerve fibers for muscle contraction
2-7 cycles
131
How does nerve block pain modulation work?
Creation of action potential failure
132
What is action potential failure?
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
What kind of nerve stimulation hyperpolarizes the membrane creating an inhibitory effects for a nerve block?
Comtinued stim of a nerve at a fast pace of >1000 pps
134
What is wedenskis inhibition?
When the membrane is unable to keep up with stimulation and the AP fails
135
What is the most valid and reliable measure for DPTs to diagnose MSK problems and for directing, progressing, and assessing the efficacy of treatment?
Pain
136
Pain is a _____ complaint that must be _____ measured
Subjective, objectively
137
What characteristics of pain do we want to include in a pain assessment?
The location, description/quality, frequency, provocation
138
What form can be used to assess the location, description, and quality of pain?
The brief pain inventory short form
139
If pain is constant, is the pain number ever zero?
Nope
140
If pain is present for a % of the day, what kind of pain is it?
Intermittent pain
141
When pain is present <20% of the day, what kind of pain is it and how should we document that?
It is episodic pain
We should document the number of episodes per day and how long the episodes last
142
What do we want to know about pain provocation?
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
What is fear avoidance?
The description of how people with chronic pain believe increased activity, movt, or exercise will not only increase pain but further damage tissues
144
What questionnaire can be used to quantify fear avoidance?
Fear avoidance beliefs questionnaire
145
With increased fear avoidance, there is ____ physical activity, ____ participation in rehab and ____ outcomes and chronic conditions
Decreased, decreased, poor
146
What is pain catastrophizing?
Negative cognitive effective response to actual or potential pain
147
What are the three main categories seen in pain catastrophizing?
Magnification, rumination, feeling of helplessness
148
What should we look for if a pt can’t communicate that they are in pain?
Look at their facial expressions, VSs, and signs of muscle guarding
149
What technique in our toolbox can we use to help calm pts with high fear avoidance?
TM
150
What is pain catastrophizing associated with?
Pt reported higher pain severity
Greater disability
Greater illness behavior
Higher chronic pain after injury
Higher opioid use
151
What questionnaire can we use to help chronic pain pts understand how to overcome pain?
Self efficacy questionnaire
152
What is covered in the self efficacy questionnaire?
Pain management
Physical fxns coping
