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Neuro Dev/Control II > Current Perspectives on Pain Management > Flashcards

Current Perspectives on Pain Management Flashcards

1
Q

Multiple factors influence how patients understand and respond to pain including

A
  • Media
  • Marketing of healthcare options: pharmaceutical interventions
  • Mental makeup: beliefs, culture, social environment
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2
Q

How is modern medications dealing poorly with pain

A
  • 50% felt they had little for no control over their pain
  • 1 in 5 with chronic pain do’t seek medical help
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3
Q

Fentanyl in relationship to morphine

A
  • Fentanyl is 50-100 times more potent pain killer than morphine used for treating severe pain, typically advanced cancer pain
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4
Q

Describe the anterolateral columns (nociceptive pathways)

A
  • Convey nociceptive, temperature, & crude touch info to brain
  • Spinothalamic: fast, discriminative nociception & temperature & crude touch, somatotropin arrangement in S1
  • Divergent: slow, non-specific nociception
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5
Q

Describe the spinathalamic pathway

A
  • Free nerve ending carry fast nociception by A & C fibers
  • 2d order neuron crosses midline
  • Travels up spinothalamic tract, trigeminal lemniscus
  • VPL and VPM nucleus in thalamus
  • Thalamocortical radiations
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6
Q

Describe the divergent pathways

A
  • Activated by C fibers: use interneurons to release substance P
  • Connects to brainstem = spinomesencephalic (turning head/eye towards painful stimuli) and spinoreticular (arousal, attention changes due to pain)
  • Connects to cortex = spino-emotioal (anterior cingulate, insula, anygdala, dorsal prefrontal cortex, affect emotions, behavior, & personality)
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7
Q

Which pathway may be more responsible for behavioral aspects of chronic pain

A
  • Divergent pathways due to slow scarring speed to different higher centers
  • The pathways can also get sensitized by repeated stimulation during injury
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8
Q

Describe the gate theory of pain

A
  • Info from 1st order low-threshold mechanical afferents & 1st order nociceptive afferents converge non the same 2nd order neurons ion dorsal horn
  • Competition of 1st order pathways determine signals that are transmitted up the chain & the other gate is “closed”
  • Explains sharp, acute type pain but chronic
  • Has been found too be inaccurate
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9
Q

Describe the counterirritant theory for pain

A
  • Gating happens via interneurons
  • Interneurons connect non-nociceptive to nociceptive pathways afferents via substance P interneurons
  • Interneurons release NT encephalin/endorphins which has anti-nociceptive activity, hyper polarize substance P interneurons
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10
Q

Descending pathways that provide anti-nociception

A
  • Descending pathways from cerebral cortex, amygdala
  • Neurohormonal pathways from hypothalamus, adrenal medulla
  • Descending tracts from brainstem areas: PAG, locus coerulus in pons (release norepinephrine), Raphe nucleus in rostral ventromedial medulla (release serotonin)
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11
Q

Describe the levels of antinociception

A
  • V: cortex/amygdala; dopamine/serotonin; emotions, motivation, memory, personality, stress, sleep
  • IV: hormonal system; PVG, pituitary, adrenal medulla
  • III: descending pathways from brainstem to dorsal horn - serotonin, norepinephrine, endorphins
  • II: dorsal horn – by activating local inhibitory interneurons – enkephalin, dynorphin
  • I: – at periphery by inhibiting nociceptor activity (NSAIDS)
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12
Q

Which brain centers are both pro and anti nociceptors

A
  • Lateral prefrontal cortex
  • Amygdala
  • Rostural ventromedial medulla
  • PAG
  • Locus coeruleus
  • Medial prefrontal cortex
  • Anterior cingulate cortex
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13
Q

Current knowledge of pain regulation

A
  • Pain signals ascend up different pathways
  • Higher centers then generate a top-down response that regulate the afferent nociceptive pathways
  • Top-down response can inhibit or amplify the afferent nociceptive signals
  • Depends on the genetic, physiological and psychologic factors of an individual and can be influenced by prior experience through plasticity
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14
Q

What determines whether the sensory processing remains normal, becomes suppressed, sensitized, or reorganized

A
  • Genetics and prior experience
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15
Q

Describe a normal state of pain regulation

A
  • Signals are transmitted accurately, real nociception felt as pain
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16
Q

Describe a suppressed state of pain regulation (antinociception)

A
  • Touch, pressure, vibration transmitted normally but nocieptive signals inhibited
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17
Q

Describe a sensitized state of pain regulation (temporary pro-nociceptive)

A
  • Repeated tissue irritation changes NTs and receptor activity, enhancing nociceptive signals (hyperalgesia)
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18
Q

Describe a reorganized state of pain regulation (persistent pro-nociceptive)

A
  • Loss of tissue causing degeneration of pain pathways, structural reorganization of synapses at dorsal horn, axonal sprouting from mechanical receptors pathways, touch beams painful (allodynia)
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19
Q

What are the peripheral neuropathic states of pain regulation

A
  • Sensitized and reorganized states
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20
Q

Define peripheral neuropathy

A
  • Sensitization or maladaptive neuroplastic changes in the peripheral somatosensory pathways from trauma, compression, inflammation, or ischemia
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21
Q

Symptoms of peripheral neuropathy

A
  • Burning, tingling, paresthesia, hyperalgesia, allodynia, pain in dermatomal or cutaneous distribution
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22
Q

Describe the peripheral neuropathic pain mechanisms

A
  • Ectopic sites (sites of nerve injury generating impulses abnormally independent from peripheral stimuli)
  • Ephaptic transmission (cross-excitation between injured and uninjured nerves)
  • Peripheral sensitization (sensitization of nociceptive pathways due to continued activity – causing hyperalgesia)
  • Structural reorganization (continued sensitization causing axonal sprouting from non-nociceptive fibers activating nociceptive tracts – causing allodynia)
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23
Q

Describe CRPS pain

A
  • Pain in whole limb along with dystrophic changes in skin/muscles
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24
Q

Describe fibromyalgia pain

A
  • Complaints oof aching all over with or without movements, multiple trigger points all over body, increased sensitivity to almost all kinds of sensory stimulus, sleep disturbances, mood, memory issues
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25
Q

Describe the pain neuromatrix theory

A
  • Chronic pain is a multidimensional experience produced by patterns of nerve impulses generated by a widely distributed neural network (“body-self neuromatrix”) in the brain
  • Neural network patterns may be triggered by sensory, cognitive or emotional inputs, but they may also be generated independently
26
Q

Generalization of the neuromatrix model

A
  • A neuromatrix not just for pain…but for all other sensory, cognitive and behavioral aspects that shape our life
  • They talk to each other and influence each other so, pain has bidirectional relationships
27
Q

Mechanism of chronic pain

A
  • Malfunctioning/maladaptive triggering of pain neuromatrix: pain triggered by cognitive and emotional inputs
  • Disruption of top-down regulation of pain: down regulation of antinociception & up regulation of pro-nociception
  • These explain: Pain in absence of sensory stimuli, or disproportionate to, or inconsistent with sensory stimuli and Widespread pain NOT in any dermatomal/cutaneous distribution
28
Q

Maladaptive changes in neuromatrix in people with chronic pain

A
  • The pain neuromatrix shifts to a distinctly different space as pain turns from acute -> subacute -> chronic
  • Triggers similar brain areas that are involved in addiction
29
Q

Describe normal acute pain

A
  • A properly functioning burglar alarm system
  • We need it
30
Q

Describe chronic pain

A
  • Malfunctioning alarm working at a high alert level raising false alarms int eh absence of threats due to being sensitized
  • Abnormal alterations in pain processing pathways due too maladaptive neuroplastic changes in it
  • No biologic purpose: chronic pain not a symptom of disease but the disease itself
  • We don’t need it
31
Q

Describe reorganization/smudging of body maps in chronic pain

A
  • Maladaptive plasticity after injury, disuse, immobilization, neglect, etc.
  • Can last ability to detect L from R
32
Q

Describe the degenerative process in the brain of chronic pain patients

A
  • Gray matter atrophy equivalent to 10-20 years of aging
  • Likely relates to cognitive and emotional impairments
  • Hippocampus may increase volume: always thinking about pain
  • Gray matter atrophy accompanies changes in white matter connectivity
33
Q

Describe fibromyalgia

A
  • Wide spread pain: no dermatomal distribution, no peripheral injury
  • Increased sensitivity to all kinds of sensory stimuli
  • Less gray matter in cingulate gyrus, insular cortex
  • Unpredictable pain flare ups
  • Pain associated with stress, sleep deprivation, negative emotions
  • Muscle fatigue and tender spots/trigger points
34
Q

Describe chronic LBP

A
  • Unpredictable pain, pain w/ or w/o movement, diffuse non-dermatomal, persistent long after healed pathology
  • Strongly associated with negative emotions, maladaptive fear-avoidance beliefs, poor stress response (catastrophization), fatigue, sleep disorders.
  • Similar maladaptive cortical reorganization in the pain neuromatrix – shown by thumbnail pressure stimulation study below by comparing CLBP and Fibromyalgia
  • Heightened pro-nociception compared to control
35
Q

Describe phantom pain

A
  • Deafferentation leads to functional/structural maladaptive neuroplastic reorganization
  • Changes in M1/S1 after arm amputation – the face/lip area takes over hand area – causing phantom sensations
  • Burning, cramping, other sensations
36
Q

Describe CRPS pain

A
  • May have hx of injury: fracture, surgery, minor injuries, stroke
  • Widespread pain in the whole region, no dermatomal distribution
  • Nociceptor deafferentation: pain w/o peripheral stimulus
  • Sensitization and maladaptive reorganization of the pain neuromatrix
  • Vascular changes, muscle atrophy, bony changes (due to altered autonomic and motor systems)
37
Q

Define nociceptive pain (acute or chronic)

A
  • Tissue damage/potential tissue damage
  • Accurate activity or nociceptive receptors & pain pathways
  • Pain driven by activation of peripheral nociceptive sensory receptors and pathways
  • Acute pain resulting from noxious chemical, mechanical, thermal stimuli
38
Q

Define non-nociceptive chronic pain

A
  • Unpleasant sensory ADN perceptual, emotional, cognitive, & behavioral experience
  • With or without activity in nociceptive pain pathways
39
Q

Define peripheral neuropathic pain (PNP)/peripheral sensitization

A
  • Pain attributable to dysfunctional sensitization or lesion in peripheral nerves, DRG or dorsal root from trauma, compression, inflammation or ischemia
  • CTS, Neuralgia, diabetic neuropathy, GB syndrome
40
Q

Define central sensitization pain (CSP)

A
  • Pain due to maladaptive amplification of neural signaling within widely distributed pain-related CNS networks caused by enhanced synaptic excitability, lowering of activation thresholds and expansion of receptive fields
  • cLBP, Fibromyalgia, phantom pain, CRPS, migraine headache, OA, chronic tendon problems, etc
41
Q

Cluster of 3 symptoms and 1 sign predicted CSP-dominant mechanisms with high degree of accuracy

A
  • Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple/non-specific aggravating/easing factors
  • Pain disproportionate to the nature & extent of injury or pathology
  • Strong association with maladaptive psychosocial factors
  • Diffuse/non-anatomic areas of pain/tenderness on palpation
42
Q

Cluster of 2 symptoms and 1 sign predicted PNP-dominant mechanisms with high degree of accuracy

A
  • Pain referred in a dermatomal or cutaneous distribution
  • Hx of nerve injury, pathology or mechanical compromise
  • Pain/symptom provocation with mechanical/movement tests that move/load/compress neural tissue
43
Q

Cluster of 3 symptoms and absence of 3 symptoms and 1 sign predicted NP-dominant mechanisms with high degree of accuracy

A
  • Pain localized to area of injury/dysfunction
  • Clear, proportionate nature of aggravating/easing factors
  • Intermittent, sharp pain with movement, constant dull ache/throb at rest
  • Absence of dysesthesias, night pain/disturbed sleep, burning/shooting/sharp/electric-shoock-like pain, antalgic postures
44
Q

Assessment tools for pain

A
  • Visual analog scale
  • McGill pain questionnaire
45
Q

Assessment tools that can differentiate between neuropathic and non-neuropathic pains

A
  • PainDETECT
  • DN4
  • LANSS
  • ID pain
46
Q

Assessment tools that specifically detect CSP

A
  • Central sensitization inventory
  • OSPRO-YF
47
Q

Objective tests for neuropathic and central sensitization pain

A
  • Pain pressure threshold testing: using algometer
  • Temporal summation: 10 reps pin prick with a freq. of 1/sec; subject rates pain intensity of first & last prick from 0-10
  • Conditioned pain modulation: noxious stimulus (thermal or mechanical) applied before and during applying a second stimulus (cold or hot water bath applied to a distal contralateral extremity)
  • 2 point discrimination
48
Q

General guidelines fro chronic pain patients

A
  • Exercise should be done: aerobic endurance, strength conditioning, stabilization, walking, Tai Chi, Pilates, Yoga
  • Passive modalities only as an adjunct to exercise
  • Manual therapy for short term relief
  • Advice to stay active
  • TENS: high or low
  • Low level laser therapy
  • Strong evidence for NO effect of traction
49
Q

What should you start your chronic pain patient treatment with

A
  • PNE
  • Explaining to patients their pain experience from a biological and physiological perspective of how the nervous system/brain normally processes pain, explain using the ‘cranked-up alarm/heighted state of alarm’ example, ‘going off’ all the time and explain how the ‘alarm’ ‘wiring’ has gone ‘bad’ in them, and how it is not ‘working correctly’….this might allow patients to move better, exercise better, think different about pain, push further into pain, etc
50
Q

Describe the steps in graded motor imagery

A
  • 1) Left/right discrimination (laterality training) or implicit motor imagery
  • 2) Explicit motor imagery
  • 3) Mirror therapy
51
Q

Describe L/R discrimination training

A
  • Strat with determining whether the body part is from the L/R side
  • Progress to “has it moved to the left or right
  • Online softwares/Apps: Recognize, Orientate
52
Q

Normative data for L/R discrimination

A
  • Accuracy of ≥80%
  • Norms: speed 1.6 secs +/- 0.5 sec for necks & backs; 2 secs +/- 0.5 sec for hands & feet
  • Accuracies & response times should be reasonably equal for the left & right
  • Results should be stable & are consistent for at least a week
  • Clinical judgement needed at times
53
Q

Describe explicit motor imagery

A
  • 25% of neurons are mirror neurons & start firing when you imagine movement, or watch others move; you also use the same brain areas when you imagine moving vs when you actually move
  • Imagine affected body part stationary at rest then imagine body part moving
  • Start by increasing self awareness of stationary body part
  • Progress to imagining relevant/salient functional movements that are painful
54
Q

If needed, to help with imagining a stationary body part

A
  • Start with imagining unaffected contralateral body part
  • Or, start imagining proximal body part
  • Or, can start by observing stationary body part flash cards
55
Q

If needed, to help with imagining moving body part

A
  • Start with flash card showing a moved/twisted body part
  • Or, observe others moving the same body part
56
Q

Describe Body-scan mental exercise for relaxation

A
  • Concentrate on sensations of fingers from each area of the body consecutively including the phantom arm & hand
57
Q

Describe Imagined movements of phantom limb

A
  • To stretch away the pain & finally allow the fingers, hand, and arm to rest in a comfortable position
58
Q

Training guidelines for mirror therapy

A
  • No jewelry, watches on either limb, cover tattoos: need symmetrical images
  • Depending on the pain and disability state, decide on an appropriate activities to perform with the unaffected limb.
  • Start with exercises involving no or little movement.
  • Gradually progress to moving the affected limb in a similar way
  • Gradually increase the difficulty of exercises for both the unaffected and affected limbs.
59
Q

Immediately after a soft tissue injury, soft tissues need PEACE

A

P - Protect
E - Elevate
A - ‘Avoid’ anti-inflammatory agents
C - Compress
E- Educate

60
Q

After the first days have passed, soft tissues need LOVE

A

L - Load (PA and movements)
O - Optimism
V - Vascularization (cardio-type activities)
E - Exercise

Neuro Dev/Control II (19 decks)

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