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Neuro Exam 2 > Neurophysiology of Pain > Flashcards

Neurophysiology of Pain Flashcards

1
Q

The International association for study of pain definition

A

unpleasant sensory or emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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2
Q

6 key notes of pain

A

1) pain is a personal experience
2) pain and nociception are different phenomena.
3) pain is learned through life experiences
4) pts report of pain should be respected
5) usually serves as an adaptive role but may have adverse effects
6) verbal description is only one of the several behaviors to express pain

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3
Q

biopsychosocial model of pain

A
  • complex multifaceted phenomena
  • addresses pain with social, biologic and psychological factors
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4
Q

biological factors of pain

A
  • genetics
  • physiology
  • neurochemistry
  • tissue health
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5
Q

social factors of pain

A
  • SES
  • Social
  • Skepticism (due to negative feedback loops)
  • operant
  • social learning
  • social support
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6
Q

psychological factors of pain

A
  • perceived control of self-efficacy
  • catastrophic thinking
  • hyper vigilance
  • depression
  • anxiety
  • anger
  • can change the way we think of pain in the brain through spinothalmic offshoot to anterolateral tract
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7
Q

Guidlines for PTs using the biopsychosocial model

A

1) biological, physcial, psychological, social, and environmental factors are specific to each individual
2) pain must be addressed in a comprehensive, safe, ethical, and consistent manner using valid and reliable measuring tools.
3) comprehensive pain management should be underpinned by sound theoretical models and empirical evidence
4) PTs should be empathic and compassionate to pt in communication

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8
Q

IASP article 1

A

the right of all people to have access to pain management without discrimination

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9
Q

IASP article 2

A

the right of people in pain to have acknowledgement of their pain and to be informed about how it can be assessed and managed

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10
Q

IASP article 3

A

the right of all people with pain to have access to appropriate assessment and treatment of the pain by adequately trained health care professionals

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11
Q

factors that can lead to chronic pain

A

diet, sleep, stress, physical inactivity, sedentary behavior, smoking

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12
Q

chronic pain is a major health crisis

A

it affects more people then CVD, cancer and diabetes combined

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13
Q

delta fibers

A
  • large in diameter
  • myelinated
  • high conduction velocity
  • sharp and localized pain
  • mechanical or pressure
  • “prickly”
  • Stabbing or shooting
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14
Q

C fibers

A
  • unmyelinated
  • dull pain
  • diffuse pain and longer in duration
  • pressing, aching, dull
  • thermal, chemical, or mechanical
  • referred pain from organs
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15
Q

Peripheral nerve distinction

A
  • burning, tingling, pins and needles
  • extremities
  • follows peripheral nerve pattern
  • Tinels sign (tapping) increases pain
  • constant pain
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16
Q

muscle pain distinction

A
  • localized
  • palpation over muscle increases the pain
  • tender, throbbing, and stiffness
  • increase with lengthening or contracting muscle
  • reduced pain at rest
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17
Q

normal pain processing pathway

A

1) stimulus from peripheral nerve
2) dorsal horn depolarization: Ca 2+ diffuse into neurons causing the release of glutamine and substance P
3) signal sent via the ascending tract to the brain is perceived as pain
4) the descending tract carries modulating impulsed back to dorsal horn (brains natural way from reducing pain)

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18
Q

acute pain

A

contributes to survival by protecting the tissue from further damage. Normal response to painful stimulation

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19
Q

adaptive pain

A

protect tissues and promotes healing

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20
Q

maladaptive pain

A

process representing as a disease and represents the pathological functioning of the nervous system

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21
Q

chronic pain

A

pain lasting longer then 3 months. Tissue is no linger in protective mode but has a maladaptive process. may involve neuro pathways

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22
Q

negative neuroplasticity

A

chronic pain the involves alternative neuro pathways

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23
Q

what is prostaglandin

A

substance that causes inflammation and pain to promote healing

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24
Q

Substance P: neuropeptide

A
  • the first responder to stress or pain in the periphery. released by variety of cells (dorsal horn, mast cell, and blood)
  • immediate and on going
  • caused vasodilation and histamine release
  • strongly correlated with NS pain
  • associated with glutamate: facilitator of neurotransmission
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25
Q

what is CGRP

A

vasodilator released form sensory nerves

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26
Q

Substance P pain pathway

A

stimulas - nociceptor - release of substance P - dorsal root excitatory interneurons - reticular formation (increases alertness) - hypothalamus and the limbic system ( behavioral and emotional responses to pain) - thalamus (perception of pain)- somatosensory cortex (localization of pain)

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27
Q

allodynia

A

pain from a non painful stimuli

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28
Q

analgesia

A

absence of pain sensation

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29
Q

hyperalgesia

A

increased sensitivity to painful stimuli

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30
Q

sensitization

A

increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally sub threshold inputs

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31
Q

IASP classification of pain 3 types

A

1) nociceptive
- adaptive and “regular pain”
2) neuropathic
- damage to the NS
3) nociplastic
- Negative neuroplasticity

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32
Q

neuropathic pain classifications

A

1) peripheral nerve
2) central (brain and spinal cord)

33
Q

nociplastic pain classifications

A

1) peripheral sensitization
2) central sensitization

34
Q

Nociceptive pain : normal response to tissue damage

A
  • pain arising from a noxious stimulus in somatic tissue or organ
  • somatic and non-neural tissue will present as localized, musculoskeletal pain
  • organ and visceral pain will present as poorly localized deep dull ache
35
Q

nociceptive pain pathway

A

1) stimulus is felt
2) information is transmitted to brain where sensation is felt
3) the motor response of the brain is to move away from the stimulus

36
Q

Neuropathic pain definition

A

pain initiated or caused by a primary lesion or dysfunction in the nervous system

37
Q

peripheral neuropathic pain definition

A

pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system. can be a nerve root or peripheral nerve

38
Q

Central neuropathic pain definition

A

pain initiated or caused by a primary lesion or dysfunction in the central nervous system. Can be brain structures including cognitive behavioral and anterolateral pathways

39
Q

nociplastic pain definition

A

pain that arises from altered nociception despite no clear evidence of actual tissue damage. Causes activation of peripheral nociception despite no evidence of disease or lesion of the somatosensory system causing the pain

40
Q

peripheral sensitization

A

increased responsiveness and reduces threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields. Can show hyperalgesia or allodynia. Due to “chemical soup”

41
Q

central sensitization

A

increased responsiveness of nociceptive neurons in the CNS to their normal sub threshold afferent input
due to dysfunction of endogenous pain control systems in peduncle gray area

42
Q

what is “chemical soup” in peripheral sensitization

A

increase in substance P, CGRP, Histamine and prostaglandin in an injured area

43
Q

spinoreticular tract and brainstem reticular formation role in centralized nociplastic pain

A

awareness and arousal to pain. RF connects to hypothalamus. Helps with sleep wake cycle

44
Q

periaqueducal gray role in Nociplatic centralized pain

A
  • modulation and perception of pain
  • lesson or increase in pain perception
  • key in defensive behaviors (elevates HR, BP and RR)
  • Defensive mechanism for future pain (why people are anxious about pain)
45
Q

Thalamus role in centralized pain

A

connects to the somatosensory cortex, prefrontal cortex, limbic (for thinking) and hippocampus (memory)

46
Q

central sensitization pathways

A
  • Thalamus (send to Anterior Cingulate which sends to amygdala and prefrontal cortex)
  • Hypothalamus (send to hippocapus, amygdala, Anterior cingulate)
  • Hippocampus
  • take away: the amygdala gets a lot of information which is why people are fearful of pain
47
Q

descending pathway 2 way of pain modulation/ inhibition

A

Serotonergic pathway: cortical influence - periaqueducal gray - Nucleus Raphe (inhibition) - dorsal horn
Cattecholaminergic pathway: cortical influence - periaqueducal gray - Rostal ventromedial medulla - inhibition at the dorsal horn

48
Q

what does the periaqueductal gray provide

A

provides endogenous opioids and serotonin

49
Q

Ascending pathways of pain modulations

A

ventrolateral pain pathway

50
Q

the IASP definition of chronic pain

A

definition addresses both duration and appropriateness, defining chronic pain as pain without apparent biologic value that has presisted beyond the normal tissue healing time (3 mo)

51
Q

chronic pain sensory pathway

A

1) stimulus: enhanced responsiveness of nociceptive endings
2) dorsal horn: hyperexcitability increases discharge from second -order neurons
3) overactive ascending pain fascilatory pathway
4) brain: malfunctioning of central pain inhibitory pathways arising from the periaquaducal gray matter and RVM in brainstem
5) brain: cognitive-emotional sensitization or brain: sensory-motor conflict
6) malfunctioning of descending pain-modulating pathways

52
Q

what does chronic pain involve

A

thoughts, memories, behaviors, and emotion

53
Q

behaviors of chronic pain

A

avoidance, withdrawal, overcompensation

54
Q

emotions of chronic pain

A

depression, anger, anxiety

55
Q

thoughts of chronic pain pts

A

catastrophising, hopelessness, helplessness

56
Q

Sensory/discriminative components of the pain matrix

A
  • thalamus
  • somatosensory cortex
57
Q

Affective components of the pain matrix

A
  • brain stem
  • thalamus
  • limbic system
  • BG
  • Prefrontal cortex
  • anterior cingulate cortex
  • insula
58
Q

associative components of the pain matrix

A

posterior parietal cortex

59
Q

Physical / biological factors that lead to persistent pain

A
  • nociceptive
  • injury
  • trauma
  • infection
  • illness
  • cancer
  • nerve damage
60
Q

Psycolgical factors that lead to persistent pain

A

sleep, concentration, irritability, negative thoughts, helplessness, anxiety and depression, fears, beliefs, coping skills, trust issues

61
Q

psychosocial factors that lead to persistent pain

A

relationships, work and employment, social network, isolation

62
Q

other factors that lead to persistent pain

A
  • drug dependance / abuse
  • financial difficulties
  • cultural barriers
  • litigation
  • language barriers
  • lack of health insurance
63
Q

Pain management with phsyical activity

A

continuous exercise contributes to the brains release of endorphins. endorphins reduce the intensity of pain sensed by the brain

64
Q

Non- pharmacologic therapy

A
  • pt education
  • self management programs
  • personalized social support via the telephone
  • weight loss if overweight
  • aerobic exercise program
  • physical therapy
  • ROM exercises
  • muscle strengthening exercises
  • assistive devices for ambulation
  • patellar taping
  • appropriate footwear
  • lateral wedged insoles
  • bracing
  • OT
  • joint protection and energy conservation
  • assistive devices for ADLS
65
Q

How to build positives behaviors as a PT

A
  • acknowledge pain and listen to the pt
  • promote socialization and activity (belief system, family, start hobbies, Altruism (helping someone else, your pain goes away))
  • provide insight to changes in body schema, pain and increase activity
66
Q

Neuro pain education involves

A
  • listening
  • idividualising and context
  • experiences as well as words
  • seen as an ongoing process
  • tailored to level of health literacy
  • asking if it is wanted
  • validation of someones pain experience
  • reflective questions
  • Finding out is information is correctly interpreted
  • pain science concepts consistant throughout treatments
67
Q

Gate theory for pain reduction

A
  • unmodulated pain pathway: C fiber - inhibitory interneuron - second order neuron - strong signal to thalamus
  • Modulation of pain: Ab fibers from skin mechanoreceptors excite the inhibitory neuron which then will send a weak signal to the thalamus (want to fire ruffini texture and merkel pressure
68
Q

over the counter pain reduction

A

non-steroidal anti-inflammatory NSIDs: reduces prostaglandins which are part of the peripheral and central sensitization process. target COX2 (inflammatory process) mediate analgesia

69
Q

over the counter capsaicin

A

works by depleting Substance P
takes several weeks
PT can use to dampen pain for exercise

70
Q

peripheral sensitization pharmacologic agents

A
  • local anesthetics
  • topical analgesics
  • anticonvulsants
  • tricyclic antidepressants
  • opioids
71
Q

Central sensitization pharmacologic agents

A
  • anticonvulsants
  • opioids
  • NMDA-receptor antagonists
  • Tricyclic/SNRI antidepressants
72
Q

Descending modulation from brain pharmacologic agents

A
  • anticonvulsants
  • opioids
  • tricyclic/SNRI antidepressants
73
Q

other pain condiations

A
  • phantom limb pain
  • hand shoulder syndrome (post mastectomy with lymphedemea)
  • pelvic pain
  • chronic low back or cervical pain
  • autoimmune conditions
  • fibromyalgia: brain processes pain signals
74
Q

phantom limb

A

characterized by missing sensory input to the somatosensory cortex. negative neuroplasticity

75
Q

mechanism of CRPS

A

1) original injury initiate pain impulse from brain and carried by sensory nerves to CNS
2) in the spinal cord the pain impulse triggers an impulse in the sympathetic nervous system which returns to the original site of injury
3) in blood vessels: the triggering of the sympathetic nervous system causes vessels to spasm and lead to swelling and increased pain
4) pain triggers another response establishing a cycle of pain and swelling

76
Q

what is CRPS

A

a conditions that results with burning, extremity pain, red mottling of the skin. Can lead to central desensitization if not treated

77
Q

treatment of CRPS

A

1) wrap extremities with ace wrap to reduce sensory input and use dorsal columns (20-30 mins)
2) movement to increase the use of MS and bloodflow
3) tactile information (self initiated): skin movement targeting the ruffini NOT CRUDE TOUCH

78
Q

what is mirror therapy used for

A

used to trick the brain into thinking that the involved limb is back to normal by moving the uninvolved limb in the mirror

79
Q

reconceptualising pain according to modern pain science

A

-in the brain: receives sensory info determines how dangerous is this?
-pt pulls from previous experience, cultural factors, social/work environment, expectations about consequences, beliefs, knowledge and logic to determine severity
-pt created meaning for pain
-determine to be anxious or fear pain or sets expectations for pain

Neuro Exam 2 (4 decks)

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