pain review Flashcards

1
Q

pain define

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

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

  • Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.
  • Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
  • Through their life experiences, individuals learn the concept of pain.
  • A person’s report of an experience as pain should be respected.
  • Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.
  • Verbal description is only one of several behaviors to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.
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2
Q

models of pain

A

How can it be possible
to experience pain
without tissue damage?

How can it be possible to
experience tissue damage
without pain?

How can it be possible to
experience pain after
tissue damage has healed?
i.e. chronic pain

Pain system can be overrrided for short period of time to allow you to get to safety

clinical relevance
insidious onset of pain - muscle recognise presence of ongoing irritant and remove to stop cycle of tissue micro trauma

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3
Q

models of pain - chronic / persistent

A

biopsychosocial model
social - culture
social interactions

psycho - illness behaviour
beliefs, coping strategies
emotions, distress

bio - neurophysiology
physiologic dysfunction
(tissue damage)

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4
Q

pain pathways

A

Nociceptors are free or bare nerve endings that respond to painful stimuli.
Joint capsule & periosteum are most sensitive tissues, followed by subchondral bone, tendons and ligaments.
Pain receptors are supplied by variety of different nerve fibres

only when it hits cerebral cortex do you perceive pain

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5
Q

nociceptors

A
A delta fibres 
(smaller than a beta)
Mechanical
1st / Fast Pain
Well-localized
Sharp / Prickling
Glutamate neurotransmitter
C fibres - slow fibres
Polymodal
2nd / Slow Pain
Diffuse
Dull
Aching
Burning
Substance P neurotransmitter
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6
Q

spinothalamic

A

pain signals are filtered selected and modulated at every level

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7
Q

pain signals

A

descending innibitory system

primary source is periaqudcutal grey matter
inhibit downward towards the dorsal horn

direct structural components from limbic system

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8
Q

neuromatrix

A

Spinal cord & brain are best seen as integrated Neuromatrix not simply tracts – i.e. computer

Other inputs can modify pain signals – basis for Rx
Pain strongly linked with emotions – limbic system
Stress, endocrine responses, autonomic & immune system inputs & mental functions
CNS is plastic – neurophysiology changes over time with development of chronic pain
Pain and nociception are different phenomena: the experience of pain cannot be reduced to activity in sensory pathways

CNS very plastic
related to pain
neuroplasticity + pain
system has potential to experience chronic pain
pain and nociception are different phenomena

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9
Q

hyperalgesia

primary and secondary

A

Hyperalgesia: increased pain from a stimulus that normally provokes pain
more nociceptive drive from periphery causing more irritation

Primary Hyperalgesia: increased sensitivity to input at the site of the injury and due to processes in damaged tissues. It is largely due to the sensitisation of peripheral nociceptors.

Secondary Hyperalgesia: sensitivity in uninjured tissues around the original injury. This is most likely to arise from central mechanisms.

Allodynia: pain evoked by stimuli that are not normally painful
e.g. touch or cold / heat

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10
Q

neuropathic pain

A

Neuropathic Pain: Pain caused by a lesion or disease of the somatosensory nervous system.
Peripheral Neuropathic Pain: Pain caused by a lesion or disease of the peripheral somatosensory nervous system.
Central Neuropathic Pain: Pain caused by a lesion or disease of the central somatosensory nervous system.

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11
Q

nociplastic pain

A

Nociplastic pain: Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.

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12
Q

central sensitisation

A

Central sensitization: Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.

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13
Q

peripheral sensitisation

A

Peripheral sensitization: Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields.

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14
Q

neuropathy

A

a disturbance of function or pathological change in a nerve. eg radiculopathy
in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy

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15
Q

nociceptive pain

A

Nociceptive Pain (Somatic Pain):
Dull, deep, aching type pain.
Mechanical / physiological processes in injured tissue: tends to be localised.
Predictable response to stretch, compression or movement
Responds to simple painkillers & NSAIDs
Improves with appropriate passive (manual) treatment

types of spinal pain Referred / nonradicular pain = any somatic structure of spine causing pain with referral
Radicular pain = caused by spinal nerve or root e.g. radiculopathy – disc bulge irritating nerve root in foraminal space e.g. L5/S1

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16
Q

7 predictive clinical criteria of nociceptive pain

A

Cluster of 7 clinical criteria predictive of Nociceptive Pain, including:
Pain localised to the area of injury/dysfunction,
Clear, proportionate mechanical/anatomical nature to aggravating and easing factors,
Usually intermittent and sharp with movement/mechanical provocation; may be a more constant dull ache or throb at rest,
Absence of:
Pain in association with other dysaesthesias,
Night pain/disturbed sleep,
Antalgic postures/movement patterns and
Pain variously described as burning, shooting, sharp or electric-shock-like’.

High levels of classification accuracy (sensitivity 90.9%, specificity 91.0%).

17
Q

peripheral neuropathic pain

predictors of neuropathic pain

A

Superficial, burning, shooting, cramping within all or part of nerve innervation field (dermatome or cutaneous field).
+/- Paraesthesiae and possible muscle weakness and autonomic changes.
Allodynia
Often difficult to ease with rest or simple painkillers & NSAIDs.
Provoked by neurodynamic tests, compression or nerve palpation
Response to passive treatment varies.

predictors of neuropathic pain
Pain referred in a dermatomal or cutaneous distribution
e.g. L5 dermatome in L5 radiculopathy, median N distribution in hand in CTS
History of nerve injury, pathology or mechanical compromise and
Pain/symptom provocation with mechanical/movement tests (e.g. Active/Passive, Neurodynamic) that move/load/compress neural tissue

High levels of classification accuracy (sensitivity 86.3%, & specificity 96.0%)

18
Q

types of spinal pain
non-radicular
radicular

A

Nonradicular pain = any somatic structure of spine causing pain with referral
Radicular pain = caused by spinal nerve or root e.g. radiculopathy – disc bulge trapping nerve root in foraminal space e.g. L5/S1

19
Q

central sensitisation pain

predictors of central sensitisation pain

A

Widespread, non-anatomical distribution
Ongoing pain after healing with hyperalgesia, allodynia
Inconsistent response to stimuli & tests
Pain seems to have a ‘mind of its own’
Simple pain meds ineffective & exacerbated by emotion
Unpredictable or no response to passive treatments
Abnormal Impulse Generators (AIGs) in sensory nerves – spontaneous pain impulses
Abnormal neural activity due to disease/injury – peripheral or central e.g. phantom limb pain, post stroke pain, ongoing peripheral nerve injury

Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple/non-specific aggravating/easing factors,
Pain disproportionate to the nature and extent of injury or pathology,
Strong association with maladaptive psychosocial factors (e.g. negative emotions, poor self-efficacy, maladaptive beliefs and pain behaviours)
Diffuse/non-anatomic areas of pain/tenderness on palpation.

High levels of classification accuracy (sensitivity 91.8%, specificity 97.7%).

20
Q

define central sensitisation

A

Def: Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.

Def: changes occurring at a cellular level to support the process of neuronal plasticity that occurs in nociceptive system neurons in SC & in supraspinal centres because of activation of nociceptive system:

neurons in SC become hypersensitive to stimuli from involved tissues &
increase their response to both noxious and innocuous stimuli from remote uninvolved tissues
sprouting of A fibres in dorsal horn developing new synaptic connections with nociceptor system neurons
WDR range cells in DH (processing nociceptive & non-nociceptive impulses) become sensitised

21
Q

central sensitisation

neurotransmission

A

NMDA receptor activation in postsynaptic neuron by glutamate (excitatory amino acid)
Release of Ca2+ postsynaptically – modulates ion channel activity making neuron more excitable to subsequent glutamate release.
Increased intracellular Ca2+ triggers production of nitric oxide – diffusing out to make presynaptic neuron more excitable.

22
Q

examples of clinical syndromes

–> pain mechanisms

A

discogenic LBP - nociceptive
radiculopathy - peripheral neuropathic or nociceptive or mixed
postural LBP - nociceptive

23
Q

low sensitisation

A
sub acute neck pain 
clear eggs and eases 
low responsiveness to stimuli 
posture 
mvmt 
palpation of local neck structures

persistent knee pain
local sensitised palpation
pain with postures and mvmt

mgmt implications
as per guidelines for condition

24
Q

high sensitisation - helpful / protective

A

acute supination ankle sprain
clear sensitisation
and hyperalgesia localised to affected ankle structure

sub acute back pain + painful radiculopathy
can be considered protective in acute + sub acute stages

25
Q

high sensitisation - unhelpful

A

acute low back pain
no red flags with allodynia +/_ hyperalgesia
Chronic OA heightened responsiveness to touch movement
load
pressure

address factors contributing to increased sensitisation
neuropathic pain, psycho factors and lifestyle

26
Q

pain Ax

A

assess pain experience and personal impact of pain
self report - gold standard

distribution body chart
acute
sub acute
chronic

severity
quality

27
Q

VARs / NPRS

A

valid and reliable
1-3 = mild
4-6 = moderate
7-10 = severe

pain drawings

28
Q

mcGill pain questionnaires

A
SENSORY Descriptors
Dull
Throbbing
Sharp
Shooting
Burning
Pounding
Stabbing
Prickly
Hot
Deep
EMOTIONAL Descriptors
Tiring
Exhausting
Sickening
Fearful
Punishing
Cruel
Attempt to raise yellow flags
29
Q

pain questionnaires examples

A

Other QUESTIONNAIRES:
Örebro MSK Pain Screening Questionnaire - SF
Keele STarT Back Questionnaire (available as app) Yellow flag
Fear-avoidance belief questionnaire Yellow flag
Quality of Life (QoL) questionnaires e.g. SF-12 or 36
Illness behaviour questionnaire Yellow flag
Coping strategies questionnaire Yellow flag
Pain beliefs and perceptions inventory Yellow flag
Pain self-efficacy questionnaire (PSEQ) Yellow flag

30
Q

neuropathic questionnaire

A

self-LANSS

painDETECT

31
Q

disability / functional Ax

A

Questionnaires (disability commonly combined with pain for different regions / clinical syndromes)
e.g. Oswestry LBP Q 2.0, Roland-Morris Scale (LBP), Neck Disability Index, Patient Specific Functional Scale

Physical performance measures
Less useful for predicting prognosis

Work loss
Capacity for work
e.g. FCE

32
Q

ODI 2.0

A
Interpretation of ODI score:       
40-60% = high level disability
 20-40%  = moderate level disability
 0-20% = mild level disability
Reference data: 
Metastatic Disease mean score: 48% (Range 18-23/50)
Primary Care mean scores: 
Acute LBP = 27% (Range 6-24) 
Chronic LBP = 43% (Range 10-21)                    Roland & Fairbank (2000)

Beaumont Pain Clinic CLBP pts’ mean ODI score = 46% (SD14) Kearon et al (2012)

33
Q

quantitative sensory testing

A

QST which is a psychophysical method used to quantify somatosensory nerve function in both healthy subjects and patients with neuropathic pain
Backonja et al, 2013
Example – Pressure Pain Threshold measured with pressure algometer: Pressure (kPa) at which stimulus changes from pressure to pressure and pain
Can discriminate altered central pain processing

IASP - Attempt to establish somatosensory profiles in neuropathic pain to stratify patients based on mechanism-based classification

34
Q

tools to assess domains/ drivers of chronic pan

A

BIO:
Diagnostic imaging
Physical exam: AROM, MUSCLE AX (CONTROL, STRENGTH, ENDURANCE, LENGTH), PPIVMs, PAIVMs, NDT, Neuro exam etc
Central Sensitisation Inventory (score >40 on part A)
Pain Sensitisation Assessment
Clinical Quantitative Sensory Tests (QST) - PPT, Cold Pressor test (5s icecube)

PSYCHO:
Anxiety & Depression e.g. HADS
Beliefs & Attitudes questionnaires e.g. STarT Back tool, FABQ
Fear of movement e.g. Tampa Scale for Kinesiophobia

SOCIAL:
Work status
Sports status