pain review Flashcards
pain define
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.
models of pain
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
models of pain - chronic / persistent
biopsychosocial model
social - culture
social interactions
psycho - illness behaviour
beliefs, coping strategies
emotions, distress
bio - neurophysiology
physiologic dysfunction
(tissue damage)
pain pathways
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
nociceptors
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
spinothalamic
pain signals are filtered selected and modulated at every level
pain signals
descending innibitory system
primary source is periaqudcutal grey matter
inhibit downward towards the dorsal horn
direct structural components from limbic system
neuromatrix
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
hyperalgesia
primary and secondary
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
neuropathic pain
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.
nociplastic pain
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.
central sensitisation
Central sensitization: Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.
peripheral sensitisation
Peripheral sensitization: Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields.
neuropathy
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
nociceptive pain
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
7 predictive clinical criteria of nociceptive pain
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%).
peripheral neuropathic pain
predictors of neuropathic pain
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%)
types of spinal pain
non-radicular
radicular
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
central sensitisation pain
predictors of central sensitisation pain
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%).
define central sensitisation
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
central sensitisation
neurotransmission
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.
examples of clinical syndromes
–> pain mechanisms
discogenic LBP - nociceptive
radiculopathy - peripheral neuropathic or nociceptive or mixed
postural LBP - nociceptive
low sensitisation
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
high sensitisation - helpful / protective
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
high sensitisation - unhelpful
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
pain Ax
assess pain experience and personal impact of pain
self report - gold standard
distribution body chart
acute
sub acute
chronic
severity
quality
VARs / NPRS
valid and reliable
1-3 = mild
4-6 = moderate
7-10 = severe
pain drawings
mcGill pain questionnaires
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
pain questionnaires examples
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
neuropathic questionnaire
self-LANSS
painDETECT
disability / functional Ax
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
ODI 2.0
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)
quantitative sensory testing
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
tools to assess domains/ drivers of chronic pan
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
