Lecture 28 - Management of chronic musculoskeletal pain (24 MINUTES)
Pain definition Classification and Causes
 IASP: unpleasant sensory or emotional experience associated with actual or potential tissue damage, or
described in terms of such damage.
 Pain Classification
o Temporal
 Acute < 6 weeks
 Subacute 6 weeks – 3 months
 Chronic > 3 months (occurs in the absence of ongoing pathology; something has changed in
the nervous system, so the individual is still experiencing pain, even though no pathology )
o Aetiology
 Malignant VS Non Malignant
o Physiologic
 Nociceptive: irritation/damage of nociceptors (in periphery)
 Somatic; skin + soft tissues + muscles + bone + joints (sprain, fracture, inflammation)
 Visceral (Colic, MI); internal organs  presents as dull, ache, cramp, poorly localised
 Neuropathic
 Pressure on/Destruction of  PNS / CNS / ANS  e.g. Peripheral Neuropathy, Post
Herpetic Neualgia (after shingles), Spinal Cord Injury, CVA (thalamic)
 Mixed(Chronic) Pain: nociceptive + neuropathic
Arthritis Classification
 Immune mediated: RA, Psoriatic arthritis
 Reactive: Reiters
 Crystalline: Gout, pseudogout
 Infective: septic arthritis
 Degenerative: OA, following any of the above, or trauma
Aetiology of Pain
 Trauma: bone, muscle, joint, ligament
o Acute (Inflammation) VS Chronic (OA)
 Immunologic: RA (also infection component)
 Infection: bone (osteomyelitis), soft tissue (cellulities), disc
 Neoplasm: primary or metastatic (expansion of tumour within enclosed space; e.g. liver tumour stretches
Gleason’s Capsule  characteristic pain)
 Hypoxia (e.g. gangrenous limb)
 Referred Pain: somatic, visceral (angina) or neuropathic (e.g. in distribution of nerve OR dermatome)
Pain Pathways (Propagation)
I.
Tissue damage  inflammatory soup – K+, PG, histamine, Leukotrienes, TNF, substance P, Thromboxane
II.
Detected by Nociceptors in periphery  trigger pain nerves (A delta + C)
III.
Travel to dorsal horn of spinal cord lamina 1 and 2
IV.
Interact with wide dynamic response neurones in lamina 5
V.
Crossover to anterolateral side of Spinothalamic Tract
o NB: pain messages are also carried by the Spinoreticular tract // Spinomesencephalic tract //
Spinocervical tract // Dorsal columns
VI.
Travel up to thalamus
VII.
Synapse onto Somatosensory cortex
VIII.
Post central gyrus
Pain Pathways (Modulation)
 Frontal / temporal lobes
o Emotional and cognitive responses (interpretation) to pain
 Descending inhibitory pathways
o Hypothalamus, Periaqueductal grey, Locus ceruleus, Ventromedial and ventrolateral medulla
 Gate Control theory
o modulation of nociceptive input by descending influences at dorsal horn
 Other influences
o Pain triggers arousal (Autonomic Nervous System aroused)
o Withdrawal – reflex (if danger, automatic withdrawal) and higher level (behavioural; if someone
trying to hurt you)
o Autonomic stress response
 primitive responses from brainstem eg nausea, sweating (particularly with visceral pain)
o Hormonal stress response
Chronic Pain: No Nociception
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“Wind up” – sustained nociceptive input (eg damaged nerves) [due to changes in Spinal Cord + Brain]
I.
CNS becomes sensitised to experiencing pain
II.
Activates NMDA receptors dorsal horn (NB: important for treatment)
III.
Lower threshold for pain in injured and surrounding tissue
 NB: also spontaneous nociceptive activity
IV.
Expansion of nociceptive field (in 2 ways):
 Allodynia (perception of pain, from a not normally painful stimulus)
 hyperalgesia (increased sensitivity to pain, which may be caused by damage to nociceptors
or peripheral nerves)
Chronic Pain: Psychosocial
 Physical Changes (following can magnify pain they are experiencing right now) (people with pain tend NOT
to move around as much  causes secondary effects )
o Weakness, poor fitness, joint stiffness
o Fatigue, insomnia, appetite changes
o Iatrogenic complications (medications)
 Psychological Changes – mood, anxiety, grieving
 Social Changes – sick role, illness behaviour, secondary gain, financial, employment changes
Why Pain is Important: Epidemiology
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Common: 70% > 65 = pain in the previous year // 30% report persistent pain (>6 mo)
Personal - aim to avoid chronicity – physical, functional, psychological and social impacts
Economic - $34 000 000 000 / year
o 20:80 rule (80% of costs come from 20% of chronic patients)
o Off work 1 year, 2% chance of ever Returning To Work
Importance of Assessing Pain
o 70% of Answers from History
o 20% from Examination
o 10% from Investigation
Pain History Taking
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SOCRATES
o Description of Pain
 Nociceptive
 Somatic: ache, sharp, throbbing, well localised
 Visceral: throbbing, deep
 Organ capsule: sharp
 Obstruction: crampy, colicy
 Neuropathic
 Burning, stinging, lancinating, electrical qualities, allodynia, deep aching. Along
peripheral nerve, dermatomal distribution
o Associated Symptoms
 Systems review, fevers, chills, night sweats, weight loss, weakness, sensory changes, bowels,
bladder sexual dysfunction
Other Important Points
o Past and present treatments for pain
o Co-morbidities – HIV, Cancer, IVDU
o Medications – past and present, Prescription, and over the counter, side effects, steroids?
o Social History – where, with who, financial,
o Smoking, Alcohol, Caffeine, Illicit drugs (may lower threshold of pain)
Functional Assessment
o Sleep
o Appetite
o Mood / anxiety
o Mobility
o Activities of Daily Living
 Personal – eat, dress, shower, toilet
 Domestic – cook, clean, wash,
 Community – Work, drive, shop,
recreation
Pain Assessment in the Elderly
o NB: important to get the carer input
o Atypical Presentations
 Confusion, Delirium, Fatigue, Insomnia,
↓ Appetite, Weight loss, Constipation,
Frustration, Withdrawal, Anxiety, Depression, Agitation, Stop walking, Refuse to self care
Impact of Pain on Person (Pscyhosocial)
o Finances
o Expectations for treatment
o Responses of others to pain (family, friends, colleagues, HCW)  hostile, helpful, supportive?
Red Flags
o Major/minor trauma
o Steroids in past
o Systemically unwell; fevers, chills, night sweats, weight loss
o History of cancer, bacterial infection
o IVDU, HIV
o Night pain
o Severe localised pain
o Neurological changes
Tools for Assessing Pain
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Visual Analogue Scale: 10cm line, patient says how bad it is
Numeric Rating Scale: out of 10
Verbal descriptor – 7 point scale (mild, modersate, severe etc.)
Abbey pain scale – cognitive impairment – includes behaviours
Brief Pain Inventory
McGill Pain Questionnaire
Psychology and Pain
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Psychosocial Yellow Flags
o Attitudes and beliefs
 Incorrect: pain is dangerous, movement will cause damage, rest and passive modalities best
o Behaviours
 fear avoidance, reliance of medications, 5 Waddell signs
o Compensation issues
 ½ rate full recovery // Catastrophisation
o Diagnosis (unclear) and treatment (passive); different doctors say different things
o Emotions
 anxiety, depression
 Employment risk fx = 
 Poor job satisfaction, Unstable job history, Stress at work, Poor work relationships,
Unsupportive work envt, Low education, low SES, Bad previous injury mx, Heavy
work, shift work
o Family and social support – too much / little
Examination
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Usually focus on MSK / neurological
Functional assessment – walking, ADL
Palpation, Percussion
Observe behaviour, non verbal cues
Waddell signs
 Tenderness tests: Superficial, diffuse, non anatomic
o Simulation: pain with no movement  axial loading, simulated rotation (hurting in wrong place =
faking LOLOL)
o Distraction: SLR in seated position
o Regional Disturbances: deviation from accepted neuroanatomy
o Over Reaction
Mental state examination – psych issues
Multi-disciplinary assessment – medical, PT, OT, Psychology
Investigation
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Rational use of Ix – will the result affect your clinical decision making and management?
Overexpectations
X-rays – functional views; flexed etc. // Ultrasound – soft tissue // CT – bone, when MRT c/i
MRI – tumor, infection, soft tissue, acute bony injury // PET: malignancy // Bone Scan – fracture, malignancy
Others for red flag conditions
Rainbow Flags
Faking Pain