JOINT AND MUSCLE PAIN

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JOINT AND MUSCLE PAIN
Jane Greening
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Physiology Joint and Muscle pain
Specific muscle pains
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JOINT PAIN
C and A? fibres (IV and III) found in all soft
tissues associated with joint EXCEPT cartilage

• Sensitization of nociceptors following
  inflammation
• respond to lower levels of stimulus
• increased firing rate
• increase in resting activity

CENTRAL SENSITISATION
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Sensitization of joint nociceptor by inflammation
Spike firing, imp/s
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Flexion
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30s
10
5
0
72
87
90
105
125
147
170
173
198
205
Injection of kaolin
minutes after kaolin
Responses of a high threshold group III unit to
flexion in the normal range before and during
arthritis. Recording from the knee joint nerve in
the anaesthetized cat.
From Schaible, H-G Schmidt, R.F. Proc Vth World
Congress on Pain, 1988
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SENSORY NERVES
NOCICEPTORS in MUSCLE

• Type III or A? - small myelinated
• Type IV or C - unmyelinated

• Dense in - myotendinous junctions
• fascial sheaths
• muscle arterioles and small arteries
• Not found in muscle fibres or around capillaries

• Most are polymodal, activated by mediators,eg
  bradykinin, histamine, 5HT, H, K

• May become sensitised fire to low threshold
  stimulation. Muscle C fibre firing effective in
  producing
• central sensitisation Wall, Woolf J Physiol 356
  443-458 1984

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• C fibre sub populations
• Mechanical Stretch
• Ergoreceptors may sense effort in muscle (Mc
  Closky Mitchell J Physiol 224173-186 1972)
• thermoreceptors
• Silent nociceptors

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Pain from cutaneous and muscle tissues

• Localisation good for superficial tissue skin
  poor for muscle

• Muscle pain described as deep ache
• associated with tenderness, cramping, weakness,
  fatigue, exercise intolerance

• C fibre input from muscle central
  sensitisation
• Aß input perceived as painful

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Muscle hyperalgesia and referred pain

• Inject hypertonic saline
• Intramuscular Electrical stimulation
• Intramuscular injection of algesic substances
• Responses to pressure algometry /clinical
  palpation

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Muscle hyperalgesia Results

• Would expect to find hyperalgesia
• Studies find both hyperalgesic responses to
  pressure plus unchanged and reduced responses
• Extent of referred pain appears correlated to
  the intensity of induced muscle pain

Laursen RJ et al. Pain1 105-113
1997 Graven-Nielsen T et al. Pain 69111-117 1997
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Somatosensory changes (pressure) segmentally and
extrasegmentally after injection of hypertonic
saline into Tibialis Anterior
Inject hypertonic saline
Graven-Nielsen et al. European Federation of IASP
Chapters, Nice France 2000 p.213
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Specific muscle pain

• Ischaemic
• DOMS
• Inflammatory/ degenerative
• Neurogenic
• Exs Induced muscle cramp

• Fibromyalgia
• Myofascial Trigger
• points

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CAUSES OF MUSCLE PAIN
Muscle pain associated with exercise or pathology

• Pain with exercise
• Ischaemia during high intensity exercise.
  Metabolic build up, fatigue develops - Not
  lactate muscle remains acidic 1-2 mins post exs.
  McArdles, no lactate still get pain
• K, ADP, AMP, H acting in combination on
  nociceptors

Peripheral vascular disease intermittant
claudication Angina ischaemic pain from heart
muscle
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Delayed Onset Muscle Soreness

• Particularly post eccentric / high force
  loading/low metabolic cost (so unlikely to be
  consequence of metabolic depletion)

• Release CK into bloodstream 4-6 days post exs
• ( changes to permeability of muscle cell
  membrane). CK levels not related to onset pain

• Effects on force production at low frequencies

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? Effects of NSAIDs reduce muscle soreness (in
jaw not limb muscles) but no change in function
? Inflammatory reaction of muscle and connective
tissue
Tokmakidis SP et al. J Strength Cond Res.
17(1)53-59 2003 Tegeder l et al. Inflamm Res
51(8) 393-402 2002
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Muscle Pathology 1) myositis infective 2)
inflammatory myopathies (muscle weakness) 3)
impaired energy metabolism Metabolic muscle
disease eg Mc Ardles disease anaerobic
dysfunction
Neurogenic origin 1) referral from nerve root
injury 2) spontaneous firing of C fibres in
peripheral nerve neuritis
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Muscle Trauma

• Inflammatory mediators C fibre firing

• Crush trauma on hard surface hours later
  Myogloblinuria
• die from kidney failure

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Indications of damage in skeletal muscle

• Decreased force generation

• Sarcolemma changes holes in membrane
  increased permeability
• measure blood levels of myoglobin / CK
• Biopsy samples architecteral disruption
• degeneration / regeneration
• inflammatory changes

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FIBROMYALGIA

• Classification by American College of
  Rheumatology Chronic multifocal pain and
  generalised allodynia/hyperalgesia
• Widespread pain and tenderness in 11 out of 18
  defined
• musculoskeletal sites

• Associated symptoms poor sleep, mood changes,
  headache, fatigue
• May coexist with other disorders

• Lack of clinical signs in NSAP may be diagnosed
  as fibromyalgia ( Reilly 1993)
• No peripheral pathology identified in this
  syndrome
• (Cohen Quintner 1998). ?Disorder of central
  processing of
• sensory information (Littlejohn 1998)

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Central sensitisation may be reason why local
pain condition can spread and become generalised
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? Local MS disorder
Bengtsson et al. Pain 39171-180, 1989 Muscle
pain and tender points disappeared during
epidural lignocaine. ?? Impulses in primary
afferent neurones evoke pain in FMS
Neumann L et al. Semin Arthritis Rheum. 2003
Apr32(5)320-5 report increased rate FMS among
persons subjected to neck trauma
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?

• Organic cause
• Initiated and maintained by
• Longstanding nociceptive input
• Changes within the CNS
• Changes in stress regulatory systems
• Changes in serotonin metabolism
• Genetic factors

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MF TRIGGER POINTS
taut band in muscle
locus of sensitivity
Local and referred pain
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Consensus of poor inter-observer reliability in
identifying Trg.pts

• Pearce JM Eur Neurol
• 52 (2)67-72 2004
• no hard physical signs or laboratory evidence

• Simmonds Muscle pain, myofascial pain
  Fibromyalgia recent advances 1999 Haworth Press
  spontaneous electrical activity and contraction
  knots

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Myofascial Trigger Points treatment

• Mechanical
• Thermal
• Chemical

Chemical lignocaine Botulism toxin 5-HT3
receptor antagonist (tropisetron) (also used in
treatment for Fibromyalgia)
Farber et al. Int J Clin Pharmacol 21(1) 1-13
2001
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Muscle Cramp
Exercise induced painful, involuntary muscle
contraction
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Risk factors older age, fatigue, poor
stretching, higher BMI, repetitive exercise
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faulty posture, shortened muscle length
intense exercise and exercise to fatigue
Disturbance in the activity of muscle spindles /
golgi tendon organs
relaxation phase of muscle contraction is
prolonged in fatigued muscle, likelihood of fused
summation of action potentials
increased motor neuron activity and motor unit
recruitment
CRAMP
treatment of cramp reducing muscle spindle and
motor neuron activity by reflex inhibition and
afferent stimulation
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Muscle damage does not always pain
Muscle pain does not always muscle damage