joint mobilisation 3 Flashcards
indications for joint dysfunction and pathology
analgesia
improve joint hypomobility
improve functional ability
joint pathology involves what 3 systems
muscle
neural
articular
stokes and young effects of joint injury
joint injury
immobilisation
muscle atrophy
muscle weakness
mechanism of action of joint mobilisation
mechanical
neurophysiological
types of nociceptors
a delta fibres
c fibres
what type of fibre is a delta fibre
mehcanical
a delta fibre is responsible for what kind of pain
1st / Fast Pain
Well-localized
Sharp / Prickling
a delta neurotransmitter
Glutamate neurotransmitter
what type of fibre is c fibre
polymodal
c fibre is responsible for what kind of pain
2nd / Slow Pain Diffuse Dull Aching Burning
c fibre neurotransmitter
Substance P neurotransmitter
spinothalamic signals waddel 2004
pain signals are filtered, selected and modulated at every level spinal cord spinothalamic medulla midbrain primary somatosensory cortex thalamus corpus callosum
grades in glides that are large amplitude
grade 2 and 3
mobilisation effects
end of range EOR passive movemnts
increase joint ROM
decrease peri articular muscle spasm, intra articular pressure, joint afferent nociceptor activity
stimulates large diameter joint afferents for increased movement
end of rang joint rehabilitation
muscle inhibition - decrease in peri-articular tension
decrease in intra articular pressure -|> decrease in pain
decrease in nociceptor activity
local mechanical effect to joint mobilisation
CHANGE TO COLLAGEN EXTENSIBILITY
effect on immobilisation on joint
permanent length change - micro trauma 0 force needed
how is immobilisation of joint settle
adhesions form within 15 days and are dense at 2/12
neurophysiological effect of joint mobilisation
MOTOR EFFECT – CHANGE IN SPASM most likely due to analgesia removal of pain stimulus
analgesia
neurophysiological effects of analgesia
SPINAL CORD – Type I Mechanoreceptors in joints have inhibitory effect at SC on type IV nociceptor activity: PAIN GATE Mechanism
neurophysiological effects of analgesia in higher central nervous system
HIGHER CNS – ACTIVATION OF DESCENDING INHIBITION OF PAIN
SYMPATHETIC EFFECTS – initial hypoalgesia associated with increase in SNS activity (↓ skin temp & ↑ skin conductance) demonstrated after Gr III PA x 1 min x 3 sets in CxSp higher CNS involvement & probably dPAG stimulated
psychological effects of manual therapy
positive placebo response
biomechanical effects of manual therapy
altered tissue extensibility - > repair and tissue remodelling
altered fluid dynamics
physiological effects of manual therapy
stimulation of gating system and descending endogenous opioid system -> pain relief
muscle inhibition
reduced intra articular pressure
CONTRAINDICATIONS TO JOINT MOBILISATIONS
Joint dislocation or unhealed fracture
Immediate post-op to tendons, muscle, joint capsule or skin
Acute joint flare-up e.g. RA
Malignancy / bone disease
JOINT MOBILISATION PRECAUTIONS
Infection / inflammatory process in or close to joint Early stage of healing Analgesia or Muscle relaxants taken ?response Bone fragility e.g. osteoporosis for high grades only hypermobile or subluxed joint haemophilia
TECHNIQUE SELECTION DEPENDS ON
DIAGNOSIS HISTORY & STAGE OF DISORDER: PRESENTING SIGNS & SYMPTOMS*** contraindications or precautions response to techniques
for pain recommended techniques
Accessory mobilisations in neutral without pain (Gr I – II)
Physiological (large amplitude) without pain (Gr II)
recommended techniques for stiffness
Physiological mobilisatons at limit of range (Gr III – IV) Accessory Rx in Physiological range / at limit (Gr III – IV) Grade V (accessory & physiological Manipulations)
recommended techniques for stiffness and pain
Rx primary component first
Primary Pain – Accessory or Physiological (Gr II)
Primary Stiffness – Accessory or Physiological (Gr III – IV) at limit, respecting pain
TO CAUSE PAIN OR NOT TO CAUSE PAIN WITH JOINT TECHNIQUES?
severity
irritability
nature of condition - stage of healing
