Control system - peripheral

Question 1

What peripheral elements will we consider in the relationship between peripheral control system, pain, injury and pathology?

Answer 1

• Muscle
• Sensory receptors
• Associated spinal circuits

Question 2

Muscle as a source of pain

Answer 2

• Pain receptors
• Group III and IV “pain” afferents (Aδ & C fibres)
• Hyperalgesia

Question 3

nociceptors

Answer 3

nociceptors tells threat not pain

Question 4

Changes in muscle as a result of pain, injury and pathology

Answer 4

•  Atrophy
–  Immobilisation – injury, surgery
–  Dennervation – injury, surgery (won't be the same as before)
–  Disuse – pain, fatigue
–  Inflammation
–  Reflex inhibition – joint injury, surgery
–  Other causes
•  Neural pathology – poliomyelitis
•  Muscle pathology – muscular distrophy

Question 5

Muscle atrophy

Answer 5

• Occurs rapidly
– Poorly understood
– Microgravity loss of muscle volume
– Significant changes in muscle weight and fibre size are reported in the first week of immobilization {Appell, 1990}
– due to disuse following spinal cord injury occurs within days {Taylor, 1993}

Question 6

muscle atrophy - what changes?

Answer 6

– Contractile protein loss
– Decreased muscle fibre
– Not uniform > greater change in slow muscles (i.e. more type I muscle fibres)
- functional implications

Question 7

Changes in muscle as a result of pain, injury and pathology

• Fatty infiltration

Answer 7

– Accompanies atrophy

start to get fatty infiltration, damaged connective tissue

Question 8

Mechanisms = acute

Answer 8

people with low back pain have atrophy of multifidus
Acute inhibitory/ regeneration phase
Muscle inhibition
Acute size reduction (?vascular/other mechanism)
Acute adipose activation
Regeneration pathway activation

Question 9

Mechanisms sub-acute

Answer 9

6 weeks - 3months have other changes = muscle had recovered in size however more was fat
so early inhibition start to create fatty change and connective tissue change

Pro-inflammatory cytokine phase
Slow-to-fast muscle fiber transformation
Fibrosis
Fatty infiltration

Question 10

Sub-acute/chronic phase: Muscle structural change

Answer 10

increase in TNF and Cytokines

Question 11

Where do the cytokines come from?

Answer 11

• Acute inflammation, typically short-lived & reversible event - remove injured cells
– Injured cells – release factors – hypersensitivity
– Macrophages & Mast cells - inflammatory cytokines
• Persisting stimuli - little chance to complete healing processes = persistent inflammation
– Macrophages > tissue damage

Question 12

Where do the cytokines come from?

• Macrophages

Answer 12

– Macrophages changed by micro- environment
• Muscle fibre types
– Less fatigue resistant – acidic environment`
more short twitch fibre = more fatigued = more lactate = more acidic = drives macrophages

Question 13

chronic injury

Answer 13

(>6 months): Extensive atrophy & structural change
• Extensive muscle atrophy – Disuse?
• Extensive structural change

Disuse/deconditioning phase
Muscle/muscle fiber atrophy
Fibrosis
Fatty infiltration

Question 14

Implications for treatment

Answer 14

• Does not simply mean anti-inflammatory drugs are required!
• Exercise can change macrophages
– Exercise promotes M2 (anti-inflammatory)
– Muscle fibre-type changes micro-environment
• Treatment targeting depends on timing based on different mechanisms
– Acute – inhibition – activation
– Sub-acute – pro-inflammatory – change fibre type – Chronic – disuse - hypertrophy

Question 15

exercise response

Answer 15

Exercise reduces cytokine response in multifidus muscle near degenerating discs

Question 16

Other Changes in muscle as a result of pain, injury and pathology

Answer 16

•  Contracture
–  Immobilisation –  Pain
• Muscle shortening
–  Maintained period of reduced length –  Splinting
–  ?Functional/postural

Question 17

Summary - Muscle

Answer 17

• Can be a source of pain
• Muscle can change as a result of pain, injury and pathology
– Requires specific attention in rehabilitation programs