L20 - LBP, management of pain Mechanisms Flashcards
Management of pain mechanisms: back pain
- Central sensitization
- Motor control
- Spinal muscles
- Intervertebral discs
- Fact joints
- Physical fitness
- Job satisfaction
- Job support
- Social interaction
- Family support
- Poor sleep
- Catastrophizing
- Self-efficacy
- Fear of pain
- Depression
- Inflammatory system response
- Kinesiophobia
Pain neurobiology: description with all type of pain
PAIN NEUROBIOLOGY
Not all pain is same, IASP pain mechanisms:
- Nociceptive pain: Movement-related. Predominantly driven by activation of peripheral nociceptive fibers
- Neuropathic pain: pain attributable to a lesion or dysfunction in Peripheral NS & Central NS
- Nociplastic pain: Central/central sensitization. Amplification of neural signaling within central
nervous system eliciting pain hypersensitivity, from cellular to widespread network.
Possible assumptions based on mechanism
Possible assumptions based on mechanism
- Nociceptive: movement-related modify tissue loading
- Neuropathic: modify nerve loading & reduce amplification
- Nociplastic : central/central sensitization, reduce amplification, psychological, education, …
Muscle changes: description
Muscle changes
- Structural remodeling of muscles without atrophy
- Increased adipose & connective tissue content
- Alteration in muscle fiber types
- Fatty infiltration
- Fibrosis
Actively regulated by muscle inflammatory mechanisms
Inflammatory dysregulation: description
Inflammatory dysregulation
- Elevated pro-inflammatory cytokines like TNF and IL-6.
- Acute inflammation promoting hypersensitivity in tissue.
- Chronic inflammation linked to fibrosis and structural damage
IVD: description & at 6 months
Intervertebral discs
- Degenerative changes in IVDs correlate with adjacent muscle alterations.
- Secreted proteins like SPARC impact collagen synthesis and disc integrity
At 6 months:
⇧ CSA of adipose & connective tissue
⬄ CSA muscle and individual muscle fibers ⇩ slow fiber proportion (both sides)
⇧ fast fiber proportion (injured side)
⇧ expression of collagen-1 (injured side)
⬄ expression of collagen-3
Sources of cytokines:
- injured cells
- macrophages
Different parts / roles
Injured Cells:
- Cells subjected to acute mechanical stress or injury release pro-inflammatory mediators.
- Mediators initiate inflammation & hypersensitivity to promote healing & repair
Macrophages:
- M1 Macrophages: Produce pro-inflammatory cytokines such as:
o Tumor Necrosis Factor-alpha (TNF-α).
o Interleukin-1 beta (IL-1β).
- M2 Macrophages: Release anti-inflammatory cytokines, including:
o Interleukin-10 (IL-10).
o Interleukin-1 receptor antagonist (IL-1RA).
Balance between M1 (pro-inflammatory) & M2 (anti-inflammatory) subtypes depends on
microenvironment, influencing tissue repair or chronic inflammation.
Possible mechanisms linked to cytokines
Paracrine Effects and Microenvironmental Changes:
- Cytokines produced as paracrine response to immediate environment.
- Injured cells release factors altering behavior of nearby cells, leading to local inflammation.
- Muscle fiber type changes in injured areas create acidic environment, which influences cytokine production.
Adipose Tissue:
- Fatty infiltration, particularly in multifidus muscle, associated with higher levels of TNF-α & other
inflammatory markers. - Observed in individuals with degenerative disc conditions or chronic low back pain.
Mast Cells:
- Mast cells, activated during acute inflammation, contribute by releasing inflammatory cytokines
Process in acute phase
Part of strategy to develop mechanical support in
response to injury
If so, it is simple, passive & non adaptative
Human IDD: relationship between fat & expression TNF
- Multifidus muscle harvested as surgery
- TNF expression in multifidus is greater in
individual with higher clinical grade of fat
Evidence of inflammatory dysregulation in epidural adipose tissue has potential for broad impact on
tissue health & LBP symptoms.
Can inflammatory processes & structural changes in multifidus be prevented or reversed with exercise?
- short term exo
- long term exo
Short term exercise (acute):
- Collagen synthesis/degradation to assist remodeling.
Long-term exercise
- Prevents aging-dependent fibrosis
Anti-inflammatory effects of exercise might prevent and/or reverse fibrotic changes
Physical activity: decrease cytokine in multifidus near degenerating disc:
Experiment on SPARC-null mice:
- SPARC=Secreted Protein, Acidic, Rich in Cysteine.
- SPARCisdecreasedin degenerating discs
- Effectsoncollagen1
- Progressive, accelerated disc degeneration
Aim of model: parallel effect of normal aging on SPARC expression
IVD degeneration: greater connective tissue thickness in multifidus near degenerating discs
Time dependent: multifidus muscle plasticity- different mechanisms
- description
- implications for rehabilitation
Image
Implications for rehabilitation
Changes in muscle structure have different time dependent mechanisms
- Acute: inhibition, exercise, activate
- Sub-acute: pro-inflammatory, exercise, train to active then load
- Chronic: disuse, exercise activate, train for hypertrophy
Pain: BPS problem
Role of interaction between biology & psychology in back pain
55 controls
109 LBPs
- 15 recovered
- 55 partially recovered
- 14 unrecovered
Cytokines: baseline analysis:
CRP: C-reactive protein = marker for inflammation
+ image
Longitudinal cluster analysis of pain / BPS model
Longitudinal cluster analysis:
- Elevated CRP & IL-6 plus poor sleep associated with best recovery, whereas high TNF combined
with depression-like symptoms was associated with worst recovery
at 6 months
- Early identification & management
Cluster 1: “inflammatory & poor sleep”
Role of CRP
Cluster 2: “higher TNF & depression”
Role of TNF
Pain sensitivity:
- longitudinal cluster analysis
- implications for rehab
Longitudinal cluster analysis
- Pain sensitivity in acute phase related to recovery if associated with poor sleep & depression (not
sensitivity alone)
Implications for rehab
Biology & psycho interact
Treatment needs to be multifactorial
How can we identify pain mechanisms in clinical practice
Table
