Chronic Pain & Central Sensitization Flashcards
Number of people worldwide who suffer from chronic pain.
More than 1.5 billion
Hours of productive time workers lose on average due to a pain condition
4.6 hours
International Association on the Study of Pain defines pain as:
(plus 3 things about pain)
“An unpleasant sensory and emotional experience which follows actual or potential tissue damage or is described in terms of such damage.”
■ Pain is complex and poorly understood.
■ Physical pain is equal to emotional pain
■Threat or potential for injury can cause pain
Moseley defines pain as:
“A multiple system output that is activated by an individual’s specific neural signature. This neural signature is activated whenever the person perceives a threat.”
Pain is the end result of
Central processing of sensory stimuli.
Description of Chronic pain:
Pain that persists for more than 3 months or pain that persists after the ‘usual’ time for tissue healing or pain in the absence of obvious nociception.”
4 types of acute pain: FINN
- Functional
- Inflammatory
- Nociceptive
- Neuropathic
All 4 types of pain typically contribute to chronic pain syndromes.
Peripheral or central sensitization
Mechanism of Pain: Neuroplasticity- How does a chronic pain state develop?
Peripheral Sensitization
- Injury causes release of “sensitizing soup”
- Reduction in threshold and increase response of nocioceptors
Central Sentisization
- Membrane excitability, synaptic recruitment and decreased inhibition.
- Uncoupling of pain from peripheral stimuli
2 ways that the brain controls pain
- Facilitatory System- “Accelerator”
- Inhibitory System
“Brake”
Malfunctioning in people with chronic pain
How is pain processed by the brain? (5)
- Entire brain is active during pain- No specific “pain areas”
- Brain has a particular “Pain Map” that occurs regardless of the specific tissues injured
- “Smudging” in the cortex with distorted pain maps
- A representation of pain can be caused in the brain by anticipating pain or giving the illusion of pain- Distraction or anxiety can contribute
- Emotional Pain uses similar brain areas to physical pain- Why we use a Biopsychosocial approach to pain
When does sensitization occur?
after repeated or intense noxious stimulus
Sensitization Lowers threshold for activation. True / False
True
Types of Sensitization
Peripheral
- Increased responsiveness nociceptors
Central
- Changes to the synaptic transmission to the spinal cord
- With or without real tissue damage
Sensitization Produces: ASH
- Allyodynia- Pain produced by a normally innocuous stimuli
- Hyperalgesia or hypersensitization- Exaggerated and prolonged response
- Secondary Hyperalgesia- Spread beyond site of stimulation or injury. Also known as “referred pain”
Allyodynia
Pain produced by a normally innocuous stimuli
Hyperalgesia or hypersensitization
Exaggerated and prolonged response
Secondary Hyperalgesia
Spread beyond site of stimulation or injury. Also known as “referred pain”
Mechanisms of peripheral sensitization
(4-5ish)
Brief (lasting days) muscle hyperalgesia
- Induced after eccentric exercise
- Soreness after 1-2 days (DOMS)
- Occurs at different sites among subjects
- Model for hyperalgesic trigger points in MPS
Central Sensitization (4)
- Amplification of response
- Novel inputs to nociceptive pathways- Actives A-beta large low-threshold mechanoreceptor pathways
- Pain in non-inflamed tissues- Central pain in absence of peripheral injury
- Functional shift- High threshold mechanoreceptors now respond to low threshold inp
Conceptual framework for Understanding pain in the Human:
Inputs to body-self matrix from:
- Cognitive-relatied brain areas- memories from past experiences, attention, meaning & anxiety
- Sensory signalling systems- Cutaneous, Visceral & MSK inputs
- Emotion-related brain areas- Limbic system and associated homeostatic/stress mechanisms
Outputs to brain areas that produce:
- Pain perception- Sensory, Affective & Cognitive dimensions
- Action programs- Involuntary & voluntary action patterns
- Stress-regulation programs- Cortisol, Noradrenalin, and endorphin levels immune system activity
Facts about sensitization (6)
- Occurs after repeated or intense noxious stimulus
- Lowers threshold for activation
- Amplifies subsequent inputs
- Nervous system adapts and becomes over effective where anything can cause a big reaction
- Adaptive
- Hyperalert to potentially damaging conditions
NO LONGER ABOUT PROTECTION!
What happens during normal sensation?
Central sensitization? Receptive Field Expansion
- Sleeping neurons become activated
- Over efficiency of all neurons
Conclusion
- Somatosensory Neuron Receptive Fields are Malleable (Plastic)
- Plasticity is the basis for the effects of central sensitization
Mechanisms of Central Sensitization: SIR
ENHANCEMENT
Synaptic efficacy
- Neuronal plasticity
- Nervous system becomes too efficient and responds to things it normally doesn’t respond
Increase in membrane excitability at the dorsal horn
Reduced inhibition of descending system
- Periaquaductal grey matter doesn’t inhibit pain as it should (Blocks unnecessary information & If not working, all information ends up in cortex)
- Some studies show PAG is smaller in individuals with chronic pain- Also linked with depression in chronic pain
