Lecture 11 - pain modulation + analgesia Flashcards
(30 cards)
What is meant when it is said “Pain is not simply a sensation”
Unpleasant sensory & emotional experience
* e.g. pain “feels” sharp and is “distressing”
Presentation of pain from deeper structures
Difficult to accurately localise
* Dull, aching
* Dormant period
* Slow pulse, BP (you can’t run away from threat - internal)
* Sweating, nausea
Presentation of pain from human skin
Can accurately localise
* Sharp, hot, pricking
* brisk movements
* Rise of pulse (fight or flight > sense of invigoration
Why woul our brain want to inhibit pain?
In extreme situations (escaping), temporarily supress pain to allow you to focus on immediate needs
* may even inhibit certain parts of body to focus on the most urgent pain
Gate Control Theory
Noxious stimuli transmitted by afferent fibres to spinal cord are blocked by a gating mechanism @ dorsal horn
* Gate “open” > pain perceived
* Gate “closed” > pain supressed
What fibres are activated by non-painful stimuli?
A-beta (large diameter)
What fibres are activated by painful somatosensory stimuli?
A-delta and C (small diameter)
Which fibres “close the gate” at the spinal cord?
A-beta
* Activate it at the same time > activate an inhibitory neuron and inhibit the output neuron (projection)
What is the purpose of the spinal cord pain gate?
Fine-tuning system
* ensures pain is a protective warning, without dominating the sensory experience.
What soothing actions for pain would make sense base don the gating mechanisms?
Rubbing a wound
Conditioned pain modulation (CPM)
Multiple noxious stimuli present, inhibit most to focus on a primary source
* Occuring in the lower brainstem
Circuitry in CPM (areas)
Midbrain PAG lesions had minimal effect (modulate it, but doesn’t drive)
Caudal medulla SRD lesions had a huge effect
CPM and chronic pain
Those with chronic pain are less likely to have conditioned pain modulation
7T fMRI
Clearer picture of neural circuitry
* cannot compare each scan BUT can compare % changes
What areas would go on and off between scans (looking at CPM)
SRD and A5
* correlated with % change in pain
* project directly down to dorsal horn
* DRIVE CPM
CPM pathways from PAG
Goes to RVM then to dorsal horn
* more modulatory
Drug efficacy and CPM
More CPM predicts HIGHER analgesic drug efficacy in chronic pain individuals
What kind of cell group is A5?
Noradrenergic
Upper brainstem role in pain mod/analgesia
Drive defensive behaviours and analgesia
* lateral/dorsal column in PAG
What effect can the upper brainstem have on fight or flight?
- Hypervigilance
- Increased sensitivity, BP, HR, respiration rate (support MOTOR output)
- Analgesia
Where are ACTIVE coping strategies evoked from?
LATERAL PAG
* fight or flight
Where are PASSIVE coping strategies evoked from?
VENTRAL PAG
* Visceral input
* Withdraw/inactivity
What physiological changes occur when we want to fight?
The ROSTRAL part of the lateral PAG is stimulated
* Extracranial vasoDILATION
* Hindlimb and renal vasoCONSTRICTION
What physiological changes occur when we want to run away (flight)?
The CAUDAL part of the lateral PAG is stimulated
* Extracranial vasoCONSTRICTION
* Hindlimb and renal vasoDILATION
