Lecture 10 - acute injury to chronic pain Flashcards
(20 cards)
“Onion ring” mapping of face
Starts @ nose
* Synapse rostral or caudal in MEDULLA based on this position
Def. sensitisation
Increased responsiveness of nociceptive N. to their normal input, and/or recruitment of a response to normally subthreshold inputs.
Central sensitization
Repeated noxious stim. (no injury) > flexor motor output (which indicates sensitization in the CNS)
* Keeping pain system on high alert
Prevalence of chronic pain
3.4m AUS (1 in 7)
* Economic disadvantages
* Reduced quality of life
Required duration for chronic pain
> 3 months
Nociceptive pain
Pain arising from actual or threatened damage to non-neuronal tissue
* Due to activation of nociceptors
* E.g. Low back pain
Neuropathic pain
Pain caused by a lesion or disease of the somatosensory NS
* E.g. Carpal Tunnel
Nociplastic pain
Pain arising from altered nociception despite NO clear evidence of tissue damage or evidence of disease/lesion of the somatosensory NS
Diagnosing neuropathic pain
- Accidental (e.g. fracture or stroke)
- “Planned” (e.g. amputation or hernia repair mastectomy)
Distinguishing if the pain is neuropathic:
History > Examination > Diagnostic Test
Symptoms of neuropathic pain
VERY diverse
* E.g. shooting, heat/cold, pins, electric, numb
Status of treatment of chronic pain
Not very effective (side-effects)
* limited understanding of neurobiology
When does chronic pain develop?
Unknown when the ‘transition’ from acute pain to chronic pain occurs after an injury.
Current knowledge of neurobiology of chronic neuropathic pain
- NO peripheral N. activity required
- NOT associated w/ constant pain pathway activation (Thalamic activity changes not present in controls)
- Altered rhythms in pain pathways
- Non-neuronal (glial) changes in pain pathways
Astrocytes changes in pain pathways
Increase in GFAP-pos astrocytes (POST MORTEM)
* Due to injury
* Morphology and shape changes to astrocytes
TSPO changes in pain pathway
TSPO binding in lower back pain
* Radioligand
* Activation in thalamus
Pro-nociceptive cytokines
Released from microglia (overtime they disapear) and astrocytes (increase overtime) which increase pain intensity after periphery injury
Affective pain circuits in animals
Often see guarding, attending or escaping/jumping
What is the main difference between peripheral and central sensitisation?
- Location
- Peripheral becomes HEAT-sensitive
- Central amplifies signal
What is the benefit of sensitisation?
- Allows the injured tissue to heal
- Continuous warn/remind the brain to avoid further injury here
