What do A delta fibres and c fibes detect
ADelta- thermal, mechanical stim
C- dull pain, unmyleanated
What is hyperalgesia and what does it causes/what causes it
Hyperalgesia occurs when tissue damage occurs and several chem mediators (histamine, bradykinins, Atp released) sensitizes area
What is Substance P
-Released w tissue damage
Sensitizes pain receptors and increases vasodialation to injured region (increases input of chem mediators)
What does NGF do
When released in tissue damage response it acts as a pain mediator (enhances perception of pain)
Which rexxed lamina will pain typicall go into
Specifically rexxed lamina 1 + 4 + 5
What rexed lamina does the spinoreticular tract enter and what does it do
Recieves pain info that projects into lamina 7+8 and up to thalmus
Provides more autonomic response to pain (emotional etc)
why does refered pain occur
Viscera project to same a + c fibres and both project to cortex (cant tell dif)
Pain travels back along autonomic neurons to specific levels
What brain regions attempt to modulate pain
Venterobasilar complex of thamus
- internal capsul
- periaquaductal + periventricular grey
Where do opiots have a great affect in the CNS
Dorsal horn has high density
=decreases release of NT and neuromodulators +decrease calcium to terminals ( prevents docking)
How does TENS work (and how long till it takes affect)
20 mins min
Stims a alpha and beta fibres which stims inhibitoru interneurons (closes gate)
What part of brain has a big impact of pain + fear and what receptors does it have that can be blocked
Ant cingulate cortex (which communictes w amygdala and limbic system)
-Has NMDA receptors (which if blocked may block emotional tag to pain.)
What are some characteristics of someone with chronic pain
- Burning/shooting pain
- Summation- progressive worseing by slow repetatie stim
- Hyperalgesia- increased response to painful stim
- allodynia- pain to normally non painful stim
What are some aspects that change in chronic pain (3)
- Overly actie dorsal horn neurons
- NMDA and AMPA receptors are phosphorylated (lose ability to inhibit pain)
- Inability to block signals (GABA input diminishes)
What is nociplastic pain
Pain that arises from altered nociception despite no clear evidence of actual or thretend tissue damage
