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Pain (Overview (Hyperalgesia, Allodynia, Somatic (muscle, CT), vs visceral…
Pain
Overview
Hyperalgesia
Allodynia
Somatic (muscle, CT), vs visceral
Spontaneous pain
Acute pain from
noxious stimulus
Fibres
C (small, unmyelinated, dull burning pain), polymodal -
second pain
Ab (large, myelinated, non-noxious light touch)
Ad (small, myelinated, initial reflex to acute pain) -
first pain
Free nerve endings. Stimuli are thermal (eg
TRPV1
), mechanical (eg
TRPA1
), or chemical (eg
capsaicin
)
Cell bodies in dorsal root ganglia
Pain categories
2. Inflammatory pain:
innocuous stimuli, plasticity, mediators released in terminal
SP, CGRP, Globulin, PKs, NGF, Histamine, 5-HT, low pH, ATP, Arachadonic acid (-> PG),
1. Nociceptive
: C or Ad, mainly TRP channels, acute (->) chronic
3. Neuropathic pain
: actual nerve damage, maladaptive plasticity
4. Dysfunctional pain
: chronic diffuse hyperalgesic pain, absence of obvious periperal origin
Ascending pathways
Spinoreticular
:
fibres decussate
-> contralateral cord -> brainstem reticular formation -> amygdala, hypothalamus, thalamus -> cortex (emotional)
Spinomesencephalic
:
2ndary neurons decussate
-> contralateral anteriolateral column -> periaqueductal grey -> PAG inhibitory neurons descend
Spinothalamic
:
2ndary neurons decussate
-> contralateral tract -> synapse thalamus -> somatosensory cortex (pain localization)
Ad and C fibres activate AMPA, NK1, and CGRP channels in dorsal horn
Endogenous opioids
Enkephalins (pro-enkephalin)
Dynorphins (prodynorphin)
Endorphins (pro-opiomelanocortin)
(pre-pro): endoprotease -> endopeptidase -> active form
Descending inhibition
PAG contains many brain region inputs + high conc
endogenous opioids + opioid receptors
Gate control theory: Ab activation (rubbing injury) inhibits C fibre transmission
Opioid receptors
Open K+(ir) and close VGCCs ->hyperpolarization
μ, δ, κ :, ORL1
: inhibitory GPCRs