Pain (nociception) Flashcards
what is the somatosensation of pain called
nociception
examples of other somatosensations
touch
temperature
proprioception
pressure
what does neurophysiology of pain involve?
(3 STEPS)
1- initiation 2- propagation 3- perception
what causes initiation of pain sensation
activation/depolarization of pain receptors at the site of injury
where does perception of painful stimuli take place
somatosensory, emotional, and cognitive regions of the brain
describe propagation of pain sensation
depolarization along nerves to spinal cord (switch over in spinal cord:contralateral) and then ascend up spinal cord to thalamus which relays the information to the somatosensory, emotional, and cognitive regions of the brain
how does anesthesia and pain medications work in reference to the ascending pain pathway
block the ascending pain pathway at various locations so the pain sensation does not reach the brain
Dorsal column-medial lemniscal pathway (DCML) does what sensations
carries the sensory modalities of fine touch (tactile sensation), vibration, and proprioception
The anterior spinothalamic tract of the anterolateral system does what sensations
Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.
The lateral spinothalamic tract of the anterolateral system does what sensations
Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.
why is nociceptive fibers being slow adapting good
because it is a protective mechanism you want the pain signal to keep firing so as to learn painful stimuli and not forget the tac in your foot etc
where does the lateral spinothalamic tract cross over
spinal cord
what are the two pain fibers of the ascending pain pathway
A-delta fibers and C fibers
what chemical stimulates A-delta fibers
glutamate
what chemical stimulates C fibers
mostly substance P but some glutamate
What binds to receptors of the A-delta and C fibers that leads to sensitization and exacerbation
prostaglandins
which fiber A-delta or C fibers has faster conduction and why
A-delta fibers be myelinated vs C fibers which are unmyelinated
what “kind” of pain does A-delta fibers elicit
sharp, stinging, intense pain (myelinated fast fibers)
what “kind” of pain does C fibers elicit
dull, achy, chronic, burning, less intense pain (unmyelinated slow fibers)
what are the three types of pain
nociceptive
inflammatory
neuropathic
What is nociceptive pain defined by
external irritating or harmful stimulus like heat, cold, acid/chemicals, getting hit with hammer or getting a shot
what does the transduction of nociceptive pain rely on
activation of distinct TRP channels and other peripheral nocireceptors
what is the main TRP channel to know
TRPV1 (activated by heat or acid/chemicals like capsaicin)
pain treatment options for nociceptive pain
local anesthetics
Cox2 inhibitors
opioids/opiates
what does TRP stand for
transient receptor potential
what activates TRP channels
heat or capsaicin
what is capsaicin
compound found in hot peppers that can bind to TRP receptors/channels and elicit sensations of pain
how can capsaicin be used for pain management
use capsaicin to target TRP channels for low long activation which then leads to desensitization and management of pain
what causes inflammatory pain
tissue or internal organ damage that causes a local or systemic immune response (i.e. release of inflammatory mediators by immune cells)
how do inflammatory mediators stimulate pain transduction
they stimulate their respective receptors on nociceptive fibers
examples of inflammatory mediators
histamine
serotonin
bradykinin
prostaglandins
ATP
H+
nerve growth factor
TNF alpha
endothelins
interleukins
what do you treat inflammatory pain with
local anesthetics
Cox2 inhibitors
opioids/opiates
locally released inflammatory mediators not only activate pain fibers in inflammatory pain, what else can they do
sensitive pain fibers in both inflammatory and nociceptive pain
what are the two forms of sensitization
hyperalgesia
allodynia
define hyperalgesia
slightly painful stimulus is now perceived as being significantly more painful (this is primarily a peripheral component)
define allodynia
enhanced sensitivity and reaction to a stimulus that is normally NOT painful (usually-but not always- at or near the site of primary injury) (this is both due to a peripheral component as well as a central component)
how does allodynia work
inflammatory mediators can ‘non-specifically’ bind to TRP channels and decrease the threshold needed for activation
how does hyperalgesia work
inflammatory mediators activate their specific receptors on pain fibers leading to phosphorylation of VGSCs, TRP channels, and other signaling proteins which ‘sensitize’ these pain fibers thus later phosphorylation events(painful stimulus) are amplified due to increased frequency of firing of APs of these ‘sensitized’ pain fibers
describe neuropathic pain
reflects damage to peripheral or central nervous system which leads to pain perception without persistent external pain stimulus or pain perception in presence of non-painful stimulus (allodynia)
what are the treatments for neuropathic pain
atypical analgesics: tricyclic antidepressants, anticonvulsants, calcium channel blockers (drugs that sedate, change mood, or are used for general anesthesia) or opioids/opiates (less effective)
can you treat neuropathic pain with opioids/opiates
yes but way less effective
what are the two components of pain processing
discriminative (where) and affective (emotional)
what does discriminative pain processing determine
magnitude of pain
what type of painful stimulus
where is the pain coming from
what does affective pain processing determine
emotions
how unpleasant is the pain
how uncomfortable is the pain
what is the target of descending pain inhibitory pathways from the brain
dorsal horn in the spinal cord
how does the descending pain inhibitory pathways inhibit pain transduction
descending brainstem inputs activate local dorsal horn interneurons that inhibit pain transmission
see picture
how the descending pain inhibitory pathway works
see picture
define referred pain
visceral discomfort/pain interpreted as cutaneous (skin/surface) pain
why do we have referred pain
convergence of visceral and cutaneous pain afferents in the spinal cord (onto same spinal thalamic nerves) which then activates central mechanisms that interprets visceral pain as occurring at cutaneous sites
describe gate theory
mechanoreceptor activation promotes inhibition of pain relay neurons in the dorsal horn
see picture
how does phantom limbs/pain work
mis-match between central representation and periphery due to re-wiring of pathways spinothalamic nerves lose innervation from nerves from missing limb then nerves from limb area still there (i.e. lost lower arm so “limb area still there” would be upper arm) rewire and attach to the spinothalamic nerves that once were innervated by the lost limb area now feel pain where no limb is anymore
