Pain Flashcards
Types of nociceptors
- Thermal: respond to low and high extremes (45degC). Adelta fibres.
- Mechanical: respond to P, nociceptive mechanical, pinch, pin prick. High threshold. Adelta fibres.
- Polymodal: respond to mechanical, chemical or thermal. C fibres - diffuse aching burning pain
nociceptive vs neuropathic pain
2 pain mechanisms:
Nociceptive: normal pain pathway. Nociceptors activated»_space;
response to tissue damage, inflammatory pain
(muscles, bones, organs, skin…)
Neuropathic: pain system malfunctioning.
- no activation of nociceptors. damage in PNS/CNS nerves> abnormal signalling > pain perception
ex: post-herpetic neuralgia, central pain, phatom limb pain, diabetic neuropathy, peripheral nerve damage, cord injury, stroke
what is axon reflex
aka neurogenic inflammation:
- lesion > signals goes to C fibres > spinal cord
1. pass the DRG on way to spinal cord to activate withdrawal reflex
2. branches in peripheral nerve terminals > release PEPTIDES: CGRP and Substance P >
a. blood vessels: vasodilate (red), increase permeability (swelling), release BRADYKININ
b. mast cells: release HISTAMINE > effects on blood vessels
c. platelets: relese SEROTONIN
what causes inflammation?
axon reflex and tissue damage
-red, warm, swelling
inflammation after tissue damage
what activitates and sensitize nociceptors
Nociceptors are activated by:
- mast cells via histamine
- platelets via serotonin
- plasma via bradykinin
Nociceptors are sensitized by:
- damaged cells via K+, prostaglndins, leukotrienes
- axons via Substance P
nsaid mechanism
decrese pain due to tissue damage
- analgesic, antipyretic, anti-inflamm
- block COX> decrease production of prostaglandins > decrese sensitization
ex: aspirin, ibuprofen, naproxen, indomethacin
PAG matter purpose in pain
Periaqueductal grey in midbrain
- descending input to dorsal horns > release ENKEPHALINS (like morphine) from dorsal horn interneurons > act on opioid receptors to inhibit pain transmission via:
1. inhibit NT release from 1ry neuron
2. hyperpolarize 2ary neuron
referred pain
convergent afferent fibres from viscer nd body surfce @ 2ry neuron so cn’t localize
(ex: diaphragm > shoulder. appendicitis > umbilicus)
gate-control theory
inhibition of touch afferents > pain signal doesn’t go.
ex: TENS, rubbing helps relieve pain
-activate Abeta (touch fibres) > activates inhibitory neuron on 2ry pain neuron on its way to STT > no pain transmission
Closes the gate which is activated by 1ry pain fibres (Adelta, C)
what is algesia
sensitivity to pain
what is analgesia
no sensitivity to pain
what is hyperalgesia/hypoalgesia
increased/decreased sensivitity to pain
what is allodynia
pain from usually non-painful stimulus
what is dysesthesia
abnormal unpleasant feeling
what is noxious
stimulus causing tissue damage
Types of cutaneous fibres: Abeta, Adelta, C
Abeta: touch via DCML.
Adelta: fast pain. well localized.
C: slow pain: distressing, emotional, achy
what is pain sensitization?
ex mech
decrease threshold for activation
> hyperalgesia
ex: prostglandins enhance response to bradykinin > activate nociceptors to fire
Pain pathway
explain dull, achy pain
C and Adelta fibres > spinal cord > decussate > ascend via STT > Spinal Lemniscus > thalamus > 1ry somatosensory cortex
1ry: C fibres
2ry: in SL
3ry: branch off in thalamus to reticular nuclei > CINGULATE GYRUS of LIMBIC SYSTEM
Tension Headaches describe
- most common
- bilateral, non-throbbing
- featureless
- not disabling > dont’ seek help
Migraines describe
- throbbing
- starts on 1 side
- photo/phonophobia
- nausea
- aura/non aura
- disabling, need help
-episodic headache, 4-72hrs with
any 2: unilateral, throbbing, worse iwth activity, moderate/severe
and any 1: nausea/vomitting, photophobia and phonophonia
Epi of migraines
- common, higher than other common diseases (>10% prev globally, most burden brain issue)
- more in women, peak in reprod yrs
- higher in boys
- genetic link
- develop with other associated disorders: depression, anxiety, sleep
- risk factors: female, young, low SES, trauma, concussion, obesity, medications, stress, bad SLEEP, depression/anxiety, allodynia
what is aura
- most ppl do not have aura
- at least 2 ttacks
- visual, sensory, speech, motor (positive or negative)
- 5min-60min
Course of a migraine
Prodrome: 12-24hr before. mood changes, yawning, crave carbs, maybe aura, DOPAMINE
Headache: sensory hyper-excitability
Resolution: like being drunk
postdrome
Triggers of migraines
- wheather change
- poor sleep
- weekends/holidays
- menstruation
- stress
- strong smells
- skipping meals
- foods: dyes, msg, wine, caffeine
