Pains Flashcards
Loss of pain is caused in diabetes and Leprosy because of what?
Nerve damage
What can happen if there is an absense of pain?
unaware of minor injuries
What is pain?
mystifying symptoms?
discriminative sensation and a graded motivation(behavioural drive) = different from classical senses
Can attain intolerable intensity, but can disappear in heat of battle
its an enigma
Its a human exprience that is commonly generalised to psychic suffering of any sort
It’s a clinical complaint that can present mystifying symptoms
-allodynia - sensitisation to normally innoculus stimulus
-referral from deep tissue to skin (radiation over wide regions)
-temporal augmentation
-persistent after -sensations, emotional variability and hyperpathia (hysterical responses)
Specificity Vs. Convergence theories
Specificity theory- this theory treats pain as a distinct sensation - detected and transmitted by specific receptors and pathways to distinct pain areas of the brain
-convergence theory suggests pain is an integrated, plastic state represented by a pattern of convergent somatosensory activity within a distributed network (neuromatrix)
Nociceptors
What are they?
classified by what?
2 types?
- afferents with free nerve endings
- classified according to activating stimulus, fibre-type and conduction velocity
- lightly myelinated Aδ fibres (20m/s) = FAST (mechano-sensitive, mechanothermal-sensitive)
- -unmyelinated C fibres (2m/s) = SLOW (polymodal: chemical, thermal, mechanical)
Nociceptors Vs. Thermoreceptors?
Nociceptors = respond specifically to pain and are a subset of afferents with free nerve endings
demonstrated with heat responses = some only start to fire at around 45c(when person begins to feel pain) = nociceptors, whereas others fire before pain is felt (eg,thermoreceptors)
–> clear that thermoreceptor activation has already saturated before pain is received = NOT a ‘ramping up’ response of normal receptors
Fast and Slow pain
Fast (or 1st pain) = sharp and immediate: can be mimicked by direct stimulation of Aδ fibre nociceptors
Slow (or 2nd pain) = more delayed, diffuse and longer-lasting + can be mimicked by stimulation of C fibres
Molecular pain receptors
specific molecular receptors associated with nociceptive nerve endings are activated by heat
-Capsaican receptor(TRPV1 = transient protein receptor) is activated in nonciceptive Aδ and C fibres at 45c by capsaicin (a vanilloid which is the active component in chilli)
-related receptors are activated in Aδ fibres alne at a higher threshold (52c)
-molecular receptors that respond to heat= heat-detection machine
(Capsaicin = mimics endogenous vanilloids released by stressed tissue = nociceptors may be detecing stress chemical)
Central Pain Pathways
Sensory discriminative- location, intensity, type of stimulus
affective - motivational - unpleasantness signals (what you associate pain with) and fight or flight
Discriminative pathway is the easiest to define and involves tract: spinothalamic tract (aka. anterolateral system)
Spinothalamic projections
measurements of activity in the somatosensory cortex indicates what? (2)
preserve topgraphy
measurements of activity in the somatosensory cortex indicates
1- regions responds to painful stimuli and that response correlates to intensity of pain
2- that this is spatially mapped
Complex cortical representation
-when feeling pain part of the brain corresponding lights up = cortical representation
-painful stimuli activate the same region of the somatosensory cortex as the non-painful mechanical stimuli –> however, pain activates a distinct response that includes other regions
NOTE: activation of insula and cingulate cortex - these are connected to the limbic system ( known to be involved in activation of emotional response) = affective-motivational response to pain
Affective-motivational pathways
mapping? - parabrachial nucleus?
inputs from where? (2)
unpleasantness strongly correlated with activity in cingulate cortex
-shares some paths with anterolateral system
-little or no topographic mapping - neurons in parabrachial nucleus can respond to pain stimuli from anywhere on the bodys surface
-no. of points of input to the emotional (limbic) and homeostatic(hypothalamic) systems
NOTE: this is not the intensity of pain
(intensity = somatosensory cortex activated via discriminative pathway)
Specificity theory
receptors- both cellular and molecular that respond to pain (C and Aδ fibres - TRPV1)
- specific pathways that convey pain messages
- regram of the CNS that are specifically activated in response to pain
no. of phenomena that don’t fot: - pain perceived not always proportional to intensity of stimulus
- modulation by other stimuli
- referral of pain from viscera to skin
- phantom limb
- placebo effect
What is hyperalgesia?
What is Allodynia?
h= increased response to a painful stimuli (result of lowered nociceptor thresholds = increase pain response) a= painful response to a normally innoculus stimulus
What is hyperpathia? =variant of hyperalgesia and allodynia
its underlying causes are different and so symptoms are slightly different –> happens when there is fibres/ axonal loss that results in a raising of the detection threshold (need big stimulus to detect)
so, when we do eventually feel pain = v high so results in ‘explosive pain’
