pain Flashcards
(25 cards)
what is pain essential for
-survival
what is pain
-an enigma
-both a discriminative sensation and a graded motivation
-It is a leading clinical complaint that can present mystifying symptoms, such as: allodynia, referral, placebo-effect, after-sensations, emotional variability, and hyperpathia
-universal human experience that is commonly generalized to psychic suffering of any sort
whats the Specificity theory
-holds that pain is a distinct sensation, detected and transmitted by specific receptors and pathways to distinct “pain areas” of the brain.
whats the convergence theory
-suggests that pain is an integrated, plastic state represented by a pattern of convergent somatosensory activity within a distributed network (a so-called ‘neuromatrix’).
what are nociceptors
-Afferents with free nerve endings
-Classified according to activating stimulus, fibre-type and conduction velocity
-Lightly myelinated Adelta fibres, FAST* ~20m/s
=Mechano-sensitive
=Mechanothermal-sensitive
-Unmyelinated C fibres, SLOW ~2m/s
=Polymodal: mechanical, thermal and chemical
what do nociceptors respond to
-respond specifically to pain and are a subset of afferents with free nerve endings
-heat responses: clear that thermoreceptor activation has already saturated before pain is perceived
what are the type different types of pain
-fast
-slow
whats fast pain
-first pain
-sharp and immediate; can be mimicked by direct stimulation of Adelta fibre nociceptor
what is slow pain
-second pain
-more delayed, diffuse and longer-lasting; mimicked by stimulation of C fibre nociceptors
how can Specificity be demonstrated
-experimentally by selectively blocking the fibres in turn
-stimulation of Aalpha or Abeta(proprioceptive and mechanoceptive) fibres never elicits the pain sensation
-Thus, there are a distinct set of Adelta and C fibres, nociceptors, specifically associated with pain detection
what are Molecular Pain Receptors
-Specific molecular receptors associated with nociceptive nerve endings are activated by heat
-The capsaicin receptor (TRPV1) is activated in nociceptive Adelta and C fibres at 45°C, and by capsaicin, a vanilloid which is the active component in chillis
-Related receptors (other TRPs*) are activated in Adelta fibres alone at even higher thresholds (52°C)
-These molecular receptors are known to respond directly to heat, i.e. they themselves are the heat-detection machines
-However, capsaicin is thought to mimic endogenous vanilloids released by stressed tissues
-Thus, nociceptors may also work by detecting release of chemicals from stressed cells
what are the two components of the central pain pathway
-Sensory discriminative:
=signals location, intensity and type of stimulus
-Affective-motivational:
=signals ‘unpleasantness’, and enables autonomic activation, classic flight or fight response
what does the discriminative pathway involve
-the spinothalamic tract, also called the anterolateral system
what does the Measurement of activity in the somatosensory cortex indicate
-That this region does indeed respond to painful stimuli and that response correlates to intensity of pain
-That this is spatially mapped. This can be shown experimentally
what does comparison of cortical activation by painful or innocuous mechanical stimuli to skin show
-demonstrates that painful stimuli activate the same region of the somatosensory cortex as the non-painful mechanical stimulation applied to the same region of skin
whats the affective-motivational response to pain
-pain activates a distinct response that includes other regions
-Notable is the activation of the insula (red) and the cingulate cortex (green)
-These regions are connected to the limbic system and known to be involved in the activation of emotional responses
-Little or no topographic mapping
=Neurons in parabrachial nucleus can respond to painful stimuli from anywhere on the body’s surface
-this is not the intensity of pain. Intensity activates the somatosensory cortex via the discriminative pathway
what are the phenomena that appear not to fit with the specificity theory
-Pain perceived is not always proportional to intensity of stimulus
-Modulation by other stimuli (e.g. acupuncture)
-Perception of pain in severed limbs (phantom limbs)
-Referral of pain from viscera to skin
-Placebo effect
whats hyperalgesia
-increased response to a painful stimulus
-Hypersensitivity of damaged skin to a normally tolerable painful stimulus (e.g. light skin prick)
whats allodynia
-painful response to a normally innocuous stimulus
-Painful sensitivity of sunburnt skin to gentle mechanical stimulus (e.g. light brushing) or mild temperature
what are the peripheral effects of an inflammatory response
-Hyperalgesia: result of lowered nociceptor thresholds which heightens pain response
-Peripherally, tissue damage releases a ‘soup’ of inflammatory substances which affect nerve function, recruit mast cells and neutrophils, and increase local blood flow
-Bradykinin, for example, directly affects the function of nociceptive molecular receptors such as TRPV1
-Prostaglandins lower the threshold for axon potential generation.
-Some painkillers (analgesics), notably aspirin and ibuprofen, act on cyclooxygenase (COX), an enzyme important in prostaglandin biosynthesis
whats central sensitisation
-Centrally, sensitisation can also result from the activity-dependent local release of substances like prostaglandins from nociceptive dorsal horn neurons.
-As in the periphery, this can lower the thresholds for action potential generation for neurons relaying nociceptive information, also giving rise to hyperalgesia
-However, another consequence of this is that these relay neurons also become sensitive to nearby non-nociceptive inputs (e.g. mechanoceptors)
-The result of this is that normally innocuous stimuli (e.g. gentle brushing of the skin) can be perceived as painful
-allodynia
whats hyperpathia
-a variant of hyperalgesia allodynia, but its underlying causes are different and so the symptoms are also slightly different.
-Hyperpathia results when there is fibre/axonal loss/damage (either centrally or peripherally) that results in a raising of the detection threshold (ieyou need a greater level of stimulation before the stimulus is detected).
-The result, however, is that when the detection threshold is exceeded, the subsequent excitability is much greater and patients report ‘explosive’ pain
whats phantom limb pain
-Phantom limbs are experienced after amputation
-Patients have the illusion that the limb is still present
-Indicates that central representation of the body is not passive, ie that it persists in the absence of peripheral input
-Surprisingly, children born without limbs can also have phantoms, suggesting that central maps may be partly pre-formed.
-clearly does not fit simply with specificity theory
whats referred pain
-Another phenomenon not easily explained in terms of the specificity theory
-Pain due to damage in the viscera is often perceived as coming from specific locations in the skin according to what organ is affected. (e.g. heart attack is often preceded by pain in the left shoulder and arm)
-Not well understood but thought to reflect convergence of visceral afferents onto the same pathways as cutaneous afferents in the CNS
-Extremely useful, however, in aiding clinical diagnosis of organ dysfunction
