Pain Neurophysiology and Subtypes Flashcards
what do low and high threshold receptors transduce
what are fibre types are high threshold and thin diameter afferents and what do they have as their end organs
low: touch, vibration, coolness, warmth
high: pinch, crush, laceration, chemicals
A delta or C polymodal, free nerve endings as end organs
the axon of a peripheral nerve will only open in response to what type of stimuli
T or F: free nerve endings express a number of receptor terminals
high noxious mechanical, thermal or chemical stimuli
T, we have different gaits embedded within nerve membranes
once the gaits on a free nerve ending opens what may happen to them
what is a nerves resting membrane potential and what threshold must it reach to send an AP
they may not close right away so they remain sensitized and less stimuli is required to reopen the gaits
-70 is resting, -55 to send AP
explain the components of a nerve axon beginning with the myelinated axon
what is embedded within the epineurium
myelinated axon with Schwann cells is wrapped in endoneurium
endoneurium is a fascicle of axons which is wrapped by the perineurium
multiple fascicles of the perineurium are wrapped up by the epineurium
arteries and veins
what innervated the epineurium and perineurium
what does the presence of blood vessels within a nerve create the potential for and what would this cause
thin diameter free nerve endings
blood products to spill into a nerve when there is a crush or laceration causing a compressed nerve to be sensitized enough to be painful
where does the cell body of the first order neuron live
the dorsal and ventral roots carry what types of nerves
in the dorsal root ganglia
dorsal: sensory
ventral: motor
what is the primary order nerve in the dorsal horn of the spine
what two types of second order neurons can the primary order neurons synapse with in the spine
either A delta or C polymodal
either nociceptive specific or wide dynamic range neurons
what do nociceptor specific neurons interface with
what do wide dynamic range neurons interface with
only high threshold nerves coming into the periphery (need intense stimuli to depolarize)
lower threshold touch based fibres (coolness, warmth, vibration)
the A delta, C fibre or A beta fibres coming in from the dorsal root may both synapse with what
when might both of these synapse onto the same neuron
an interneuron in the spinal cord
if the second order neuron is a wide dynamic range neuron
how does descending input affect the likelihood an AP will travel back up the spinal cord to the brain
how may glial cells play a role in chronic pain
through descending noxious inhibitory control
substance P can activate glial cells to release a pro inflammatory mediator which stimulates the second order neuron in the spinal cord causing it to fire making the brain think there’s something happening out in the periphery
A delta and C fibres overlap with type 1 and 2 mechanoreceptors in which of the dorsal horn laminae (layers)
which brain structure is an essential component to determining whether or not we should be experiencing pain
laminae 2-5
the prefrontal cortex because it’s the judgement making centre
why have prior attempts to treat pain by removing parts of the brain been unsuccessful
in the case of chronic pain, what happens to the boundaries somatosensory cortex
because we do not have a singular pain centre in the brain, its a distributed experience among many different parts of the brain
the boundaries may start to smudge and we lose the ability to know these boundaries (other parts of the somatosensory cortex start to take over)
how does brain activity change when touching an area of pain in individuals with chronic pain and what does this tell us
the brain becomes more activated and deactivated in certain areas
tells us that reaction to stimuli of the painful area can be very different for someone with chronic pain
what is complex regional pain syndrome (CRPS) and what causes it
what happens when testing two point discrimination in someone with CRPS
how can you improve two point discrimination and brain activity in an individual with CRPS
when you feel pain in an entire limb, have weakness or swelling
caused by dysfunction of the CNS
2 point discrimination is impaired and there is less brain activity in the brain when 2 point discrimination is done on the affected side (brain disowns the hand)
desensitization (stroke hand with feather)
describe nociceptive pain (driven by, AP direction, responds to what treatment)
pain driven by tissue stimuli that is intense enough to cause potential or actual damage
AP start at the end organ of the high threshold afferent and travel orthodromically (in the right direction) towards the spinal cord and brain
amenable to NSAIDs, analgesics, non pharmaceutical peripheral therapies, surgery
describe neuropathic pain (driven by, AP direction, symptoms)
driven by APs arising from a damaged nerve
AP arise somewhere along the path of the nerve other than the physiological end organs
AP travel both orthodromically (right way) and antidromically (wrong way)
strange sensations (allodynia, pricking, cold, weak)
in neuropathic pain, how does the AP travelling both orthodromically and antidromically impact the target tissue
it causes neurogenic inflammation in the target tissue
describe central/nociplastic pain (driven by, causes)
driven by abnormal CNS activity, may begin as a peripheral driver but is maintained through changes to the function of the CNS after peripheral input is solved
glial cell activation, changes in thresholds, NTs (release of substance P), peripheral nerves that activate NS or WDR neurons
alterations in brain structure, connections or chemistry
describe emotional pain (driven by, mechanisms)
what is linked to emotional pain
what is the placebo/nocebo phenomena
driven by strong negative emotions
mechanisms similar to nociplastic but is less about peripheral input and more about chronic distress, depression, fear, anxiety
endocrine function (stress pathways)
the experience of pain can be modified through manipulation of context and expectation
describe visceral pain (driven by, type of symptoms, DOES NOT respond to what treatment, type of stimuli causing pain)
driven by stimuli arising from the viscera
poorly localized diffuse symptoms (associated with other symptoms depending on the organ affected)
NSAIDs, analgesics, peripheral mechanical therapies
inflammation, chemical irritation, ischemia (a special case of nociceptive pain but stimuli aren’t purely mechanical)
what are the clinical indicators of nociceptive pain
predictable, consistent, associated with movement or pressure
most likely to find tissue based abnormality, amenable to NSAIDs
what are the clinical indicators of neuropathic pain
related to nerve pathology, inconsistent and unpredictable association with movement, usually localized, strange symptoms, not amenable to NSAIDs
what are the clinical indicators of nociplastic pain
more chronic, poor association with movement, less predictable
difficult to localize, no clear association with tissue abnormality
may be amenable to opioids but not NSAIDs
what are the clinical indicators of emotional pain
pain related to strong negative emotions, no clear association with movement or tissue abnormalities, not amenable to NSAIDs
what are the clinical indicators of visceral pain
poorly localized, not related to movement but may be worse in certain postures depending on the organ, co-occurring with other symptoms, not amenable to NSAIDs or mechanical therapies
describe acute, subacute, and chronic pain
what differentiates acute and chronic pain
acute: lasting 3-6 weeks from onset, is adaptive or protective
subacute: lasts between 3-6 weeks to 3-6 months from injury
chronic: over 3-6 months from onset, non adaptive or non protective
the inability of the body to restore normal homeostasis
