Pain & Nociception Flashcards
nociception
activity in the nociceptors and nociceptive pathways (central and peripheral)
- initiated by a noxious stimulus
- involves pain processing pathways
- causes physical changes (BP, HR, cortisol)
pain
perception of the noxious stimulus; the unpleasant feeling and behavioral response to a noxious stimulus
5 key factors of pain
- has a physical cause
- it is a feeling (sensory and emotional experience)
- requires consciousness
- it is subjective
- it is unpleasant
reason for pain
overall protective and critical for survival
alerts the body of the threat and triggers protective behaviors to limit damage and promote healing
allodynia
pain experienced in response to a non-noxious stimulus
hyperalgesia
exaggerated response to a noxious stimulus
acute pain
pain that follows tissue damage (has a specific cause)
- short lived - resolves as tissues heal
- has protective function
nociceptive and physiologic/adaptive
chronic pain
pain that persists when the initial cause is gone
- long lasting
- no protective function
- difficult to treat
pathologic/maladaptive pain
somatic pain
pain from the skin, muscles, bone, soft tissues, teeth, etc
can be precisely localized/perceived at the affected area due to a LARGE # of fibers that go to SPECIFIC parts of the spinal cord that innervate the area
visceral pain
pain from internal organs, glands, smooth muscle
diffuse and poorly localized due to a SMALL # of fibers that spread extensively in the spinal cord that innervate the area
referred pain
visceral pain that can be felt at somatic sites due to viscero-somatic convergence
viscero-somatic convergence
the overlap of somatic and visceral nerve fibers in the spinal cord that causes altered processing of visceral and somatic pain inputs
viscero-somatic convergence
the overlap of somatic and visceral nerve fibers in the spinal cord that causes altered processing of visceral and somatic pain inputs
viscero-somatic convergence
the overlap of somatic and visceral nerve fibers in the spinal cord that causes altered processing of visceral and somatic pain inputs
viscero-somatic convergence
the overlap of somatic and visceral nerve fibers in the spinal cord that causes altered processing of visceral and somatic pain inputs
neuropathic pain
pain caused by a lesion/disease of peripheral nerve fibers
can be acute or chronic
ex. amputation, spinal cord injury, diabetic neuropathy, cancer
neuropathic pain
pain caused by a lesion/disease of peripheral nerve fibers
can be acute or chronic; often involves nervous system hyperexcitability
ex. amputation, spinal cord injury, diabetic neuropathy, cancer
nervous system hyperexcitability
bombardment of excitatory signals to CNS + a decrease in inhibitory signals that causes hyperexcitability
pain processing pathway
transduction –> transmission –> modulation –> perception
transduction
conversion of a noxious stimulus into an electrical signal (AP)
where does transduction occur
peripheral nociceptors
noxious stimulus triggers depolarization –> activates nociceptors –> generates AP
what is action potential frequency proportional to
intensity and duration of the noxious stimulus
nociceptors
peripheral endings of nociceptive A-delta and C fibers in their target tissues
have a HIGH activation threshold - requires very intense/prolonged stimuli
what type of signals do nociceptors detect
mechanical, temperature, and chemical
unimodal nociceptors
only get activated by 1 type of stimulus
usually A-delta fibers
polymodal nociceptors
activated by a wide variety of noxious stimuli
usually C fibers
silent nociceptors
MIAs - mechanical insensitive afferents
nociceptors with an extremely high activation threshold that are usually inactive and require previous sensitization to be activated
transmission
action potential propagation from periphery to the CNS
where does transmission occur
along A-delta and C fibers
process of transmission
AP generated at nociceptors travels along nerve fibers causing voltage gated Na channels to open –> AP propagates down fiber
A-delta fibers
FAST, medium sized, lightly myelinated nerve fibers involved in IMMEDIATE SHARP pain
C fibers
SLOW, small, unmyelinated nerve fibers involved in slow burning/dull pain
what type of fiber is more abundant in somatic tissues
A-delta fibers
causes somatic pain to be more immediate/sharp
what type of fiber is more abundant in visceral tissues
C fibers
causes visceral pain to be more slow/dull
A-beta fibers
FASTEST, large, myelinated nerve fibers involved in NON-PAINFUL touch
NOT involved in nociception
dorsal horn of the spinal cord
site of A-delta/C fibers synapsing with secondary afferents
main neurotransmitter released by A-delta/C fibers
glutamate
main neurotransmitter released by A-delta/C fibers
glutamate
main receptor on secondary afferent neurons in the spinal cord
AMDA receptors
AMDA receptors
glutamate receptor on the secondary afferent neuron
causes depolarization and further propagation of AP to the CNS
secondary pain afferents
located in the dorsal horn of the spinal cord
types:
1. interneurons
2. propriospinal neurons
3. projection neurons
interneurons
major target for primary afferent neurons (A-delta/C)
can be excitatory or inhibitory to pain transmission to CNS
used as a target for pain meds
propriospinal neurons
transfer inputs between spinal cord segments
projection neurons
transfer inputs from spinal cord to supraspinal centers in the brain via ascending tracts
wide dynamic range neurons (WDRn)
special projection neurons (or interneurons) that receive information from all primary afferents (A-delta, C, A-beta) to detect noxious and non-noxious stimuli
receptors cover a large area with high overlap –> many WDRns activate in response to single stimulus
modulation
up or down regulation of action potential transmission; affects how much of the action potential reaches the brain to determine amount of pain experienced
where does modulation occur
dorsal horn of the spinal cord
function of ascending tracts
transmit the action potential from dorsal horn of the spinal cord to supraspinal centers
gate control mechanism
activation of nerves that do not transmit pain signals (A-beta) to alleviate the final pain feeling
non-painful mechanical stimuli –> activates A-beta (FAST) fibers –> activates inhibitory interneurons at the dorsal horn –> decreases painful signals sent to the brain
descending modulation
feedback mechanism from supraspinal centers to the dorsal horn of the spinal cord that change pain perception in the brain
supraspinal centers send excitatory/inhibitory interneurons/projection neurons to dorsal horn –> facilitates amount of pain signal that gets sent back up to the brain
how does emotional state/manipulation of attention alter pain perception
descending modulation
not focusing on pain/positive thoughts –> increased inhibitory signals sent from supraspinal centers –> less pain felt
focusing on pain/negative thoughts –> decreased inhibitory signals sent from supraspinal centers –> more pain felt
what are two descending modulary systems
- PAG-RVM (tonically active - inhibitory)
- Pontine-NE Cell Groups (activated by PAG-RVM)
sensitization
increased responsiveness of the nervous system (PNS or CNS) to noxious stimuli
makes nervous system hyperaware during pain to decrease further damage –> results in allodynia and hyperalgesia
produces reversible changes in nervous system (if long lasting, can become chronic)
peripheral sensitization
sensitization that occurs at the site of injury
caused by local inflammation that changes the environment of the nociceptors
results: allodynia and primary hyperalgesia (at site of injury)
central sensitization
sensitization that occurs at the dorsal horn neurons in the spinal cord
caused by sustained noxious stimulation leading to neuronal hyper-responsiveness
results: allodynia and secondary hyperalgesia (spreads to surrounding areas)
WIND-UP phenomenon
an increase in neuron responsiveness after sustained noxious stimulation leading to an increased number of APs generated following each individual stimulus
increased efficacy of synaptic transmission leads to central sensitization of WDRns (less glutamate required to transmit pain)
what receptors and nerve fibers are involved in the WIND-UP phenomenon
NMDA receptors
C fibers repetitively firing
perception
awareness of the feeling of pain leading to negative emotions, behavioral responses, and learning
where does perception occur
cortical regions of the brain
subcortical regions project to the cortex to modify
pain experience
multidimensional experience of pain based on the characteristics:
1. sensory-discriminative
2. emotional-motivational
3. cognitive-evaluative
sensory discriminative aspect of pain experience
somatosensory cortex
involves pain intensity, location, quality and duration
emotional motivational aspect of pain experience
limbic system
emotional reaction to pain
cognitive evaluative aspect of pain experience
prefrontal cortex
pain meaning and its possible consequence
