central mechanisms of pain Flashcards
the spinal trigeminal nucleus is located where
the medulla
the spinal trigeminal nucleus has 3 subdivisions, what are they
- oralis (light touch)
- interpolaris (temp perception)
- caudalis (pain perception)
what is another name for nucleus caudalis
medullary dorsal horn…pain perception located
describe the organization of the medullary dorsal horn
-nociceptors are restricted to the more superficial layers (I and II)
non-nociceptive terminate in the deeper layers ( III, IV, V)
-there is some overlap b/w these fibers, in layers II and V
what are the cell types of the medullary dorsal horn
- nociceptive specific neuron (specific for pain)
2. wide dynamic range neuron
what is a wide dynamic range neuron
responds to non-noxious and noxious stimuli (gets input from both of these afferents)
what layers have noxious/non-noxious overlap
II and V
what aspects of the medullary dorsal horn CONVERGE
- nociceptive and non-nociceptive afferents
- peripheral afferents that have different receptive fields (detect sensory for different areas…like joints vs. muscle sensory)
is this convergence responsible for referred pain
yes? lol sorry, sucked at notes this day
referred pain is partially explained by this convergence under PATHOLOGICAL CONDITIONS when pain and non-pain afferents converge on a pain-signalling neuron
what occurs during central sensitization
- c-fiber stimulated causing acute pain and inflammation
- substance-p is released from the c-fiber and acts on the medullary dorsal horn neuron causing its depolarization
- the depolarization of the MDH neuron causes the NMDA receptor to be modified by the removal of its Mg2+ block
- this “activates” the NMDA receptor
- glutamate released (during innocuous…non-noxious…stimuli) from the a-Beta-fiber (neuron) can bind to the NMDA receptor and cause pain (where it normally wouldn’t)
is pain confined to the medullary dorsal horn/nucleus caudalis
no….during a trigeminal tractotomy (input to nucleus caudalis as well as C1-C3 afferents cut) you get anesthesia (bc of cut C1-C3), analgesia (pain removed in face), and hypolgesia (less pain detection in intraoral areas)…but still have pulpal pain!….this pain must be coming from somewhere else
if there is a lesion in the pons, what sensory is diminished
intraoral touch, thermal, pain is gone….this indicates that maybe there is some pain detection occuring in the SUBNUCLEUS ORALIS (in the pons)
what is the pathway for emotional pain input
afferent fibers–> medullary dorsal horn–>nucleus submedius–> cingulate cortex
what is the pathway for sensory pain input
afferent fibers–>MDH–>VPL (thalamus)–>cortex
what are the reflexes associated with pain pathways (in the mouth/face)
jaw opening, sweating, increased HR and BP
describe the receptive field in the VPL (sensory pain)
small receptive field…good localization of pain
describe the receptive field in the nucleus submedius (emotional pain)
large receptive field…poor localization of pain
describe the response the VPL gives to the cortex during the stimulus
tracks and detects the onset and offset of the stimulus. (once the stimulus starts it responds, and when the stimulus stops, the responses to the cortex stop)
describe the response of the nucleus submedius to the cingulate cortex during the stimulus
the n.submedius sends signals to the cingulate cortex even after the stimulus stops (response outlasts the stimulus)
describe the relationship b/w the stimulus and response for the VPL
the stimulus and response is LINEAR
describe the relationship b/w the stimulus and response for the n.submedius
the neural response yielding a “negative emotion” (unpleasant) OUTLASTS the stimuli
forebrain pathways can modulate pain perception….how
- anxiety can increase pain perception
2. the placebo effect can decrease pain perception
induction of anxiety and the placebo effect increase brain activity in the ….
anterior cingulate cortex
name 3 CNS sites that have the ability to modulate descending pain (back to the periphery)
- forebrain/anterior cingulate cortex
- midbrain (PAG)
- rostral ventromedial medulla
what molecules are released from the CNS to SUPPRESS PAIN
endogenous opioids
what is the mechanism for descending control of pain (suppression)
- descending projections from the CNS to the periphery send opioids (to enkephalinergic/opioid interneurons..with opioid receptors)
- these interneurons work pre and post synaptically to suppress pain
how do enkephalinergic interneurons work to suppress pain
- PRESYNAPTICALLY: they suppress the Ca2+ channels so that no Ca can influx and cause n.t release
- POSTSYNAPTICALLY: they open K+ channels (which I think would hyperpolarize the cell so no a.p can occur)
what is the local control of pain/GATE CONTROL THEORY
potential circuit that explains how non-noxious stimuli can suppress pain (a-beta fibers). basically a-beta fibers (detecting non-noxious stimuli) ACTIVATE inhibitory interneurons, these activated inhibitory interneurons can then INHIBIT c-fibers so that no pain signal can be released from the c-fiber to the periphery
