Modulation of Pain Flashcards
What is the role of non-nociceptive fibers in pain modulation?
They contribute to the normal perception of stimulus quality, even though they do not respond directly to noxious stimuli.
When something hurts, there is regular discriminative touch input being conveyed as well.
Pain modulation at the level of the receptor:
What is peripheral sensitization? When does it occur? What is the result?
Following repeated exposure to a noxious stimulus, the receptors become more sensitive to that stimulus (meaning there is a lower threshold for depolarization) and therefore more responsive to it (an action potential is more likely to be fired).
as the injured tissue heals, the sensitization typically declines and the threshold for pain returns to pre-injury levels
Pain modulation at the level of the receptor:
What is the hypothesized mechanism of peripheral sensitization?
PS is thought to result from the exposure of receptors to chemicals released by damaged tissues and sensory nerve endings in the vicinity by injury. (Chemical mediators cause hypersensitivity)
Pain modulation at the level of the receptor:
What condition may be caused by peripheral sensitization?
Hyperalgesia (excessive response to noxious stimuli)
Pain Modulation at the level of the receptor: Opoids
Where are endogenous opiods and opiod receptors most concentrated and why?
In the dorsal horn of the spinal cord and in brain stem regions involved in modulation of pain because that is where pain modulation occurs.
What are the 3 ways in which opiods decrease pain?
Opiods decrease pain by INHIBITION in these 3 ways:
- They hyperpolarize the peripheral processes of the primary afferent neurons so they are not as responsive to noxious stimuli
- release of neurotransmitter from the presynaptic membranes of sensory neurons is reduced
- 2nd order neurons are hyperpolarized.
Pain modulation at the level of the spinal cord:
What are the two neurotransmitters in the spinal cord that modulate pain and what are their mechanisms?
1) Gluatamate - it is a SMALL MOLECULE neurotransmitter. its action is confined to postsynaptic neurons in its immediate vicinity. It mediates RAPID synaptic transmission.
2) Substance P - it is a neuropeptide neurotransmitter. Levels of substance P elevate with chronic pain. It enhances and prolongs the effect of glutamate. It can diffuse and affect neurons at a considerable distance. it mediates SLOW synaptic transmission.
Pain modulation at the level of the spinal cord:
What is central sensitization?
After repeated activation by primary afferent fibers, dorsal horn nociceptive neurons become more sensitive (hypersensitivity of 2nd order neurons) meaning that heir threshold decreases. Threshold can decrease so much that they can be activated by non-nociceptive primary afferent fibers.
Pain modulation at the level of the spinal cord:
What is the hypothesized mechanism of central sensitization?
Windup: repeated input to the secondary neuron in the spinal cord increases the discharge rate, changing the make up within the cell in such a way that gene expression is changed, which could constitute a memory of the input at the cellular level.
As the tissue heals sensitization typically goes back down and the threshold decreases.
Pain modulation at the level of the spinal cord:
What conditions are possibly caused by windup?
hyperalgesia - excessive reaction to noxious stimuli
allodynia - an innocuous stimulus produces severe pain
phantom limb pain
Pain modulation at the level of the spinal cord:
What is gate control theory?
Non-nociceptive fibers can inhibit nociceptive fibers by activating inhibitory neurons (this is closing the gate)
nociceptive fibers also interact with the interneuron, so they can inhibit the interneuron, thereby opening the pain gate
Pain modulation at the level of the brain: descending systems.
Where do the descending systems for pain modulation originate? what can information descending from these areas do?
primary somatosensory cortex amygdala midbrain pons medulla
Info from these areas can inhibit the activity of nociceptive projections in the dorsal horn of the spinal cord
