Neuromodulation Of Pain

Question 1

Pain

Answer 1

Unpleasant sensory and/or emotional experience associated with actual or potential tissue damage

Pain is always subjective

Question 2

Noxious stimulus

Answer 2

A stimulus that is damaging or threatens damage to normal tissues

Question 3

Nociception

Answer 3

The neural process of encoding noxious stimuli

Question 4

Nociceptors

Answer 4

Receptors that, when activated, cause the sensation of pain

Question 5

Hyperalgesia

Answer 5

Increased pain sensitivity

Question 6

Hypoalgesia

Answer 6

Absence of pain in response to stimulation that would normally be painful

Question 7

Allodynia

Answer 7

Painful response to non-nociceptive stimulation

Question 8

Dysesthesia

Answer 8

An unpleasant abnormal sensation, whether spontaneous or evoked

Question 9

Acute pain

Answer 9

Direct result of tissue damage or potential tissue damage, and is a symptom
Serves a protective mechanism

Question 10

Chronic Pain

Answer 10

Does not serve a biological purpose

Considered chronic if:
It outlasts normal tissue healing time
The impairment is greater than would be expected from the physical findings or injury
Pain occurs in the absence of identifiable tissue damage

Question 11

Gate control theory

Answer 11

Specialized nerve endings, nociceptors, response is modulated in the dorsal horn of the spinal cord
“Small” fibers open the pain gate
“Large” fibers close the pain gate

Question 12

Other Pain Control Theory’s

Answer 12

Peripheral: change environment
Segmental: not just simple gate control
Supraspinal: brainstem and cortical
Neuromatrix theory: Pain is a multidimensional experience - Neurosignature patterns of nerve impulses generated by a widely distributed neural network in the brain
Biopsychosocial model

Question 13

Pain Sensory Afferents

Answer 13

Aδ - Fast pain (sharp, pricking)
C fibers - Slow pain (burning pain, dull/achy)

Question 14

Pain Pathway

Answer 14

Noxious Stimulus -> Nociceptors -> Primary afferent neurons (Aδ and C fibers) -> Dorsal root ganglion -> Spino-thalami tract -> Secondary afferent neurons (RVM & PAG) -> Thalamus -> Third order neuron (Limbic system)

Question 15

Inhibition of Nociceptive System

Answer 15

Hypoalgesia (decreased) - Endogenous Modulation

Peripheral and Central/Descending
Neurotransmitters (Norepinephrine, Serotonin, GABA)
Neuromodulators (Endomorphins/enkephalins, δ and μ opioid receptors)
Endocannabinoids

Pain to pain inhibition
Nociceptive input targets cortical, midbrain, and medullary areas to inhibit the transmission neurons

Question 16

Facilitation of Nociceptive System

Answer 16

Hyperalgesia (increased) - Endogenous modulation

After Injury:
Sensitization of neurons in the dorsal horn
Increase in receptive field size
Increased responsiveness to innocuous or noxious stimuli
Decreased threshold to innocuous or noxious stimuli

Neurotransmitters (Serotonin, Glutamate)
Neuromodulators (Substance P, Calcitonin gene-related peptide, H+/lactate/ATP or by-products)
Non-neuronal activators (Cytokines, Nerve growth factor)

Question 17

Opioids

Answer 17

Work to reduce neuronal cell excitability which results in reduced transmission of nociceptive impulses

Four classes
1. Endorphins: β (hypothalamus, pituitary)
2. Enkephalins: δ
3. Endomorphins: μ
4. Dynorphins: κ

• May produce analgesia through a peripheral mechanism
• Inhibit ascending transmission of nociceptive information in the dorsal horn
• Activate pain control pathways centrally

Question 18

How Does PT Modulates Pain

Answer 18

Exercise/physical activity
Manual therapy
Cognitive behavioral therapy
Other: Instrument-assisted soft-tissue mobilization (IASTM), Heat/cold, Electrical stimulation, Laser, Acupuncture/dry needling, Placebo

• Exercise reduces nociceptor activity
• Exercise restores normal movement of joint and tissue, which could remove a mechanical irritant to a nociceptor
• Exercise decreases nociceptor excitability, increases peripheral inhibition, and promotes healing of injured tissues