Neuromodulation Of Pain Flashcards
Pain
Unpleasant sensory and/or emotional experience associated with actual or potential tissue damage
Pain is always subjective
Noxious stimulus
A stimulus that is damaging or threatens damage to normal tissues
Nociception
The neural process of encoding noxious stimuli
Nociceptors
Receptors that, when activated, cause the sensation of pain
Hyperalgesia
Increased pain sensitivity
Hypoalgesia
Absence of pain in response to stimulation that would normally be painful
Allodynia
Painful response to non-nociceptive stimulation
Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked
Acute pain
Direct result of tissue damage or potential tissue damage, and is a symptom
Serves a protective mechanism
Chronic Pain
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
Gate control theory
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
Other Pain Control Theory’s
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
Pain Sensory Afferents
Aδ - Fast pain (sharp, pricking)
C fibers - Slow pain (burning pain, dull/achy)
Pain Pathway
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)
Inhibition of Nociceptive System
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
Facilitation of Nociceptive System
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)
Opioids
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
How Does PT Modulates Pain
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
