Pain
A physiologic response that serves as a warning
Nociception
The perception of pain
Nociceptors
Pain receptors
Gate control theory
Pain transmission occurs because of the signals sent to the spinal cord where the cells in the substantia gelatinosa work as a gate.
Neurochemistry
neuroanatomy
The gate control theory of pain involves what? [2]
Thalamus
Major integration center for pain
Higher brain centers: Brainstem, reticular area, thalamus
Synapse happens at the substantia gelatinosa, where do messages get sent?
C-fibres
Fibres that send slower, duller pain messages associated typically with chronic pain
Hypoxia
Lack of oxygen to tissues
Lactic acid. This stimulates nociceptors
When the body switches to anaerobic metabolism, what is created as a result?
Prostaglandins
These are synthesized from exposed phospholipid of broken cell membranes, and stimulate nociceptors and increase sensitivity to pain
Inhibitory
Signal that tries to stop pain message from getting sent higher, or reduce severity
Substance P
Glutamate
aspartate
calcitonin
pG
Histamine
Bradykinin
Excitatory neurotransmitters: [7]
chemical mediators
pressure
temperature
How are pain receptors stimulated? [3]
Serotonin
GABA
glycine
norepinephrine
endogenous opiods
Inhibitory neurotransmitters [5]
depolarization, AP generated
impulse transmission in nerve along a delta or c fibers
Stimulation of pain receptors initiates what? [2]
A-delta fibres
Large, myelinated pathway for fast, sharp, localized pain
C fibres
small, unmyelinated pathway for slow, dull, burning, diffuse pain
Dorsal horn
Impulses from a-delta/C fibres are sent to this relay station between peripheral and central nervous systems
Synapse in the substantia gelatinosa
for impulses to travel up the spinothalamic tract, it needs to travel across where?
Release in inhibitory or excitatory neurotransmitters.
When an impulse reaches the end of a presynaptic neuron, what does that cause?
Neurotransmitters cross the synapse in the substantia gelitanosa and bind to receptors on post-synaptic neurons to send message to CNS
What initiates depolarization of post-synaptic neurons in dorsal horn?
Neurotransmitter binding to receptors
What initiates deplarization of post synaptic neurons?
Neo: sharp, fast
Paleo: slow, dull
Two tracts from dorsal horn to CNS
reticular system
limbic system
cerebral cortex
Pain perception centres whre learned behaviours, cultural aspects, and previous experiences shape emotions associated with pain: [3]
HPA axis views pain as a stressor, and HPA gets activated
Why might patients in pain have increased pulse, sweating, tachypnea?
Motor response
Different than a reflex arc, normally if touching something painful for longer than a millisecond. It removes the body part that is painful at the time
Reticular and limbic system
cerebral cortex
HPA axis
Muscles
The thalamus sends messages to various effectors: [4]
Descending pathway of pain modulation
Increases or decreases the transmission of pain signals in the periphery, spinal cord, and brain
The synapse of pain. If we stop the synapse (aka modulating pain) then we stop the brain from perceiving there is pain
Where is the “gate” in gate control theory?
Segmental pain inhibition.
How do a-beta fibres modulate pain?
Once pain is perceived in CNS, message is sent back for a motor response and stimulation.
A-beta fibres take over and send non-painful messages (squeezing, tapping, etc) to the brain via the ascending pathway and inhibitory neurotransmittors are released.
pain gate gets closed
How segmental pain inhibition inhibits pain: [3]
PAG (periaqueductal grey)
Region of the midbrain that receives pain messages has axons connecting it to dorsal horn in spinal column. Stimulates NRM area to release endorphnis in dorsal horn
Endorphines
the feel-good morphine in he body
Endorphines bind to and inhibit ion channels in post-synaptic neurons OR
Inhibitory neurotransmitters inhibit the ion channels and
Post-synaptic transmission of pain impulses from periphery decreases so pain decreases
How do endorphines decrease pain?
Diffuse noxious inhibitory control (DNIC)
Activates when another area is receiving noxious (painful) stimuli at the same time as the original painful area, and A-beta fibres are stimulated and help with the pain (ex: deep massage, acupuncture, heating pad).
Somatic
Visceral
Referred
three classifications of acute pain:
a-delta or C-fibres
Somatic pain (joints, skin, muscles) sends signals along which fibres?
C-fibres
Visceral pain sends signals along which fibres?
Chronic Pain
Pain lasting longer than 3-6 months. Can be ongoing or intermittent
Intractable pain
Chronic pain associated with metastasis in cancer
Neuropathic pain
Chronic pain caused b damage to/dysfunction of nerves/nervous system. Described as burning, shooting, shock-like, tingling
Phantom limb pain
diabetic neuropathy
post-herpetic neuralgia
multipl sclerosis
parkinson’s disease pain
Examples of neuropathic pain:
Post-herpetic neuralgia
When herpes zoster virus lives in nerve ganglia after the chicken pox. When reactivates, causes inflammation f neuron with prolonged impulses
Cutaneous
“superficial”
Dermatome
Region of the body wall supplied by a single pair of dorsal root ganglia
Pain threshold
Lowest amount of pain a person can recognize
Pain tolerace
Greatest amount of pain a person can endure
before treatments
after treatments
with vitals (are you feeling any pain?)
When should pain be assessed? [3]
mild
moderate
severe
Descriptive scale of pain: [3]
Stimulates a-beta fibres to close pain gate
How do massage and tens machines treat pain?
Numbs nociceptors so the don’t fire
How can cold treat pain?
Stops lactic acid production
How can oxygen treat pain?
It removes stimuli
How can increased circulation (massage, heat, ultrasound) tret pain?