Descending Modulation Of Pain Flashcards
1
Q
What is neurogenic inflammation?
A
- normal transmission of the sensation/anticipation of pain through nociceptors from PNS to CNS
- normal inflammatory action
2
Q
What is peripheral sensitisation?
A
- a reduction in the threshold of receptor sensitivity
- an increase in the magnitude of responsiveness from nociceptors
- results in allodynia
- heat sensitivity, but not mechanical
- requires ongoing stimulation to lower activation threshold and increase responsiveness of nociceptors
- requires ongoing peripheral pathology for sensitisation to be maintained
- localised to site of injury
3
Q
What is central sensitisation?
A
- increased responsiveness of nociceptors in the central nervous system to either normal or sub-threshold stimulus
- hypersensitivity to stimuli
- response to non-noxious stimuli
- increased pain response evoked by stimuli outside of the injury (expanded receptive field)
- a-beta mechanoreceptors become involved => hypersensitivity in non-inflamed tissue
- sensitive to touch
- non-mechanical/non-anatomical pattern of pain provocation in response to movement
- diffuse
- psychological factors involved
4
Q
What is the result of central sensitisation?
A
- recruitment of additional, sub threshold nociceptors => increased field of receptivity
- increased output of Nociception
- effects persist beyond tissue healing => allodynia
- over-activation of ascending pathway and under-activation of inhibiting pathways
5
Q
How does central sensitisation occur?
A
- inputs = C fibres + a-beta mechanical fibres (don’t usually get involved)
- C fibres release substance P, CGDP to dorsal horn
- a-beta fibres release glutamate (excitatory) to dorsal horn
- under normal circumstances NMDA is blocked, however, sustained release by nociceptors of glutamate, substance P and CGDP forces Mg2+ from NMDA receptor (unblocking)
- this boosts synaptic efficacy and allows Ca2+ into the dorsal horn neurons => activates Intracellular pathways to CNS => maintaining central sensitisation
6
Q
What is the role of glial cells (Astrocytes) in normal neuronal transmission?
A
- Astrocytes take part in glutamate (excitatory) and GABA (inhibitory) reuptake
- Astrocytes are activated by neurotransmitters
- Once activated Astrocytes experience an increase in Ca2+ and release transmitters of their own; enhancing or inhibiting synaptic activity
7
Q
What is the role of glial cells (Astrocytes) in central sensitisation?
A
- Astrocytes become activated and upregulate neuronal transmission => less re-uptake of glutamate (excitatory), more re-uptake of GABA (inhibitory)
- works with microglia which release chemicals to increase/decrease re-uptake
8
Q
What is the physiology of the pain-gate mechanism?
A
- located in dorsal horn of spinal cord (Substantia gelatinousa SG)
- primary neurons:
—> a-beta = quick + non-noxious => light touch, pressure, hair movement
—> a-delta = slower + noxious => pain + temperature => sharp, intense, tingling sensations
—> C fibres => very slow => pain + temperature + chemical => prolonged burning sensations
- if interneurons (inhibitory) in SG stimulated by a-delta + C fibres => excitatory response => pain modulated
- activation of large diameter a-beta fibres can reduce and inhibit transmission of small diameter a-delta and c-fibres (pain gating)
9
Q
How do a delta fibers inhibit activation of c (pain) fibres in pain gating?
A
- c-fibbers are slow, caring pain signals in 1st order neuron => excitatory stimulates 2nd order neuron and switches off interneuron
- if a-delta fibers are activated using mechanical pressure or temperature => activates interneuron stopping transmission of pain signals
10
Q
How is pain gating relevant to treatment?
A
- adding pressure
- cold/heat
- TENs => delivers small electrical current to activate non-nociceptive receptors in skin => signal to interneuron in spinal cord then activated to inhibit pain signals
- brain sends endorphins to the pain gate => lower transmission of pain signals between 1st and 2nd order neuron (prevents substance P release + inhibits synaptic potentials in post synaptic neurons) + reduced pain perception in brain
11
Q
What can create endorphins?
A
- pleasurable activities
- excitement
- meditation
- laughter
- intense exercise
12
Q
What is descending pain modulation?
A
- a delta/c nociceptive input into dorsal horn
- goes to medulla (rostral ventro-medial medulla RVM or dorsolateral pontine segment)
- into midbrain via periaqueductal gray (PAG)
- into thalamus + cortex + insula + amygdala + hypothalamus
- descending pathways go via PAG (midbrain)
- medulla (RVM)
- down to spinal segment and where 1st order neuron meets 2nd order neuron; serotonin + noradrenaline released => opioids released into interneuron resulting in inhibition of Spinothalamic fibers of pain
13
Q
What is Diffuse Noxious Inhibitory Control (DNICS)?
A
- 2 noxious stimulants
- 1st is inhibited by descending modulation to that segment of the spine e.g. lumbar decreasing stimulation of nociception
- 2nd noxious stimulant is facilitated by descending modulation to that segment of the spine e.g. cervical increasing stimulation of nociception
14
Q
What is another name for DNIC (diffuse noxious inhibitory control)?
A
- lateral inhibition
- listen to a specific sound and see how other sounds reduce
15
Q
What is disinhibition?
A
- failure of normal descending pain inhibitory system
