Descending Modulation Of Pain Flashcards
(30 cards)
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
16
Q
What is a major factor in heightened pain response?
A
- DNIC - descending noxious inhibitory control
17
Q
What occurs simultaneously with central sensitisation?
A
- DNIC (descending noxious inhibitory control)
- not synonymous
18
Q
How does DNIC (descending noxious inhibitory control) present?
A
- can be local, bilateral, segmental or whole body
- linked to fibromyalgia, RA, chronic pain
19
Q
How is DNIC (descending noxious inhibitory control) tested?
A
- can be tested with QST (quantitative sensory testing)
20
Q
Pain can be modulated in 2 ways
A
- descending facilitation
- descending inhibition (endogenous analgesia)
21
Q
What are the psychosocial factors affecting pain experience by modulation?
A
- context => pain beliefs/expection/placebo
- cognitive set => hypervigilance/attention/distraction/catastrophising
- chemical + structural => neurodegeneration/metabolic e.g. opiodergic, dopaminergic/maladaptive plasticity
- mood => depression/anxiety/catastrophising
22
Q
Which pathways are mainly serotonergic?
A
- pro-nociceptive pathways
23
Q
Which pathways are mainly noradrenergic?
A
- anti-nociceptive pathways
24
Q
Which brain areas are involved with the modulation of pain?
A
- periaquaductal grey (PAG)
- rostroventral medulla (RVM)
25
How do descending pathways bring change in the dorsal horn?
- release of serotonin and noradrenaline into interneuron which either inhibits or facilitates
- serotonin facilitates in DNIC
- noradrenaline inhibits in DNIC
26
What happens to the ascending input from nociceptors?
- a beta fibres become stimulated and transmit mechanical nociceptive signals when they wouldn’t usually
27
What factors produce either a descending facilitation or inhibition of nociception?
- mechanical stimulation e.g. pain gating
- descending inhibition from nociceptive stimulation to the brain
28
What is DNICS?
Descending noxious inhibitory control
29
When might we use DNICS in practice
- if a patient has an primary and secondary injury, know that the primary injury is being inhibited by noradrenaline and secondary injury is being stimulated by serotonin
30
What are the clinical implications of disinhibition?
- a patient can experience 2 injuries, the first one might disappear when the second one gets more intense
