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Definition
Activation of nociceptive primary afferents
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Conscious, affective unpleasant somaesthetic percept localized to the body.
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Increased sensitivity to noxious stimuli
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| We often identify damaged tissue via identifing... |
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Definition
| Redness, Swelling, Heat and Pain |
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| Substances released after tissue damage are ... |
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Definition
| Substance P, Potassium, Serotonin, Bradykinin, Histamine, Prostaglandins. These often act to vasodilate. |
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| Nociceptors can detect mechanical, thermal and chemical changes above a set threshold. True or False? |
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Definition
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| All nociceptors are free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglia and are named according to their appearance at their sensory ends. True or false? |
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Definition
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There are 10 layers to a spinal cord. I-VI is dorsal horn, VII and X is Intermediate zone and VIII-IX is ventral horn. The layers are known as lamina. L1 is known as the ... L2 is known as the ... and L3-4 is known as the ...
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Marginal layer, Substantia Gelatinosa, Nucleus porprius.
Remember as MSN :) |
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L1 - Marginal layer = ...
L2 - Substantia Gelatinosa = ...
L3,4 - Nucleus proprius = ... |
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Definition
L1 - A delta fiber: Nociceptive and WDR neurons with ascending axons
L2 - C fiber: Nociceptive and WDR interneurons
L3-4 - A beta fibwer: Somatotopic low threshhold inputs - ascending dorsal column axons
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| The spino-thalamic tract/pathway goes right through medulla and pons and to the midbrain then the thalamus. These thalamic neurons project to the cerebral cortex. |
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The “central matrix” mediating the experience of pain...
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Definition
• somatosensory cortex I & II
• anterior cingulate cortex (blue)
• ventrolateral prefrontal cortex
• insula cortex
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1) How good is pain localisation?
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| This is due 2 poor or mis-localised visceral pain may be due 2 convergance of somatic and visceral inputs to ascending nuerons. We have a viscerotopic map but dont really use it and instead they just sort of piggy back on the cutaneous map. |
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2) Can nociceptive activity be modulated, centrally and peripherally?
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Definition
We can reduce pain by rubbing surrounding area, this is known as counter irratation.
Nociceptive activity “opens” the gate, and non-nociceptive activity “closes” the gate. This is done via the non-nociceptive fibre innervating an inhibitory interneuron and therefore weakening the activation.
Inhibiting GABA in the insular produced a lasting analgesia, by enchancing
descending inhibition of spinal neurons (via PAG, medulla?)
Increasing the activity of neurons that expressed GABA receptors produced a
hyperalgesia through activation of the amygdala.
When Enkephalin is released there is a decreased response. The descending inputs reduce it via interneuron’s. These Enkephalin’s effect the pre and post synaptic sites.
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| 3) Is the increased sensitivity to somatic stimuli fully explained by peripheral sensitization? Central sensitization ‐ change in efficacy at the first synapse |
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Definition
The threshold of the cell is altered after a lot of C fibre input. LTP is to do with glutamate receptors and works over a long period of time.
Early gene c-fos is a marker of nociceptive activation and is indicative of long-term changes in excitability.
Secondary hyperalgesia:
- Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues.
- Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.
In addition to analgesic mechanisms involving opioids and descending inhibition,
the are descending facilitatory (algesic) pathways.
Facilitatory effects seem to parallel, and apparently overlap with, inhibitory effects
(dorsal reticular nucleus; nucleus giantocellularis).
The origin of facilitatory activity may be the cingulate and insular cortex. The effect
seems to be associated with
secondary hyperalgesia: an increased sesnitivity to
somatic stimuli applied to regions near regions that are injured / inflamed
It is the normal sequel of a cutaneous injury, but is not seen if descending inputs to
DH are blocked.
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Definition
The generation of pain by normally innocuous stimuli. This is a Chronic pain state associated with dorsal horn hyper-excitability
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| Mechanism behind allodynia.... |
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Definition
Damage to peripheral nerves results in retrograde signals to microglial cells in the spinal cord
Microglia become activated, secreting growth factor BDNF, which down regulates KCC2 chloride transporters in SDH neurons GABAergic inhibition of SDH neurons opens Cl
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channels, but the lack of KCC2 activity means the Cl-
equilibrium potential is above resting membrane potentials - therefore GABA is excitatory
Now low threshold activity in A
β
fibres activates rather than inhibits SDH neurons
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| Thermo grill experiment shows.... |
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Definition
An example of pain but not nociception. There is an inhibition between the warm and cool. They sort of cancel each other out. There is no damage to the skin but there is a feeling of pain.
We have dedicated receptors to cool and receptors to noxious hot/cold.
Receptor fields are opened in close proximity and this reveals inhibition in the cool and warm receptors. The cancel each other out. There is now no signal to inhibit the nociceptive signal and so Nociception happens. Look closely at diagram. Cool would inhibit the noxious stimulus. Cool is cancelled out by warm. Therefore there is not cool signal and so there is nothing to inhibit noxious stimulus.
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| Pain can be localised to one area? True or false? |
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Definition
| False, it is locasiled to many areas that is collectivley known as the 'pain matrix' |
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| How does the prefrontal cortex involve itself in pain? |
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Definition
The PFC involves itself in our expectation of pain. Just the thought of pain activates descending inhibitiory pathways.
There is also a placebo effect. If we are told something is going to be painful then we do experience more pain, and the reverse works as well, if we say take this pill it will reduce the pain, the empty capsule in fact does nothing but makes us think less pain therefore less pain.
The anticipation of pain does in fact modulate the final pain effect and it is believed that is due to descending inhibitory pathways. Placebo effects are real. The encephalin and endorphin pathways are modulated and actually minimise the effect of pain.
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Many components of the pain matrix are active when we
experience pain empathetically, which are these and how do they work?
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Definition
Many components of the pain matrix are active when we experience pain empathetically.
When people watch a loved one experience receive a painful stimulus, there is activation (in the observer) of cingulate, insula and prefrontal regions - but not somatosensory regions, suggesting that somatosensory cortex confers sensory / discriminative dimension of the pain experience rather than the affective dimension.
There are studies where the brains of both the person experiencing pain and the person they love is experiencing pain and they are watching it. Similar areas are activated. Areas that are activated when you feel pain is the somato-sensory cortex because it is where you feel the pain in your body. |
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