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PainPain
What is pain?
Pain is a sensation that you feel when
there is damage to your body
Although this applies to normal
circum...
Nociceptive pain
 As mentioned before, this is the pain that is felt
when there is damage to your body and the
pain serve...
Nociceptive pain
Brain
1. You stand on a needle
which causes tissue
damage at the point of
impact
2. This information is t...
Pain transmission
 Nociceptive pain is sensed and transmitted by two types
of nerve fibres; A-delta and C fibres:
 A-del...
Pain transmission
 C fibres are unmyelinated, with a slow conduction velocity and
terminate in the skin as free nerve end...
Pain transmission
 Transmission of pain from the periphery to the brain
can be outlined in the following steps:
Step 1:
...
Pain transmission
Step 2:
 The thermal stimulus needs to be converted (transduced) into
an electrical signal so that it c...
Step 2:
TRPV1
TRPV1
Specialised ending of
A-delta fibres
TRPV1
TRPV1
Free nerve
endings of
C fibres
Impulse towards the br...
Pain transmission
Step 2:
 A-delta fibres are activated first because of their low
threshold and they transmit the impuls...
Pain transmission
Step 3:
The impulses travel along the axons of
both A-delta and C fibres towards the
spinal cord
In th...
Step 3:
1. A-delta fibres enter
the dorsal horn and
synapse in lamina I
2. Neurones from
lamina I cross the
midline via th...
Step 3: C fibres (both peptide-rich
and peptide-poor) enter
the dorsal horn and
immediately travel in
Lissauer’s tract to ...
Step 3:
1. C fibres ascend up
Lissauer’s tract
2. Peptide-rich C fibres synapse in
lamina I
3. The majority of these
pepti...
Step 3:
1. C fibres ascend up
Lissauer’s tract
2. Peptide-poor C fibres synapse on
interneurons in lamina II
3. The intern...
Summary of pathways
Type
of
fibre
Synapse
in the
dorsal
horn
Tract Connections Function
A-delta Lamina I Spinothalamic
Ven...
Pain modulation
 Once pain has been sensed and the
danger averted, pain sensation needs to
be depressed
 This is so that...
Gate control
 This is a theory that A-beta fibres (which carry
sensations other than pain) can control the
transmission o...
Gate control
A-beta fibres synapsing in lamina V
Pain projection
neurone
Interneuron in lamina III.
This interneuron inhib...
Pain projection
neurone
‘Opening the gate’
1. Activity in the C
fibres is higher than
activity in A-beta
fibres
2. This ac...
‘Closing the gate’
Pain projection
neurone
1. Activity in the A-
beta fibres is higher
than C fibres
2. This activates the...
Descending analgesia
 Activated by the spinoreticular tract, as it
synapses at the locus coeruleus, nucleus raphe
and the...
Descending analgesia
Periaqueductal
grey
(midbrain)
ThalamusAmygala
Nucleus rapheLocus coeruleus
Dorsal horn of the spinal...
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Pain

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Pain

  1. 1. PainPain
  2. 2. What is pain? Pain is a sensation that you feel when there is damage to your body Although this applies to normal circumstances, pain can be felt when there is no damage when the mechanism becomes pathological Therefore, pain can be described as nociceptive (in normal situations) or neuropathic (in pathology)
  3. 3. Nociceptive pain  As mentioned before, this is the pain that is felt when there is damage to your body and the pain serves as a mechanism to bring your attention onto the site of injury  The response can then be to limit injury by moving away from the noxious stimulus  If you couldn’t experience pain, you would not be aware of any tissue damage and such individuals die early
  4. 4. Nociceptive pain Brain 1. You stand on a needle which causes tissue damage at the point of impact 2. This information is transmitted to the brain (the transmission is known as nociception), where a sensation of pain is then felt 3. The response is to limit tissue damage by moving your leg away from the needle
  5. 5. Pain transmission  Nociceptive pain is sensed and transmitted by two types of nerve fibres; A-delta and C fibres:  A-delta fibres are myelinated, with a fast conduction velocity and a low threshold for activation i.e. the stimulus doesn’t need to be strong to activate it  In the skin, A-delta fibres terminate as specialized receptors  A-delta fibres can sense mechanical or thermal stimuli i.e. excessive stretching of the skin or extreme temperatures
  6. 6. Pain transmission  C fibres are unmyelinated, with a slow conduction velocity and terminate in the skin as free nerve endings. They have a high threshold for activation i.e. the stimulus needs to be very strong to activate it  C fibres can sense mechanical, thermal and chemical stimuli. There are two types of C fibres:  Peptide-rich  Peptide-poor  The differences between the two types are related to the type of neurotransmitter they release (alongside glutamate) in the spinal cord  For example, peptide-rich C fibres release glutamate and substance P in the spinal cord while peptide-poor C fibres release glutamate and ATP  Another difference is where the two types synapse in the dorsal horn of the spinal cord
  7. 7. Pain transmission  Transmission of pain from the periphery to the brain can be outlined in the following steps: Step 1:  Tissue damage occurs – this can be due to excessive stretch of the skin, extreme temperatures or irritant chemicals SkinThe World Excessive heat damages tissue
  8. 8. Pain transmission Step 2:  The thermal stimulus needs to be converted (transduced) into an electrical signal so that it can be transmitted to the brain  This tranduction is done by specific membrane channels and receptors  For example, heat is sensed by the TRPV1 (capsaicin) receptor, pH is sensed by the ASIC receptor while receptors for inflammatory mediators also play a part (bradykinin, TNF etc)  In this case, the TRPV1 receptor senses the extreme heat and induces a membrane potential in both the A-delta and C fibres
  9. 9. Step 2: TRPV1 TRPV1 Specialised ending of A-delta fibres TRPV1 TRPV1 Free nerve endings of C fibres Impulse towards the brain Peptide rich Peptide poor
  10. 10. Pain transmission Step 2:  A-delta fibres are activated first because of their low threshold and they transmit the impulse as fast as possible to the brain  Therefore, A-delta fibres tell you where the pain is coming from i.e. where the damage is  C-fibres are activated slower (high threshold) and transmit slower because they will allow you to actually feel the pain i.e. generate an emotion (fear, anxiety etc)  It is essential that A-delta fibres are activated first because it is more important to know that there is pain, and where it’s coming from so that you can produce a response  Feeling emotional can come after the danger has been removed
  11. 11. Pain transmission Step 3: The impulses travel along the axons of both A-delta and C fibres towards the spinal cord In the spinal cord, they have their own separate point of synapse
  12. 12. Step 3: 1. A-delta fibres enter the dorsal horn and synapse in lamina I 2. Neurones from lamina I cross the midline via the anterior white commissure 3. These neurons enter the contralateral side and go up the cord in the spinothalamic tract, to the thalamus. In the thalamus, they synapse in the ventroposterolateral nucleus Thalamus Primary somatosensory cortex 4. From the thalamus, they travel to the somatosensory cortex, where the location and intensity of the pain become known
  13. 13. Step 3: C fibres (both peptide-rich and peptide-poor) enter the dorsal horn and immediately travel in Lissauer’s tract to 1-2 spinal segments above the level of entry For example, if C fibres enter at L4, they would ascend up Lissauer’s tract and synapse in L2
  14. 14. Step 3: 1. C fibres ascend up Lissauer’s tract 2. Peptide-rich C fibres synapse in lamina I 3. The majority of these peptide-rich C fibres cross the mid-line and ascend in the dorsolateral funiculus, as the spinoparabrachial tract Pons 4. They synapse in the lateral parabrachial nucleus, in the pons Hypothalamus Amygdala 5. From the pons, they go to the hypothalamus and the amygdala. This tract is responsible for the emotional response to pain
  15. 15. Step 3: 1. C fibres ascend up Lissauer’s tract 2. Peptide-poor C fibres synapse on interneurons in lamina II 3. The interneurons travel down to lamina V 4. From lamina V, the fibres cross the mid-line and ascend up the spinoreticular tract Medulla Nucleus raphe Locus coeruleus Thalamus 5. Fibres synapse in the reticular formation of the medulla, nucleus raphe and the locus coeruleus 6. Finally, these fibres synapse in the intralaminar nuclei of the thalamus and the cingulate cortex. All these connections activate the descending analgesic pathways Anterior cingulate cortex
  16. 16. Summary of pathways Type of fibre Synapse in the dorsal horn Tract Connections Function A-delta Lamina I Spinothalamic Ventroposterolateral nucleus in the thalamus Localisation of stimulus Peptide- rich C fibre Lamina I Spinoparabrachial Lateral parabrachial nucleus in the pons Emotional aspects Peptide- poor C fibre Lamina II -> Lamina V Spinoreticular Reticular formation, locus coeruleus, nucleus raphe, intralaminar nuclei in the thalamus, anterior cingulate cortex Emotional aspects and descending analgesic activation
  17. 17. Pain modulation  Once pain has been sensed and the danger averted, pain sensation needs to be depressed  This is so that tissue repair can carry on without having to feel pain  Pain modulation occurs at two main sites: 1. In the periphery i.e. gate control 2. From the brain/brainstem i.e. descending analgesic pathways
  18. 18. Gate control  This is a theory that A-beta fibres (which carry sensations other than pain) can control the transmission of pain in the dorsal horn  When the activity of A-beta fibres are high, they stop the transmission of pain (as well as transmitting their own stimulus) – the ‘gate is closed’  When the activity of C fibres are higher than A- beta, they ‘open the gate’ and allow pain transmission to occur
  19. 19. Gate control A-beta fibres synapsing in lamina V Pain projection neurone Interneuron in lamina III. This interneuron inhibits the projection neurone, when A-beta is active C fibres synapsing in lamina I and II C fibres act on inhibitory interneurons This interneuron acts to inhibit the interneuron in lamina III, which has an inhibitory block on the projection neurone
  20. 20. Pain projection neurone ‘Opening the gate’ 1. Activity in the C fibres is higher than activity in A-beta fibres 2. This activates the interneuron in lamina II. This interneuron inhibits the interneuron in lamina III 3. The block on the pain projection neurone is removed Glu Glu Glu GABA or Gly
  21. 21. ‘Closing the gate’ Pain projection neurone 1. Activity in the A- beta fibres is higher than C fibres 2. This activates the interneuron in lamina III. This interneuron inhibits the projection neurone Glu GABA or Gly Glu Glu GABA or Gly
  22. 22. Descending analgesia  Activated by the spinoreticular tract, as it synapses at the locus coeruleus, nucleus raphe and the thalamus  The locus coeruleus inhibits nociceptive fibres with Noradrenaline  Nucleus raphe inhibits nociceptive fibres by using 5-HT and the opioid, Enkephalin  The thalamus and amygdala activate the periaquductal grey, which activates both the locus coeruleus and the nucleus raphe
  23. 23. Descending analgesia Periaqueductal grey (midbrain) ThalamusAmygala Nucleus rapheLocus coeruleus Dorsal horn of the spinal cord 5-HT and EnkephalinNoradrenaline

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