The Physiology of Pain Flashcards
What is pain?
What does it trigger?
- A mental process, serving as an essential warning system
- Emotional and behavioural responses
Nociceptors:
What are they? What path do they take?
What are the 2 types of nociceptive fibres?
Aδ fibres:
What type of pain does it signal?
What type of axons does it have?
What are they sensitive to?
Which neurotransmitter is used?
C fibres:
What type of pain does it signal?
What type of axons does it have?
What are they sensitive to?
Which neurotransmitter is used?
- Somatosensory primary afferents; peripheral endings are the
sensory receptors, cell body in dorsal root ganglion, and synapses in dorsal horn - Aδ fibres, C fibres
- IMMEDIATE, SHARP 1st pain
- Myelinated, Thck
- Mechanical trauma, Noxious heat
- Glutamate
- DELAYED, ACHING 2nd pain
- Unmyelinated, Thin
- Mechanical trauma, Noxious heat/cold, INFLAMMATION
- Substance P (as well as others)
Sensory responses:
Which pathways does it use?
Where does this pain pathway go?
What does it do/allow one to know?
What does electrical stimulation of the SS cortex cause?
What does electrical stimulation of VPN cause?
What occurs with a Primary SS Lesion?
- Lateral Pain Pathways
- Synapse and ascend in the anterolateral tract of spinal cord, to the thalamic VPN, before ending at a primary SS area
- Awareness; What the pain is, Where it is, What does it mean, What to do
- Localised sensation felt over area stimulated
- Localised “sharp/hot/electric” pain
- Loss of sensation in the affected area
Emotional/Behavioural:
Which pathways does it use?
What do the nociceptors trigger?
Where does this pain pathway go?
Which centres in the brain receive these nociceptor inputs?
What does electrical stimulation of the medial thalamus cause?
What occurs with a Primary SS Lesion?
- Medial Pain Pathways
- Sympathetic NS, and triggers effective, preventative, and recuperative responses
- Synapse and ascend in the anterolateral tract of spinal cord, to non-specific thalamic nuclei, before either ending in the anterior cingulate or insular cortex’s
- Modulatory and autonomic control centres
- Unpleasant feeling, yet HARD TO DESCRIBE
- Loss of sensation, but still an unpleasant feeling
How does referred pain work?
- Pain afferents from organ enter spinal cord dorsally and synapse with afferents that innervate specific areas of skin (dermatomes); dermatomal afferents then send info to the brain
What can descending control of pain lead to?
Which pathway is used?
How does it cause Analgesia?
How can it also cause Hyperalgesia?
What can be given directly into the spinal cord to suppress pain? How does it do this?
- Stress-induced Analgesia, Anxiety-induced Hyperalgesia
- Medial Pain Pathway
- RV medulla, DL pontine tegmentum in Midbrain synapse with spinal cord (NA/Serotonin) = Inhibition of Nociceptor system = Analgesia
- Serotonin can also have a stimulatory effect = Hyperalgesia
- Opioids; mimics the NA/Serotonin
What is Nociceptive pain?
What does Inflammatory pain cause?
Why does inflammation cause more pain?
Pathological pain e.g. Diabetic Neuropathy:
What can abnormal activity trigger?
What can abnormal CNS processing of pain lead to?
- Normal pain due to tissue damage
- Hyperalgesia or Allodynia (light touch becomes painful)
- Inflammation depolarises and hypersensitises the Type C nociceptors; release of inflammatory mediators = more pain
- Centrally-mediated hypersensitivity
- Neurogenic pain = pain w/o apparent cause
Treatment:
What can chronic pain often lead to? How can this be treated? How does the treatment affect the descending control?
What else can be given for the anxiety felt? How does this affect pain pathways?
What else can be given? How do they work?
- Depression; treated with Antidepressant - reduce pain by improving mood and coping ability
o But, these also ↑transmission in the descending anti-nociceptive pathways - Benzodiazepines (anxiolytics)
o But, these also ↓activity in pain pathways by enhancing spinal cord inhibition - Anticonvulsants; block high frequency AP firing during seizures, ↓NT release at potentiated synapses
