Session 6 - Pain Pathways Flashcards Preview

Semester 5 - CNS > Session 6 - Pain Pathways > Flashcards

Flashcards in Session 6 - Pain Pathways Deck (23):
1

What is pain?

A complex, unpleasant awareness of a sensation (modified by experience, expectation, immediate context, culture etc

2

What is the stimulus threshold for pain?

o The range where tissue damage occurs, e.g. temperature activated nociceptive pathways between 44-460C
oThe same in everyone

3

What is pain tolerance?

o Variable reaction to a painful stimulus

4

What modifies pain tolerance? (4)

Environment
Situation
Psychological/Emotional factors
Increases with age

5

Give the four stages of nociception

o Transduction – Activation of Nociceptors by a stimulus
o Transmission – Relay of action potentials along nociceptive fibres to CNS
o Modulation – By other peripheral nerves or CNS mechanisms
o Perception – The interpretation by the brain of the sensation as painful

6

How is nociception activated?

Noxious thermal, chemical or mechanical stimuli can trigger firing of primary afferent fibres through the activation of Nociceptors (pain-specific receptors, mostly polymodal) in the peripheral tissues.

7

How is pain transmitted?

Transmission of pain information from the periphery to the dorsal horn of the spinal cord is via A Fibres (Sharp Stabbing Pain) and C-Fibres (Dull Nagging Pain).

8

How is pain information modulated?

Pain Information can be inhibited or amplified by a combination of local (spinal) neuronal circuits and descending tracts from high brain centres. This constitutes the ‘Gate-Control Mechanism’.

9

How is perception of pain information moderated?

Thalamocortical projections carry information on location, intensity and nature of pain. An emotional response is then made via the limbic system, and a stress response is made via the hypothalamus.

10

Outline the gate control mechanism of pain awareness

o Primary afferent fibres synapse in Lamina I, II and V of spinal cord dorsal horn
o Transmitter peptides are involved in ascending pain pathways
 Substance P, Calcitonin, Bradykinin, Glutamate, Nitric Oxide
o The activity of the dorsal horn relay neurons is modulated by several inhibitory inputs. These include:
 Local inhibitory interneurons, which release opioid peptides
 Descending inhibitory noradrenergic fibres from the locus ceruleus area of the brainstem
 Activated by opioid peptides
 Descending inhibitory serotonergic fibres from the Nucleus Raphe Magnus and Periadueductal grey areas of the brainstem
 Activated by opioid peptides

11

What do visceral receptors respond to?

o Muscle contraction and distension
o Rapid stretching of capsules of viscus organs
o Ischaemia of smooth muscle
o Compression or stretching of ligaments
o Chemical irritation

12

What do visceral receptors not respond to?

o Cutting
o Pinching
o Burning.

13

Why is referred pain felt in an area away from the painful stimulus?

Visceral receptors converge on spinal cord 2nd order neurones shared by somatic nociceptive fibres (lamina V). Therefore the brain perceives the pain as coming from that spinal nerve’s dermatome.

14

How is pain information passed on?

The onward passage of pain information is via the Spinothalamic Tract, to the higher centres of the brain. Here, there is coordination of the cognitive and emotional aspects of pain and control of appropriate reactions.

15

How is pain sensation modulated?

Opioid peptide release in both the spinal cord and brainstem can reduce the activity of the dorsal horn relay neurons and cause analgesia, known as ‘shutting the gate’

16

Define analgesia

Inability to perceive pain when tissue damage is occurring

17

What is local pain modulation?

o Local inhibitory interneurons, which release opioid peptides

18

Where is central pain modulation centred?

Fibres from the Periaqueductal Grey Matter (PAG) of the mid-brain regulate descending pain modulation pathways. The PAG consists of a collection of cells highly sensitive to opiod neuropeptides (enkephalins, endorphins, dynorphin) and direct stimulation of this area can have an analgesic effect.
o Descending inhibitory noradrenergic fibres from the locus ceruleus area of the brainstem
 Activated by opioid peptides
o Descending inhibitory serotonergic fibres from the Nucleus Raphe Magnus and Periadueductal grey areas of the brainstem
 Activated by opioid peptides
 End on cells in the Substantia Gelatinosa, causing the release of Enkephalin, which modulates the activation of ascending pain pathways

19

What happens in damage to the thalamus?

The experience of pain in areas of the body can be due to neural damage to the posterior Thalamus, e.g. by blockage of the posterolateral branch of the posterior cerebral artery.
Symptoms:

20

Give four symptoms of thalamic damage in terms of pain

o Loss of sensation from contralateral side
o Followed by extreme pain, regardless of stimulus type
o Pain is insensitive to opioids (lesion above their point of action)
o Pain is sensitive to anti-epileptic drugs

21

What is phantom limb pain?

Some patients retain sensations (sometimes painful) of their limbs after amputation. The sensations are not responsive to morphine, suggesting they arise centrally.

22

What is peripheral nerve pain?

Arises from peripheral nerve lesions such as in peripheral neuropathy, e.g. in diabetes. This type of pain is normally localised in the territory of the affected nerve.

23

Outline migraine

Migrates cause moderate to severe headaches, associated with nausea, vomiting and photophobia. Patient may perceive an aura prior to onset, a visual, sensory, language or motor disturbance. The pain is central, as it is unresponsive to morphine.