Lecture 14- Pain

Question 1

What is pain?

Answer 1

-“An unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential tissue damage.”

Is context dependent

Question 2

What are the three types of pain recognized?

Answer 2

-Acute: arises suddenly and has a specific cause, resolves quickly
-Chronic: long-term (months) pain that persists long after the
original stimulus has subsided
-Intermittent: pain that comes and goes

Question 3

What receptors are the ‘pain receptors’?

Answer 3

Nociceptors

Question 4

What is the purpose of feeling pain?

Answer 4

Alerts us that something is wrong so we can seek attention/ help or change our behaviour to prevent tissue damage. It serves as a learning tool.

Question 5

What congenital disease is associated with a lack of pain sensation?

Answer 5

• CIPA= Congenital Insensitivity to Pain with Anhidrosis
• Caused by mutation in a gene that codes for a nerve growth factor receptor, resulting in developmental failure of a subset of sensory and autonomic nerves (nociceptors)
• Absence of pain leads to repeated self mutilation and injuries

Question 6

Where are nociceptors found?

Answer 6

• Widespread, esp. in skin, joints, muscles, viscera
• Absent from brain!
• Usually free nerve endings of primary sensory neurons

Question 7

What are the three main classes of Nociceptors + How they are activated?

Answer 7

• Thermal: activated by high (>45C) and low (<5C) temps
• Mechanical: activated by intense pressure
• Polymodal: activated by high intensity mechanical, thermal, or chemical stimuli

Question 8

Which of the types of nociceptors are thinly myelinated and what is the consequence of this?

Answer 8

• Thermo & mechanoreceptors (A6 fibers)

- Signal acute onset

Question 9

Which of the types of nociceptors are unmyelinated and what is the consequence of this?

Answer 9

• Polymodal receptors (C fibres)

- Signal ongoing slow dull pain

Question 10

Which of the three ascending pathways to the brain are nociceptors/ pain sensation associated with?

Answer 10

The spinothalamic tract/ anterolateral pathway

Question 11

What is hyperalgesia?

Answer 11

Persistent or enhanced pain sensation often due to inflammation and release of chemicals from damage site

Question 12

What is allodynia?

Answer 12

Pain in response to innocuous sensory stimuli

Question 13

In hyperalgesia what chemicals activate the nociceptor as a result of tissue damage?

Answer 13

Potassium, Prostaglandin, Serotonin, Bradykinin

Question 14

What does substance P do during hyperalgesia?

Answer 14

• It’s released from nerve endings and increases capillary permeability (contribution to inflammation)
• Also causes mast cells to release histamines which in turn activates the nociceptor endings (to release more substance P). The histamines cause itch

Question 15

What is analgesia?

Answer 15

Selective suppression of pain without effects on consciousness

Question 16

List the three ‘methods’ of analgesia…

Answer 16

• Pain signaling can be ‘gated’ by stimulation of non-pain sensory fibres from the same area
• Pain signaling modulated by descending pathways (endogenous opioids)
• Pharmacological intervention

Question 17

What is the gate control model?

Answer 17

-Pain info, carried by C fibres, activates projection neurons in SC,
signals sent via anterolateral tract to thalamus
-Activation of non-pain sensory fibres from same region (i.e rubbing the area of the wound) activates inhibitory interneurons in dorsal horn, reducing output of projection neurons and therefore reducing the intensity of the pain that reaches the brain.

Question 18

What technology did the idea of ‘gating’ lead to?

Answer 18

Therapies such as TENS (Trans Epidermal Nerve Stimulation)

Question 19

How does pain inhibition work via the descending pathways?

Answer 19

Works to inhibit the nociceptor/ C-fiber reducing the activation of the dorsal horn projection neuron and resulting in decreased sensation in the brain

Question 20

What do endogenous opiates interact with and what is the result of this?

Answer 20

• Opiate receptors in CNS

- These inhibit pain signaling (previous card)

Question 21

How are prostaglandins invovled in pain relief?

Answer 21

-Major strategy is to inhibit cyclooxygenase enzymes to reduce
prostaglandin synthesis
-Limiting the amount of prostaglandin produced has pain- suppression effects both at site of injury and in sensory neurons in DRG and CNS

Question 22

Can we usually localize pain?

Answer 22

• Normally specific somatotopic mapping of sensory input (including pain) from the body onto somatosensory cortex means we can normally localize the origin of somatic sensations accurately.
• However, many spinothalamic tract neurons also receive input from nociceptors in muscle, joints, or viscera. In these cases it can be hard to distinguish the source of the pain

Question 23

What is it called when the origin of the pain is wrongly identified?

Answer 23

Referred pain: the brain can’t tell where the source of the pain came from so it ‘refers’ it to the most common site of stimulation (skin)

Question 24

If the brain as no pain receptors how come we get headaches?

Answer 24

Intracranial & head tissues (meninges, blood vessels, head & neck muscles, eyes, ears, teeth, mouth) do have pain receptors (not localizing pain correctly?)

Question 25

What are phantom pains?

Answer 25

-Pain felt in a region that no longer exists (amputated limb)

Question 26

What are the two causes of phantom pains?

Answer 26

1. Ongoing activity of nerves that used to lead to that part of the body
2. Invasions of cortical representation for that part of the body by intact body regions e.g. touch face but it feels like it came from the hand as neurons from face have spread into hand region in brain