Pain

Question 1

Why do we need pain?

Answer 1

• Without it we would be unaware of minor injuries

- Minor injuries could become infected resulting in loss of finger etc

Question 2

How does pain differ from classical senses?

Answer 2

It is both a discriminative sensation and a graded motivation

Question 3

Specificity theory

Answer 3

Pain is a distinct sensation, detected by and transmitted by specific receptors and pathways to distinct pain ares of the brain

Question 4

Convergence theory

Answer 4

Pain is an integrated plastic state represented by a pattern of convergent somatosensory activity within a distributed network

Question 5

What is a nociceptor?

Answer 5

A sensory receptor for painful stimuli

Question 6

How are nociceptors classified?

Answer 6

According to activating stimulus, fibre-type and conduction velocity

Question 7

Nociceptors are a subset of?

Answer 7

Afferents with free nerve endings

Question 8

Fast pain

Answer 8

First pain, sharp and intermediate

Can be mimicked by direct stimulation of A-delta fibre nociceptors

Question 9

Slow pain

Answer 9

Second, more delayed, diffuse and longer-lasting

Mimicked by stimulation of C fibre nociceptors

Question 10

Hyperalgesia

Answer 10

Increased response to a painful stimulus

Question 11

Allodynia

Answer 11

Painful response to a normally innocuous stimulus

Question 12

Peripheral effects of inflammatory response

Answer 12

• Tissue damage releases inflammatory substances which affect nerve function
• Prostaglandins lower threshold for action potential
• Lowered nociceptor threshold heightens pain in hyperalgesia

Question 13

Central sensitisation

Answer 13

• Local release of prostaglandins from nociceptive dorsal horn neurons
• Lower threshold for action potential - hyperalgesia
• Neurons also become sensitive to non-nociceptive inputs
• Normally innocuous stimuli perceived as painful - allodynia

Question 14

Hyperpathia

Answer 14

• Variant of hyperalgesia and allodynia, underlying causes different
• Results when there is fibre/axonal loss (central or peripheral)
• Raising of detection threshold (greater stimulation before detected)
• When detection threshold is exceeded, subsequent excitability is much greater - patients report explosive pain

Question 15

Phantom limb pain

Answer 15

• After amputation, patients have illusion that limb is still present
• Central representation of the body persists in the absence of peripheral input
• Attempts to block pain pathways usually fail, this pain may also be centrally represented
• Pain may be a representation of what we expect pain to be

Question 16

Why may children born without limbs experience phantoms?

Answer 16

Central maps may be partly pre-formed in the womb

Question 17

Referred pain

Answer 17

• Pain due to damage in the viscera is often perceived as coming from specific locations according to what organ is affected
• Heart attack often left shoulder/arm pain
• Thought to reflect convergence of visceral afferents onto similar pathways as cutaneous afferents in the CNS
• Useful in aiding clinical diagnosis

Question 18

Perception of pain varies according to its context

Answer 18

• WWII soldiers with severe wounds experienced little/no pain
• Indian fakirs demonstrate mind over matter when walking on fire
• Suggestion that pain will be relieved results in pain relief - placebo effect
• Mechanisms exist to overcome even severe pain

Question 19

Physiological basis of pain modulation

Answer 19

• Stimulation of periaqueductal grey activated brainstem nuclei that modulate activity of dorsal horn neurons
• Descending inputs in dorsal horn activate enkephalin-releasing interneurons which presynaptically inhibit nociceptive fibres
• Enkephalins are members of endogenous opioid peptides that includes endorphins and dynorphins

Question 20

Modulation may appear locally

Answer 20

• Rubbing an injury often relieves pain

- Due to local inhibition by mechanoreceptors (AB fibres) of nociceptive (C fibre) inputs in the spinal cord