Pain

Question 1

Definition of pain

Answer 1

The sensory and emotional experience associated with actual tissue damage.

Question 2

Pain threshold

Answer 2

The point at which a stimulus is perceived as pain

Question 3

Pain tolerance

Answer 3

The duration or intensity of pain one can tolerate before the start of overt pain responses

Question 4

What is nociception and what can be said about nociceptors

Answer 4

Nociception is the sensory process of detecting tissue damage

Nociceptors: Free nerve endings of primary sensory neurons, afferent Adelta and C fibres. Located throughout the body and react to mechanical, chemical (excitatory NT’s, ischaemia, toxins) and thermal stimuli. Have a high threshold

Question 5

What are the four main processes involved in nociception?

Answer 5

Transduction (conversion of pain t electrical signals by receptors), transmission, perception and modulation

Question 6

C fibres vs A-delta fibres

Answer 6

C-fibres: most numerous, small diameter, unmyelinated (slow). Are polymodal. Pain is diffuse, dull, aching. Slow pain.

A-delta: medium diameter, myelinated. React to mechano-thermal stimuli. Well localised sharp fast pain

Question 7

Transduction

Answer 7

The conversion of painful stimuli to electrical signals.

Question 8

Transmission

Answer 8

Composed of electrical (AP’s) and chemical (NT) transmission.

Primary afferent to dorsal horn to brain stem to thalamus to sensory cortex

Question 9

What are the two main classes of dorsal horn cells in relation to pain

Answer 9

1) Nociceptive specific in lamina’s 1 and 2. Activated by only noxious stimuli. A-delta and C
2) wide dynamic range in lamina 5. Activated by nociceptive and innocuous (touch), A-delta, C and A beta

Question 10

What are the two divisions of the spinothalamic tract?

Answer 10

Neo-spinothalamic: Typically A-delta afferents (lamina 1) runs to PCG where pain is perceived

Paleo-spinothalamic: Typically C fibres, lamina 2 and 3, and takes info to reticular formation and limbic system. emotional part of pain

Question 11

How is pain perceived?

Answer 11

Reticular formation: autonomic response and motor response
Limbic: emotional response
Somatosensory: interpretation of the pain

Question 12

What is the transmitted signal liable to?

N.b a lot occurs in the dorsal horn

Answer 12

Dampening and amplificaton

Question 13

How can pain be dampened?

Answer 13

• By segmental inhibition

- Descending inhibitory nerves

Question 14

What is the gate control theory of pain (pain dampening)
premise
Three variables
Mechanism

Answer 14

• Based on the premise of a ‘gate’ in the dorsal horn modulating afferent nerve impulses.
• A-delta and C fibres open the gate; A-beta of light touch close the gate; brain messages can open or close gate
• Inhibitory interneurons in the dorsal horn keep gate closed by producing enkephalin (opiate like), stopping signals from A-delta and C fibres. The interneurons are stimulated by A-Beta fibres of touch, and descending inibitory information

E.g rub forehead when sore

Question 15

Detail of descending inhibitory information

Answer 15

When pain signals pass through the midbrain, the periaqueductal area is stimulated causing neurons in the locus ceruleus(pons) and nucleus raphe magnus to transmit fibres to these interneurons and release serotonin or noradrenaline

Question 16

Pain amplification and Windup (hypersensitivity)

Answer 16

Windup is the process of increased AP output from dorsal horn cells due to sustained low input from C fibres

Excessive calcium influx, lowering receptor threshold

Question 17

Nociceptive pain

Answer 17

Tissue damage, opioid sensitive

Question 18

Neuropathic pain

Answer 18

Damage to nerve fibres themselves. Opioid resistant.

Sensitive to membrane stabilisers (gabapentin, carbamazepine) ; tricyclics; spinal cord stimulators

Question 19

Types of neuropathic pain

Answer 19

Peripheral: e.g diabetic neuropathy, trigeminal neuralgia. Described as burning tingling stinging

Central: spinal cord damage, thalamic pain syndrome

Question 20

Complex regional pain syndrome

Answer 20

Can occur following injury major or minor, causing severe debilitating pain. Sympathetic NS also affected so abnormal circulation and increased temp. Loss of function

Question 21

Inflammatory pain

divided into?

Answer 21

Post trauma pain associated with tissue damage and inflammatory mediators.

Neurogenic inflammation: release of neuropeptides from nerves C fibres (substance P etc). Axon reflex, cause more inflammatory mediator release (Primary hyperlagesia) and cause oedema and dilation. Can eventually cause WINDUP or central sensitisation (secondary hyperalgesia)

Non neurogenic inflammation: release of inflammatory substances from vessels and CT. peripheral sensitisation, primary hyperlagesia.

Both contribute to hyperalgesia (lowering pain threshold)

Question 22

Primary and secondary hyperalgesia

Answer 22

Primary is peripheral sensitisation by inflammatory mediators lowering the pain threshold of the receptors.

Secondary is windup when afferents are constantly being stimulated so dorsal horn cells fire more, lower threshold due to excessive calcium

Question 23

Chronic pain mechanism

Answer 23

Constant pain stimulation at dorsal horn causes excess NT to affect glial cells in the dorsal root. They release cytokines.
Causes more NT release. Can change physiology such that pain signal is generated in dorsal horn due to vicious circle

Associated with depression and bad sleep etc