Psychophysiology of Pain

Question 1

Define hyperalgesia

Answer 1

increased sensitivity following tissue injury

Question 2

Define primary hyperalgesia

Answer 2

local to site of damage

Question 3

Define secondary hyperalgesia

Answer 3

extending to surrounding undamaged areas. inappropriate involvement of mechanosensory fibres

Question 4

Define allodynia

Answer 4

increased sensitivity to non-noxious stimulus

Question 5

Define nociception

Answer 5

name for pain signals

Question 6

What is pain?

Answer 6

An unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential damage

Question 7

What is somatic superficial pain?

Answer 7

It is skin or tissue damage, and is a sharp, fast pain which is localised

Question 8

What is somatic deep pain?

Answer 8

It is deeper skin, muscle, or joint pain, with tissue damage and inflammation. It is burning, itching and aching slow pain and is long-lasting.

Question 9

What is visceral pain?

Answer 9

It is organ pain, with distension, ischemia, inflammation, and it is a dull ache or burning slow pain and often long lasting

Question 10

What is acute pain?

Answer 10

Momentary or severe pain for weeks to months (less than 3 months), which is resolvable, the damage heals, and the pain goes away.

Question 11

What is chronic pain?

Answer 11

Persistent pain which remains despite the healing process, it is long lasting for longer than 3 months.

Question 12

Why do we feel pain?

Answer 12

It is an early warning system which alters us to danger for actual or potential harm.

Question 13

What is the SCN9A gene?

Answer 13

Congenital absence of pain disorder - it is totally immune to pain, no pain signals arrive at the CNS, the ion channels are non-functional and there is a lack of neuronal signalling

Question 14

How do pain signals get to the brain?

Answer 14

The 1st order neuron takes the nociceptor and it gets into the spinothalamic tract. The second order neuron then carries the signals to the thalamus via the spinal cord. Then the third order neuron carries the signal to the sensory cortex.

Question 15

What does the spinothalamic tract feel?

Answer 15

Temperature, pain and crude touch

Question 16

How does the encoding of pain signals work?

Answer 16

Action potentials carry the nociceptors to the spinal cord, then the activators and sensitises are the inflammatory mediators which activate free nerve endings.
Activators = histamine and serotonin
Sensitisers = prostaglandin and bradykinin

Question 17

Explain free nerve ending activation when tissue is damaged.

Answer 17

The tissue is damaged and inflammatory mediators are then released by the tissue. The activators activate the free nerve endings. Prostaglandin can cat as a sensitizer an increased the activation, therefore, the free nerve endings are now acting as nociceptors. The free nerve endings send nociceptive signals to the brain via the spinal cord which creates redness, swelling, heat and pain.

Question 18

What are the consequences of continued damage or infection?

Answer 18

Persistent activation causing free nerve endings to release substance P. Substance P is a powerful vasodilator and mast cell activator. Mast cells then degranulate, causing more activation of free nerve endings and more release of substance P. This causes a peripheral sensitisation and a positive feedback loop.

Question 19

What happens in the spine in the pain pathway?

Answer 19

The 1st order neuron synapses with the 2nd order neurons in the spinothalamic pathway. Action potentials are carried to the spinal cord and ascends the spine to the thalamus.

Question 20

Describe the process of central sensitisation

Answer 20

1st order neuron nociceptive neurons respond to the noxious mechanical or chemical stimuli, when this is activated the neurons release glutamate in the spinal cord. The glutamate activated the 2nd order neuron, which carries the nociceptors via the spinothalamic tract. The glutamate releases AMPA glutamate receptors on the 2nd order neurons which goes into the spinothalamic tract. However, NMDA glutamate receptors are also activated if there are high levels of glutamate. Once the NMDA receptors are activated, they allow calcium ions to enter the 2nd order neuron. The calcium can trigger long term changes in the 2nd order neuron leading to central sensitisation. The 2nd order neurons will respond stronger, so any nociceptors will be amplified before they arrive to the brain, making the pain perception increase.

Question 21

What are the four main types of nociceptor fibre?

Answer 21

Mechanical, thermal and mechanothermal, and polymodal.

Question 22

Explain the fibre group sensation for each type.

Answer 22

Mechanicals fibre group is delta A, and its sensation is sharp, pricking, and fast pain. Thermal and mechanothermal is delta A, and its sensation is slow burning, cold sharp and pricking. Polymodal is fibre group C, and its sensation is hot and burning, cold, mechanical stimuli and slow, deep pain.

Question 23

What are delta A fibre group and C fibre group?

Answer 23

Delta A is myelinated (insulated) and large diameter axons which creates rapid conduction speed. C is unmyelinated (not insulated), and small diameter axons which create slow conduction speed.

Question 24

Explain the indirect spinothalamic pathway

Answer 24

It has slow C fibres, and connects with the limbic system and hypothalamus. It is part of the reticular activating system and is linked to emotional aspects of pain, linked to understanding salience/significance, linked to the memory of pervious painful experiences, and is linked to autonomic responses. It also has poor spatial discrimination.

Question 25

Explain the direct spinothalamic pathway

Answer 25

It has faster A delta fibres, and connects to cortical areas. It has good spatial discrimination and has discriminatory sense of pain sensations. It is where on the body the damage or danger is happening.

Question 26

What is referred pain?

Answer 26

Referred pain is the pain felt in a part of the body other than the actual source of pain signals. For example gallbladder pain may be felt in the shoulder, and heart pain ,au be felt in the left arm.

Question 27

Why do we have referred pain?

Answer 27

Pain and nociception are different phenomena, pain cannot be inferred solely from activity in sensory neurons. Nociception is the warning signal, pain is our brain telling us how important those signals are, or our brain generates the pain experience, therefore ain is individual and subjective.

Question 28

What factors can open the pain gate?

Answer 28

Stress, tension, depression, worry, boredom, lack of activity, feelings of lacking control

Question 29

What factors can close the pain gate?

Answer 29

Relaxation, contentment, happiness, distraction

Question 30

What is the cognitive modulation of pain?

Answer 30

The 4 key psychological factors that can affect pain perception is attention, experience, expectation, perceived threat. This cam amplify or attenuate pain perception.

Question 31

Explain the descending inhibitory pathways.

Answer 31

The spinothalamic tract afferents up the spine to the brain, enkephalins can reduce the incoming nociceptive signals and therefore help reduce the central perception of pain. Neurons in the brain stem send efferent fibres to the spine, and they pass downwards in the spine. Descending modulatory fibres release serotonin and norepinephrine, and powerful endorphins are releases, known as enkephalins. So even if the signals are being generated, they can’t get through.

Question 32

Explain the pain gate theory by Melzack and Wall 1965.

Answer 32

Delta A fibres are mechanosensory and they encode touch sensations, but when activated they can cause enkephalins to be released in the spine, as we know, enkephalins inhibit the transmission of nociceptive signals to the brain. Therefore applications to the pain gate theory is to rub the pain better like massaging and acupuncture.

Question 33

Why do we need pain?

Answer 33

Nociception and pain perception are processes that help us monitor physical threats, potential damage, or actual damage.

Question 34

What is central damage?

Answer 34

A stroke, spinal cord injury, tumour growth centrally, and central inflammation. This links to central sensitisation, and can become pathological

Question 35

What is peripheral damage?

Answer 35

Physical trauma to nerve, degenerative damage, and disease pathologies. Links to peripheral sensitisation and can become pathological

Question 36

What is pathological pain?

Answer 36

Central and peripheral damage are pathological pain that creates neuropathic pain. It is damage to somatosensory system.

Question 37

What are the 4 inflammatory mediators?

Answer 37

Prostaglandin, histamine, serotonin, Potassium ions

Question 38

Define nociception

Answer 38

The neural process of encoding noxious stimuli