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Neurophysiology > Pain > Flashcards

Pain Flashcards

1
Q

What is pain

A

An unpleasant sensory or emotional experience associated with actual or perceived tissue damage- a product of higher brain processing

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2
Q

What is congenital insensitivity to pain

A

Don’t feel pain, can easily injure yourself

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3
Q

What can cause congenital insensitivity to pain

A

Na+ channel mutation, nerve growth factor mutations, overexpression of opiods

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4
Q

Congenital insensitivity to pain- Na+ channel mutation

A

Mutations in the voltage-gated Na+ channel in pain afferent neurons, means info about noxious stimuli is not transmitted

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5
Q

Congenital insensitivity to pain- nerve growth factor mutations

A

Mutations in NRTK1, the nerve growth factor necessary for the growth and survival of nociceptive neurons

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6
Q

Congenital insensitivity to pain- opiods

A

Overexpression of opioids, the brain’s natural pain relief

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7
Q

How does congenital insensitivity to pain suggest pain and touch pathway are separate

A

Sensation of touch is normal in these disorders

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8
Q

What are the 3 main types of nociceptors

A

Adelta mechanosensitive, Adelta mechanothermal, and C fibre polymodal receptors

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9
Q

What sort of structure do Adelta and C fibres have

A

Free nerve endings, thin, Adelta is slightly wider and myelinated

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10
Q

What types of temp do Adelta and C fibres detect

A

Adelta- cold thermoreceptors

C fibres- warmth receptors

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11
Q

What sort of touch and pressure do Adelta’s free nerve endings detect

A

Crude touch- we’d only be aware of it if our dorsal columns were damaged

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12
Q

What are nociceptors

A

Sensory receptors that respond to dangerously intense stimuli to signal that tissue is at risk of being damaged

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13
Q

What is the threshold of nociceptors

A

High thresholds of stimulation

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14
Q

What is the receptive field size of nociceptors

A

Large receptive fields

A delta < C fibres

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15
Q

What neurotranmitters do Adelta and C fibres release at the first synapse

A

Adelta- glutamate

G fibres- glutamate and substance P

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16
Q

What is the consequence of the large receptive field sizr of nociceptors

A

Make fine localisation difficult, but this isn’t really necessary, more important you feel the pain

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17
Q

What stimulation do Adelta mechanothermal nociceptors respond to

A

Dangerously intense thermal stimulation

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18
Q

What stimulation do Adelta mechanosensitive nociceptors respond to

A

Dangerously intense mechanical stimulation

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19
Q

What do C fibre polymodal receptors respond to

A

Have lots of receptors that bind to different ligands produced in tissue injury, and report back using EPSPs from all the different ligands present

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20
Q

Where do the nociceptors first synapse

A

Substantia gelatinosa in spinal cord

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21
Q

What is substance P

A

Neuropeptide, no obvious clearance mechanism so hangs around a lot longer, can cause prolonged depolarisation when they bind to the NK1 receptor AKA hyperalgesia

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22
Q

What is the result of the different fibres having different conductino speeds

A

First pain- sharp, brief better-localised pain (Adelta)

Second pain- duller, poorly -localised long-lasting pain with a burning quality (C fibre)

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23
Q

How can we isolate the effect of Adelta vs C fibres

A

Can selectively block either pharmacologically, can separately stimulate each fibre to elicit 1st vs 2nd pain

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24
Q

Experimental demonstration that nociception involves specialised neurons NOT greater discharge of neurons that respond to normal stimulus intensity

A

Applying increasing heat to a hand gradually increases firing rate of thermoreceptors, but thermosensitive nociceptors only become active when the heat becomes noxious (45degC), at which point the normal thermoreceptors are at max rate

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25
Q

How do we know where pain comes from

A

By the location the fibres enter the spinal cord, the nerves the info is sent in, the separate pathways for different fibres despite them mixing together in the same nerve

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26
Q

How does pain in the face and neck differ from in the rest of the body

A

The face and neck take a different path to the thalamus

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27
Q

What do second-order neurons go from the substantia gelatinso

A

Decussate and enter the anterolateral quadrant, then travel up the spinothalamic tract contralaterally

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28
Q

What happens to the 3rd neuron in the pain pathway

A

Neuron sends info from the thalamus to the somatosensory cortex

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29
Q

How are the pain and touch relays similar despite being completely separate pathways

A

Pain and touch are both 3 neuron relays with 2 synapses

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30
Q

What is referred pain

A

Pain detected by nociceptors in internal organs is often sensed on the surface of the body

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31
Q

What is a possible explanation of referred pain

A

Nociceptors from several locations converge on a single ascending tract- since pain signals are more common than pain from internal organs, the brain associates activation of the pathway with pain in the skin (McGraw Hill 1987)

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32
Q

What is Brown-sequard hemiplegia

A

Lateral hemisection of the spinal cord- loss of motor function and touch on the same side as the injury, loss of pain sensation on the opposite side to injury

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33
Q

What does Brown-sequard hemiplegia demonstrate

A

Touch is carried on the same side as it is detected, whereas pain info crosses over and is carried on the opposite side of the body

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34
Q

What are the main ascending pathways for pain

A

Spinothalamic tract (MAIN), spinoreticular tract, spinotectal tract

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35
Q

What is the main descending pathway for pain

A

Spinomesencephalic

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36
Q

What does the spinothalamic tract do

A

Important in localisation of painful or thermal stimuli- principal ascending pathway

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37
Q

What does the spinoreticular tract do

A

Causes alertness in response to painful stimuli

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38
Q

What does the spinotectal tract do

A

Orients eyes/head towards stimuli

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39
Q

What does the spinomesencephalic tract do

A

Important in descending modulation- main descending pathway

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40
Q

How have we identified the pain matrix

A

Scientists give people painful stimuli and see which parts of the brain light up- very many areas!

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41
Q

Why does the pain matrix involve so many brain areas

A

Due to evolutionary importance of pain

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42
Q

What do polymodal C pain fibres do instead of adapting to stimuli

A

They become sensitised to subsequent pain- for a lower stimulus intensity we get a greater pain intensity pain perception

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43
Q

What is allodynia

A

When we experience pain from normal touch, well before normal pain response would be generated eg putting on clothes

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44
Q

What can cause hyperalgesia in C fibres

A

Sensitisation of the peripheral nerve endings or at the first/second synapse as info travels to the brain

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45
Q

What is hyperalgesia

A

increased amount of pain associated with a mildly noxious stimulus

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46
Q

What 2 differently located effects does hyperalgesia involve

A

Sensitisation of peripheral nociceptive nerve terminals

Central faciliation of transmission aka ‘wind up’

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47
Q

What do C fibres have receptors for

A

eg bradykinin, serotonin, ATP, H+ released in response to tissue injury

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48
Q

Peripheral hyperalgesia- what transmission occurs as a result of mediators released by injured tisse binding to C fibres

A

Generated EPSPs on each C fibre summate to form APs that go up into the spinal cord and down the many branches of C fibres

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49
Q

Peripheral hyperalgesia- what is the result of APs being sent down lots of C fibre branches

A

Neurotransmitters stored in these branches eg substance P and CGRP are released at the nerve ending

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50
Q

Peripheral hyperalgesia-What is the effect of neurotransmitters eg substance P and CGRP released by the nerve endings

A

They act on mast cells and cause them to release histamines, and act on blood vessels to make more blood come to the damaged tissue area and make them leaky

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51
Q

Peripheral hyperalgesia- what is the result of mast cells releasing histamines and increased leaky blood flow

A

NEUROGENIC INFLAMAMTION
Histamines sensitize polymodal C fibres
Swelling and reddening, allowing the area to fight damage and infection

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52
Q

Peripheral hyperalgesia- why can pain be felt over large distances of the body

A

Mediators released by the injured tissue can diffuse to non-injured areas, and CGRP and substance P can be released at sites distance from the injury since the C fibres are so branches

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53
Q

What is the protective function of pain being felt over long distances away from the injury

A

Forces you to protect the tissue and prevent further damage

54
Q

What is central hyperalgesia

A

Central sensitisation to pain by facilitation of pain transmission particularly in extended pain states eg chronic pain, aka ‘wind up’

55
Q

Why is central hyperalgesia/chronic pain bad

A

Untreated pain becomes worse, no longer helpful as an illness signal

56
Q

Where does central hyperalgesia occur

A

In the dorsal horn of the spinal cord (1st synapse), in the thalamus (2nd synapse)

57
Q

What is central hyperalgesia a form of

A

Neuronal plasticity

58
Q

Central hyperalgesia- what happens in terms of receptors under low levels of stimulation

A

Glutamate binds to AMPA receptors and signals pain to the brain
NMDA receptors bind glutamate but remain inactive due to the Mg2+ block

59
Q

Central hyperalgesia- what happens under repetitive stimulation

A

C fibres fire repeatedly, causing the release of glutamate AND substance P (which binds to NK1 receptors) causing slow prolonged depolarisation

60
Q

Central hyperalgesia- what is activated as a result of prolonged depolariation due to substance P

A

NMDA receptors (coincidence receptors) are activated as glutamate is bound AND depolarisation has removed the Mg+ block

61
Q

Central hyperalgesia- what is the result of NMDA receptors opening

A

Influx of Na+ down its conc gradient, but more importantly Ca2+ which activates calmodulin kinase and protein kinase C

62
Q

Central hyperalgesia- what is the result of activation of calmodulin kinase and protein kinase C

A

Phosphorylation/transcription/insertion of AMPA receptors, increasing sensitivity to glutamate
The whole process is a loop, causing hyperexcitability of nociceptive receptors after severe or persistent injury

63
Q

Central hyperalgesia- what is the effect of NK1 antagonists in animals

A

Have tried to reduce wind up in animals, reducing the chance NMDA will open to allow Ca2+ in, but these haven’t translated well to humans

64
Q

Central hyperalgesia- how can chronic pain be treated?

A

By giving NK1, NMDA or AMPA antagonists- however, these can cause side effects eg blockage of NMDA receptors can cause memory loss as the receptor is involved in memory

65
Q

Pain medications for inflammatory pain- what are NSAIDS

A

Non-steroidal anti-inflammatory drugs

eg can reduce prostoglandin (receptor) synthesis to reduce pain

66
Q

Pain medications for inflammatory pain- how do local anaesthetics work

A

Block VGNa+ channels in primary afferent fibres, preventing APs travelling up the spinal cord to create the perception of pain

67
Q

Pain medications for inflammatory pain- how do opiates work

A

Can can hyperpolarisation/IPSP by binding to u receptors to open K+ channels and close Ca2+ channels, reducing the amount of neurotransmitter released

68
Q

What are alternative pain medication examples

A

Acupuncture, TENS machines, deep brain stimulation, antidepressants, hypnosis

69
Q

What is acupuncture

A

Invasive procedure where small needles are inserted below the skin to relieve pain

70
Q

Study into how acupuncture works as pain relief

A

Goldman (2010)- acupuncture causes the release of adenosine that binds to A1R causing analgesia (pain relief)

71
Q

What is TENS

A

Transcutaneous electrical nerve stimulation- delivery of mild electric current through patches attached to the skin

72
Q

How is TENS believed to reduce pain

A

By creating electrical impulses in Abeta fibres, we can affect pain fibres via interneurons that connect the two

73
Q

What are 2 theories of the physiology behind TENS

A

Gating of pain transduction, production of natural endorphins

74
Q

What is the gate theory of pain

A

Melzack and Wall 1960s- Abeta fibre releases glutamate to stimulate an inhibitory neuron in the dorsal horn that releases GABA to cause an IPSP onto the C fibres, reducing their firing

75
Q

Major criticism of the gate theory of pain

A

No concrete evidence that this circuit exists

76
Q

Alternatve theory for gate theory of pain- cortical mechanism

A

Inui et al (2006)- suggests TENS relieves pain by cortical mechanisms with minimal spinal involvement

77
Q

Study supporting alternative theory for gate theory involving cortical mechanisms

A

Inui et al (2006)- using the different speeds of conductinon of Abeta and Adelta fibres, they stimulated them to ensure their signals never passed through the dorsal horn at the same time so the inhibitory circuit could not work- YET Abeta fibres still relieved pain despite only crossing the Adelta fibres in the cortex

78
Q

Examples when our perception of pain is altered

A

Beecher- WW2 soldiers with severe battle wounds experienced no pain
May not notice an injury while playing sports

79
Q

What are opioids

A

Natural pain relievers produced by our body, mimiced by manmade opiate drugs

80
Q

What placebo effect can occur if we think we’ve taken pain relief

A

We produce natural opioids, producing a real effect that can be blocked by opiate receptor antagonists

81
Q

What structures can enable descending modulation of pain

A

Collaterals from the relay neuron go to individual sites in the brain that determine how much pain is perceived
Can affect PAG, NRM, LC, NRPG

82
Q

Descending pain modulation- what is the PAG

A

Periaqueductal grey

83
Q

Descending pain modulation- what is the LC

A

Locus coeruleus

84
Q

Descending pain modulation- what is the NRM

A

Nucleus raphe magnus

85
Q

Descending pain modulation- what is the NRPG

A

Nucleus reticularis paragigantocellularis

86
Q

How does the PAG modulate pain

A

PAG can be stimulated or inhibited by the cortex depending on emotional state, can stimulate the NRM

87
Q

How does the NRM modulate pain

A

NRM can be stimulated by the NRPG or PAG, releases 5HT and enkephalin through dorsal lateral verniculus that comes into the dorsal horn to reduce pain transmission up the relay neuron

88
Q

How does the LC modulate pain

A

LC produces noradrenaline, which can inhibit pain transmission in the dorsal horn

89
Q

Evidence of the PAG being able to reduce pain

A

In animal models, stimulation of the PAG allows painless surgery on animals

90
Q

Where can opioids act in the body to modulate pain

A

Can reducing firing of nociceptive afferent neurons in the periphery, can cause IPSP in dorsal horn, can stimulate NRPG, can stimulate PAG by inhibiting an interneuron that usually inhibits PAG

91
Q

How do opioids have an effect on target areas

A

When opiates bind to a u receptor, they can open K+ channels to cause hyperpolarisation or close VGCa2+ channels to reduce the amount of neurotransmitter produced

92
Q

What is deep brain stimulation used to treat

A 
Chronic neuropathetic (nerve) pain
Successful in 60% of patients halving pain
93
Q

What is deep brain stimulation

A

Electrodes implanted into the brain which send electrical current to stimulate brain areas to relieve pain (eg PAG, thalamus)

94
Q

How is is thought that deep brain stimulation reduces nerve pain

A

Increases levels of opioids, cause release of adeosine, or modify brain circuits to reduce transmission of pain

95
Q

What is the nocebo effect

A

When you feel a stimulus as painful because you expected it to be painful

96
Q

Study showing effect of nocebo effect on pain perception

A

Yoshida et al (2013)- a group who saw ‘participants’ screaming out in pain when touching a hot stimulus reported very high levels of pain when touching the stimulus themselves, compared to a group who just watched a nice film beforehand

97
Q

How can the nocebo effect be caused in pain perception

A

PAG can cause descending FACILIATION of pain rather than inhibition

98
Q

Where is the pain gate that determines how mcuh pain we feel

A

In the substantia gelatinosa of the dorsal horn, at the first synapse between the Ad or C fibres and the relay neuron

99
Q

Examples of factors that close the pain gate

A

Mechanosensitive stimulation, placebo, distraction, opiates, environmental danger etc

100
Q

Examples of factors that open the pain gate

A

Infection, depression, anxiety, nocebo effect, inflammation

101
Q

How is the intensity of pain encoded by the relay neuron

A

Frequency of AP firing

102
Q

What has to happen in the relay neuron for pain to be perceived

A

The relay neuron must reach threshold for an AP to fire to allow perception of pain

103
Q

What may cause phantom limb pain

A

When the severed ends of nerves that believe they are still connected to the limb are abnormally stimulated, causing the sensation of pain in the missing limb- missing limb may feel twisted, contracted etc
Cortical reorganisation

104
Q

What is mirror box therapy for phantom limb pain

A

Individual sees both of their hands as if they’re intact, move the intact hand but look in the mirror so it appears as the severed hand, tricks the brain into thinking the severed arm is no longer bent into the abnormal shape (Ramachandran et al, 2000)

105
Q

What is nociception

A

Refers to the peripheral and CNS processing of info about the internal or external environment, as generated by the activation of nociceptors

106
Q

How are nociception and pain different

A

Pain is the feeling, while nociception is the sensory process that provides signals that trigger pain

107
Q

What does congenital insensitity to pain suggest about the importance of pain

A

Low levels of nociceptive activity are important to tell us when a particular movement/posture is putting too much strain on our body- patients often injure themselves a lot, bite their tongue/lip

108
Q

How are Adelta mechanosensitive receptors activated

A

Mechanically gated ion channels in their membrane are bent by eg stepping on a thumbtack, depolarising the channel and generating APs

109
Q

What effect can proteases released at the site of injury have

A

Proteases can break down extracellular peptide kininogen to form bradykinin, that binds C fibre receptors

110
Q

How does ATP affect the C fibres

A

ATP depolarises receptors by binding directly to ATP-gated channels

111
Q

How are Adelta mechanothermal receptors activated

A

Heat above 43C burns tissues, causing heat-sensitive ion channels to open, leading to depolarisatino and APs

112
Q

Evidence for H+ acting on C fibres

A

Anaerobic metabolism causes a build up of lactic acid leading to an excess of H+ in the extracellular fluid, activating H+ gated ion channels on C fibres, causnig the dull ache associated with exercise

113
Q

Evidence for the role of histamines

A

Creams that contain antihistamines block histamine receptors, reducing pain and swelling

114
Q

What is primary vs secondary hyperalgesia

A

Primary- within area of damaged tissue

Secondary- tissues surrounding the damaged area

115
Q

Peripheral hyperalgesia- how can bradykinin have long-lasting effects

A

Bradykinin makes heat-activated ion channels more sensitive

116
Q

Peripheral hyperalgesia- what are prostaglandins

A

Chemicals generated by the enzymatic breakdown of lipid membrane, that greatly increase the sensitivity of nociceptors to other stimuli

117
Q

How can secondary hyperalgesia interact with CNS mechanisms

A

Following injury, activation of mechanoreceptor Abeta axons by light touch can evoke pain, allowing cross-talk between the touch and pain pathways in the spinal cord

118
Q

What do the pain fibres do before synapsing on cells in the substantia gelatinosa

A

Branch and travel a short distance up and down the zone of Lissauer

119
Q

What add neurotransmitter of the pain afferents appears necessary to experience moderate to intense pain

A

Substance P- stored in storage granules in the axon temrinals, released by high frequency trains of action potentials

120
Q

Example of referred pain

A

Pain in the heart from angina is often reported in the upper chest wall and left arm

121
Q

Which pathway conveys info about pain and temp from the spinal cord to the brain

A

The spinothalamic pathway

122
Q

Where does the second-order neuron synapse

A

The spinal thalamic fibres project through the spinal cord, medulla, pons and midbrain without synapsing until they reach the thalamus

123
Q

Where do the pain and touch pathways get close to each other

A

The pain pathway eventually comes to lie alongside the medial lemniscus, and some spinothalamic axons terminate in the VP nucleus but the two pathways remain distinct (different region of the nucleus)

124
Q

How great a region of the thalamus do the spinothalamic tract/trigeminal lemniscal axons synapse on compared to those of the medial lemniscus (touch pathway)

A

A much wider region- also project over a wider area of the cerebral cortex

125
Q

Which regions of the thalamus do the spinothalamic axons terminate in

A

Ventral posterior nucleus, small intralaminar nuclei of thalamus

126
Q

What is the trigeminal pain pathway

A

Fibres in the trigeminal nerve synapse on second-order sensory neurons in the spinal trigeminal nucleus of the brain, that then cross and ascend in the trigeminal lemniscus to the thalamus

127
Q

What is the role of pain pathways other than the spinothalamic and trigeminothalamic

A

Send axons to a variety of structures at all levels of the brain stem before they reach the thalamus- some important in generating sensatinos of slow, burning pain, while some trigger behavoural arousal and alertness

128
Q

Examples of opioids

A

Morphine, codeine, heroin

129
Q

Evidence of role of endorphins in pain relief

A

Small injections of endorphins into the PAG can produce analgesia by binding to opioid receptors

130
Q

Evidence of role of endorphins in pain relief from a blocker

A

Administering the blocker of opioid receptors, naxolone, blocks the effects of endorphins

Neurophysiology (23 decks)

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