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Somatosensory & pain systems Flashcards

1
Q

What is pain?

A

Derives from POENA(L) & means penalty or punishment = suffering, distress of body or mind

Sensory & emotional, makes u feel bad w the emotional component

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2
Q

Define pain exactly:

A

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

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3
Q

Why does the deifinition of pain mention it resembling pain?

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

A

“Or resembling that associated with” = lots of ppl in pain aren’t actually suffereing from an obvious cuase

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4
Q

Where are our thresholds for pain set (e.g. mechanical or thermal) & why?

A

Series of sensory thresholds that are set just below where the tissue damage would occur

This is a survival mechanism –> bc if the tissue is damaged it may become infected etc

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5
Q

What is nociception?

A

The perception (detection) of noxious events in our environment

Has no emotional component to it, need this to drive the emotional component of pain

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6
Q

What is pain?

A

The “feelings” associated with nociception

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7
Q

What are the 3 things that pain always is?

A
  • Subjective
  • A learned experience
  • UNPLEASANT
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8
Q

What do we mean when we say pain is subjective?

A

Everyone experiences pain differently

e.g. Could be suffereing from severe arthritic damage & be experieincing very little pain while other would experience a lot

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9
Q

What do we mean when we say pain is a learned experience?

A

We need to experience pain thru childhood to learn how to process pain

Pain experiences when you’re younger influence your pain response when ur older

However pain during critical stages in child development can alter developemnt

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10
Q

How can pain during critical stages in child developemnt alter pain reception?

A

Children who go thru surgery when young, have dampened pain reception (e.g. thresholds are higher)

However if they’re re-injured they feel more pain & are more susceptible to chronic pain later in life

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11
Q

What NS in involved in pain?

A

Both the PNS & CNS

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12
Q

What is the overall role of the PNS in pain?

A

Detection of noxious events (nociception) involves the PNS which relays info to the CNS (specifically the spinal dorsal horn)

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13
Q

What is the overall role of the CNS in pain?

A

Interpretation of noxious inputs takes place in the CNS (specifically in the brain)

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14
Q

Is the brain needed for reaction to a painful stimulus?

A

No - brain is for interpretation of noxious info

Reaction to painful stimulus this is not needed –> brain & SC can be seperated

The body will still react as the unconscious reaction does not req the brain but the reaction to how it makes us feel involves the brain

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15
Q

What are nociceptors?

A

Peripheral nerves that detect noxious stimuli

Are activated by intense chemical, thermal or mechanical stimuli

& They feed that info into the dorsal horn of the spinal cord

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16
Q

Where is the ventral & dorsal horn of the SC found?

A

Dorsal = at the top

Ventral = at the bottom

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17
Q

Where does info enter & exit the SC?

A

Dorsal horn = info enters the SC thru here at the top

Ventral horn = reflexes flow out of here at the bottom

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18
Q

What is the main focus/role of the dorsal horn of the SC?

A

Pain & nociception

This is where the sensory info arrives, info is relayed from here up to the brain & the brain in turn sends the info back down the SC, thru to the ventral horn

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19
Q

If the dorsal horn is more/less excited what do you feel?

A

More excited = more pain

Less excited = less pain

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20
Q

How do analgesics work to dampen pain?

A

They dampen excitement in the dorsal horn of the SC

Less excitement = less pain felt

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21
Q

What are the elements of the “pain pathway”?

A
  • Peripheral nociceptors
  • Primary afferent neurons
  • Intrinsic spinal dorsal horn neurons
  • Ascending projection neurons
  • Higher centre neurons
  • Descending neurons

(Works like a circuit)

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22
Q

What are the 3 types of pain reception fibres?

A
  • A-beta fibres
  • A-delta fibres
  • C fibres
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23
Q

How big are A-beta fibres & why is this helpful?

A

Have the largest diameter & are wrapped in lots of myelin, so they conduct quickly by saltatory conduction

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24
Q

What sort of signals so A-beta fibres carry?

A

Transduce & encode info abt light touch, pressure, vibration & some pain

Use these most when interacting with stuff in our environment

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24
Q

What is the stucture of A-delta fibres like?

A

Myelinated like A-beta, but less so

Smaller in diameter than A-beta too

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25
Q

What sort of info do A-delta fibres carry?

A

Convey info such as sharp pain or fast pain, also temp & touch

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25
Q

What is the structure of C-fibres like?

A

Thin & unmelinated

So slower conduction

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26
Q

What are C-fibres activated by?

A

Activated by high threshold info, so high temp & dull pain

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27
Q

What NTs do A-beta & A-delta fibres use?

A

ATP & glutamate ATP

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28
Q

What NTs do C-fibres use?

A

They also use ATP & glutamate like Delta & Beta

However, a subset of C fibres use neuropeptides –> CGRp & substance P

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30
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31
Q

Give an example of an area that uses C fibres for pain

A

Testicles –> these are only activated by C fibres, thats why there is a prolonged aching pain

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31
Q

How does C fibres use of neuropeptides (CGRp & substance P) help their function?

A

CGRp & substance P are slow acting NTs so they hang around for a while

This creates a dull aching pain in the affected area, like when you stub your toe & it hurts for a while after

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32
Q

Where are the 2 terminals of peripheral afferent neurons found?

A

One in dorsal horn in the SC

One in the distal terminal in the target tissue (e.g. in the skin)

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32
Q

How many terminals do peripheral afferent neurons have?

A

2 terminals

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33
Q

Name some of the distal terminals found in the skin (epidermis)

A

Epidemis:
- Free nerve endings

Sub-epidermis
- Meisner corpuscle
- Root hair plexus
- Merkel disks

Dermis:
- Pacinian corpuscle
- Klause’s end bubbles

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43
Q

Describe the pain response that happens when you stub your toe:

A
  • Initially A-beta fibres you feel pain from stubbing ur toe
  • Shortly followed by A-delta fibres which is sharp pain & then a second(ish) later..
  • C fibres will arrive, which is the slow, dull & achy pain
44
Q

What are primary afferent fibres (PAFs)?

A

Are the neurons which innervate our skin, muscle, viscera & bones

45
Q

What are the 3 types of PAFs?

A
  • A-Beta
  • A-Delta
  • C fibres
46
Q

What are the properties of A-delta & C-fibres?

A
  • High threshold
  • Can respond to single or multiple modalities
  • Activation leads to different qualities of pain
  • Have specific transduction channels responding to noxious stimuli
  • Can have both afferent & efferent functions
47
Q

What are the 5 key parts of the spinal cord when looking at pain?

A
  • Dorsal horn
  • Ventral horn
  • Superficial laminae
  • Intermediate laminae
  • Deep lamina
48
Q

What is the superficial laminae in the SC made up of?

A

Pain specific neurons

Pain inputs from c-fibres, A-delta fibres, interneurons & projection fibres that process painful info

(Top 2 layers)

49
Q

What is the intermediate laminae in the SC made up of?

A

Touch specific neurons

Receive input from A-beta fibres so process tocuh specific innocuous info

(Layers 3&4)

50
Q

What is the deep lamina in the SC made up of?

A

Intergrative neurons

Deepest part of the spinal cord is intergrative - get info from all 3 sensory neurons types

(Layer 5)

51
Q

What appears white & grey in SC stains?

A

White - myelin

Grey - neurons

52
Q

What flows thru white matter in the SC?

A

Neurons that are myelinated carrying info up to brain

53
Q

How many layers (laminae) are there in the grey matter of the SC?

A

We have 10 laminae (layers)

54
Q

What are the 10 laminae in the SC grey matter divided into?

A
  • Superficial laminae (top 2 layers)
  • Intermediate laminae (3&4)
  • Deep lamina (layer 5)
55
Q

What is the spinal cord dorsal horn the site of?

A

It is the first site of processing cociceptive info

56
Q

Describe how the dorsal horn is innervated:

A
  • Peripheral nerves have their cell bodies in the dorsal root ganglia - adjacent to but outside the SC
  • Sensory neurons innervate their target tissue & the dorsal horn of the SC entering via the dorsal root
  • Different types of sensory neurone terminate in different parts of the dorsal horn
57
Q

Why would be lamina 1&2 but also 3&4 be activated during a high magnitude noxious stimulus?

A

Noxious stimulus will activate lamina 1&2

3&4 will be activated too bc pain will also activate the low threshold fibres

High magnitude stimulus will activate all fibre types so you see bigger vol of dorsal horn being activated

58
Q

What happens in the SC when a noxious stimulus is detected?

A
  • PAFs synapse w doersal horn neurons (second order neurons)
  • These are either projection neurones or spinal interneurones
  • Projection neurones convey info to the brain
  • Interneurones relay & intergrate noxious info to projection or motor neurones
59
Q

What is the best way of classifying projection & interneurones?

A

Based on the NTs the neuron releases & other proteins they express (may produce nitric oxidr for example)

(Not best for them to be classified by apperance or electrophysiological properties as they aren’t always consistent or easy to detect)

60
Q

What happens when the PAF arrives at the dorsal horn?

A

When it arrives it will send an axon into the dorsal horn –> but it doesn’t make synaptic connection w just 1 second autoneurone

May contact 1000s of autoneurones –> projections ficate in many ways & make connections in a large vol of dorsal horn tissue

61
Q

Why is there a large amt of substance P found at the top of the dorsal horn?

A

Many C-fibres enter here in the dorsal horn & C-fibres produce lots of substance P

62
Q

What is the receptor for substance P?

A

NK1 receptor

(Neurokinin 1)

63
Q

Where do each of the nociceptors terminate in the laminae of the dorsal horn?

A

A-Delta = I & V

C = II & V

A-Beta = III, IV &V

64
Q

How does nociceptive info get to the brain?

A

Uses projection neurones –> summarises the 3 main concs of neurones that form the spinothalamic tract

65
Q

Where are projection fibres found in the SC?

A

Some in lamina 1, a few in 3&4 & LOTS in lamina 5

66
Q

How do projection neurones work?

A

Their cell bodies are found in the SC but they send axonal projections all the way up to ur brain

67
Q

Where do the projection neurones in the SC send info to & why?

A

The thalamus

It is a relay & distribution centre for all physical info –> makes sure info is sent to the correct bit of the cerebral cortex

68
Q

Where would somatosensory info in the spinothalamic tract go to?

A

Somatosensory info in the spinothalamic tract recieves info from the SC

The part of the thalamus that receives it sends it to e.g. the somatosensory cortex or the anterior cingulate cortex

69
Q

How does pain info flow thru the brain?

A
  • Info arrives in the thalamus
  • It sends info to the primary somatosensory cortex
  • In turn it sends info to the secondary somatosensory cortex (thalamus would also send info directly here too
  • Thalamus also sends info to anterior cingulate cortex & the prefrontal cortex
70
Q

What are the anterior cingulate cortex & the prefrontal cortex involved in?

A

The more conscious perception of emotions of pain (how we feel in the long term)

71
Q

What is the role of spinoparabrachial tract?

A

Another ascending tract - this is the main one involved in the emotion of pain

72
Q

How does the spinoparabrachial tract send emotional info about pain & how is the response generated?

A
  • It sends info from lamina I & lamina II (bits of the dorsal horn that get the pain info)
  • Sends info up to PARABRACHIAL NUCLEUS (has large output to amygdala)
  • AMYGDALA activated when soemthing unpleasant happens, in turn sends info to the BASAL GANGLIA
  • THALAMUS sends info to the INSULA
  • CEREBELLUM is also involved in pain processing (not just coordianting movement)
73
Q

What is the role of the parabrachial nucleus?

A

Not involved in where in my body I’m hurt but how does it make me feel

(Has a large output to the amygdala - involved in fear and aversion)

74
Q

What is the insula?

A

It is an interaction point between sensory & emotional points of pain

It is incredibly important

75
Q

What are the 2 main factors that can affect how much you feel pain?

A
  • Attentional modulation
  • Emotional modulation
76
Q

How does emotional modulation affect the way you feel pain?

A

If u have low mood u will feel pain more intensely that if ur happy

Good mood = less pain

Your emotional brain centres are able to modulate the way you feel pain

77
Q

What is attentional modulation & how does it affect how u feel pain?

A

The attention you pay to the pain affects the way you experience pain

If ur the sort of person that catastrophises things & you worry too much about the pain it will feel worse

If ur distracted pain = less

78
Q

Babies pain perception:

A

Low cortison babies (less stressed babies) feel less pain –> proves this is not just true in adults

Could test cortisol in their saliva

79
Q

Describe the periaqueductal grey (PAG):

A

Midbrain centre involved in descending pain modulation

Involved in sending info back down the SC, not just to do with movement but to do w modulating the excitability of the dorsal horn

80
Q

What is the earliest evidence of the PAG?

A

From Mayer & Price –> they electrically stimulated the PAG of rats

Rats elicited stimulation produced analgesia

Following the noxious stimulus they didn’t try to move away or squeal

They managed to completely remove thier experience of pain

Works the same in humans

81
Q

Why can’t we use electrical stimulation of the PAG as a therapy option for pain?

A

Although it removes our experience of pain when stimulated

The PAG is also invovled in more than jsut pain responses –> involved in many AUTONOMIC proesses
e.g. HR, BP, respiration rate

Can’t be used as a theraputic option

82
Q

Where is the PAG found in ur brain?

A

Lies right in the centre of our brain, next the the periaqueduct & appaears grey, hence the name

83
Q

Name some of the inputs into the PAG:

A

Gets info directly from the SC but also from the;
- Cingulate cortex
- Frontal cortex
- The hippocampus
- Amygdala
- Hypothalamus

84
Q

What is the main role of the PAG?

A

Much like the thalamus is a relay centre for info coming into the brain;

The PAG is a relay centre for info leaving the brain

85
Q

Describe the connectivity of the PAG:

A

PAG intergrates inputs from the limbic forebrain & diencephalon –> w inputs from dorsal horn or SC

Major inputs arise from;
Amygdala, prefrontal cortex (anterior cingulate & insular cortices), nucleus accumbent, hypothalamus, locus coerulus & dorsal horn of SC

86
Q

What can microinjection of opiods or electrically stimulating the amygdala cause?

A

This results in analgesia

Can be reversed by lidocaine injection into the PAG

87
Q

What can happen in you have a stroke occur in ur thalamaus or PAG?

A

Obvious effects such as issues w speech & movement

But it can also cause abonormal processing of pain –> bc the lesions occur in the area of the brain which impacts pain processing

88
Q

What is the dorsal part of the PAG involved in?

A

More autonomic functions

89
Q

What is the ventral part of the PAG involved in?

A

More invovled in pain modulation

90
Q

How does the PAG connect to the SC?

A

PAG controls the dorsal horn Does but does not connect directly to the SC

PAG sends projections to a part of the braintem called the rostral ventral medulla

This sends neuronal projections down to the dorsal horn

91
Q

Where do the specific areas of the PAG project to & how does this relate to their roles?

A
  • Ventrolateral PAG (pain modulation) projects to the rostral ventral medulla (RVM) & to the dorsal lateral & ventrolateral pontine tegmentum
  • Dorsolateral PAG (autonomic functions) projects to the ventrolateral medulla, a region critical for autonomic control
  • Rostral PAG projections also exist particularly to the medial thalamus & orbital frontal cortex - areas involved in ascending nociceptive pathways
92
Q

What is the role of the rostral ventral medulla?

A

Sends projections down the breain stem between the PAG & dorsal horn

93
Q

What recent development has been made on the PAG?

A

Shown recently that specific regions of the PAG recieve input from specific regions of the dorsal horn;

e.g. second order neurones activated by C-fibres projected preferentially to the VL-PAG, whereas larger A fibres projected mainly to the DL/L PAG

94
Q

What is the rostral ventral medulla (RVM)?

A

The rostral part of the ventral medulla

Not a specific brain region like nuclues accumbens or the thalamus –> RVM is an area

AKA the nucleus raphe magnus (NRM)

95
Q

Where does the RVM (NRM) recieve a major input from?

A

The PAG

The RVM then sends projections down to the dorsal horn of the SC

96
Q

What happens if you activate the RVM (NRM)?

A

Activating the RVM can make pain better by inhibiting the excitability of the dorsal horn

(can make pain worse too by facilitating excitability in the dorsal horn)

Brain bidirectionally controls the way we experience pain

97
Q

Name 3 areas that contain opioid peptide transmitters (e.g. enkephalins)?

A
  • PAG
  • NRM (RVM)
  • Dorsal horn
98
Q

What % of the pop suffer from chronic pain?

A

25-30% of the pop in developed countries experience chronic pain

99
Q

Chronic pain = ?

A

NOT USEFUL (maladaptive)

100
Q

Define hyperalgesia:

A

Inc responsiveness to a normally noxious stimulus

If stimulus hurt before it will rlly hurt now

101
Q

Define allodynia:

A

Pain or unpleasant sensation evoked by a normally non-painful stimulation

102
Q

Define spontaneous pain:

A

Pain w no obvious immedaite cause

103
Q

What causes chronic pain?

A

Arises from damage to tissues (inflammation) or nerves

The cause of pain may have gone but the SC is still sending signals of this pain

Physiological properties of the SC ahve undergone change & means pain is felt all the time

(Changes in perception arise thru changes in neuronal properties)

104
Q

Why is spontaneous pain so bad?

A

You can’t escape spontaneous pain, chronic pain makes u miserable & is a vicious cycle:

Can lead to social isolation as the pain in public makes you withdraw, then alongside the physical pain u feel u also feel emotional pain,

e.g. low mood or anxiety, we know when your mood is worse you feel pain more & you also think about the pain all the time (attention to pain).

105
Q

What can be used to treat chrionic pain short term?

A

Opioids (these dampen the pain signals firing in the dorsal horn)

106
Q

Why can opioids only be used short term to treat pain?

A

They become ineffective after a short period of time –> higher dose is needed

This can lead to addiction

107
Q

What are the characteristics of primary hyperalgesia?

A
  • Thermal (heat & cold), and mechanical hyperalgaesia & allodynia
  • Small region surrounding injury
  • Within minutes
  • Peripheral neuronal changes

(Response to a painful stimuli)

108
Q

What are the characteristics of secondary hyperalgesia?

A
  • Mechanical hyperalgesia & allodynia
  • Larger region
  • Within minutes/hours
  • CNS changes
109
Q

Why have we developed the system of secondary hyperalgesia?

A

To protect us from further injury

Our thresholds are lowered in the larger zone so the chances of us being injured further in the primary region is reduced

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