The Somatosensory System: Pain Flashcards

1
Q

What is pain?

A

Pain is a protective sense that protects you from damaging your tissues

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2
Q

How is pain defined?

A

Pain is a response to a sensory input that has the potential to damage your tissue.

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3
Q

What is involved in pain?

A

A combination of sensory (discriminative) and affective (emotional) components.

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4
Q

What is an important note for future doctors regarding pain?

A

Pain is always subjective; never dismiss a patient’s report of pain.

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5
Q

What is nociception?

A

The sensory component of pain alone.

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6
Q

How is pain perceived?

A

A sensory stimulus that has the potential to cause damage activates free nerve endings (nociceptors) found all over the body.

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7
Q

What types of stimuli can activate nociceptors?

A

Blunt force injury, cutting injury, high heat, extreme cold, inflammation, low pH.

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8
Q

What are the two types of nociceptors?

A

Mechanical nociceptors and polymodal nociceptors.

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9
Q

What do mechanical nociceptors respond to?

A

Strong shearing force in skin, causing sharp well-localized pain.

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10
Q

What do polymodal nociceptors respond to?

A

Many stimuli including sharp blows, damaging heat, and chemicals released by damaged tissue, resulting in poorly localized dull burning pain.

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11
Q

What are the common features of primary sensory neurons?

A

All primary afferent fibers are excitatory, their cell body is in the dorsal root ganglion, and they have a single axon that splits.

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12
Q

What is the axon type of mechanical nociceptors?

A

Mechanical nociceptors are found on A-δ (delta) axon fibers.

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13
Q

What is the axon type of polymodal nociceptors?

A

Polymodal nociceptors are found at the end of C axon fibers.

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14
Q

How do A-δ and C fibers differ?

A

A-δ fibers are myelinated and have faster conduction.

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15
Q

What is the result of different conduction rates in A-δ and C fibers?

A

They result in feeling two different types of pain from the same stimulus.

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16
Q

What is first pain?

A

A sharp pain experienced quickly due to A-δ fibers.

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17
Q

What is second pain?

A

A dull, burning pain experienced later due to C fibers.

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18
Q

Where does a primary sensory neuron have its cell body?

A

In the dorsal root ganglion (outside CNS).

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19
Q

Where does a primary sensory neuron synapse in the spinal cord?

A

With a second-order neuron in the substantia gelatinosa (lamina 2 of dorsal horn).

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20
Q

Where do noxious fibers synapse in the dorsal horn?

A

C fibers synapse in lamina 2 and A-δ fibers synapse in lamina 1.

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21
Q

Where do primary afferent neurons providing cutaneous innervation terminate?

A

At lamina I-II.

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22
Q

Where do primary afferent neurons providing visceral innervation terminate?

A

In lamina I, V, X.

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23
Q

What is the consequence of the difference between visceral and cutaneous innervation?

A

It is easier to localize pain from cutaneous sources than from visceral sources.

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24
Q

What neurons make up the majority of the dorsal horn?

A

Local interneurons.

25
What is the function of interneurons in the dorsal horn?
They modulate the activity of projection neurons.
26
What must happen for a pain signal to reach the brain?
The pain signal must overcome inhibition by interneurons.
27
How does a noxious stimulus overcome inhibitory drive of interneurons?
Nociceptor fibers synapse with interneurons to inhibit other inhibitory inputs.
28
How can rubbing a painful area help relieve pain?
It activates non-noxious primary afferent fibers, increasing inhibition and closing the spinal gate.
29
What is the clinical significance of gate control theory?
Increased non-noxious afferent input can provide analgesic effects.
30
Which ascending tract carries pain information to the brain?
The spinothalamic tract (lateral part).
31
Where does pain information end up in the brain?
In the cortex via tertiary neurons and in subcortical areas.
32
When is pain actually perceived?
Pain is perceived once it reaches the brain.
33
When is pain actually perceived?
You only perceive pain when subcortical areas of the brain are activated (pain is perceived at subcortical level, localised in cortical level).
34
Where is the input localised in the brain?
You localise the input at the cortical level at the somatosensory cortex. This occurs to inputs that come from cutaneous afferents.
35
How are the emotions associated with pain added?
You add the emotion associated with the pain through activation of the limbic system – a subcortical region of the brain.
36
How can we see which parts of the brain are activated?
With Functional MRI you can see different parts of the brain that are activated. ## Footnote E.g. we know the cortex is involved in localisation and limbic area is big on emotion.
37
How does the brain stem communicate with the spinal cord?
Brain stem nuclei (rich in opioids) send axons down to the dorsal horn of spinal cord via descending pathways.
38
What are some neurotransmitters released in the dorsal horn of the spinal cord?
In the dorsal horn of the spinal cord we can get release of endogenous opioid: 5-HT (serotonin), noradrenaline, enkephalin from neurones that have cell bodies in the brain stem.
39
What is this descending system involved in preventing pain called?
This is called the Intrinsic Analgesia System. ## Footnote E.g. battlefield injury when soldier stands on land mine and leg is blown off they are capable of getting up, picking up amputated leg and hopping off to hospital without feeling pain.
40
Describe the rate of afferent input in normal physiological pain.
In normal physiological pain (non-facilitated) the sensation of pain is directly proportional to afferent input firing rate.
41
How is chronic pain different from non-facilitated pain?
In Persistent/chronic pain states we see an increased sensitivity to pain.
42
What are the two mechanisms underlying the increase in sensitivity to pain in chronic pain?
Process of peripheral and central sensitisation.
43
What is this change in sensitivity known as?
This is known as neuroplasticity.
44
Define hyperalgesia and allodynia.
HYPERALGESIA: enhanced painful response to a normally painful stimulus. ALLODYNIA: painful response to a normally non-painful stimulus.
45
What are the mechanisms underlying heightened pain?
Process of peripheral and central sensitisation.
46
What is the response to antidromic AP conduction?
In response to antidromic AP conduction you get the release of substances at the peripheral nerve ending called substance P & CGRP.
47
What is the effect of the inflammatory soup on the nerves?
What they do is lower the threshold at which the nerve ending will fire the AP.
48
What are the consequences of this decreased threshold?
Once they have been sensitised however, their thresholds are lowered and they will start firing AP that are at a much lower stimulus threshold.
49
Which nociceptors show sensitisation in response to inflammatory soup?
It is the polymodal nociceptors (C fibres) that show the sensitisation in response to inflammatory soup.
50
What is this sensitisation to inflammatory soup called?
This whole process is called neurogenic inflammation.
51
What type of hyperalgesia does peripheral sensitisation result in?
Primary hyperalgesia: Due to damaged tissue we have a sensitised nerve ending which has got a lower threshold at which it fires AP.
52
How does peripheral sensitisation result in allodynia?
In peripheral sensitisation we have more AP being fired and so more noxious information is going into the SC and you will be feeling more pain as a result.
53
What causes secondary hyperalgesia?
Secondary hyperalgesia is thought to be due to changes happening in CNS.
54
Describe the mechanism of central sensitisation.
Peripheral sensitisation promotes central sensitisation.
55
What neurotransmitters can be found in pre-synaptic nerve?
In the primary afferent nerve ending you can see common things: Glutamate (excitatory NT), Substance P.
56
What receptors are found on second order neurones membrane?
The second order neurone has a number of receptors: AMPA, NMDA, NK-1.
57
What is the excitatory neurotransmitter normally released from primary afferent nerve?
Glutamate is released and it acts on AMPA and NMDA receptors.
58
Describe the signalling between primary and secondary neurone in acute pain.
Normal signalling at a primary afferent synapse in the dorsal horn with a second order neurone – This is called signalling of acute pain (normal).