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Clinical Teaching > Transduction, Transmission, Perception and Modulation of Pain > Flashcards

Transduction, Transmission, Perception and Modulation of Pain Flashcards

1
Q

Which fibres carry immediate fast pain to the CNS?

A

A-delta fibres.

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2
Q

Which fibres carry slow, persisting pain to the CNS?

A

C fibres.

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3
Q

Describe how somatosensory information travels to the somatosensory cortex.

A
  • Primary afferent is the first order neuron and terminates in the spinal cord or the brainstem.
  • Second order neuron projects from here into the thalamus.
  • Third order neuron projects to the cortex.
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4
Q

What are the four stages in the process of experiencing pain?

A
  1. Transduction
  2. Transmission
  3. Modulation
  4. Perception
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5
Q

Decribe A-delta fibres.

A
  • Myelinated
  • Sharp, localised pain
  • Minority of the nociceptors are A-delta fibres
  • Fast conduction (6-30 m/sec)
  • Polymodal (but usually mechanical & thermal)
  • Not usually visceral
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6
Q

Describe C fibres.

A
  • Unmyelinated
  • Dull, throbbing, diffuse pain
  • Majority of nociceptors are C fibres
  • Slow conduction (0.5-2 m/sec)
  • Polymodal
  • C fibres respond to chemical stimulation (inflammatory etc.)
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7
Q

What is transduction of pain?

A
  • Conversion of a noxious stimulus (heat, mechanical, chemical) into an action potential in a nociceptor.
  • Heat - >45°C or <15°​C
  • Chemical - K+, ATP, bradykinin, histamine, substance P
  • Mechanical
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8
Q

Which substances have a sensitising effect on nociceptors?

A
  • Prostanoids
  • Leukotrienes
  • Substance P
  • CGRP
  • Glutamate

They cause hypersensitivity in tissues which have been damaged. E.g. taking a hot shower after having sun burn.

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9
Q

Describe the transmission of pain between the first and second order neurons.

A
  • No single excitatory substance
    • Glutamate
    • Substance P
    • CGRP
  • No single ‘pain receptor’ but glutamate binds to:
    • AMPA
    • NMDA (sleeping during acute pain but important)
    • G-protein coupled receptors
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10
Q

Where do local anaesthetics work?

A

Sodium ion channels.

If you are trying to block sensation the local anaesthetic acts on the ion channels.

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11
Q

Describe the pain pathway

A
  • Normally, an AP comes into the CNS via the dorsal horn and synapses on a second order neuron.
  • The second order neuron crosses over (because the spinothalamic tract crosses over immediately - pain and temperature make me cross).
  • The second ordern neuron ascends to the thalamus.
  • Another synapse happens on the thalamus which sends the third order neuron to the cerebral pathway.
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12
Q

What is the main excitatory substance in the CNS?

A

Glutamate

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13
Q

On what does glutamate act in normal (nociceptive) pain?

A

AMPA receptor

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14
Q

Which substances are at work in chronic pain?

A
  • Glutamate
  • Substance P
  • NMDA receptors are awoken
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15
Q

Why are NMDA receptors important in clinical practice?

A

This is where ketamine acts. Ketamine is an anaesthetic with very significant analgesic properties.

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16
Q

How is pain modulated at the dorsal horn?

A
  • Accentuation of pain by waking of NMDA receptors
  • Descending inhibition (dampening of pain) (3 mechanisms):
    • GABA is the principal inhibitor in the CNS - release.
    • Descending inhibition from periaqueductal gray matter - rostral medulla - dorsal horn.
  • Endogenous opioids
  • Also higher order brain function (distraction)
17
Q

Describe the gate control theory of pain.

A
  • Initial damage to nociceptor fibre (either A-delta or C fibre).
    • So, example, little kid tumbles and hurts knee.
  • Naturally, the response is to ‘rub it better’.
  • This sets up stimulation in the mechanoreceptor fibres (A-beta fibres). These are thickly myelinated so they conduct impulses much faster.
  • This sensation also travels into the dorsal horn and synapses on second order neurons.
  • But, this sensation also synapses on an inhibitory neuron before it reaches the spinal cord and this effectively blocks the transmission of the nociceptor fibre.
18
Q

What is pain perception?

A
  • The end result, where the neuronal activity becomes a conscious experience.
  • Past experience, current situation and understanding all modulate that conscious experience (somatosensory cortex).
  • By focussing all your attention on the pain, it is worsened.
  • Reticular system elicits an autonomic response.
  • Limbic system links perception of pain with mood.
19
Q

Describe the characteristics of visceral pain.

A
  • The receptors on visceral organs tend to be C fibres.
    • These respond to distension and ischaemia.
  • They activate multiple second order neurons (not a 1:1 relationship, therefore there is poor localisation).
  • The C fibres converge on second order neurons which also have input from A-delta fibres from the periphery (somatic body).
    • This results in referred pain due to the convergence.
20
Q

Describe the autonomic response elicited by the reticular system in response to pain.

A
  • Pain causes increased heart rate, increasing blood pressure (these things make the heart work harder).
  • Uncontrolled pain in the thorax making patient unable to take a deep breath in can cause chest infection.
  • Slowing of gut emptying - after trauma if patient has had food you are more likely to aspirate because your gut motility has slowed and the gut had not emptied.
21
Q

What are the associated autonomic symptoms of acute severe pain.

A
  • Sweating
  • Pallor
  • Nausea
  • Tachycardia
  • Hypertension
22
Q

Which groups of patients are more difficult to assess with respect to pain?

A
  • Non-verbal patients
    • Very young children
  • Patients with severe learning difficulties
    • Change in pattern of behaviour
  • Elderly patients
    • Dementia patients can find it difficult to articulate that they have pain.
  • Pain can be seen as an acceptable symptom to present to the GP with but may not be what you actually want to talk about - it is the permission slip to talk about other issues.
23
Q

How do you recognise pain in a patient who won’t tell you that they are in pain?

A
  • Assess:
    • How do they look?
    • How are they behaving?
    • Actively ask
24
Q

How do you assess pain?

A
  • USE SOCRATES
    • Site & radiation
    • Onset & duration
    • Character
    • Associated features
    • Exacerbating & relieving factors
    • Impact of the pain - what does it stop the patient doing?
    • Red flags
    • Co-morbidities
    • Treatment history - compliance, S-E, benefits
    • Psycho-social history & awareness of yellow flags (markers that the acute pain will transition to chronic pain).
25
Q

What are the key factors in pain prevention and preparation?

A
  • Anticipation and simple adjustments
    • RICE - rest, ice, compression, elevation
  • Distraction
  • Education
    • Explain to the patient what is underlying the pain
    • If they think it is cancer pain they focus on it and it becomes worse.
  • Challenge misconceptions
  • Re-branding:
    • “Pain should be too strong a word but you will be tender” - ‘tender’ has positive connotations.
    • “You shouldn’t feel pain but you will feel heavy, heavy pressure”
  • Put the patient in control of the pain - if you know you are going to do something that will hurt a patient, tell them that if it gets too much they can put their hand up and you will stop.
  • Topical anaesthetics - ametop, EMLA
26
Q

What is neuropathic pain?

A
  • “A pain arising as a direct consequence of a lesion or a disease affecting the somatosensory system”.
    • The lesion is in the nervous system.
  • Difficult to describe.
  • Spontaneous & evoked pains
  • Allodynia
    • If you touch or blow on skin, the patient with neuropathic pain might perceive that as neuropathic pain as opposed to light touch.
  • Relatively common (3-18%)
  • Abnormal or unpleasant or unpleasant sensations rather than pain.
  • Challenging to manage.
    • Normal anaesthetic agents (paracetamol, NSAIDs) probably won’t have the same effect.
27
Q

What are the causes of neuropathic pain?

A
  • Traumatic (phantom limb pain)
    • Can be other unpleasant sensations (itch, crawling)
  • Diabetic neuropathy
  • Postherpetic neuralgia
    • Can happen following shingles
  • Trigeminal neuralgia
  • Post-stroke pain
28
Q

What might you find upon examination of a patient with neuropathic pain?

A
  • Changes in colour
  • Vasomotor differences
  • Changes in sweating (profuse) or dryness (dry and thick skin)
  • Oedema
  • Changes in sensation
29
Q

How is neuropathic pain usually managed?

A
  • Tricyclic anti-depressants
  • Anticonvulsants
    • Pregabalin
    • Gabapentin
30
Q

What are the positive phenomena of neuropathic pain?

A
  • Things which are present which are not normally present:
    • Pain without any apparent stimulus
      • Can be continuous
      • Or can happen at random (paroxysmal)
    • Evoked pain
      • Pain from a stimulus that is not normally painful
      • Exaggeration of painful response either in intensity or over a time period (pain resonates and lasts longer than normal relative to the stimulus).
31
Q

What are the negative phenomena associated with neuropathic pain?

A
  • Sensory loss
    • Thermal
    • Vibration
    • Soft touch
32
Q

What is the definition of chronic pain?

A

Pain persisting beyond the usual healing time of the acute injury (3 months is normally the benchmark).

33
Q

Describe the neuroplasticity behind chronic pain.

A
  • There is actually a change in the CNS.
    • There is a retrograde inflammatory at the site of injury; normally when the tissue heals the inflammatory response is dampened. Sometimes it is not.
  • Prolonged inflammatory response results in decreased pain threshold in primary afferents.
  • Increased production of substance P & CGRP.
  • Recruitment of NMDA receptors
    • Wakes up Wide Dynamic Range (WDR) neurones.
      • ‘Wind-up’ phenomenon
  • Spinal cord - changes in gene & receptor expression in DRG & dorsal horn neurons.
34
Q

What are the non-modifiable yellow flags for chronic pain?

A
  • Gender (female)
  • Age
  • Genetic predisposition
  • Lower socio-economic status
  • Occupational factors
  • History of abuse
35
Q

What are the modifiable yellow flags for chronic pain?

A
  • Past experience of pain (that site and others)
  • Anxiety and depression
  • Catastrophising beliefs
  • Surgical approach
36
Q

What is complex regional pain syndrome?

A
  • One example of a neuropathic pain - relatively common. Tends to hapen after trauma.
  • Abnormal sensation
  • Vasomotor change
  • Sudomotor change
  • Motor / trophic change
  • Regionally restricted e.g. hand
  • Disproportionate to the trauma
37
Q

Describe the Budapest criteria.

A
  1. Patients must report continuing pain disproportionate to the trauma.
  2. Patients must report at least one symptom in 3 of the 4 following categories:
    1. Sensory
    2. Vasomotor
    3. Sudomotor / oedema
    4. Motor / trophic
  3. Patients must display one sign in 2 of the categories above.
  4. Signs and symptoms must not be better explained by another diagnosis.

Clinical Teaching (12 decks)

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