Transduction, Transmission, Perception and Modulation of Pain Flashcards
(37 cards)
1
Q
Which fibres carry immediate fast pain to the CNS?
A
A-delta fibres.
2
Q
Which fibres carry slow, persisting pain to the CNS?
A
C fibres.
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.
4
Q
What are the four stages in the process of experiencing pain?
A
- Transduction
- Transmission
- Modulation
- Perception
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
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.)
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
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.
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
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.
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.
12
Q
What is the main excitatory substance in the CNS?
A
Glutamate
13
Q
On what does glutamate act in normal (nociceptive) pain?
A
AMPA receptor
14
Q
Which substances are at work in chronic pain?
A
- Glutamate
- Substance P
- NMDA receptors are awoken
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.
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
What are the key factors in pain prevention and preparation?
* 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
What is neuropathic pain?
* "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
What are the causes of neuropathic pain?
* 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
What might you find upon examination of a patient with neuropathic pain?
* Changes in colour
* Vasomotor differences
* Changes in sweating (profuse) or dryness (dry and thick skin)
* Oedema
* Changes in sensation
29
How is neuropathic pain usually managed?
* Tricyclic anti-depressants
* Anticonvulsants
* Pregabalin
* Gabapentin
30
What are the positive phenomena of neuropathic pain?
* 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
What are the negative phenomena associated with neuropathic pain?
* Sensory loss
* Thermal
* Vibration
* Soft touch
32
What is the definition of chronic pain?
Pain persisting beyond the usual healing time of the acute injury (3 months is normally the benchmark).
33
Describe the neuroplasticity behind chronic pain.
* 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
What are the non-modifiable yellow flags for chronic pain?
* Gender (female)
* Age
* Genetic predisposition
* Lower socio-economic status
* Occupational factors
* History of abuse
35
What are the modifiable yellow flags for chronic pain?
* Past experience of pain (that site and others)
* Anxiety and depression
* Catastrophising beliefs
* Surgical approach
36
What is complex regional pain syndrome?
* 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
Describe the Budapest criteria.
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.
