Pain Flashcards
What are the 4 types of pain?
Acute: Post-operative, trauma, medical emergencies, sickle cell crisis
duration less than 3 months
Chronic Back pain, neck pain, vascular, neuropathic pain, headaches, phantom limb pain, complex regional pain syndrome,
visceral - usually trauma or repeated infections
Cancer pain
What are the 7 classes of pain?
Nociceptive - tissue damage - nociceptors
Inflammatory - inflammatory mediators - Peripheral and central sensitization
Neuropathic - nerve injury - Including ectopic activity, neuroimmune int. central sensitization
Mixed
Visceral
Sympathetically maintained
Psychological
See diagram in intro lecture on first page for the pathogens is of pain
-
Is the PAG important in pain pathways?
Very
Page 2 of intro lecture for mood and state of mind diagram
-
Summarise how pain is managed?
Understanding and explaining the mechanisms of pain
Diagnosis of the pain
Investigations
Advice about managing pain on a daily basis
Pacing of activities, goal setting, relaxation, doing something for enjoyment, coping with bad days
Simple pharmacotherapy
Physiotherapy
Summarise specialised pain management
TENS
Acupuncture
Physical therapies
Psychological therapies
Pharmacotherapies
Tricyclic antidepressants, gabapentinoids,
Analgesics, opioids
Topical agents
Combinations
Injections
Trigger point, nerve blocks, epidurals, facet joint injections
Can we test for pain?
No
Read notes on final page of intro lecture
-
What is the intensity theory of pain?
Intensity theory (pain not a unique modality but emotional state produced by stronger than normal stimuli)
What is today’s pain definition?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
How does nociception work?
Noxious stimuli detected by damage-sensing neurons, nociceptors whose specialized free nerve endings are in skin, muscle and viscera and cell bodies in the dorsal root ganglia (DRG);
They respond to multiple types of stimuli (high mechanical pressure, high/low temperatures, chemicals) which will only generate electrical activity if they are over a certain threshold.
Receptors at sensory terminals convert such stimuli into electrical activity (e.g. TRPV1): the larger the change in voltage at the terminal, due to influx of Na+ and Ca2+ through receptors forming ion channels, the greater the number of action potentials generated.
What are the 4 main modalities of nociception and what type of fibres carry them?
A-Delta:
Mechano nociceptors:
- Tissue damaging stimuli.
- Pressure
C (most common) Thermal nociceptors -(N.B. 10% of C-fibres signal innocuous thermal information) - > 45 degrees Chemically sensitive Nociceptors - (Mechanically insensitive) - Algogens, pH irritants Polymodal nociceptors (N.B. Most abundant) - Thermal, mechanical, chemical
Where do pain pain pathways from the periphery end up?
Termination points of sensory neurons in the spinal cord. Most neurons involved in pain signals terminate in laminae I and II at the top, or dorsal end of spinal cord contacting cells transmitting information in regions of brain involved with the responses to pain and its perception
What are the main 2 ascending pain pathways?
Spinothalamic: Discriminative aspect of nociception. Fast pain
Spinoreticular: Responsible for arousal and affective (unpleasantness) aspects. Dull pain
Where is pain processed in the brain? (L02)
Pain matrix (areas in the brain responsible for processing nociceptive inputs and generating the pain experience; for more details see Prof Thompson’s lecture)
Pain matrix revisited (see papers from G Iannetti, UCL)
What is the Gate Control theory?
Melzack and Wall suggested that small interneurons in the dorsal horn act as a gate which controls the amount of excitation of the transmission cells.
What factors regulate the gate control mechanism?
- Amount of activity in pain fibres
- Amount of activity in other peripheral fibres (activation of mechanoreceptors Aß fibres)
- Messages descending from brain, e.g. emotions (anxiety, relaxation), mental conditions (boredom, learning)
Thus: psychological factors influence pain perception by regulating the gate mechanism
What do you know about the PAG?
PAG: periaqueductal gray, rich in opioid receptors and enkephalins(electrical stimulation of PAG produces analgesia); PAG neurons’ axons end on serotoninergic neurons in the medulla
What do you know about the RVM?
RVM: rostro ventromedial medulla: important area both for inhibition and facilitation of nociceptive processing; bidirectional central control of nociception
Pain is a subjective experience and has what three components?
sensory-discriminative:
- sense of intensity, location and duration
affective-motivational:
- unpleasantness and desire to escape it
cognitive component:
- involving judgments, beliefs, memories, perception of environment and patient’s own history
Are pain pathways rigidly hardwired?
Neural substrates that mediate pain are plastic, i.e., modifiable depending on use or modulatory influences
To note: the central role of the dorsal horn which integrates peripheral, local and descending input. Change in excitability at this level will control output to the brain
How can we divide up types of pain?
Nociceptive
Clinical
- inflammatory
- neuropathic
- functional
What are the 2 forms of pain hypersensitivity?
◦ Thresholds are lowered so that stimuli that would normally not produce pain now begin to, so called ALLODYNIA
◦ Responsiveness is increased, so that noxious stimuli produce an exaggerated and prolonged pain or HYPERALGESIA
What is peripheral sensitisation to pain and what causes it?
Reduction in threshold and increase in responsiveness of peripheral ends of nociceptors.
Sensitization arises due to the action of inflammatory chemicals (ATP, PGE2, NGF)
What is central sensitisation to pain and how is it caused?
an increase in the excitability of neurons within the central nervous system, triggered by a burst of activity in nociceptors, which alters the strength of synaptic connections (activity-dependent synaptic plasticity) between nociceptors and spinal cord neurons
What does a SCN9A channelopathy cause?
- congenital inability to experience pain
- SCN9A codes for an α-subunit of a voltage-gated Na channel, Nav1.7, strongly expressed in nociceptive neurons (autosomal-recessive trait to human chromosome 2q24.3).
In three consanguineous families from Pakistan, this gene presents homozygous non-sense mutations which result in total absence of nociception
What’s the difference between A-Beta and A-delta and C fibres
A Beta
- Big
- Sensitive mechanoreceptors
Ie. to coral columns
A Delta/C
- Small
-Thermoreceptors, Nociceptors
Ie. to spinothalamic tract
Aδ: large (2-5 mm), fast conducting, myelinated
C: small (0.4-1.2 mm), slower conducting, non-myelinated fibres
(Stub toe etc - sharp pain and then throbbing - a delta and then c fibres)
What part of the brain is responsible for pain?
Area of the brain activated by the nociceptors
- was said to be the primary sensory cortex
- now use fMRI - pain matrix
- cant tell you which area is responsible for the actual perception of pain
But pendulum is swinging back
- maybe pain is in old brain parts
- maybe posterior insula
