Pain Flashcards
name the two descending pain pathways
serotonergic
noradrenergic
How does the descending pain pathway work
fibres project down the spine, and release serotonin and noradrenaline which impinge on the pain gate to close it
True or False: pain is the most common reason people seek clinical advice
True
Describe Aσ fibres (mechanical)
- sharp pricking, fast pain
- larger diameter due to myelination
- Faster conduction velocity
Give 2 ways pain can be managed/treated
- drugs
- local anaesthetics
- physical therapy to retrain nerves/NS
- psychotherapy and associated psychological support
- holistic approaches i.e. CBT/accupuncture/meditation
- Guided physical activity
- Surgery
Define nociception
The neural process of encoding noxious stimuli.
Describe SOMATIC Superficial pain
- Tissue Damage
- Skin
- Sharp/fast pain
- Localised
In inhibitory interneurons, what are the two neurotransmitters likely to be
GABA
Enkephalin
What is the role of the Putamen and Primary motor cortex in the pain response
the motor response i.e. move away from pain source
Many neuropathic conditions result from changes in the electrical activity of peripheral neurons.
What do these cellular level changes do?
- Facilitate sub-threshold depolarisation
- Increase action potential duration
- Increase the excitation threshold
- Lower the excitation threshold
- Reduce neurotransmitter release
Facilitate sub-threshold depolarisation
Define neuropathic pain
Pathological damage to somatosensory system
What is outlined here?
The descending pain pathway
Describe the endogenous opioids theory.
- The brain releases endogenous opioids in response to pain perception
- Internally produced molecules with opioid-like action to regulate transmission of nociceptive signals
- Similar brain regions that modulate the signal from nociceptive afferents
How does nociception information ascend the spine?
Pain fibres (A or C) ascend the spinal cord via the direct spinothalemic pathway
Define pain catastrophising
the concept of an irrationally negative forecast of future events
negative cognitive affective response to anticipated or actual pain
Sensitisation molecules (prostaglandin, bradykinin and nerve growth factor) are all produced by damage to the skin and activate what
nociceptors
What is the purpose of us experiencing pain?
- Warning of ‘actual or potential harm’
- Actual or potential tissue damage
- Elicits changes in behavior
Give 2 ‘objective’ measurements of pain
- cold pressor test
- VAS
- Numerical scale i.e. 1-10
- Smiley face (abbey pain) scale
What functions does Substance P have
- activation of vasodilation
- activation of degranulation of mast cells (contains histamine)
contributes to neurogenic inflammation
Define Allodynia
Extreme increased sensitivity following tissue injury
- Central mechanism
- Microglia – activated during inflammation
- Switch inhibitory input to excitatory
What is the difference between nociception and pain perception
Pain perception is key to defining the series of AP propagating to the spinal cord
Nociception is the process of encoding the noxious stimuli
Outline the fear avoidance model
A psychiatric model that describes how individuals develop and maintain chronic musculoskeletal pain as a result of attentional processes and avoidant behavior based on pain-related fear.
Describe the indirect spinothalemic pathway
- Slower C fibres
- Limbic system
- Hypothalamus
- Reticular formation
- Reticular activating system
- Poorer spatial discrimination
How does physical activity ease pain physiologically
- causes a decrease in hormones associated with inflammation
- chronic pain is linked to tight, week muscles so PA can help to relieve this
- increases blood and oxygen flow to muscles
- stress reduction
- distraction technique
What is the scientific reasoning behind TENS machines?
Based on pain gate theory- by vibrating at the frequency of the Aσ fibres, this closes the pain gate and activates the inhibitory interneuron in the dorsal horn zone
In clinical practice, how could you help someone come to terms with their chronic pain and its psychological impacts
- teach them avoidance isn’t always the answer as pain doesn’t always = damage
- Involve patients in their care
- Help them make sense of the pain (what’s causing it)
- Be consistent
- Show them techniques for coping with anger and other reactions
Describe a strong stimulation of nociception spinal pathway
- Glutamate released from the pre-synaptic cell (i.e. C fibre)
- Binds to AMPA receptors
- Causes influx of Na+ at post-synaptic cell
- =AP to thalamus
But also
- under heavy activation glutamate also binds to NMDA
- Causes influx of Ca2+ also
- Changes the sensitivity of the 2nd order neuron
- Releases substance P
Describe SOMATIC Deep pain
- Tissue Damage
- Deeper layers of skin, muscle and joints
- Burning, itching, aching
- Diffuse
What 4 molecules are activated by a leison, and have an effect on free nerve endings
K+, H+, histamine, serotonin
What are the three stages of pain catastrophising
- magnification
- rumination
- helplessness
State 2 factors which close the ‘pain gate’
- Relaxation
- Contentment
- Optimism
- Happiness
- Distraction
- Pro-activity
Describe a transient spinal nociceptor synapse pathway
- Glutamate released from the pre-synaptic cell (i.e. C fibre)
- Binds to AMPA receptors
- Causes influx of Na+ at post-synaptic cell
- =AP to thalamus
What is the role of the periaqueductal gray
its the brainstem centre, causing the descending pain pathway
Describe C fibres
- Polymodal
- Hot burning, cold, mechanical stimuli, slow, deep pain
- Smaller in diameter
- Slow conduction velocity
Describe Peripheral sensitisation
Substance P mediated feedback loop
Presynaptic (i.e. 1st order sensory neurons) sensitised
What 4 molecules are involved in sensitisation at a free nerve ending following a leison
prostaglandin , bradykinin, nerve growth factors, substance P
Describe Aσ fibres (thermal/mechanothermal)
- slow burning, cold prick
- larger diameter due to myelination
- Faster conduction velocity
State 3 inflammatory mediators which may be present in a free nerve ending
- Histamine
- Nerve growth factor
- Bradykinin
- Prostaglandin
- Substance P
If the threshold level of activation is reached following a leison, what molecule is produced?
Substance P
Explain why we might have referred pain
Visceral pain can manifest on different areas of the body i.e. gall bladder = shoulder pain
In the developing embryo, areas of the internal organs and external skin started in the same embryonic area, before migrating away, Therefore, nerves are related and project to tha same area of the nervous system
Describe the substance P feedback loop (peripheral sensitisation)
- Nociceptor activated by molecules produced in response to skin leison
- Substance P produced by activation of nociceptors
- Degranulates mast cells to release histamine
- Histamine activates nociceptors
Define acute pain
- momentary (mild) or severe
- weeks / < 6 months
- readily resolvable
What is the role of the primary somatosensory cortex in the pain response
identifies where on the body the pain signal is coming from
State 3 factors influencing pain
- past experience
- mental health state
- culture
- gender
- genetics
- placebo effect
- cause
Define chronic pain
- persistent - remains despite healing processes
- long lasting
- complex emotional effects
- complex social / lifestyle implications
What is the pain toolkit
A resource written for patients, by patients with tips and tricks for self-managing chronic pain
How does the nociception signal get to the spine?
the free nerve ending registers damage and sends a response to the CNS to activate the withdrawal reflex
What happens when glutamate binds to a NMDA receptor
When glutamate bindss to the NMDA receptors the conformation of the protein changes and Ca2+ permeable ion channels open.
Describe briefly the pain gate theory
By activating inhibitory neurons, this inhibits the nociception signal more i.e. stops the pain signal passing through
Define pain
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Where does the spinothalemic pathway lead to?
The somatosensory cortex of the brain
define Hyperalgesia
Increased sensitivity following tissue injury
- Primary - local to site of damage
- Secondary - extending to surrounding ‘undamaged’ areas
What is the role of the amygdala in the pain response
develop conditioned response to pain i.e. to avoid situations where pain is a likely outcome
What 4 factors can amplify or attenuate pain, by the neuromatrix theory
- attention
- experience
- expectation
- perceived threat
State 2 factors which open the ‘pain gate’
- Stress
- Tension
- Depression
- Worry
- Boredom
- Lack of activity
Describe Central sensitisation
NMDA receptors activated with strong or repeated activation
Post-synaptic neurons (e.g. 2nd order sensory neurons) sensitised
How does the gate control theory work?
The concept of the gate control theory is that non-painful input closes the gates to painful input
Ascending Aβ fibers block pain impulses at the spinal cord level carried along Aδ and C fibers
Results in prevention of the pain sensation from traveling to the central nervous system
Why isn’t tissue damage always felt as pain?
“pain receptors” not uniformly distributed
Give an example of the types of receptors in a free nerve ending
- TRP Proteins i.e. TRPV1 (Heat and pH)
- Mechanoreceptors
- GPCR
- TKR
- CGRP
What is the descending pain pathway
A modulatory pathway which works to close the pain gate i.e. in survival war situations
Describe the direct spinothalemic pathway
- Faster ‘Aδ’ fibres
- Cortical areas
- Better spatial discrimination
- Discriminatory sense of pain sensations
Describe VISCERAL pain
- Caused by distension, lack of O2, inflammation
- organs
- dull ache, burning or gnawing
- Can cause nausea and sweating
- Can be referred
What are the three classes of endogenous opioids?
Three classes:
Enkephalins
Endorphins
Dynorphins
What is the role of the insula in the pain response
allows for pain signalling/computation- affective response
links to autonomic response
Describe the process of the activation of a free nerve ending during a leison
- Skin cells, and small blood vessels are damaged/ripped by the leison
- K+ concentration in the cells is high in a cell, so leaks out from the damaged cells
- This change in potential activates the free nerve endings
(increased by H+, histamine and serotonin)
