Case 2 - Pain Flashcards
Define pain
Unpleasant sensory or emotional experience associated with, or resembling that associated with, actual or potential tissue damage
List the steps involved in pain processing
1- Detection - a noxious stimuli is detected by nociceptive fibres
2- Transduction - thermal / mechanical/ chemical signals changed into electrical signal
3- Conduction - along a peripheral nerve, i.e. sciatic
4- Transmission - lateral spinothalamic tract transmits pain
5- Perception - biopsychosocial model, i.e. effect of catrophising
6- Modulation - i.e. move foot away from pain
What are the 4 types of pain?
Nociceptive pain
Inflammatory pain
Neuropathic pain
Nociplastic pain
What is nociceptive pain?
Is it good or bad pain?
Pain from actual or threatened damage (noxious stimuli) due to direct activation of nociceptors by high-threshold stimuli. Pain is evoked in a graded response by high-intensity stimuli, and lasts longer if the pain is more severe (appropriate response).
Good pain - adaptive and serves a protective response
What is inflammatory pain?
Is it good or bad pain?
Associated with regions of acute inflammation and peripheral sensitisation. Inflammation leads to the release of histamine, prostaglandins, ATP and 5-HT, which leads to increased nociceptive excitability/ responsiveness. this can cause pain even with innocuous stimuli.
Normal signs = heat, redness, swelling
Good pain - adaptive and protective during healing, and is reversible
What is neuropathic pain?
Is it good or bad pain?
Pain caused from lesion or disease of the somatosensory nervous system. It is persistent and has maladaptive amplification. Pain can be spontaneous, i.e. evoked from both low-intensity and high-intensity stimuli
Bad pain - no useful purpose
What are some features of neuropathic pain?
Sensitisation - either peripheral (increased responsiveness of nociceptors) or central (increased excitability of CNS neurons).
- Hyperalgesia = abnormal increased sensitivity to painful stimuli
- Allodynia = lower threshold of nociceptors, so stimuli that don’t normally cause pain do - example is tactile allodynia (pain of brushing the skin, central sensitisation)
What is nociplastic pain?
Is it good or bad pain?
Altered nociception despite no evidence of tissue damage or disease/ lesions. Activates peripheral nociceptors. E.g. fibryomyalgia
Bad pain - not useful
Name the two ascending sensory tracts
Spinothalamic
Dorsal columns
What information do spinothalamic tracts transmit?
Lateral spinothalamic = pain and temperature
Ventral spinothalamic = crude touch and pressure
Describe where neurons synapse within the spinothalamic tract
Receptor is in periphery, axon in spinal cord
1- First order neurone = dorsal horn of grey matter
2- Second order neurone = decussates and ascends to the thalamus
3- Third order neurone = synapses in ventral posterior nucleus of thalamus, which then goes to somatosensory cortex (S1 and S2)
What information do the dorsal columns transmit?
Information from discriminative touch, fine touch, vibration and proprioception
Describe where neurons synapse within the dorsal columns
1- First order neurone = from periphery, moves ipsilaterally and ascends up towards the medulla.
- Fasciculus Gracilis tract - info from lower limbs, synapses in the nucleus gracilis
- Fasciculus Cuneatus tract- info from upper limbs, synapses in the nucleus cuneatus
2 - Second order neurone = decussates in the medulla (forms the medial lemniscus) which ascends to the thalamus
3- Third order neurone = goes to the somatosensory cortex
Name the descending tract and where the neurons synapse
Corticospinal tract
1- Precentral gyrus, through internal capsule
2- In the medulla, 85-90% decussate (lateral corticospinal tract), and 10-15% continue ipsilateral (ventral corticospinal tract) before decussating in the sispinalnal cord
3- Synapse with a lower motor neurone
What is acute pain? Give some of its characteristics
Provoked by disease or injury (damage) and serves a useful biologic purpose (protective).
- Intensity correlates with the triggering stimulus
- Can be clearly located
What is chronic pain? Give some of its characteristics
Pain that outlasts the normal time of healing, due to altered nerve signals. It can be considered a disease state and is persistent. Includes neuropathic and nociplastic pain. .
- Uncoupled from causative agent (intensity doesn’t correlate)
- Lasts 3-6 months +
- No adaptive or protective function
What is the basis behind chronic pain?
Neuronal plasticity:
- Peripheral sensitisation: lower threshold and increased responsiveness of peripheral ends of nociceptors
- Central sensitisation: Increased excitability of neurons in the CNS to normal inputs, so abnormal responses (i.e. hyperalgesia)
What are the characteristics of AA and AB fibres?
Large cell body (40-80 um)
Myelinated axons
Fast nerve conduction velocity (40-120 m/s)
What is the function of AA and AB fibres?
AA= Proprioception
AB= mechanoreceptors
What are the characteristics of A-delta fibres?
- Small to medium cell body (15-50 um)
- Thinly myelinated
- medium nerve conduction velocity (10-30 m/s)
What is the function of A-delta fibres?
Respond to mechanical and thermal stimuli
What are the characteristics of C fibres?
Small cell body (10-25 um)
Not myelinated
Slow nerve conduction velocity (0.2-2 m/s)
What is the function of C fibres?
Responds to thermal, mechanical and chemical stimuli
Which fibres transmit fast and slow pain, and hot and cold temperatures? What neurotransmitter do these fibres use?
A delta = fast pain, cold - use glutamate
C fibres = slow pain, heat - use substance P
What are the differences between slow vs fast pain?
Slow pain = aching, burning - poorly localised
Fast pain = rapid onset (like a pin prick) - precisely localised
What is a silent polymodal nociceptor?
Type of C fibre that is only activated if inflammation is present
What Rexed laminae do A delta and C fibres send branches to innervate?
A delta = rexed laminae I and III-V
C fibres = rexed laminae I - II
How do A delta fibres transmit pain?
A delta = first order neurone, synapses in the dorsal horn then decussates
Terminates in the thalamus
Goes to somatosensory cortices to interpret pain quality and localisation
How do C fibres transmit pain?
C fibre = first order neurone, synapses in the dorsal horn then decussates
Terminates in the thalamus
Goes to reticular formation and the periaqueductal grey (PAG) area, this is less precise but important for pain perception
What is the role of the reticular formation?
Keeps you alert
What is the role of the PAG?
Pain relief - releases endogenous opioids
What are Rexed laminae?
Grey matter of the spinal cord is characterised into different parallel laminae by the size of the neurons present and the packing density.
Describe the changes beween the superficial dorsal horn, mid dorsal horn and then ventral horn of the rexed laminae?
Superficial dorsal = packed and small sensory neurons
Further down the dorsal horn = sensory neurons get bigger and are less packed
Vental horn = motor neurons so are bigger cell bodied, and less tightly packed
What is the pain gate theory?
Suggests inhibitory interneurons are inhibited by AB fibres. Therefore, can get pain relief by increasing AB input (‘rubbing it better’) - this is theorised to shut the pain gate that was opened by C-fibres, as rubbing floods the hurt area with tactile AB encoded stimulation = reduces pain
What are 4 receptors involved in pain?
TRPM8 - activated by a decrease in temperature
TRPV1 - activated by an increase in temperature
ASIC - activated by an increase in H+
P2X and P2Y - activated by ATP
Why do mints feel cold and hot chilli peppers feel hot when you eat them?
Mints feel cold because menthol activates TRPM8, the receptor activated by a decrease in temp (percieved as cold)
Peppers feel hot because capsaicin activates TRPV1, the receptor activated by an increase in temp
What are the mechanisms behind neuropathic pain?
- Increased inflammatory cells and mediator response: resident mast cells release histmaine and cytokines, causing release of action potential. this increases vascular permeability= inflammatory soup
- Altered nociceptors activity: increased ectopic firing, altered receptor/ ion channel expression (peripheral sensitisation)
- Altered spinal processing, central sensitisation and synaptic reorganisation: increased nociceptor activity, leads to central sensitisation (spinal hyperexcitability)
- Altered central processing and descending inhibition
What are the effects of spinal hyperexcitability?
Increased activity of C fibres
Increased neuropeptides, i.e. substance P and glutamate
Glutamate activates NMDA receptors and second order neurons