What is pain?
Pain is an unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage or both
What is noiciception?
The detection of tissue damage by specialized transducers connected to A - delta and C fibers
What part of the noiciceptor detects pain?
Free nerve endings
What type of stimuli do noiciceptors respond to?
Which type of nerve fibre is responsible for fast pain? Slow pain?
Fast pain - A delta
Slow pain - C fibres
What are the three types of neurone found predominantly in the grey matter?
Low threshold mechanoreceptive neurons (layer 3 and 4) - receive input from A beta fibres
Noiciceptive specific neurons (layer 1 and 2) receiving input from C and A delta fibres
WDR (wide dynamic range) (layer 5) - main input is A beta responds to both noxious and non-noxious stimuli via interneurons.
Where do primary noiciceptive afferent impulses primarily end?
In the dorsal horn
What is the anterior spinothalamic tract responsible for?
Sensation of simple touch
What is the lateral spinothalamic tract responsible for?
Conveys fast and slow pain
(pain and temperature sensation)
Which rexed lamina does the spinothalamic tract arise in?
Arises in the rexed lamina 1,2 and 5
Where does the lateral spinothalamic tract end?
Terminates in the ventroposterior thalamic nuclei
Where does the ventroposterior thalamic nuclei feed into?
The somatosensory cortex to facillitate the spatial, temporal and intensity discrimination of painful stimuli
Where does the ventral spinothalamic tract project?
To the medial thalamic nuclei
Where does the medial thalamic nuclei project to?
Cortical regions such as anterior cingulate and insular cortex as well as other parts of the limbic system
Where does pain perception occur?
In the somatosensory cortex
Where do descending pathways arise from that usually descrease the pain signal?
Arise from the periaqeductal grey matter
travel from the brain to the dorsal horn
What is hyperalgesia?
Increased perception of pain or even perception of non-noxious stimuli as noxious stimuli
When does hyperalgesia happen?
Happens when there is a tissue injury and inflammation
What do the terms primary hyperalgesia and secondary hyperalgesia mean?
Primary - hyperalgesia at the site of injury
Secondary - hyperalgesia in surrounding uninjured tissue
Central pain sensitization following normally non-painful stimulation
Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.
What is the difference between allodynia and hyperalgesia?
Allodynia - decreased threshold for response
Hyperalgesia - Exaggerated response to stimuli
How does spontaneous pain compare to allodynia and hyperalgesia?
Spontaneous pain doen't affect the sensation of pain - it results in spontaneous activity in nerve fibres
What is the main difference between peripheral sensitization and central sensitization?
Central sensitization happens at the level of the spinal cord
Peripheral sensitization causes sensitivity to heat
What are the three components of central censitization?
What happens during Wind up?
C fibres are influenced by substance P (their threshold is lowered)
C fibres are now more sensitive and are more likely to depolarize
There is also an increase in the receptive field of C fibres
Which neurones are involved in wind up?
Only the neurones taking part in the synapses with primary afferent input
When does wind up manifest and when does it terminate?
Manifests over the course of a stimulus and terminates with that stimulus
How does the classical - central sensitisation mechanism work?
Involves opening up of new synapses as a result of a strong enough stimuli to elicit the response.
If the intensity is strong enough then it occurs immediately with the stimuli and can outlast the duration of the stimuli
Results in secondary hyperalgesia
Once activated, it can be maintained even by low intensity of the offending stimuli
What neurotransmitters and receptors are associated with classical sensitization?
NMDA receptor activation by glutamate is known to trigger a series of changes resulting in classical central sensitization
Which synapses are involved in long-term potentiation?
Involves mainly the activated synapses
What type of stimuli does long - term potentiation result from?
Results from very intense stimuli
What are the receptors and transmitters for long-term potentiation?
The mechanism is involves both AMPA and NMDA receptor activation by glutamate.
What is the result of suprasegmental central sensitization of pain?
What is the difference between chronic pain and acute pain?
In chronic cases the presence of noxious stimuli is not essential and the source can be nociceptive, neuropathic or mixed
What is nociceptive pain?
A sensory experience that occurs when specific peripheral sensory neurones (nociceptors) respond to noxious stimuli
When does nociceptive pain normally end?
Usually resolves when damaged tissue heals
What is neuropathic pain?
Pain initiated or caused by a primary lesion or dysfunction in the somato-sensory nervous system
Where does neuropathic pain occur?
•The painful region may not necessarily be the same as the site of injury – pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain)
Is neuropathic pain more likely ot be acute or chronic?
Ulinke nociceptive pain it responds poorly to conventional analgesics
How can we reduce transduction of pain?
How do we reduce transmission of nociception?
- DREZ - dorsal root entry zone (The surgery destroys the area where damaged nerves join the central nervous system, thereby interfering with inappropriate pain messages from nerves to the brain.)
- Cordotomy - cutting nerves of spinal cord
How do we alter the perception of pain?
Cognitive behavioural therapy
Graded motor imagery
Mirror box therapy
How can we manipulate descending modulation?
- Spinal cord stimulation