Session Six (Pain Perception) Flashcards
What is the difference between an exterospective and interospective sense, and which category does pain fit into?
- Extero = Inform us about the world around us e.g. vision and smell
- Intro = Inform us about our own body state e.g. hunger and proprioception
- Unclear which pain is, as technically it is an internal sensation but relating to external stimuli
What is nociception and how is it distinguishable from pain?
- Nociception = a neural processing of stimuli likely to cause tissue damage
- Distinct from pain as we don’t always feel ‘pain’ when our tissue is being damaged (e.g. battlefield wounds) and we don’t always have tissue damage when we feel pain (e.g. chronic pain disorders)
- Pain is therefore a sensation that comes from nociception but is not the exactly the same.
- Nociception cannot completely account for the entirety of the pain experience
Briefly outline the neuroanatomy behind nociception and pain.
Nociception occurs peripherally, and involved the detection of noxious stimuli (+/- motor reflex):
- Alpha-Delta fibres are myelinated and respond rapidly
- C fibres are unmyelinated so respond more slowly and are responsible for a prolonged pain sensation
- These then feed into the Dorsal Root Ganglion and are integrated at the Spinal Cord
Pain is the Cognitive Processing of Nociception, happens in the brain’s pain matrix, which involves:
- Insula
- Thalamus
- Hypothalamus
- Rostro ventromedial medulla
- Anterior cingulate cortex
- Amygdala
- Prefrontal cortex
There is also a decending pain inhibition pathway:
- Starting at the Ralph nuclei and the Locus Coreolus
- Sends projections down dorsal horn
- Inhibits C fibres of pain
- System poorly understood, likely linked to cognitive processes such as emotional state
What does Craig and Bushnell’s (1994) hot plate study show?
- Cold stimulus + Moderately hot stimulus = Burning sensation
- Suggests cold can somehow modulate the pain sensation
- Clinical evidence of Allodynia, increased pain perception in the presence of normally non-painful stimuli as a result of central sensitisation to pain.
How does the placebo effect work?
A mental representation of an impending sensory event can significantly shape neural processes that underlie the formulation of the actual sensory experience.
What does Benedetti et al (2005) show about the placebo effect?
- Demonstrated the placebo effect
- Patients were subjected to a pain trial after being given a control or a placebo analgesic cream
- Found lower self reported pain levels in the placebo group
- Benedetti suggests that this is due to 3 processes; Attention, Reappraisal, Expectation
- They also showed that if the patient is given a Naloxone spray, the placebo effect disappears, suggesting that whatever mechanism attention affects pain sensation by, it is opiod dependent.
What 3 processes are involved in the placebo effect?
- Attention (e.g. self-distraction) (DLPFC, ACC)
- Reappraisal (e.g. of control and threat of situation) (VLPFC)
- Expectations (DLPFC, VLPFC, ACC)
What effect does Naloxone administration have on the placebo effect?
Makes it almost disappear. Suggests the cognitive processes involved in creating the placebo effect are somehow opioid dependent.
What are some limitations with EEG use?
- Measures overall activity, not in any way specific to location
- In a sulcus, where two active areas directly face each other, the pulses basically cancel each other out.
- EEG can only pick up cortical activity, sub-cortical stimuli don’t get picked up.
- Gives us a wide picture with a lot of ‘background noise’ so hard to tell what is specific to the condition being studied, but this can be worked around by measuring event specific potentials
What are event-related potentials?
- EEG potentials that are specific to a given event e.g. pain
- Acquired by exposing the patient to a stimulus again and again and measuring the time
- Compare the brain signals that occurred at these times and look for things that happened specifically then
- Allows us to identify what is specific about a stimulus while ignoring the brain background noise.
- Time locked and phase locked to a stimulus
What have event specific EEG studies into pain shown us?
- Identified the N2P2 complex, thought to be a brain wave closely related to pain
- Multiple studies have found this complex
- Also shows an N1 peak hidden within N2 that occurs on the contralateral side to where the pain is occurring
- e.g. Pain in left hand shows up the N2P2 as well as N1 in the left brain (right brain processes left hand)
- Also shown differences in pain response between stimulus in the feet and in the hands
- Feet takes longer and at different location in brain (homunculus)
What have studies into the relationship between how we perceive our bodies and pain shown?
What is the clinical use of this information?
- Crossing arms and putting someone through a pain test appears to reduce pain.
- Using mirrors to artificially make a persons hand seem larger and inflicting pain increases the pain sensation
- Doing the same but making them smaller decreases the pain response
- This suggests there is a link between the way our brain perceives our body and how it interprets pain.
- Useful in phantom limb pain, can be used to create a fake arm and treat the pain there.
Event related studies have identified the N1 and N2P2 complexes, how does this fit into the pain/nociception distinction?
- It is believed that the N1 response it the basic pain response, consistent regardless of how we affect the pain stimulus.
- N2P2 however appears to represent a later stage of processing related (directly or indirectly) to the perceptual outcome of this nociceptive input
- We know from studies where we altered the timing between two jolts of pain, N1 was always consistent but N2P2 varied heavily.
- Furthermore, amplitude of N1 was consistent with how they rated the pain (again suggesting it is related to objective pain sensation)
- This was not the case with N2P2
Conclusion:
- Pain causes an initial;, predictable pain response (N1) that is followed by a loess predictable, highly variable response (N2P2)
What have studies trying to identify a “pain matrix” shown?
There isn’t really one.
- Studies compared what happens in the brain (via EEG, fMRI…) when exposed to auditory, visual, nociceptive and tactile stimuli.
- Actually very little difference (except for significant occipital lobe activation in visual)
- No pain matrix, per se
- Whatever we experience as pain is not entirely tied to a pain matrix but more of a salience matrix.
What does most recent evidence suggest the role of the brain’s “pain network” is?
- Detecting salient sensory stimuli
- Prioritising these sensations’ access to attentional and executive functions
- May still contribute to the experience of pain but unclear how
