L18 - Chronic Pain and Sleep Flashcards
what is chronic pain?
pain that outlasts the expecting healing time of an injury - usually 3-6 months.
generally not due to residual injury or inflammation.
- 20-25% osteoarthritis patients who have knee/kip replacement don’t get improvement in pain.
- depends on type of pain.
- increased pain sensitivity is a good indicator of chronic pain.
What are predisposing factors to chronic pain?
- Women - 1.5-2 times higher pain sensitivity and about double rate of chronic pain
- early life pain/stress and prior injury increases adult pain sensitivity
- stress
- psychological/personality factors such as fear of pain, catastrophising.
Describe chronic pain pathophysiology.
Due to neuroplastic changes in the peripheral and central NS.
- peripheral changes in multiple receptors - eg. nociceptors receptors become more sensitive, and upregulate receptor expression
- glial cells in the spinal cord remodel to intensify pain transmission - receptor modification, they start responding to pain, when in acute pain they usually dont respond. thus, extra pain signal.
- pain neurons grow and increase synaptic connections to second order neurons in the medulla.
- CNS changes resulting in central sensitisation - glial cells, astrocytes, microglial - physiological changes that contribute to increase in sensitivity of pain receptors and neurotransmitters… increased activity of Insula and primary SSC and other pain regions .. so more active that they shoudl be for any given stimulus.
- —> allodynia
the pain is the disease.
What’s allodynia
increased pain sensitivity, where light touch becomes painful.
brain think’s benign stimuli is painful.
Why is treatment of chronic pain so difficult?
- don’t know what’s going on
- PAG reduces pain from the descending pathway.. but if this pathway is not really working… then morphine etc is really ineffective!!!!!!!
Relationship between sleep and pain?
- approx 20% of population
- chronic insomnia approx. 10% of pop
55-88% COMORBID!
- prospective studies show sleep disruption and insomnia in particular increase the risk of dev chronic pain.
PAIN CAN ALSO INHIBIT SLEEP.
reciprocal relationship!
- reduced SWS an REM cause hyperalgesia whereas warmth detection and other tactile stimuli are unchanged.
4 mechanisms:
- descending pain inhib pathway
- inflammation
- attentional regulation
- central sensitisation
What are the possible mechanisms for the relationship between sleep and pain?
4 mechanisms:
- descending pain inhib pathway - may not be working properly. PAG not able to reduce pain as it should. sleep might be why
- inflammation - sleep dep changes pro inflammatory mediators - inflammation increases pain receptor sensitivity, and also cause activation itself.
- attentional regulation - possibly with lack of sleep, difficult to switch attention elsewhere
- central sensitisation - PAG may be less active to reduce pain with sleep loss.
How can conditioned pain modulation (CPM) be seen via the descending pain inhib pathway?
- 2 pain stimuli at once.
- increase in pain threshold can be seen when one pain stimuli is already present (pinching thumb, then putting hand in ice water).
- can tolerate more pain due to release of endogenous opioids already, due to the first stimuli
if you give the two stimuli at the same time, the pain will be higher.
Effect of sleep on Conditioned Pain Modulation (CPM)?
- 3 days of restricted sleep, one group 6.5 hours and another 8.5 groups.
- found 30% increase in pain threshold if thumb was squished whilst being in cold water at baseline (no sleep restriction)
- found a decrease in conditioned pain modulation with reduced sleep - oreducted a bility for the PAG to inhibit the actual signals coming through the pain pathway.
Inflammation in sleep deprivation?
- Sleep dep or restriction increases inflammatory markers
- Inflammation increases nociceptor sensitivity
- Those who slept less experienced an increase in total body discomfort
Inflammation and social pain?
- placebo or endotoxin (bacteria) in healthy subjects
- cyberball social exclusion experiment in fMRI.
- endotoxin group showed greater social distress, depression, but same brain activations
- increase in IL-6 activation of the anterior cingulate and insula within endotoxin group –> inflammation
therefore inflmmation plays a role in social pain
How does sleep affect attentional regulation?
- sleep loss impairs neurocog function, maybe distraction is poor when tired.
- subjects were sleep restricted, and measured pain whilst/whilst not playing a video game.
- measured pain, and redness, and area of sensation alteration.
- distraction reduced pain ratings in well-slept subjects, and more redness, and larger zone of altered sensation in low sleep group
INDICATES INFLAMM AND SPINAL MODIFICATIONS
(SINCE sleep also affects inflam)
What are they ways that sleep loss may increase pain?
- reducing descending pain inhibition
- increasing pro-inflammatory mediators
- reducing ability to regulate attention - be distracted
- modified central pain sensitisation
Describe sleep treatment for pain
- double blinded study, post-docs were lied to that they were investigating insomnia
- did two intervention techniques - CBTI and Behavioural desensitisation in 100 patients with knee osteoarthritis.
- both groups had similar decrease in clinical pain
- reported that for CBT-I group, Wake after sleep onset pain levels correlated with pain change at 3 and 6 months but not behavioural desensitisation.
QUESTIONABLE CONCLUSION?
What is fibromyalgia
chronic widespread pain in different areas, not necessarily permanent.
- unrefreshing sleep.
- Fatigue
- GI symptoms
- allodynia
- cog impairment, lifetime depression
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