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Summary Pain Perception & Treatment
This summary contains all of the material covered in the lectures of Pain Perception & Treatment.
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Summary Pain Perception and TreatmentLecture 1. Introduction Pain Perception and Treatment
Definition of pain by IASP: ‘’An unpleasant sensory and emotional experience associated
with, or resembling that associated with, actual of potential tissue damage.’’
- Pain is a personal experience that is influenced to varying degrees by biological
psychological and social factors
- Pain and nociception are different phenomena. Pain cannot be inferred solely from
activity in sensory neurons
- Through their life experience, individuals learn the concept of pain
- Although pain usually serves an adaptive role, it may have adverse effects of function
and social and psychological well-being
- Verbal description is only one of several behaviors to express pain: inability to
communicate does not negate the possibility that a human or nonhuman animal
experiences pain
Alternatives to normal pain
1: Injury without pain
- Congenital analgesia
- Episodic analgesia
2: Pain without injury
- Poststroke central pain
- Low back pain
3: Pain after the injury healed
- Phantom pain
4: Pain somewhere else then the injury
- Referred pain
Congenital analgesia: due to a hereditary change, so not temporary
- They can understand that others are in pain → their emotional processing is still intact.
But they cannot identify painful situations in themselves
Episodic analgesia: More temporary
- NO shock and not related to the severity of trauma
- Release of endorphins in brain that
- Localized to their injury, so they might be able to feel pain in other locations
Central poststroke pain
- Pain following a stroke, often in or surrounding the thalamus
- Heightened sensitivity to pain and find non painful things painful, like a simple touch
- Difficult to treat
- Hypothesis: damage reduces inhibitory power to suppress pain → hyper excitability
,Phantom (limb) pain:
- patients reporting serious pain in an amputated limb
- nerves are damaged, and they might be hyperexcited
- Other studies suggest that it happens in the spinal cord level, the receptive fields of the
receptors are expanded
- most popular hypothesis = Reorganization in the brain: overlap in regions in the brain
- It is not entirely clear why this causes pain
- Doing exercises in the remaining limb can
relieve pain in the missing limb
- If you imagine a movement, the motor cortex is
activated
Pain on a neuronal level
A-delta fibers: immediate,
localized pain
C fibers: later often throbbing,
less localized pain
After the first peak, you start to have more cognitive, evaluative
processes that happen in the brain
How does pain work?
At the spinal cord we have a control system what enters our brain our not
= gate control theory
If the inhibitory neuron is active, it will inhibit the projector neuron to the
brain.
So normal touch will not lead to a pain signal being processed
When there is a lot of pain the inhibition system is suppressed, so the
projection neuron will no longer be inhibited.
If you rub a painful spot, pain will be relieved, because large fiber input
will be activated, which causes the inhibitory neuron to be active, and the
projection neuron to be inhibited.
When the signals are too strong (too much
pain) this does not work.
the different do relate, but also work independently.
How we deal and think about pain is dependent on the Prefrontal
cortex. There is no ONE pain region in a brain, it is more of a
network.
,Vicious cycle
Negative mood → increased sensitivity to pain
Pain → Negative mood
Cognitions
- Prior experiences
- Attention/expectation
- Mood
- Neurochemical and structural changes
- Genetics
- Sensitization
Catastrophizing predicts
- Acute pain sensitivity
- Pain chronification
- Future pain
When you pay attention to your pain, the intensity and unpleasantness is higher than when
you are distracted from your pain
When you are in a bad mood, the unpleasantness of the pain is higher than when you are in a
bad mood, but the intensity is relatively the same
If you expect something to hurt, it will hurt more than when you do not expect it to hurt
- placebo: positive expectations
- nocebo: negative expectations
Chronic pain
- reduces grey matter density in the PFC and Thalamus
→ might be reversable
, Lecture 2. Pain neurophysiology & Pain pharmacology
Measuring pain in infants
Neuroplasticity: from pain to chronic pain
1. Abnormal input → Like tissue damage, abnormal behavior
2. Sensitization → Alterations in sensations
3. Reorganization → Spontaneous chronic pain (you do not need stimulation)
- Thalamic activity decreased
- S1 and S2 activity decreased
- Amygdala/limbic circuitry activity increased
(emotional experience of pain)
→ changes in brain in chronic brain
number of years in chronic pain decreases cortical gray
matter
1 year of experiencing chronic pain is just as eroding as 10
years of aging (on brain level)
neuropsychologically tested: if these people in chronic
pain have less cortical grey matter, they would perform
less on neuropsychological tests that rely on the frontal lobes.
- Psychomotor speed
- Executive functions
- Working memory
Alternative explanations for doing worse on these tests
- Opioid medication (mostly psychomotor speed)
- Alcoholism (mostly memory)
- Depression / sleeping disorder
→ would lead to different decreases in cognitive function
Nociception: The neural process of encoding noxious stimuli
Nociceptive pain: Pain that arises from actual or threatened damage to non-neral tissue and is
due to the activation of nociceptors.
Consequences of encoding may be autonomic (like elevated blood pressure) or behavioral
(reflex/more complex nocifensive behavior = defensive to protect yourself)
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