Lecture 25 - Body Maps and Plasticity Flashcards
The pain caused by excessive cold is most accurately
described as ___________ pain.
nociceptive
you have a specific nociceptive receptor that is activated by specific pain: extreme cold, extreme heat, etc…
direct pathway model
very straight forward
you have nociceptors that are stimulated and once they get that signal it’s sent eventually to somatosensory cortex
the cortex elicits a withdrawl response: you pull your hand away
gate control model
the gate is holding in the pain
when the gate closes it turns off the transmission cell and if that cell isn’t active the pain can’t be felt
• Simple version proposed by
Melzack & Wall (1965).
• The “gate” consists of
substantia gelatinosa cells in
the spinal cord (SG- closes the gate and SG+ opens the gate).
• Input into the gate comes from: – Large diameter (L) fibers - information from tactile stimuli (mechanoreceptors). – Small diameter (S) fibers - information from nociceptors. – Central control - information from cognitive factors (from the cortex).
Input into the gate comes from:
– Large diameter (L) fibers -
information from tactile stimuli
(mechanoreceptors).
– Small diameter (S) fibers -
information from nociceptors: want to open the gate!
– Central control - information
from cognitive factors (from the
cortex): where attention or your mood comes into play: it can come down and try and close the gate
gate output …
…. is transmission cell (Tcell)
activity. More T-cell activity
means more intense pain.
− Pain decreases when the gate is closed by stimulation of SG- by
central control or L-fibers.
− Pain increases when stimulation of the S-fibers activates SG+ to open the gate.
− By this model, we can regulate
amount of pain sensed through
other tactile input (rub or scratch) or cognitive factors (mood or
attention).
perception of pain decreases
when gate is closed by stimulation of SG- by
central control or L-fibers.
perception of pain increases when
stimulation of the S-fibers activates SG+ to open the gate.
Central Control
Expectation
- when you are anticipating something is going to hurt, they experience more pain and vice versa
- EX: when surgical patients
are told what to expect, they request less pain medication and leave the hospital earlier. (hypnosis)
– EX: Placebos can also be effective in reducing pain.
Central Control
Shifting Attention
if you don’t look at it, it won’t hurt as much
in burn units: virtual reality technology has been used to keep patients’ attention on other stimuli rather than the pain-inducing stimulation: playing a game so they can shift their attention away from their body and helps to lessen the perception of pain
Central Control
Content of emotional distraction
participants could keep their hands in cold water longer when pictures they were shown were positive: when they saw positive pictures they could keep their hands in the water for longer and when the pictures were negative they kept their hands in the water for less time
your mood (affected by these pictures) can control how much pain you feel
According to the gate control model of pain perception, input to
the “gate” of the substantia gelatinosa (SG) comes in from large diameter (L) fibers, small diameter (S) fibers, and ‘central
control’ areas in the cortex. Which of these inputs is most
responsible for carrying nociceptive signals to open the gate?
S-fibers
How does the brain represent pain?
the pain matrix
- Subcortical areas include the hypothalamus, amygdala, and the thalamus: activated when someone reports they’re experiencing pain
- Cortical areas include S1 and S2 in the somatosensory cortex, the insula, and the anterior cingulate and prefrontal cortices.
- These areas taken together are called the pain matrix: many cortical and subcortical regions
can’t say that there is one region that is the pain region
How can we separate the sensory and affective (emotional)
components of pain?
Experiment by Hofbauer et al. (2001)
– Participants were presented with potentially painful stimuli and asked:
• Asked To rate subjective pain intensity (sensory): on a scale of 1-100 how much does that hurt
• To rate the unpleasantness of the pain (affective element): rate 1-100 of how much you don't like it
– Brain activity (PET scan) was measured while they placed their hands into unpleasantly hot water.
– Hypnosis - suggestions - (to modulate central control) was used to attempt to increase or decrease the sensory and affective components: how intense or unpleasant it was
• Results showed that: Hypnosis had major affect!
– Suggestions to change the
subjective intensity led to:
when they were told the water is very very hot they rated the intensity AND UNPLEASANTNESS higher
• Changes in perceived intensity
• Changes in unpleasantness
• Associated with changes in S1
activation.
– Suggestions to change the
unpleasantness of pain:
- Lowered ratings of unpleasantness.
- Did not affect perceived intensity: Hypnotic suggestion to change unpleasantness didn’t affect intensity: these two things can be pulled apart
• Activation in the anterior cingulate cortex (but not S1):
!! the intensity judgment seems to driven by what’s happening in somatosensory cortex which further drives what’s happening in unpleasant rating, but it doesn’t go the other way
Intensity Vs. Unpleasantness
if you manipulate intensity it is associated with changes in S1
if you change the perceived intensity you change the perception of unpleasantness
BUT if you change the perception of unpleasantness there is activation in anterior cingulate cortex BUT NOT in S1, which means the perception of intensity DOES NOT CHANGE
dissociable: this suggests that these two elements can be separate
S1 –> ACC
but NOT ACC –> S1
Suggestions to change the
subjective intensity led to:
• Changes in perceived intensity
• Changes in unpleasantness
• Associated with changes in S1
activation.
Suggestions to change the
unpleasantness of pain:
• Lowered ratings of unpleasantness.
• Did not affect perceived intensity.
• Activation in the anterior
cingulate cortex (but not S1).
endorphins
Pituitary gland and hypothalamus
release these neurotransmitters
activate opiate receptors and reduce pain.
Injecting naloxone (with a similar molecular structure to endogenous morphin - to endorphins)
– blocks the receptor sites, resulting in more pain.
– Naloxone also decreases the
effectiveness of placebos (telling
us expectations act like/trigger
endorphins).
People whose brains release
more endorphins can
withstand higher pain levels.
Social Pain: If pain has a strong affective (emotional or cognitive) component, can it be experienced without the painful (injuring) stimulus?
Experiment by Eisenberger et al. (2003)
– Participants watched a computer game.
– Then, they were asked to play with two other “players” (but it was really automated - just the computer).
– The “players” excluded the participant: doesn’t let the subject paly
– fMRI data showed increased activity in the anterior cingulate cortex and participants reported feeling ignored and distressed. = same brain mechanism involved in the perception of unpleasantness
Empathy: Can you feel other peoples pain?
Experiment by Singer et al. (2004)
– Romantically involved couples participated.
– The woman’s brain activity was measured by fMRI.
– The woman either received shocks or she watched while her partner received shocks.
– Results: Similar brain areas (i.e. insula and anterior cingulate) were activated in both conditions (both when she was shocked and she saw her partner shocked)
– Higher levels of empathy are associated with more ACC activation.
Higher levels of empathy are associated with
more ACC activation.
Phantom Pain: Can we feel pain without either a physical sensation or
an affective cause?
In phantom limb phenomena, people (50 - 80%) report feeling pain from a limb that has been
amputated.
- It can range from mild (an itching sensation) to intense (bending in an unnatural position).
- The pain is localized to a specific place.
- They know they have a missing limb: It is resistant to top-down cognitive (central) control.
Two aspects of the phantom limb:
- Feeling sensations from the phantom, or perhaps from another body part ‘mapped’
onto the phantom (touching the face but feeling it on the phantom limb) – sensory. - Feeling the phantom move (or be cramped in a painful position) – motor.
(Note: these interact)
How can we model phantom pain?
someone loses their arm
the areas that are topographically close: face and shoulder
no longer getting info from the arm area, so the nearby areas overtake that portion of cortex
getting signals from face and shoulder: those representations overtake the arm regions (experience dependent plasticity)
Without input from the limb,
other nearby cortical regions
may begin to stimulate part of
the phantom limb’s cortical map.
The maps in somatosensory
cortex for different body parts
begin to overlap.
how regular movement works in the cortex
supplementary motor cortex sends a signal command to move to motor cortex, parietal (sensory) cortex, and cerebellum
motor cortex sends signals to body muscles
and then you get feedback (proprioceptors): “Yes we moved”
“No we didn’t”
phantom movement?
how does the phantom move?
supplementary motor cortex sends a signal command to move to motor cortex, parietal (sensory) cortex, and cerebellum
the brain says “we’re moving” but there’s no body part to initiate movement and it can’t give feedback
but as far as the brain is concerned it’s gotten the pertinent signals
Training via the mirror box:
- Create new feedback via vision.
- Synchronize movements of real hand and phantom.
• Seeing the phantom “move” in the mirror provides an update to
kinesthetic and proprioceptive
maps in the parietal cortex. This
creates the sensation of movement in the phantom.
• Visual training can relieve pain and even help eliminate the phantom limb.
Phantom limbs seem like an extreme, highly specific case.
Does it really indicate what the brain normally does?
Yes – we can change the sensory experience of a
completely ‘healthy’ and intact person in a very short
period of time.
