Principles of Sensation, Touch Flashcards

1
Q

what is the difference between sensation and perception?

A
  • usually sensation and perception are parts of one continuous process
  • sensation - how the brain represents external energy/signals
  • perception - organization and interpretation of sensory information
  • neuroscientists argue that sound is just the interpretation of energy and wavelength changes
    • if a tree falls in the woods and nobody is there, it doesn’t make any sound
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2
Q

what are the different types of processing?

A

bottom-up and top-down processing

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3
Q

what is bottom-up processing?

A
  • flow of information from sensory input to higher-level cognitive processes
  • starts with raw data (sensory input) that the brain organizes and interprets to form a perception or understanding
  • look at external world → signal is sent to the brain → sent to specialized areas → becomes a fully perceived image
    • most of our perception happens through this
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4
Q

what is top-down processing?

A
  • involves using pre-existing knowledge, expectations, or experiences to interpret and organize incoming sensory information
  • we form representations of the world in our brain and when we look at the world, we look for features related to our representations
    • ex. we have expectations about the environment/situations
    • going to a new classroom, we expect to find desks and tables
    • unique feature of humans perceptual system
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5
Q

what is transduction?

A

process of turning external energy into nervous system signals

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6
Q

how do our senses generally work?

A
  • we receive sensory stimulation (external energy) using specialized receptor cells
  • some specialized to pick up fluctuations in air pressure, others to pick up changes in electromagnetic spectrum
  • transduction turns energy into NS signal
  • turn into receptor potentials, fluctuations in resting membrane potential, not necessarily at a synapse
  • neural information is delivered to the brain
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7
Q

what are the characteristics of receptor potentials?

A
  • similar to post-synaptic potentials, but not at synapse
  • can be via ionotropic or metabotropic receptors
  • ionotropic receptors are faster than metabotropic receptor
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8
Q

what is the process of hearing?

A
  • hair cell is found in inner ear and has cilia on it
  • sound is changes in air pressure → arrives at ear → causes eardrum to flap and bones to move → causes liquid inside cochlea to move → ripples cause cilia on hair cells to move back and forth → channels are pulled open as the cilia sways
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9
Q

do we have five sense?

A
  • don’t necessarily have five senses
  • many more subcategories of senses
  • there are many other senses in animals
    • birds can orient themselves to N/S alignment even in a room
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10
Q

what is an example of how our sensory systems have a restricted range of responsiveness?

A
  • the way we sense the world is evolutionarily useful
  • visible light is a small part of the electromagnetic spectrum, we cannot see all aspects of the electromagnetic spectrum
  • we see a specific band of the electromagnetic spectrum because those bands of light bounce off us and is reflected
  • factors such as the type of sun and the light it gives off make this possible
  • gamma rays would not provide meaningful information about the world if we could sense them
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11
Q

why do some animals see different bands of the electromagnetic spectrum?

A
  • some animals can see different bands of light because it is evolutionarily important for them
  • even closely related species can have differences in sensory systems
    - for example, cats can hear higher frequencies, which helps them hunt mice
  • despite differences, there are still similarities in sensory systems between mammals, fish, and birds.
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12
Q

how does the human eye provide proof of human’s evolution? in what ways is this not optimal?

A
  • we started from light sensitive cells that developed based on evolution
  • human eyes are full of fluid because they evolved from when we were an aquatic species
    • when light travels from one medium to another (water to air), it is distorted
    • our eyes would’ve been better if they weren’t filled with fluid
  • axons and other cells and blood vessels are in front of photoreceptors
    • light has to bounce off of all these things before reaching photoreceptors
    • we use metabotropic receptors in the eye, which are slower
    • the place in the eye where all the axons leave is a blindspot
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13
Q

how did octopus’ eyes evolve?

A
  • octopus had a different lineage of visual evolution
    • water outside the octopus and water on the inside of the octopus’ eye
    • photoreceptors are the most external part of the eye
    • all the blood vessels and axons are behind photoreceptor (no blindspot)
  • their evolution was much more optimal than ours
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14
Q

if all senses are just changes in electricity, how do we know which is for what sense? what are the two theories for how we decode action potentials?

A
  1. doctrine of specific nerve endings
  2. labelled lines
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15
Q

what is the doctrine of specific nerve endings? what are its limitations?

A
  • specialized sensory cells respond only to their specific type of energy (touch-sensitive cells respond to touch, not light or sound)

Limitation:
- if you close your eye and push on it, you may see light or dark spots even without light entering
- this occurs because light-sensitive cells interpret any stimulus (pressure) as a change in light, despite no actual light change

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16
Q

what is the idea of labelled lines?

A
  • specialized sensory cells respond only to their specific type of energy (touch cells respond only to touch) AND they stay segregated as signals travel to the brain
  • each sense has separate pathways leading to specific brain areas, ensuring signals remain distinct
  • crossed pathways can cause mixed sensory experiences like synesthesia (seeing sounds, hearing colors)
  • if pathways are rewired to different targets, the brain can adapt and repurpose areas for new functions (sound-processing areas adapting to process taste)
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17
Q

what are the different layers of skin? what aspects of somatosensation do they detect?

A
  • hypodermis (deepest layer): anchors tissue to muscles and the rest of the body; detects stretch and vibration
  • dermis (middle layer): contains most sensory cells; responsible for fine touch discrimination
  • epidermis (outermost layer): contributes to fine touch discrimination
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18
Q

what is the pacinian corpuscle (lamellated corpuscle)? where is it located?

A
  • specialized skin receptor that detects vibrations
  • input layer located in the hypodermis, the deepest layer
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19
Q

in what way is the pacinian corpuscle’s structure unique?

A
  • they are pseudounipolar neurons - have a single process that splits into branches for sensory input and signal transmission to the central nervous system (output)
  • doesn’t have dendrites
  • it’s input layer is deep in the skin and connects directly to the output layer without a cell body in between
  • axon travels to the spinal cord; the cell body is located in the dorsal root ganglion
  • exception to the typical neuron structure (dendrite → soma → axon): instead, input → axon → soma
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20
Q

how do receptor potentials from the pacinian corpuscle work?

A
  • receptor potentials are also called graded potentials (similar to PSPs)
  • small vibrations produce small graded potentials; large vibrations produce large graded potentials
  • graded potentials on the input layer can depolarize the cell, then an action potential occurs in the axon
  • action potential is the same as what we know, but means of input are different
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21
Q

how does transduction happed in the pacinian corpuscle?

A
  • vibration transduction occurs via stretch receptors with mechanically gated channels
  • found in the skin and muscles, including muscle spindles (receptors for proprioception)
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22
Q

how do cells with differing thresholds contribute to sensory perception?

A
  • neurons can transmit a max of 250 action potentials (APs) per second, limiting their ability to detect the full range of stimuli
  • one neuron type cannot detect the entire range of a stimulus
  • some cells are sensitive to small changes and reach their firing ceiling early, detecting only the difference between no signal and a weak signal
  • these cells cannot distinguish between weak and moderate signals
  • a range of cells with varying sensitivities is needed for full sensory perception
  • population coding is necessary to interpret even simple touch stimuli.
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23
Q

what is intensity coding?

A
  • the brain decodes sensory information by counting the total number of action potentials reaching the next neuron (summation of responses)
  • multiple neurons work in parallel to convey the signal
  • as the stimulus strengthens, more neurons are recruited to respond
  • range fractionation: some neurons are specialized to be more sensitive to specific ranges of stimuli
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24
Q

what is sensory adaptation? what are the different kinds of sensory adaptation?

A

adaptation: progressive loss of response to maintained stimulus
- when we are touched, there is more action potentials at the beginning, even if the stimulus continues
- adaption happens at every level of sensation
- tonic receptors (slow-adapting) - persist in firing for longer
- phasic receptor (fast-adapting) - tell you about a change, then firing decreases

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25
Q

what is the benefit of sensory adaptation?

A
  • adaptation is beneficial because constant pieces of information don’t provide any new information
    • not going to be particularly useful to us
  • nervous system is more interested in changes than absolute values of stimuli
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26
Q

what are receptive fields? how would they differ for types of touch?

A
  • area on the skin in which this neuron will respond
  • modality specific - receptive field for visual neurons is part of visual field, receptive field for touch is a patch of skin
  • areas deeper in the skin have larger receptive fields (receptive fields for vibration are bigger than those for fine touch)
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27
Q

what is an “on centre, off surround” receptive field for touch? how does this increase discrimination of touch?

A
  • if you press in the centre, it’ll stimulate the cell and cause bigger potentials
  • if you press in the periphery of the receptive field, it has an inhibitory effect
  • helps with discrimination and precision
    • the centre of one cell is the periphery of another cell, increasing discrimination
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28
Q

what are the four main skin receptors? what are they responsible for? what receptors are found in different layers of skin?

A
  1. pacinian corpuscle - vibration
  2. meissner’s corpuscle - light touch
  3. merkel’s discs - fine touch
  4. ruffini’s ending - stretch
  • hypodermis (deepest): pacinian corpuscle and ruffini’s ending
  • dermis (middle): meissner’s corpuscle
  • epidermis: merkel’s discs
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29
Q

what types of receptors have the largest receptive fields? what type have the smallest?

A

in order from largest to smallest:
1. pacinian corpuscle
2. ruffini’s ending
3. meissner’s corpuscle
4. merkel’s discs
- areas deepers in the skin have larger receptive fields

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30
Q

which skin receptors are fast adapting and which are slow adapting?

A

fast adapting:
pacinian corpuscle - vibration
meissner’s corpuscle - light touch

slow adapting:
merkel’s discs - fine touch
ruffini’s ending - stretch

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31
Q

how do sensory axons differ from each other?

A
  • there are different sizes and thickness of axons
  • in order of thickest to thinnest: A alpha, A beta, A delta, C
  • A axons are myelinated and C axons are not
  • conduction speed is extremely fast in axons that are thick and myelinated
    • can’t have this for every cell, reserved for most important signals
  • proprioception has the thickest myelinated axons because they are important for knowing where your body is in space
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32
Q

what types of sensation use what types of axons?

A

A alpha: used for proprioception (muscle spindle)
A beta: used for touch (pacinian corpuscle, ruffini’s endings, merkel’s discs, meissner’s corpuscle)
A delta: pain, temperature (free nerve endings)
C: pain, temperature, itch (free nerve endings)

33
Q

what is the dorsal column system?

A
  • axons comes in from skin receptors → travels past dorsal root ganglion → travels into spinal cord
  • touch from the right side of the body moves to the right side of the spinal cord (ipsilateral)
  • the signal goes into white matter → reaches medulla in the brain
  • in the medulla, the axons switch sides to the other side of the brain
34
Q

what are dermatomes?

A
  • dermatomes are specific areas of the skin that are mainly supplied by a single spinal nerve
  • organization of spinal cord is based on our lineage as a four-legged creature
  • nerve bundles (dorsal roots) in the spine represent different patches of skin (dermatones)
  • there is overlap with adjacent dermatomes
35
Q

what is the sensory pathway?

A
  • spinal cord → brainstem (medulla) → thalamus → primary sensory cortex
    - arrive via nerves to spinal cord or brain stem
  • only sense that doesn’t go through the thalamus before primary sensory cortex is smell (because it’s the oldest sense”
  • segregated pathways (labelled lines) - somatosensory information is segregated from other sensory information
36
Q

where is the primary somatosensory cortex located?

A
  • primary somatosensory cortex is the post central gyrus
  • immediately posterior to the central gyrus/sulcus
37
Q

what are the characteristics of the primary somatosensory cortex?

A
  • perceptual processing begins because we are organizing information and making sense of it
  • contralateral organization - left side of the brain represents touch from the right side of the body
  • somatotopic organization - we maintain the map of our body inside the brain
38
Q

what are the characteristics of the secondary somatosensory cortex?

A
  • more sophisticated processing - senses bigger patterns, directional movement, hardness of object on skin
    • there is some bilateral information - sometimes when someone is touched on one side, it’ll stimulate both sides
    • makes it easier to learn how to do something on the other side of the body, after you know how to do it on one side
39
Q

what is topic organization?

A
  • refers to the way in which information or content is structured and arranged
  • cortical magnification: relative increase in the amount of cortical area dedicated to body parts that have high tactile acuity and sensory specialization
  • disproportionately large somatosensory patch in the brain because it’s evolutionary important
40
Q

what special sensory systems do animals have and how is this seen in cortical representation?

A
  • some animals have whiskers, they tell animals whether or not they will fit in small places
  • barrel cortex - disproportionately large cortical area representing whiskers
    • cortical magnification is also based on relevance for the species
41
Q

what is cortical representation?

A
  • the mapping of sensory and motor functions to specific regions of the brain’s cortex, reflecting the organization of body parts
  • neurons that are in D1 (brain area) are most receptive to touch from thumb
    • can be considered as receptive fields
    • still get signals from other fingers but they’re weak
  • size of region in the brain is based on use
42
Q

how does neuroplasticity affect cortical representation when a sensory organ is removed?

A
  • neurons in somatosensory cortex for that digit has no input
  • loses synapses from that digit
  • strengthens connections for touch in adjacent digits
43
Q

how does neuroplasticity affect cortical representation when a sensory organ is used more?

A

receptive fields related to digits that are used more become larger

44
Q

how does neuroplasticity affect cortical representation when the somatosensory cortex is damaged?

A
  • adjacent areas sometimes give up neurons so that damaged brain areas can function
    • neuroplastic and flexible process, changes how neurons are firing
45
Q

what is constraint-induced therapy?

A
  • when we constrain the functioning limb and use the less functioning limb
  • used when areas of the somatosensory cortex are damaged
  • will see that the more functioning brain area will give up neurons so that damaged area can function better
46
Q

what is phantom limb? why do we think this happens?

A
  • people who lose a hand sometimes report that they can feel their hand still
    • caused by an incomplete neuroplastic process
  • if you lose your whole hand, the neurons then go on to represent other touch areas (arm and face)
  • then, when the person is touched on their arm or face, they can mistake it as someone touching their hand
47
Q

are cortical sensory neurons specialized for their type of sensation?

A
  • yes, but wiring also seems to be an essential feature
  • ex. they are somatosensory because they’re in the skin
  • neurons can make sense of nearly any input, even artificial
48
Q

what is an example of how neurons can make sense of any input?

A
  • can put an electrode in someone’s scalp and send someone a magnetic electrical signal when they move
    • makes humans able to detect magnetic fields, north and west
  • cochlear implants pick up auditory information because electrical signal stimulates auditory nerve
    • neurons are designed to make sense of signals and patterns
49
Q

what is the benefit of flexibility in the brain while we are young, and inflexibility in the brain as we age?

A
  • most plastic brain is the young brain, makes them better at learning
    • their brains are flexible, they forget things they’ve learned sometimes
  • there is a benefit to inflexibility, we hold onto skills that we learn and valuable things
    • the brain abhors an unused neuron
50
Q

what is attention?

A
  • spending more of our brain on some processing than others
  • selective attention is our filtering mechanism for consciousness
    • a way of guiding or determining what we will spend our limited resources on
  • we have guiding mechanisms that tell sensory cortex to process things differently
51
Q

do things that we don’t pay attention to reach the brain?

A
  • unattended information, that you are not paying attention to, still reaches the brain
    • things that are strong stimuli
    • ex. someone says your name, catches your attention
  • we get bits and pieces of unattended information, reaches the cortex but is processed less
52
Q

what regions are important for attention?

A
  • posterior parietal cortex - important in guiding attention (main top-down guiding mechanism)
  • cingulate cortex - important in egocentric attention, interested in imaging ourselves in the past and future
53
Q

what is the “association” cortex?

A

also called the tertiary cortex
- pieces of cortex that are multimodal, respond to touch and sound and vision (multiple senses)
- allows us to see two simultaneous sensory experiences as one experience
- richest aspects of cognition is represented by activity in association cortex
- organization, thinking, schemas
- a lot of the brain is association cortex, motor association cortex, sensory association cortex
- a lot more related to executive function and thoughts than motor
- this is where we take in all inputs and outputs and plan what we are going to do

54
Q

what is synesthesia (cross-modal stimulation)?

A
  • when someone experiences one sensory modality, they also experience another sensory modality
  • grapheme-colour synesthesia: whenever they see a letter or number, they see it in a specific colour
55
Q

what are some ideas and theories behind synesthesia?

A
  • are they actually perceiving it as a different colour or are they just thinking it’s a different colour (association)
  • thought to be driven by learning rules rather than specific memories
    • a is for apple, apples are red
    • pre-existing multi-modality that is in all people but more emphasized in some people
  • may be related to other processes that have been evolutionarily conserved
56
Q

in what ways might multi-modality have been conserved for evolutionary purposes?

A

we are all multi-modal in some ways
- kiki vs. bouba - cross-culturally, everybody agrees on what shape is what name
- kiki is the name of the object with sharp points, bouba is the name of the object that has round corners
- we think of sounds as “sharp” or “round” even though these aren’t really qualities of sound

57
Q

how can we test grapheme-colour synesthesia?

A
  • show a picture of lots of 5s and 2s on a page in black ink
  • if they see the numbers 5 and 2 as different colours, they should be able to point them out more easily
58
Q

what is pain? how is it triggered?

A
  • associated with tissue damage, an unpleasant experience
    • signal sent to the brain to trigger pain to stop the tissue damage
    • works like other senses, pain has specialized cells with axons (nociceptors) that fire APs
59
Q

how does congenital insensitivity to pain work?

A
  • it is a voltage-gated sodium channel mutation
    • sodium channels are used in the action potentials
    • cells have proteins to transduce the information, but can’t generate AP
    • individuals frequently damage themselves and don’t realize, they don’t live too long
  • can’t feel physical pain but can still feel psychological pain
60
Q

do people with congenital insensitivity to pain still have reflexes?

A

people with inability to feel pain are still have the reflex to remove themselves from noxious stimuli
- noxious stimulus - something hot or sharp
- sensory info moves to spinal cord → synapses at an interneuron in the spinal cord
- bridges the gap between dorsal and ventral sides of spinal cord
- impacts a motor neuron that causes us to remove our hand/feet

61
Q

what are some advantages to the subjective feeling of pain?

A
  • recuperation - pain is a relatively slow signal that is useful in the long run
    • if you hurt a part of your body and there is lingering pain, you will take care of that part and protect it
  • learning - don’t want to just move away from noxious stimuli, we want to never experience it again
    • learn what is dangerous so that we don’t do it again
  • signal to others - changes in facial expression when we experience pain provide information to other humans
    • humans are prosocial creatures, signal to others regarding pain so that they don’t do the same thing
62
Q

what are nociceptors?

A
  • receptors for pain, found on cells called free nerve endings
  • pick up change in temperature or have receptors that bind to chemicals
  • if you damage skin, some cells get damaged spill chemicals
    • free nerve endings are trying to pick up these chemicals and detect damaged cells
63
Q

in what cases do cells deliberately release chemicals to evoke nociception?

A
  • histamine is released deliberately when you are exposed to something that is potentially bad
  • allergies also cause the release of more histamines
  • anti-histamine binds to even receptors in the skin, reduce inflammation and itchiness
  • we have histamine receptors on some free nerve endings
64
Q

in what way can free nerve endings detect damaged cells?

A
  • they have potassium receptors on free nerve endings to detect damaged cells
    • there is normally more potassium on the inside of the cell, so if there is an increase of K+ outside the cell, that means there has been some damage
65
Q

what are the different types of receptors the detect temperature?

A
  • TRPV1 - detect warmth
  • TRPM3 - detect HEAT
  • CMR1 - detect cold
66
Q

what are the characteristics of TRPV1 receptors?

A
  • change shape when the temperature rises, which causes change in voltage or signals GCPRs
  • will let you know when something is warm (pleasantly)
  • axons are C fibres, small unmyelinated axons (AP is slower)
  • binds to capsacin, the stuff that makes food spicy
    - we think spicy food = hot because capsacin binds to heat receptors
67
Q

what are the characteristics of TRPM3 receptors?

A
  • change shape when the temperature rises, which causes change in voltage or signals GCPRs
  • not as sensitive to lower heats, activated when things are dangerously hot
  • A delta receptors, smallest myelinated axons (AP is faster)
    - if smth is dangerously hot, we need to get the signal fast and remove ourselves immediately
68
Q

what are the characteristics of CMR1 receptors?

A
  • detects lower body temp by changing shape which changes receptive potentials
  • axons are C fibres, small unmyelinated axons (AP is slower)
  • binds to menthol, which is found in mint
    - mint has a cooling effect because it binds to our cold receptors
69
Q

at baseline, what does activity in our temperature receptors look like? how does this change as temperature gets colder then warmer?

A
  • at our baseline body temp, none of the receptors have much activity (don’t allow ions through)
  • when it is cold, only CMR1 receptors have activity
  • as it gets warmer, TRPV1 opens first because it detects warm stimuli
  • then, TRPM3 opens last because it detects hot stimuli
70
Q

what are some characteristics of cells that cause the sensation of itchiness?

A
  • also have free nerve endings
  • some itch cells have histamine receptors, and some don’t
  • they all have TRPV1 receptors (detect temperature, warmth)
    • there is an association between feeling warm and feeling itchy, but not a clear connection why
  • itch cells release a large peptide neurotransmitter - natriuretic polypeptide B (NPPB)
    • unique neurotransmitter system
71
Q

what is the spinothalamic system?

A

also called the anterolateral system
- sensory pathway in CNS responsible for transmitting pain, temperature, and itch signals
- signal crosses the midline in the spinal cord (rather than crossing after the medulla) before ascending to the thalamus
- axons of the first neuron synapse as soon as it gets to the spinal cord
- axons of the second neuron in the spinal cord immediately crosses over, then travels to the thalamus
- if you damage the right half of dorsal spinal cord, it will affect touch differently from pain and temperature
- lose right side of touch, but left side of pain and temperature

72
Q

why do we think phantom limb pain happens?

A

also called neuropathic pain
- feel tightness and immense pain in a limb that is no longer there
- caused by dysregulated peripheral neurons, where free nerve endings are lost but cell bodies in dorsal root ganglion are intact
- damaged neurons may become leaky, which can lead to dysregulation and hyperexcitability
- genetic predisposition may make some individuals more likely to experience this dysregulation.
- continuous dysregulated signals from peripheral neurons can influence the organization of pain pathways further along the nervous system
- dorsal horn neurons in the spinal cord can also become dysregulated and hyperexcitable after peripheral nerve damage, amplifying pain sensations

73
Q

what is the most effective pain management technique?

A
  • placebo is very effective for pain but has weak/no effect in other modalities
  • works for pain because it is likely top-down processed, meaning expectations play a significant role in its management
    • small intervention (pill) - less effective placebo
    • large intervention (injection) - more effective placebo
  • likely mediated by endogenous opioids because we expect pain relief
  • when we have placebo effects, there are strong BOLD activity in the basal ganglia
    • people say “must be endogenous opioids” “must be dopamine release” “must be top-down processing”
    • essentially, we use top-down perception to organize information, presuming that the placebo should relieve pain
73
Q

what are two other common ways that we manage pain?

A
  • attention and focus can modify experience of pain (psychogenic interventions)
  • we also use pharmalogical interventions and sometimes surgical interventions
73
Q

in what way is pain not just a physical sensation? what types of pain are experienced the same as physical pain?

A
  • irrespective of modality, we see common activation in the brain for every kind of pain
  • social rejection experienced and described as pain
  • all pain types seem to activate the anterior cingulate cortex
    • ACC isn’t necessarily the pain center, it is involved in other roles
    • when people feel physical, emotional and social pain, we see BOLD responses in the ACC
  • painkillers can lessen the pain of social rejection and emotional pain
    • also lessen pain of existential pain
    • suggests that when we take something that we know will impact pain, it can work as a placebo and lessen emotional pain
      • placebo still changes the way that our brain functions
74
Q

how do we use drugs for pain management? what are the two types of drugs we use?

A

analgesia - the absence or reduction of pain, two types of analgesic drugs (NSAIDS and opioids)
- non-steroidal anti-inflammatory drugs (NSAIDS)
- opioids - endogenous and exogenous

75
Q

how do non-steroidal anti-inflammatory drugs (NSAIDS) work?

A
  • work by targeting a specific pain pathway, distinct from other mechanisms previously discussed
  • NSAIDs inhibit the COX pathway and reduce prostaglandin production, thus alleviating pain
  • pain causes certain cells to activate the COX (cyclooxygenase) metabolic pathway, which produces prostaglandins
  • prostaglandins are chemicals that bind to pain receptors and amplify the sensation of pain
  • reducing the production of prostaglandins decreases the sensation of pain
  • pain caused by prostaglandins can result from both external and internal stimuli:
    - for example, menstrual pain is a result of prostaglandins acting on receptors during uterine contractions
76
Q

how do endogenous and exogenous opioids work to manage pain?

A

Endogenous Opioids: we naturally produce these neurotransmitters that reduce pain in response to stress or danger, allowing focus on survival
- Example: runner’s high happens because we are misattributing the running to a dangerous situation, causes the production/release of endogenous opioids

Exogenous Opioids: external substances (e.g., morphine, fentanyl) that mimic endogenous opioids by binding to opioid receptors
- effective in pain relief when they cross the blood-brain barrier, with stronger permeability increasing potency and risk
- act on the spinal cord, brain regions (movement, motivation, reward), and descending pain pathways to block or modulate pain signals

77
Q

what is the periacqueductal gray, and how is it involved in pain managment?

A
  • periacqueductal gray (PAG) is in the tegmentum in the midbrain
    • one of the main inputs is from the amygdala, the PAG is activated when amygdala activity is really high (ex. really scared)
  • when PAG is activated, we see very intense pain relieving effects (analgesia)
  • PAG is rich in opioid receptors and endogenous opioids
  • through the descending pain pathway, the PAG modulates pain signals all the way down to the spinal cord
  • activation of the PAG inhibits the first synapse in the pain pathway, reducing pain transmission
  • signal travels from skin to spinal cord, and opioids inhibit this synapse through heterosynaptic inhibition
  • stopping pain signals as they come into the spinal cord