psychobiology Flashcards
1
Q
divisions of the nervous system
A
- Central Nervous System (CNS)
-Brain
-Spinal Cord - Peripheral Nervous System (PNS)
divisions:
Somatic Nervous System (Controls voluntary movements)
Motor neurons
Sensory neurons
Autonomic Nervous System (Controls involuntary actions)
-Sympathetic Nervous System (Fight-or-flight)
-Parasympathetic Nervous System (Rest-and-digest)
2
Q
major structures of the brain and their function
A
- Brainstem
- location = base of brain, top of spine
- function = life supporting (breathing, heartbeat, digestion)
- made up of midbrain, pons and medulla - limbic system (emotion and memory)
- highly specialised neural structures at the top of the brain stem
- amygdala = emotion centre
- thalamus = sensory relay station
- hippocampus = memory formation - cerebellum
- function = coordination, balance, posture - cerebral cortex
- outer layer of brain
- two hemispheres left and right connected by the corpus callosum
- responsible for higher cognitive functions
3
Q
the corpus callosum
A
= is a bundle of neurons that allow right and left hemispheres to communicate
in split brain patients corpus callosum has been severed so information from one hemisphere can not go to left hemishpere
e.g. * Ball presented in left visual field
* Processed by right hemisphere (contralateral)
* Left hemisphere responsible for language
* “I don’t see anything”
4
Q
the folded appearance of the brain
A
- maximises surface area of cerebral cortex
sulci = folds
gyri = top of folds
- can get central and lateral sulcus
- e.g superior temporal gyrus, including Wernicke’s area for speech comprehension
The folds consist of many deep grooves called sulci and raised areas called gyri.
5
Q
directional terms in the brain
A
Dorsal = Top (superior)
Ventral = Bottom (inferior)
Lateral = Towards the outer cortex
Medial = Towards the center of cortex
Anterior = Front (rostral)
Posterior = Back (caudal)
e.g
Dorsolateral Prefrontal Cortex (dlPFC) = Top & outer part of the frontal cortex
Ventromedial Prefrontal Cortex (vmPFC) = Bottom & inner part of the frontal cortex
6
Q
what are the 4 lobes of the cerebral cortex
A
- frontal lobe
- parietal lobe
- temporal lobe
- occipital lobe
7
Q
describe the occipital lobe of the cerebral cortex
A
- procceses visual information (vision)
- percieves depth, distance, colour, movement
- recognising objects and faces
- includes the primary visual cortex
- the primary visual cortex receives information from the retina via the thalamus
- sends this information to the parietal lobe (object location)
- sends info to the temporal lobe ( which helps the brain to give meaning and awareness to objects in the visual field)
8
Q
describe the parietal lobe of the cerebral cortex
A
- touch and spatial positioning
= somatosensory processing - proccesses touch, pain, temperature, limb positioning
- receives sensory info from all over the body
- the somatosensory cortex interprets touch sensations
- also involved in hearing, memory, language, visual perception
- Wernicke’s area = speech comprehension
- angular gyrus = symbols and language
9
Q
describe the temporal lobe
A
= hearing and memory
- the primary auditory cortex = receives info from ears and gives them meaning
- Wernicke’s & Broca’s Areas: Language comprehension & production
-Memory formation, attention, learning (works with hippocampus and amygdala in limbic system)
10
Q
describe the frontal lobe
A
= decision making and personality
- executive functions
- Planning, self-control, emotions, problem-solving
- reward-seeking behaviour, empathy, selective attention
- personality -> impulse control and memory contribute to a persons characteristics
- damage can effect personality
primary motor cortex = controls voluntary movements
- each body part has a unique portion devoted to it
11
Q
how can we study the brain
A
- Post-mortem Dissection: Examining brain structure after death
- Animal Models: Studying similarities with human brains
- Neuroimaging:
- fMRI: Measures changes in level of naturally occuring oxygen in the blood to map which areas of the brain are more/less active during a task
- PET Scan: Injects radioactive substance into bloodstream as an indicator of metabolic activity in brain areas
- EEG: Measures electrical brain activity at the scalp
- good temporal but poor spatial resolution
temporal = when
spatial = where
12
Q
describe the structure of a neuron
A
Dendrites: Receive signals
Soma (Cell Body): Processes signals
Axon: Transmits electrical signals
Myelin Sheath: Speeds up signal transmission
Axon Terminals: Release neurotransmitters to next neuron
nodes of ranvier = allows signal rapidly to jump from node to node.
13
Q
white vs grey matter of the brain
A
Grey Matter: Cell bodies, processing centers (outer)
White Matter: Myelinated axons, transmitting signals (inner)
14
Q
functioning of the neuron
A
- dendrites receive input from other neurons via neurotransmitters
- this causes electrical changes that are interpreted in the cell body
- if the signal is strong enough it is passed on as an action potential down the axon
- myelin helps to stop the action potential degrading
- axon terminals receive the action potential and release NT across the synapse to other dendrites
15
Q
the membrane potential
A
= the difference in electrical charge between the inside and the outside of a neuron
-Inside of neuron is more negative than outside (-70mV resting potential) due to more sodium ions (Na⁺) outside the neuron and more potassium ions (K⁺) inside the neuron
-Controlled by ions (Na+, K+, Cl-)
16
Q
the action potential
electrical signals in neuron
A
- Depolarization: Neuron receives input, Na+ enters cell
- Threshold reached (-55mV) → Action potential triggered
- Repolarization: K+ exits cell to restore balance
- Hyperpolarization: Briefly becomes more negative before stabilizing
17
Q
depolarization
A
= Reaching Threshold & Sodium Influx
- A stimulus (e.g., neurotransmitter binding) opens Na⁺ channels on the dendrites.
- If enough Na⁺ enters and the voltage reaches -55mV (threshold), an action potential is triggered.
- Voltage-gated Na⁺ channels open, causing a massive influx of Na⁺ inside.
- The inside of the neuron becomes positive (~+30mV).
18
Q
repolarisation
A
= potassium outflux
-At +30mV, Na⁺ channels close, and voltage-gated K⁺ channels open.
-K⁺ exits the neuron, making the inside negative again.
-The neuron returns toward resting potential.
19
Q
hyperpolarisation
A
-K⁺ channels stay open too long, causing an overshoot (inside becomes extra negative, ~ -80mV).
-This is called the refractory period, where the neuron cannot fire again immediately.
20
Q
returning to the resting membrane potential
A
-The sodium-potassium pump restores the balance by:
Pumping 3 Na⁺ out
Pumping 2 K⁺ in
-The neuron is now ready to fire again.
-Cycle repeats when the next stimulus arrives.
21
Q
describe communication between neurons in terms of synaptic transmission
A
- Action potential reaches pre-synaptic axon terminal
- Neurotransmitters released into synaptic gap
- Neurotransmitters bind to receptors on post-synaptic neuron
- Signal is transmitted (excites or inhibits the next neuron to fire an action potential)
22
Q
what are the 7 key stages in brain development from conception to adulthood
A
- neural induction
- proliferation
- migration
- differentiation
- synaptogenesis
- cell death/ stabilisation
- synaptic rearrangement
23
Q
explain stage 1 neural induction
A
- day 18-24 of pregnancy
- genetically determined process
- neural tubes form and ends close
- neural patterning: cells aquire different identitites and dimensions
The neural tube forms very early in embryonic development, serves as the embryonic brain and spinal cord.
24
Q
explain stage 2- proliferation
A
- day 24 -125 of pregnancy
- genetically determined
- 250,000 cells produced per minute
- by day 125 (mid pregnancy) foetus has all of it’s brain cells
- Single layer of cells (Ventricular Zone) forms along the inner surface of neural tube.
25
explain stage 3- migration
- cells migrate from bottom level towards top level towards their final destination
- ventricular zone -> intermediate zone -> marginal zone
- radial cells act as scaffolding to help other cells migrate
- glial cells are support networks for neurons
26
explain stage 4 differentiation
- day 125 postnatal
- Cells differentiate into specific types (e.g., hippocampus, cerebellum).
- Cells express specific genes to make required proteins it needs for distinctive features
-Differences in connectivity, neurotransmitter molecules, receptor subtypes, proteins
- Second half of pregnancy mainly about cells differentiating and taking on their structure
27
explain stage 5- synaptogenesis
-Neurons grow more axons and dendrites, adding synapses.
-Neurons become functional cells.
1. growth cone approaches muscle fibre and makes contact
2. synaptic vesicles accumulate in axon terminal and synaptic receptors cluster at point of contact.
28
explain stage 6- cell death/ stabilisation
- Synaptic growth levels off and declines after the first year.
-Cell death prunes/sculpts synapses to bring balance.
29
explain stage 7- synaptic rearrangement
- early on axons reach out widely and form a diffuse pattern then adjustments are made ->
-Synapses strengthen or weaken based on use.
-Unused synapses die off, leading to more focused patterns of synaptic contact.
- a diffuse pattern of synaptic contact in early stages of development
- a more focused pattern of synaptic contact is present after synaptic rearrangement.
30
describe what happens from birth -> two years in terms of the brain
-Brain volume doubles in the first year.
-By age 2, reaches 80% of adult size.
Structural and functional framework in place by age 2
-Brain development after age 2 focuses on reorganising and fine-tuning circuits that are already established
-Sleep plays a role in development (babies sleep a lot).
31
brain development in childhood
- Rapid growth of cortical grey matter in first two years.
- Cortical white matter grows slowly throughout childhood and adolescence
32
Adolescence: Developing a More Streamlined Brain
-Higher ratio of white matter to grey matter.
Synaptic pruning:
Removes unused synaptic connections to refine brain function.
Occurs first in occipital/parietal lobes, then in frontal/temporal lobes.
Increase in axon myelination (white matter):
Speeds up information processing (up to 100x faster).
Improves neural efficiency.
-Prefrontal cortex (PFC) and subcortical structures still developing.
-Functional connectivity between PFC and subcortical regions stabilises only in mid-20s.
33
Imbalance Model of Brain Development (Somerville & Casey, 2010)
-Subcortical (emotional/reward) regions mature before prefrontal (cognitive control) regions.
-Adolescents rely more on emotion-driven motivational subcortical regions than rational/cognitive prefrontal control.
-Leads to increased risk-taking and emotional decision-making.
34
describe the effects of prenatal tobacco exposure on brain development
- Nicotine affects foetal brain development.
- toxins in tobacco can cross placental barrier
- dampens gene expression of foetal brain regulatory genes that are responsible for brain growth, myelination, and neuronal migration -> altering the brain structure and function
- Long-term effects: higher risk of psychiatric disorders and addiction.
35
effects of prenatal maternal stress on brain development
-foetus exposed to increased maternal cortisol
- too high cortisol impacts functional and structural brain connectivity involving amygdala, PFC and HPA axis).
- brain changes increase risk for behavioral and mental health problems later.
HPA = hypothalamic-pituitary arenal axis
36
effects of prenatal maternal depression on brain development
- associated with elevated maternal cortisol levels
- Elevated cortisol linked to larger amygdala in children.
- Higher functional connectivity in amygdala related to emotional regulation and activation. -> this is consistent with patterns of connectivity observed in adolescents and adults with major depressive disorder (areas of the PFC)
37
Effects of socio-economic status on brain development
Higher SES: prolonged structural and functional brain development, leading to more efficient cortical networks in adulthood.
Low SES: greater exposure to chronic stress accelerates brain maturation, increases allostatic load.
- Repeated activation of stress-related circuitry (e.g., amygdala, medial frontal cortex) could lead to faster maturation of that circuitry
- Stress could cause faster ageing of entire body via increased glucocorticoid levels and allostatic load (physiological "wear and tear") -> because were making the system work harder earlier.
38
effects of poverty on brain development
-Increased exposure to toxic stress in poverty affects brain development.
- affects overall mental and physical health as-well as life outcomes
- 8-9% reduction in grey matter in frontal/temporal cortex and hippocampus.
-grey matter reductions explain 15-20% of income-related achievement gaps.
39
effects of neglect on brain development
-Neglected children show reduced brain size.
- they showed a mean frontal-occipital circumference (reasonable measure of brain size) below the 5th percentile
-Brain size improved when children were removed from neglectful environment & reassessed after 1 year in foster care, especially when younger
40
changes to the prefrontal cortex with ageing
Retrogenesis: "Last in, first out" hypothesis.
= the process by which degenerative mechanisms reverse the order of acquisition in normal development.
- brain structures that mature early (e.g., sensory cortices) are more robust to ageing compared to the structures that mature later (frontal cortex)
- Grey matter in PFC declines by ~5% per decade after age 20 onwards.
41
changes to hippocampus with ageing
- Age-related decreases in hippocampal volume are associated with decline in multiple areas of cognition
-Working memory, episodic memory, processing speed, executive function
42
Compensatory Brain Activity Models: HAROLD Model
| - hemispheric reduction in older adults model
- Older adults show increased bilateral recruitment of prefrontal areas during tasks.
- More brain activity needed to maintain cognitive function (e.g., working memory).
43
Compensatory Brain Activity Models: PASA model
| posterior anterior shift in ageing model
= Older adults show recruitment of prefrontal cortex to compensate for reduced activation in the visual cortex.
- more brain activity recruited in order to maintain
44
why is studying self control important
Predicts positive life outcomes:
-Mental health
-Psychological well-being
-Better decision-making
-Stronger interpersonal relationships
Failure in self-control leads to:
-Addiction (alcohol, drugs)
-Debt & financial issues
-Obesity & poor physical health
45
definition of self control
= the ability to resist temptation and override impulsive responses in order to behave consistently with our long term goals
46
what is top down proccessing
| mechanism of self control
- abstract, rational goal directed behaviour controlled by cerebral cortex and prefrontal cortex especially the lateral PFC
-Cognitive control from the PFC over reward/threat responses.
47
bottom down processing
| mechanism of self control
- reflexive, environmentally triggered, emotioanlly driven behaviour
- more primitive structures
- from the brainstem, basal ganglia (ventral striatum), limbic system (amygdala and hypothalamus)
- Impulsive reward-seeking behaviors driven by subcortical structures.
48
successful self regulation vs self-regulatory failure(imbalance model)
successful: top-down control from the prefrontal cortex over subcortical regions involved in reward and threat processing
failure: top down control is diminished or when the balance in activity favours threat and reward systems (imbalance model)
-Weak PFC control leads to:
Stronger emotional & reward-driven impulses
More impulsive decision-making
49
Dietary Self-Control & Brain Structure
| food control
Structural MRI scans of cortical thickness and volume shows:
1. Thinner cortical thickness of PFC predicted lower dietary self-control in food choices
2. Higher volume of amygdala predicted lower dietary self-control (higher food cravings)
50
the balance model of self control study
| lopez et al., 2017
hypothesis: self control failures result from an imbalance in reward and executive control mechanisms
chronic dieters: fMRI when viewing food cues and 1 week self-report of giving into or resisting food desires
- activity in control systems(DIPFC) and reward systems (ventral striatum)
- behaviour predicted by the balance of activity, NOT the activity in one system alone
51
Cognitive Strategies to Improve Self-Control over temptation
| looking at regulating cravings for cigarettes and food images
Using fMRI, studies show:
-Thinking about long-term consequences reduces cravings.
-increase use of cognitive strategies -> increase strength of executive control -> creating habits over time
-Higher PFC activity → Better self-control.
-Lower ventral striatum & amygdala activity → Less impulsivity. (reward system)
52
the ventral striatum
- contains the nucleus accumbens
- associated with reward, reinforcement and addiction
- receives input from:
- amygdala, hippocampus and ventral tegmental area(dopamine rich area of midbrain)
53
the nucleus accumbens
- Central to addiction & cravings, responds to reward cues.
Higher nucleus accumbens activation to food cues predicted:
* Stronger food desires
* Higher enactment of food desires
* Higher amount eaten
54
Key Brain Areas in Self-Control & Reward-Seeking
1. Prefrontal Cortex (PFC) – Regulates impulses & exerts executive control.
2. Ventral Striatum – Linked to reward & reinforcement behaviors.
3. Amygdala – Processes emotions, influencing impulsivity.
4. Nucleus Accumbens – Central to addiction & cravings, responds to reward cues.
5. Ventral Tegmental Area (VTA) – A dopamine-rich region, part of the reward system.
55
Smaller Sooner vs. Larger Later Rewards
Higher impulsivity favors smaller, immediate rewards over delayed, larger rewards. -> linked to increased substance use, impatience, poorer school performance
- Linked to strong activity in the reward system (ventral striatum, amygdala, limbic system).
- greater connectivity between cortical regions within cognitive control systems -> more likely to choose larger-later reward (superior frontal cortex, dorsal anterior congulate cortex)
56
lesions and impulsivity
| Modifying brain activity in self-control
(McDonald et el., 2017)
131 combat veterans with brain injuries studied for impulsivity.
Prefrontal cortex damage → Increased impulsivity.
however:
- different areas affected in different individuals
-Possibility of functional re-organization following injury
- but there tends to be a relationship
impulsivity = behavior driven by immediate urges and executed without thoughtful deliberation or appropriate regard to consequence
57
Brain Stimulation & Self-Control Enhancement: (rTMS)
| Repetitive Transcranial Magnetic Stimulation
-Can temporarily alter brain activity by creating a temporary lesion effect
- applying it at a low frequency can reduce the likelihood of neurons firing
- applying it at low frequency to inhibit the left lateral PFC -> participants were less patient (less likely to wait for a larger reward)
58
Brain Stimulation & Self-Control Enhancement (tDCS)
| Transcranial Direct Current Stimulation
-Electrodes positioned on the scalp over cortical regions of interest
- Modifies neuron activity by altering resting membrane potentials.
tDCS over dorsolateral PFC (dlPFC) improves:
-Inhibition (Go/No-Go tasks).
-Decision-making & impulse control.
-Reduced risk-taking behavior (lasting 1-2 months).
- more top down control
59
the go/no go task
= a behavioral test for response inhibition and impulse control.
Participants are presented with two types of stimuli:
-Go Trials: A signal (e.g., a specific letter or image) instructs the participant to respond (e.g., press a button).
-No-Go Trials: A different signal instructs the participant to withhold their response.
Purpose: Measures how well individuals can suppress automatic or impulsive actions.
Findings in Adolescents:
-Increased false alarms to positive social cues (pressing a button when they should not have).
-Higher activation in the ventral striatum, indicating stronger reward sensitivity.
-Weaker PFC engagement, showing underdeveloped cognitive control.
- when emotional info is present adolescents perform worse than adults
- when no emotional info is present they perform just as well
60
meditation and self control brain circuits
-Enhances activity in executive control areas.
-Long-term meditation may alter brain circuits, improving self-regulation.
study with smokers and non smokers:
- 2 weeks of meditation training caused a 60% reduction in smoking with increased activiation in resting state anterior cingulate cortex and PFC
- smokers have lower activity in self control (ACC, PFC) areas consistent with models of addiction.
61
Marshmallow Test: Childhood Self-Control Predicting Adult Outcomes
-Those who resisted eating a marshmallow as a child had higher self-control in adulthood.
-Early self-regulation predicts long-term behavior & decision-making abilities.
- same children who did the test did tasks requiring inhibitory control as adults -40 years later
- those who were unsucessful in delayed gratification as children recruited the ventral striatum as adults
- those who were successful as children recruited the PFC as adults
62
adolescence
-Biological start: Onset of puberty.
-Social end: Establishment of independent roles in society.
-Brain connectivity between PFC & subcortical regions still developing until mid-20s
63
is it all about the prefrontal cortex?
- argued that adolescent reward seeking and risk takng behaviour was due to an underdeveloped PFC
- however children also do not have a mature PFC but do not display the same risk behaviours
- now, models consider circuitry and how different brain regions interact across development instead of just looking at the one area
64
imbalance model of brain development
Reward & emotional systems mature faster than cognitive control (PFC).
Adolescents more impulsive due to:
-Stronger ventral striatum activity (reward sensitivity).
-Weaker PFC regulation.
- greater reliance on motivational subcortical regions
65
findings of galvan et al and the nucleus accumbens
- adolescents showed stronger nucleus accumbens activation to rewards than children or adults
- activation of frontal regions was more similar to children
66
finding on manaques on how our social environment affects our brain
| Sallet et al. (2011)
- manaques living in larger social groups had larger volumes in mid-superior temporal sulcus and rostral prefrontal cortex
- each additional member of the social network contributed a 5% volume increase in these areas
- more activity in these brain areas develop it further
67
Neural Circuitry Involved in Social Cognition
| Social Brain Areas:
Amygdala: A central hub for processing social signals, connects to various cortical and subcortical regions.
Prefrontal Cortex (PFC): Key for decision-making, social reasoning, and understanding others' mental states.
ventrolateral amygdala = perception network
medial amygdala = affiliation network
rostrodorsal amygdala = aversion network
68
cortical vs subcortical meaning
Cortical links to the cortex or gray matter, while subcortical deals with the white matter in the brain
69
perception network
| social brain networks
- performs the sensory processes involved in detecting, encoding and interpreting social signals from others in the context of past experiences and current goals
- making sense of the world around you
- eg reading facial expressions
-Involves the ventrolateral amygdala and lateral orbitofrontal cortex which receive sensory input from sensory association areas of the temporal cortex, activated when responding to socially salient stimuli, e.g. facial expressions & identity
- Patients with impaired perception of facial expression and sarcasm comprehension have structural differences in e.g. amygdala, lateral orbitofrontal cortex and temporal pole.
70
affiliation network
| social brain network
=Linked to prosocial behaviors like comforting others in distress, activated by positive social feedback.
- Includes the ventromedial prefrontal cortex (vmPFC) and subgenual anterior cingulate cortex (ACC).
- e.g understanding their distressed and work out an appropriate action based on the social cue
-Decreased grey matter in vmPFC and ACC associated with diminished empathy and interpersonal warmth
- Nuclei in medial amygdala and ventromedial prefrontal cortex connect to subgenual anterior cingulate cortex and ventromedial striatum
71
aversion network
| social brain network
-Drives avoidant behavior in response to negative social cues.
e.g avoiding an untrustworthy appearing stranger
-Includes rostrodorsal amygdala and anterior cingulate cortex.
- Nuclei in rostrodorsal amygdala and caudal anterior cingulate cortex connect to pain-sensitive targets
-Regions in this network respond to untrustworthy faces and negative social feedback that elicit social aversion
- Frontotemporal dementia patients with atrophy(breaking down) in this network were more willing to trust strangers and more likely to fall for scams
72
empathy definition and it's association with pain
= natural capacity to share, understand and respond with care to the affective states of others
Empathy for Pain: Neural activation in areas like the anterior cingulate cortex and anterior insula during empathizing with others in pain
- involved in processing how unpleasant/aversive a stimulus is
- fMRI -> painful electric shock delivered to participant or romatic partner -> more pain experienced when partner received electric shock than self
73
self other distinction meaning
Ability to separate your feelings from others. Important for empathy and vicarious embarrassment.
74
when do we empathise - likeability
- participants played and economic game with confederates who played fairly(likeable) or unfairly.
- fMRI or self vs other painful stimuli
- seeing fair players experience pain activated anterior insula and anterior cingulate cortex
- for unfair players, men activated reward systems, not pain systems
-Participants saw fair player, experienced similar pain
Men delighted that cheaters got pain stimuli
75
empathy and cognitive appraisal
Study Setup: Participants watched videos of painful-looking procedures (e.g., biopsies, injections) on patients who did not actually feel pain (anaesthetised or neurological patients).
Observers felt discomfort, even though the targets were unaffected.
Key Brain Activations:
Anterior Insula & Anterior Cingulate Cortex (ACC):
Activated empathetic pain-related responses even when the target wasn’t in pain.
Reflects a bottom-up emotional response to aversive stimuli.
Temporoparietal Junction (TPJ) & Inferior Frontal Cortex:
Involved in self-other distinction and cognitive control.
Reflects a top-down response, helping us understand that the other person’s experience is different from our own.
76
Vicarious embarrassment and reality TV
= Vicarious Embarrassment: Activated by observing social norm violations.
-Involves regions like the anterior cingulate cortex (empathetic concern), inferior frontal gyrus (social identity) and middle temporal gyrus (theory of mind).
- Need to be able to put oneself in other person's shoes to experience vicarious embarrassment (doesn’t work if you can't relate to them e.g kids
77
what it psychological altruism
-Behavior that benefits others without immediate personal gain.
Involves brain areas like:
Medial Prefrontal Cortex (mPFC) and ventromedial striatum during decisions to act altruistically.
78
altruistic vs strategic choices
fMRI of altruistic vs strategic giving:
altruistic = no extrinisc reward but intrinsic satisfaction "warm glow"
strategic = extrinsic reward
both types of giving activated -> nucleus accumbens (extrinsic/intrinsic reward), anterior cingulate cortex (deciding between options) and ventromedial prefrontal cortex (social decision making)
altruistic more strongly activates:
- subgenual anterior cingulate cortex which is involved in:intrinsic motivation, charitable donations
- posterior ventromedial PFC associated with concrete primary rewards e.g warm glow
strategic more strongly activates:
nucleus accumbens -> extrinsic rewards can evoke stronger responses than intrinsic rewards
- anterior ventromedial PFC assocated with abstract secondary rewards and money.
79
the neuroscience of likes in adolescence
- fMRI of adolescents & young adults
- Reward circuits (e.g. striatum, ventral tegmental area) activated by giving and receiving Likes on Instagram
Facebook were going to release thumbs down reaction, but this was dismissed after knowing the impact it could have
80
abstract social thought in adolescents
- Adolescents' ability to interpret and react emotionally to social information becomes more sophisticated (development of PFC)
-Abstract thinking is the ability to think about concepts, ideas, and situations that are not physically present or concrete. It involves reasoning about hypothetical scenarios, understanding symbolic meanings, and thinking about broader concepts beyond immediate experiences.
81
the default mode network
= is a network of brain regions that are more active when a person is at rest or not focused on the outside world. It is often referred to as the brain's "default" mode because it activates during daydreaming, imagining
- building meaning, making social-psychological inferences
activity in the DMN predicted abstract construals:
- dorsomedial PFC
- ventromedial PFC
- inferior/posterior posteromedial cortices
- construals = an interpretation of the meaning of something
82
peer influence on risk taking
-Lateral Prefrontal Cortex: Responsible for reasoned decision-making in adolescents.
-Ventral Striatum: Drives motivation and reward, activated during peer-influenced risk-taking behaviors.
- adolescents made more risky driving decisions with peers present (two friends watching) than when alone
- with or without peers present, adolescents did not recruit the lPFC the way adults did
- peer presence heightened activity in reward circuits
- participants who showed stronger activation in ventral striatum when peers were present self reported being less resistent to peer influence in everyday life.
83
peer influence on risk taking in mice
- presence of peers increased alcohol consumption in adolescent but not adult mice
84
social exclusion
Cyberball Experiment: Shows the emotional impact of social exclusion, particularly in adolescents.
Includes activation of the insula (involved in physical pain/stress) and subgenual anterior cingulate cortex.
Interpersonal Competence: Adolescents with higher social skills and popularity show greater emotional responses to exclusion.
- Higher parent-reported interpersonal competence (social skills & popularity) associated with increased subACC activity
85
describe the cyberball experiment for social exclusion
- Participants told they are playing with two other people (really computer)
- Inclusion: other "players" equally likely to pass to participant or other
- Exclusion: after 10 passes, other two "players" pass only to each other
86
Temporoparietal junction (TPJ).
is crucial for self-other distinction, allowing us to differentiate our own thoughts, emotions, and actions from those of others. It plays a major role in Theory of Mind (ToM) and empathy.
87
Ventromedial prefrontal cortex (vmPFC).
is involved in processing rewards and reinforcing altruistic behavior, as well as making moral decisions and evaluating social interactions. It helps motivate us to engage in prosocial behaviors like helping others without expecting personal gain.
88
Anterior cingulate cortex (ACC).
is heavily involved in empathy for pain, especially when we feel distress or emotional pain in response to seeing a loved one in pain. It is part of the affiliation network and helps process the emotional experience of others' suffering.
89
what is stress
- stress as a response
- stress as a stimulus
- stress as a combination of stimulus and response
= a transaction between the individual and their environment
90
the sympathetic nervous system pathway in the stress response
-Fight or Flight" response
-Activates in response to perceived danger
process:
1. amygdala sends distress signal to the hypothalamus
2. hypothalamus sends signal through autonomic nerves to adrenal glands
3. adrenal glands release adrenaline (epinephrine) into the bloodstream
4. epinephrine circulates through the body and produces a range of physiological changes (increased heart rate, rapid breathing)
changes happen so quickly we are not aware- visuals centres not yet processed
91
the fight or flight stress response
Purpose: Evolutionary survival mechanism for physical danger (e.g., predators)
Effects on the body:
Increased heart rate and blood flow to muscles/organs
Rapid breathing & relaxed airways for more oxygen
Heightened alertness and senses (e.g., dilated pupils)
Energy release (blood sugar and fats)
Relevance: Originally for physical danger, but can also be triggered by psychological/emotional stressors (e.g., public speaking).
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Parasympathetic Nervous System (PNS) in the stress response
-"Rest and Digest" response
-Calms the body after danger has passed
-Slows heart rate, breathing, promotes digestion
- triggers responses to return body to homeostasis
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HPA Axis (Hypothalamic-Pituitary-Adrenal Axis)
| the hormonal response to stress
-Hypothalamus releases Corticotropin-Releasing Hormone (CRH)
-Pituitary gland releases Adrenocorticotropic Hormone (ACTH)
-Adrenal glands release cortisol (glucocorticoids)
Cortisol levels: Peak 15-30 minutes after stress exposure, and high in the morning, lower at night.
Chronic exposure to cortisol can be harmful.
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The Transactional Model of Stress
Stress as a Transaction: Stress responses arise when there is a perceived imbalance between situational demands and personal resources.
stress responses: cognitive, physiological + behavioural
- The stress response depends on how that individual interprets (appraises) a particular external stressor
- Interpreted different for different people ( individual level)
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what is cognitive appraisal
How we interpret or evaluate a stressor that influences our physiological and emotional response.
- can change after previous experience of a stressor (done exams before)
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types of cognitive appraisal
1. Primary Appraisal:
"Is this stimulus harmful?"
"Is this a threat or challenge?"
2. Secondary Appraisal:
"Do I have the resources to cope?"
"How can I handle this situation to get a positive outcome?"
Primary Appraisal: This involves the initial assessment of the event's relevance to one's well-being, determining if it is a threat, a challenge, or irrelevant.
Secondary Appraisal: This involves evaluating one's resources and coping abilities to address the situation, deciding how to respond.
Dynamic Process: Appraisal and reappraisal occur continuously (e.g., "I can handle this next time" or "I need a new strategy").
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what is appraisal psychology
| theory
Impact of Appraisal: The emotional reaction to stress depends on the individual’s perception of the situation, not the situation itself.
Reframing (Reappraisal): Changing the meaning of a stressful event to alter its emotional impact.
Control and Appraisal: The level of control over a situation impacts how stress is appraised—less control leads to more somatic (physical) symptoms and increased cortisol levels.
e.g a performance being judged by others
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study of controllability and threat-related activation
- participants exposed to electric shock and aversive sound(stressor)
- either controllable with button to stop or uncontrollable
- threat related regions (anterior insula) showed lower activation when participants had control over stressor
- our appraisals or a stressor affect brain activation responses
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study of appraisal and somatic symptoms
threat vs challenge appraisal of stressors in immigrants
- threat positively associated with somatic symptoms
- challenge negatively associated with somatic symptoms
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physiological impacts of acute stress on performance
= minor stress experienced on a daily basis (short term)
impairs:
- prefrontal cortex function ->impairing tasks that require complex, flexible thinking
- working memory impaired
enhances:
- amygdala and hippocampus function
- increased performance of simple, well rehearsed tasks
- classic conditoning of negative emotional stimuli enhanced
- Acute stress impairs PFC-mediated cognitive functions and switches the control of behaviour and emotion to more primitive brain circuit (keeping ourselves safe)
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PFC vs. Amygdala Response in stress and non stress
PFC (non-stress): Controls higher-order decision-making and planning.
- associated with non stressful situations where we have time to think
Amygdala (stress): Heightened emotional responses, shifts attention from task relevance to sensory salience (what's emotionally important).
- associated with stressful situations driving emotional responses
- Brain response pattern switches from slow, thoughtful PFC regulation to reflexive, rapid emotional responses of amygdala
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physiological impact of chronic stress
= Long-term exposure to stressors (e.g., financial issues, relationships)
- resulted in decreased dendrite length in the PFC in rats
- resulted in increased dendrite length in the amygdala
- this neuronal remodelling may lead to behavioural manifestations of enhanced emotionality under chronic stress
-Allostasis: Short-term adaptive responses to stress.
Allostatic Load/Overload: Long-term effects of stress that accumulate in the body ("wear and tear"), leading to health issues like immune suppression, heart disease.
Acute stress enhances immune function, while chronic stress suppresses it.
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study of chronic stress and memory
- chronic stress impairs prospective memory (remembering to perform a planned action)
- glucocorticoids bind to hippocampus which is a critical region for prospective memory
- altered hippocampal functional connectivity in chronic stress- predicted prospective memory performance
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racial discrimination as a chronic stressor
- discrimination and social exclusion provoke a stress response which has detrimental effects on health
- racial discrimination in the lab increases blood pressure and cortisol
- perceived discrimination associated with activity of pregenual ACC
- A high density of glucocorticoid receptors indicates altered stress processing
- activates brain regions involved in social distress and reduces activity in regions involved in emotional regulation
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post traumatic stress disorder
= Exposure to a traumatic event followed by development of a range of symptoms:
- Re-experiencing: Flashbacks, nightmares.
Hyperarousal: Vigilance, exaggerated startle response.
Avoidance: Avoiding reminders of the traumatic event.
- is a state of heightened responsivity to threatning stimuli
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brain changes in PTSD
- higher PTSD symptoms -> stronger activation of amygdala in response to threat
- Decrease in hippocampal volume (related to memory and stress regulation).
- however reduced volume is not a direct result of trauma exposure but more to do with the resulting ongoing symptoms
- volume lower in trauma exposed patients with PTSD but not trauma exposed patients without it
-studies suggest that smaller hippocampal volume is a pre-exisiting conditon that may make the brain more vulnerable to developing pathological stress responses
volume does not increase with successful treatment->
risk factor or result?
- interaction of genetics and environment?
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stages of sleep
- awake
- REM sleep
- non rem stage 1
- non rem stage 2
- non rem stage 3
- each stage occurs in one full cycle of sleep then repeats (without the awake)
rem = rapid eye movement
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how can we measure sleep
Polysomnography: Measures brain (EEG), eye (EOG), and muscle activity (EMG).
-People with insomnia show altered sleep architecture but still get some sleep. (spend more time in non-REM 2)
EEG = electroencephalography
EOG = electrooculography
EMG = electromyography
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the two process model of sleep regulation
Sleep is regulated by two key processes:
1. Process S (Sleep-Wake Homeostasis/Sleep Pressure): Builds up during the day, promoting sleep at night.
2. Process C (Circadian Rhythm): 24-hour biological clock that regulates sleep-wake cycles, influenced by light exposure.
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describe circadian rhythms
- daily biological cycles
- roughly 24hrs
- regulated by environmental cues (light exposure, eating, activity, socialising)
Cortisol (alertness hormone): Peaks in the morning, decreases throughout the day.
Melatonin (sleep hormone): Increases in the evening, promoting sleep.
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the suprachiasmatic nucleus (SCN)
Circadian Rhythms governed by the Suprachiasmatic Nucleus (SCN) in the hypothalamus, which receives light signals and activates melatonin secretion by the pineal gland
- is a specialised group of hypothalamic cells
- receives information about light exposure from ganglion cells in retina
- is the control centre for sleep-wake
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early animal studies on circadian rhythm
lesions = no circadian rhythm
transplant of SCN from rat with 20 hour period to a rat with 27 hour period -> recipient rat adopts the period of the transplanted SCN
master clock:
- almost all other tissues display circadian rhythm, coordinated by SCN
age:
timing of neuronal firings doesn't change with age but the strength of the signal changes (amplitude) -> weaker in older animals
- decrease in some neurochemical as age increases: glutamate, HA, NMDA, GRP
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Measuring Circadian Rhythms in the lab
Melatonin secretion timing: Helps determine an individual's sleep phase by measuirng the time at which melatonin levels rise above the threshold under dim light conditions in the laboratory
- melatonin is suppressed by light exposure so so we can measure when it starts to peak and diminish gives us an idea of an individuals phase
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measuring circadian rhythms outside the lab and social jet lag
- self reported measures -> asking people what time they would like to wake up/ go to sleep to measure circadian preference
- late/early circadian preferences become a state of dysfunction when required to work to mismatched social time
circadian preference misaligned with schedule = social jet lag
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changes in sleep-wake behaviour
Observed changes in sleep behaviours throughout adolescence / puberty:
-Later bedtimes & wake times on free days.
-Reduced sleep duration on weekdays (sleep debt).
-Weekend compensation (catching up on lost sleep).
-> characterised by short and ill timed sleep
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bioregulatory pressures to sleep-wake cycle in adolescence
-Developmental changes to both processes involved in sleep regulation (C and S)
- Delayed circadian rhythm: Melatonin release shifts later -> later sleep onset
-Slower sleep pressure build-up: Leads to extended waking hours and later sleep onset.
-Total sleep need remains ~9 hours, but sleep timing shifts.
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psychosocial pressures to sleep-wake cycle in adolescents
Bedtime autonomy: Parental control = earlier sleep onset and longer sleep duration
Academic pressure: Homework reduces sleep time.
Screen time & social media: Can delay sleep.
School start times: Misaligned with adolescent sleep patterns.
- psychosocial and bioregulatory pressures interact with each other
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impact of sleep on cognitive function
-Sleep deprivation reduces focus and sustained attention.
study:
- restricted participants school night sleep (5 days x 5 hours) plus weekend recovery (2 x 9 hours)
- attention steadily declined
- the weekend sleep was not enough to compensate
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impact of sleep on emotional wellbeing and mood
-Interrupted REM sleep impacts emotional regulation and memory consolidation.
- REM sleep important in emotional regulation
Poor sleep = higher risk of depression & anxiety.
- Treating sleep disturbance also improves depressive symptoms
Bidirectional relationship: Sleep problems worsen mood disorders & vice versa.
-Short sleep duration & insomnia symptoms linked to suicidal ideation
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consequences of social jet lag
Mismatch between social & biological clocks leads to:
-Daytime sleepiness and more napping
-Attention difficulties & lower academic performance
-Increased caffeine use & emotional instability
-Higher risk of injuries
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Shift Work Sleep Disorder
-sleep disorder caused by irregular work shifts misaligned with circadian rhythms -> body cannot adjust to schedule
-Leads to poor sleep quality & fatigue.
-Best sleep schedules shift gradually in a clockwise direction rather than shifts that change irregulary
-Switching between day and night shift does not give body time to adjust
-
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the perfect storm model
-explains why sleep problems emerge during adolescence by integrating biological, psychological, and social factors.
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zeitzebers
environmental variables that are capable of acting as circadian time cues. The light/dark cycle is the most important zeitgeber, but other stimuli such as melatonin can also function as zeitgebers.
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psychomotor vigilence test
objectively assesses fatigue-related changes in alertness associated with sleep loss, extended wakefulness, circadian misalignment, and time on task.
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the health belief model (HBM)
Assumptions: Health behaviour results from a desire to avoid or recover from illness and a belief that a specific health behaviour will prevent or cure the illness.
Original Model Constructs:
1. Perceived susceptibility – Perceived risk of illness.
2. Perceived severity – Belief about how bad the illness is.
3. Perceived benefits – Belief in the positive effects of the behaviour.
4. Perceived barriers – Perceived obstacles to engaging in the behaviour.
Example: Disagreeing with screening guidelines lowers the percentage of people getting screened.
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why is it important to understand behaviour change
Major public health problems are linked to preventable lifestyle factors, including cardiovascular disease, diabetes, and cancer.
Behaviour change plays a key role in addressing these health issues.
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Beliefs, Attitudes, Intentions, and Behaviours
Health-related behaviours are influenced by beliefs (e.g., perceived risk), attitudes (positive or negative evaluations), intentions (plans to perform a behaviour), and actual behaviours (actions taken).
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the theory of reasoned action (TRA)
Key Formula:
Attitude = Behavioral belief strength * Outcome evaluation.
Subjective norms = Normative belief strength * Motivation to comply.
Behavioural Beliefs: If I do this, then a specific outcome will occur.
Normative Belief: An individual’s perception of a behaviour influenced by the judgment of significant others (e.g., family, friends).
= a person's behavior is determined by their intention to perform the behavior and that this intention is, in turn, a function of their attitude toward the behavior and subjective norms
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critique of the theory of reasoned action
TRA assumes that intentions are the most significant determinant of behaviour.
Limitations:
-Not all behaviours are under complete voluntary control.
-Behaviour requires more than willpower (skills, resources, opportunities).
- you need to know HOW to change and what the change looks like
-Behaviours might not be easily modifiable even if intentions are present.
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suncream use example of TRA
- participants viewed slides on the importance of suncream use and reported their behaviour, intentions and attitudes before and one week after
- participants used suncream on more days (behaviour) after viewing slides
- medial prefrontal cortex activity predicted behaviour change above self-reported intentions and attitudes
- is involved in self-referential processing and implicit valuation
- whole brain search found behaviour change associated with activity in regions in taking the perspective of others (TPJ, temporal pole, posterior superior temporal sulcus)
- this is consistent with theories of persuasion -> behaviour change can result from encoding information about social norms
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two processes in TRA
behavioural beliefs -> attitude toward the behaviour -> intention -> behaviour
normative beliefs -> subjective norms -> intention -> behaviour
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theory of planned behaviour (TPB)
Perceived Behavioural Control (PBC) overlaps with self-efficacy (belief in one’s ability to succeed).
- the belief about whether one can control his or her performance of a behaviour;
PBC is influenced by past experiences and anticipated obstacles and predicts behaviour.
Example: If you believe you can control your behaviour (self-efficacy), you're more likely to perform the desired action.
The assumption: Behavioural intentions are central to the likelihood of engaging in a behaviour.
control beliefs -> perceived behavioural control -> intention -> behaviour
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Self-Efficacy and Brain Function
Self-efficacy: Belief in one's ability to perform a behaviour (e.g., resisting cravings).
-Brain regions like the mPFC and hippocampus are correlated with higher self-efficacy.
-Higher connectivity in these regions when managing cravings.
-When cravings are not perceived as an effort, brain activity in these regions is less significant.
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study of smoking cravings and self-efficacy
smoking related cues activate areas linked to:
reward = ventral tegmental area and ventromedial striatum
memory and learning = hippocampus and amygdala
motivation = anterior cingulste cortex
- the magnitude of brain resposnes to cue predicts success rates of quitting smoking
- self-efficiacy strategies reduced self-reported cravings "i can do it"
- associated with increased activation of rostral medial prefrontal cortex which is involved in appraisal of negative emotion and self assessment (components of self-efficacy)
- Positive correlation between self efficacy and mPFC and hippocampus brain regions
- When it's an effort to manage cravings, this is where we see the higher connectivity (cognitive effort to regulate cravings)
- But when its not deemed as an effort to individual, doesn’t really apply (ex-smokers with no cravings)
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The Intention-Behaviour Gap
-Intention to change alone is not enough to lead to behavioural change.
Measuring components like intentions may predict intentions better than actual behaviour.
- 40-50% of variance in intention explained
- only 20-30% of variance explained in behaviour
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Transtheoretical model (stages of change)
| motivation to change
developed by Prochaska & DiClemente in the 1970s to understand how some people quit smoking on their own and others needed support.
- a model of intentional change where stages are defined by current intention and past behaviour
example:
Motivation to change is necessary for therapeutic success in substance use disorders
Identifying neurobiological basis for motivation to chance could facilitate more effective therapeutic technique
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the six stages of change
1. Pre-contemplation: Not thinking about change.
2. Contemplation: Considering change.
3. Preparation: Making plans for change.
4. Action: Actively engaging in change.
5. Maintenance: Sustaining the change.
6. Relapse: Returning to old behaviours.
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study of motivation to change and cocaine use
- participants not seeking treatment (less motivated to change) showed increased activation to cocaine cues in a range of brain areas including the dorsolateral prefrontal cortex which is involved in cognitive control including decisions rewuiring response inhibition
- understanding why different stages of readiness to change are associated with different brain areas can help develop more effective therapeutic techniques
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Response Inhibition and Brain Function
Response inhibition: The ability to stop an undesirable action, crucial for self-regulation (e.g., avoiding harmful behaviours).
Brain regions involved in inhibition and readiness to change may indicate physiological readiness to make changes beyond just verbal communication
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stages of change readiness and treatment eagerness scale (SOCRATES)
ambivalence = wonder if they have a problem, contemplating change
recognition = acknowledging they have a problem, strong desire to make changes
taking steps = taking positive actions to stop use or to prevent relapse
- taking steps associated with increased activation in the dorsolateral prefrontal cortex
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definition of a vegatative state (VS)
Definition: A condition where a patient shows wakefulness but lacks awareness.
Diagnosis:
-No sustained, reproducible, purposeful, or voluntary behavioral response to visual, auditory, tactile, or noxious stimuli.
-Repeated examinations reveal no signs of awareness or intentional behavior.
Key Characteristic: Wakefulness without awareness.
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definition of a minimally conscious state (mcs)
Definition: A state of partial consciousness where patients show inconsistent but reproducible evidence of awareness.
Characteristics:
-Patients can exhibit sustained, reproducible, or voluntary behavioral responses to sensory stimuli (e.g., visual, auditory, tactile).
-They are not consistently responsive, but there is occasional evidence of awareness.
Key Characteristic: Some awareness of self and environment, though inconsistent.
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Distinguishing Between Vegetative State and Minimally Conscious State
Key Difference: Awareness is the critical factor.
Vegetative State: No awareness of self or environment.
Minimally Conscious State: Evidence of inconsistent awareness.
Misdiagnosis Rate:
40% of MCS patients are misdiagnosed as being in a vegetative state (Andrews et al., 1996).
Challenges in Assessment:
Major difficulty: Assessing the preserved cognitive function in patients who cannot produce behavior that is detectable with standard bedside assessments.
Neuroimaging: Essential for revealing covert cognition (awareness not observable through behavior).
Family Recommendations:
For families, it’s important to consider neuroimaging as a tool to detect potential covert consciousness in patients, as behavior alone may not fully reveal cognitive function.
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what is covert consciousness
Refers to residual awareness in patients who, despite severe brain injury or neurological disorder, still maintain cognitive function but cannot express it through typical behavior or communication.
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Neuroimaging Techniques for Detecting Covert Cognition: fMRI
In studies, patients with covert consciousness showed brain activation patterns similar to healthy controls when asked to imagine specific tasks.
Negative findings in fMRI cannot prove lack of awareness, as false negatives are common in functional neuroimaging, even with healthy individuals. Therefore, caution is needed when interpreting results.
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Identify covert cognition with fMRI
| boley et al (2017)
- healthy participants asked to do mental imagery tasks
1. motor imagery: imagine playing tennis -> normally activates the supplementary motor area
2. spatial navigation: imagine moving through the rooms in your house
- each for 30 seconds -> normally activates the parahippocampal gyrus, posterior parietal lobe and the lateral premotor cortex
findings:
- 100% accuracy when differentiating patterns of activation between rest, spatial navigation and motor imagery for all subjects
- indicative of awareness
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Identify covert cognition with fMRI
| owens et al (2006)
-23 year old women with severe traumatic brain injury from road traffic accident
- fulfilled criteria for vegetative state after 5 months
- fMRI scan performing mental imagery tasks (the same as the healthy participsnts)
- the activation in predicted cortical areas was indistinguishable from healthy controls
- same brain pattern highlighting she was consciousally aware or herself and surroundings
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Identify covert cognition with fMRI
| monti et al 2010
aim: determine what proportion of patients could reliably modulate their brain activity
- 23 VS patients, 31 mcs and controls
-5/54 patients (9%) showed brain activity indistinguishable from healthy controls.
- 1 patient used mental imagery to answer "yes/no" questions.
-Some "vegetative" patients retain awareness.
Neuroimaging better than bedside tests for detecting consciousness.
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Identify covert cognition with fMRI
| monti et el 2009
- 20 healthy volunteers and 1 MCS patient
- listening to words passively vs count a target word
- to test executive function without requiring any behavioural expression
- counting vs listening activated a fronto-parietal network associated with working memory and target detection
- the brsin response should carry the same weight with respect of evidence of areness as a motor response
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limitations of using fMRI in identifying covert cognition
- physical stress of transferring patients to fMRI facility
- Movement artefacts in imaging data from patients who are unable to remain still
-Metal implants are common in traumatically injured populations and rule out fMRI (can no longer use it)
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advantages of using EEG in identifying covery cognition
-Cheaper and more accessible for bedside use.
-Unaffected by metal implants (important for patients with traumatic brain injury who may have metal implants).
-Does not require patients to be moved, which could cause additional stress or harm.
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limitations of using EEG
-EEG results should not be generalized to all vegetative state patients, as each patient’s brain function may vary depending on the type and extent of trauma.
-EEG detects covert cognition but is influenced by task comprehension and memory. Multiple levels of understanding are necessary to produce the appropriate responses.
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Passive tasks to detect covert cognition
Studies on passive tasks show similar brain responses to healthy individuals, but the results are not consistent across all patients.
-Passive tasks (e.g., listening to soundtracks) may evoke brain activation similar to a healthy response.
Active tasks (e.g., responding to commands) have shown inconsistent results, suggesting that covert cognition detection may work better with passive tasks, though not all patients respond similarly.
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Implications and Contributions to Decision-Making of identifying covert awareness
- neuroimaging may increase opportunities for communication in behaviorally non-responsive patients with covert awareness, potentially allowing them to contribute to quality of life decisions
-Even if behavioral responses are limited, the fact that a patient is breathing and surviving indicates some level of consciousness, which is important when making decisions about long-term care.
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complex tasks and conscious awareness
complex tasks require aspects of top-down cognitive control:
- sustained attention
- response selection
- language comprehension
- working memory
- suggesting conscious awareness
however it is likely many patients lack the cognitive resources for carrying out active tasks in the scanner
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can passively watching a suspenseful short movie produce fMRI evidence of concious experience?
- one patient who was behaviourally non responsive for 16 years showed activity in the frontal/parietal network synchronised to the healthy controls
- this is evidence that the patient could engage in complex thoughts about real world events in his environment
- drawback of this study is that most VS patients do not have sustained visual fixation so they created an auditory online soundtrack from a movie
- VS patients showed similar activation
- 7 months later the patient recovered and could talk
- he could report details of the movie soundtrack despite being vegrtative at the time
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what can studying the brain and nervous system tell us about behaviour?
- why does it hurt to see a loved one in pain?
- why do teenagers do risky things when their friends are watching?
- is it possible to communicate with someone in a coma?
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Can we hold adolescents equally responsible for crimes as adults?
| Adolescent Brain Development
dual system model: sociomotional vs control systems
- rapid increase in dopaminergic activity in amygdala and ventral striatum during puberty
- structural development of prefrontal cortex and its connection to sociomotional areas, unfolds more slowly
- the temporal gap = period of heightened sensitivity to risk-taking
the context matters: emotional information and social setting
implications for juvenile crime -> usually emotionally aroused with peers
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criminal responsibility in adolescents
- if they have diminished responsibility, they should not be punished as severly as someone who does not
- diminished responsibilty = factor must be outside of a persons control
- brain regions that regulate impulse control and resistence to peer pressure are still developing -> outside of their control
- so are they less responsible for their crimes than adults?
Adolescents may struggle with impulse control and long-term planning.
Their actions are influenced more by peer pressure and emotions than rational thought.
Raises ethical and legal questions about holding adolescents to the same criminal standards as adults.
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when are brains mature?
- no single answer- it depends
- structural development continues into 20s and 30s
- subcortical and occipital regions reach a stable state earlier
- prefrontal cortex shows late development
- one study showed progressive volume changes from 15-90 that never leveled off
- brain systems in self regulation do not fully mature until early adulthood
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implications for policies
- different circumstances make different demands on adolescents brains and abilities
- state laws require a waiting period and consultations with an adult before adolescents can access abortion -> this creates a circumstance where adolescent decision making is just as competent as adults
- Roper vs Simmons case in the US supreme court got the juvenile death penalty abolished as the APA submitted a argument that adolescents are not as mature
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age ranges for responsibility
- Steinberg argues from 15-22
options for policy makers:
- select midpoint for all issues (18)
- decide on a case by case basis between 15-22years
- introduce a middle category: children, adolescents, adults
- some states have graduated drivers licence meaning you can drive but cannot carry a passenger until a certain age -> reducing peer influence on risk- taking.
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BPS guidelines for working with animals
- obligation to avoid or at least minimise discomfort to living animals
- any procedure that may cause pain or suffering is regulated under the animals act 1986
- requires a licence
- is only granted after weighing the benefits of the research against the harm to the animals
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The 3Rs Principle
1. Replacement
- Use alternatives to animal research when possible
- exisiting video material, secondary analysis
2. Reduce
- use the minimum number of animals needed for the research goals required by the animal act
- appropriate pilot studies, good experimental design, appropriate use of statistical tests, reliable measures of behaviour
3. Refine
- Improve experimental techniques to reduce suffering and improve animal welfare.
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Arguments For & Against Animal Research
For: Advances in medicine, understanding of brain functions, benefits for human & animal health.
Against: Ethical concerns, potential pain and distress, availability of alternative methods.
- illegal to test cosmetics on animals in the EU since 2009 and illegla to sell cosmetics where either the product or any ingredients have been tested on animals since 2013.
