biological Flashcards

(451 cards)

1
Q

what is cephalisation?

A

occurs in bilaterians where nervous tissue is concentrated toward one end of an organism
80% water

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2
Q

what is the CNS?

A

brain and spinal cord

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3
Q

what is the PNS?

A

NS other than brain and spinal cord

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4
Q

what are the two main types of cells in the NS?

A

neurons and glia

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5
Q

what are the functions of glia?

A

glia are essentially support cells
in the NS and have many vital roles:
1. provide structure, i.e., surround neurons and hold them in place (astrocytes)
2. insulate nerve cells with myelin sheaths
(oligodendrocytes in the CNS, schwann cells in the PNS)
3. supply nutrients and oxygen to neuron
(astrocytes)
4. removal of dead neuronal tissue & immune defence of the CNS (microglia: phagocytes)
5. during development, glial cells provide scaffolds for neurons to migrate to their final destinations (radial glia)
6. modulate neurotransmission in the synapses

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6
Q

multiple sclerosis

A

common symptoms: vision problems, fatigue, difficulties with
walking
cause: demyelination of axons in the brain and spinal cord

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7
Q

neuron structure: soma

A

contains the nucleus which contains the cell’s genetic material organised as DNA
contains mitochondria (metabolism), ribosomes (protein synthesis), ER (transports proteins to other locations)
also contains golgi and nissl bodies

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8
Q

neuron structure: axon

A

thin fibre that transmits to other neurons
the distal end has many branches that swell and form a presyanptic terminal
some axons have boutons along their fibres

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9
Q

neuron structure: dendrites

A

branching fibres reciving information from other neurons

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10
Q

neuron structure: myelin sheath

A

insulating layer that speeds up electrical transmission

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11
Q

how did myelin sheath form?

A

an ancient virus helped to form a myelin sheath around
nerve fibres

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12
Q

afferent neurons

A

sensory neurons that carry information from receptors

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13
Q

efferent neurons

A

carry signals away to the effectors (muscles/glands)

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14
Q

interneurons

A

connect other neurons

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15
Q

what is resting potential?

A

the membrane of a neuron maintains an
electrical gradient (the difference in
electrical charge) between the inside and
outside of the cell
the inside is slightly lower than outside (-70mV)

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16
Q

what are the two stages of excitation of neurons?

A
  1. transmission of information from
    the exterior through dendrites to the cell
    body
  2. transmission from the cell body through the axon out of the neuron
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17
Q

excitatory synapses

A

EPSP is a change in polarisation moving along dendrites toward the cell’s body
EPSP is positive -> provokes depolarisation

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18
Q

inhibitory synapses

A

IPSP is a change in polarisation moving along dendrites toward the cell’s body
IPSP is negative -> provokes hyperpolarisation

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19
Q

what is summation?

A

postsynaptic potentials sum up when meet
other postsynaptic potentials or if followed by others

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20
Q

what are the two types of summation?

A

over space (spatial) – from different dendrites
over time (temporal) – from the same dendrites

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21
Q

all or nothing principle

A

the amplitude of an action potential is independent of the
amount of current which produced it, i.e. larger currents do not
create larger action potentials (+30mV)
an action potential will occur fully or not at all

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22
Q

propagation of action potentials

A

first action potential – on the axon hillock
action potentials move down an axon towards another cell using saltatory conduction
APs hop along the axon recurring at successive nodes of
ranvier = fast propagation
myelin prevents any charge leakage through the axon

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23
Q

postmortem studies (19th and 20th century)

A

relationship between brain damage and loss of function
damage to broca’s area in the left frontal lobe found via PM

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24
Q

microscopic analysis of neural tissue

A

brodmann areas
6 layers of brain cortex (neocortex)
4 layers of hypothalamus (archicortex)

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25
postmortem microscopic anaylsis of tissue
5 brains of people previously diagnosed with dyslexia- smaller neurons in magnocellular layers of LGN in thalamus
26
structural imaging- in vivo examples
computerised tomography (CT) magentic resonance imaging (MRI)
27
computerised tomography
narrow X-ray beam is rotated around the patient. CT captures multiple projections from many angles on opposite side of the patient, an array of X-ray detectors measures how much radiation passes through the body at each angle bone absorbs a lot → appears white air absorbs very little → appears black soft tissue → various shades of gray many slices are taken in quick succession to form a 3D model of the area being scanned
28
contrasts and CT scans
contrast dye may be injected into the blood for better contrast (not compulsory) without contrast: a standard CT scan can show basic structures of the brain (the skull, brain tissue, and large blood vessels). it is useful for detecting issues like brain bleeding, fractures, or large tumors. with contrast: highlights blood vessels, tumors, and areas with abnormal tissue, facilitating identification of specific issues like tumors, infections, or vascular abnormalities
29
CT evaluation
fast and cost effective x-ray exposure less detailed than other methods (MRI)
30
CT scan example- hier (1978)
24 people with dyslexia atypical anatomical asymmetry in brains of some people with dyslexia
31
magnetic resonance imaging
MRI uses a very strong magnet to align the spins of hydrogen nuclei (protons) along the direction of the magnetic field radiofrequency (RF) pulse is sent into the brain, which knocks the protons out of alignment when the RF pulse stops, the protons start to relax emit signals emitted signals are detected by receiver coils around the head a computer then reconstructs these into detailed cross-sectional images of the brain
32
magnetic field of MRI
25000 times the magentic field of the earth
33
MRI evaluation
no x-ray exposure great spatial resolution expensive time consuming
34
MRI example- sun (2018)
170 children (ADHD and control) no overall difference between ADHD and controls in total bran volume or total grey/white matter volumes differences at left temporal lobe, bilateral occipital cortex and areas arounf the left central sulcus the mean classification accuracy with MRI studies classifiers to discriminate people with ADHD from control subjects=74%
35
diffusion-tensor magnetic resonance imaging (DTI)
imaging method to study white matter tracts measuring the direction of diffusion of water molecules (water diffusion in the brain tends to track along bundles of white matter fibres)
36
investigation of nervous system activity
bioelectric activity - EEG - evoked potentials energy consumption (indirectly) - fMRI - PET
37
electroencephalography
electrical brain activity measure on the scalp in living people sensitive to postsynaptic dendritic currents generated by a population of neurons that are active in synchrony
38
analysing brain waves
delta (0.5-4Hz)=sleep theta (4-7Hz)=sleep, meditation, excess theta for age is abnornmal and may be due to focal subcortical lesions alpha (8-12Hz)=relaxation beta(12-30Hz)=alertness, attention, REM sleep gamma (30-100Hz)
39
abnormal discharge on an EEG
spike and wave pattern
40
EEG example- santarone (2023)
292 routine EEG recordings of preschool children (age < 6 years) with ASD in 78.0% of cases the EEG recordings were found to be abnormal, particularly during sleep paroxysmal slowing and epileptiform abnormalities were found in the 28.4% of the subjects, confirming the high percentage of abnormal polysomnographic EEG recordings in children with ASD
41
EEG evaluation
excellent temporal resolution ( <1ms) inexpensive, accessible poor spatial resolution (scalp signal is a sum of signals from different brain sources whose locations are difficult to infer)
42
animal studies- single cell recordings
neurons behvaiour can be examined through microelectrodes but does not stimulate it
43
event-related potentials
EEG activity time-locked to an external event (e.g. sound, visual signal, response etc) averaged across multiple occurrences of the same event to reduce noise EPR peak direction (positive, negative), amplitude and timing used to investigate brain processes in different cognitive domains
44
single cell recording example- quiroga et al (2005)
single-cell recording of cells in the hippocampus that recognise sepcific people jennifer aniston neuron
45
magentoencephalography (MEG)
recording of magnetic fields produced by electrical currents in the brain using arrays of SQUIDs (superconducting quantum interference devices)
46
MEG evaluation
signal unaffected by skull, meninges more sensitive to activity at sulci millisecond temporal resolution potetntially good spatial resolution (2-3mm) expensive and limited availability
47
functional magnetic resonance imaging
activated neurons requires more oxygen blood flow increases to the active brain region, and the oxygen level in the blood goes up. fMRI detects this change in oxygen levels in the blood using a method called BOLD (Blood Oxygenation Level Dependent) imaging oxygen-rich blood has slightly different magnetic properties compared to oxygen-poor blood computer creates detailed images of brain activity plotted against structural MRI pictures. active areas of the brain appear brighter on the fMRI scan.
48
haemodynamic response function
the change in BOLD over time is known as the haemodynamic response function - makes it possible to localise active voxels - peaks in 6-8 seconds after the event and is extended over time which limits the temporal resolution of fMRI
49
fMRI evalution
excellent spatial resolution poor temporal resolutiom very expensive discomfort susceptible to artifacts (head shape, movement)
50
fMRI example- bierlich (2024)
▪ 33 persons with autism and 29 controls ▪ participants viewed short, silent videos of social interactions. ▪ a general difference in processing social interactions was found between observers with autism and controls (decreased neural activation in the right middle frontal gyrus, angular gyrus, and superior temporal areas). ▪ participants with autism showed similar neural activation patterns as control participants in areas responsible for perception of temporal dynamics of social interactions.
51
positron emission tomography
measures brain activity, local blood flow, and metabolism injection of a tracer (a small amount of radioactive material) into bloodstream (usually glucose) emission of energy: as the tracer breaks down (radioactive decay), it emits positrons (antielectrons). when these positrons meet electrons, they cancel each other out, radiating energy (gamma rays). the PET scanner detects gamma rays and creates detailed images based on where the tracer has been used most (is accumulated).
52
PET evaluation
can be used to study neurotransmitter systems (radioactive tracers can be designed to bind specifically to certain neurotransmitter receptors) sensitive to subtle changes radiation exposure low spatial/temporal resolution expensive limited availability discomfort
53
PET example- volkow (1990)
10 persons addicted to cocaine in process of detoxification and 10 controls. after 1 week of detoxification postsynaptic dopamine receptors availability was decreased in people with addiction. after 1 month of drug-free interval – similar to normal levels.
54
PET vs fMRI
PET- blood volume, fMRI- blood oxygen conc. radioactivity vs no radioactivity temp reso= 30 seconds vs 1-4 seconds spatial= 10mm vs 1mm in fMRI some brain regions are hard to image like near sinuses
55
examining the effects of brain damage: informal tasks
drawings of different emotional states by a patient with amygdala dysfunction in limbic system
56
examining the effects of the brain: observation
oberseration of phineas gage - intact speech, movement, intelligence – disinhibition of inappropriate behaviour – the injury changed his personality and behaviour the damage of ventral part of prefrontal cortex
57
modern brain stimulation
in healthy participants (noninvasive): transcranial magnetic stimulation (TMS) neurons are excited/inhibited by externally applied time-varying electromagnetic fields generated by a coil located above the head
58
split brain studies and epilepsy
large electrical discharge in focal area then spreads throughout the brain. generalized, grand mal drop seizures are potentially dangerous as they can lead to further injuries surgical intervention -> separation of the brain hemispheres
59
spilt brain studies and the visual pathway
visual information proceeds to the contralateral (opposite) hemisphere hemispheric transfer necessary for each hemisphere to perceive ipsilateral space and for midline fusion lateral & medial pathways contralateral control of distal effectors ipsilateral control of proximal effectors only can therefore use unilateral inputs and unilateral response to measure hemispheric function
60
neurotypical development
prevalence=15-20% - onset during infancy or children - impairment or delay in functions related to biological maturation of the CNS - steady course that does not involve remission or relapse - common family history (genetic factors) - possible change in pattern with age - heterogenity
61
dated dyselxia definition (morgan 1896)
originally used to describe the loss of the ability to read as the result of brain damage
62
ICD-11 definition of neurodiversity
learning difficulties result in significant impairment in the individual’s academic, occupational or other important areas of functioning. if functioning is maintained, it is only through significant additional effort
63
medical model to neurodiversity paradigm
clincial classifications (categorical) to neurodiversity spectrum comorbidity of symptoms and syndromes is the rule rather than the exception
64
prevalence of developmental language disorder
7%
65
prevalence of ASD
2%
66
prevalence of dyslexia
15%
67
prevalence of dyscalculia
6%
68
prevalence of dyspraxia
6%
69
prevalence of ADHD
4%
70
what is a single cognitive deficit model of developemental disorders?
looks for a specific cause of a syndrome and suggests a simple cause-effect relationship
71
single cognitive deficit model of dyslexia
phonological deficit
72
single cognitive deficit model of ADHD
inhibition deficit
73
single cognitive deficit model of autism
theory of mind deficit
74
prevalence of comorbid conditions and ADHD (kadesjö and gillberg, 2001)
87% of persons with ADHD have one or two other neurodevelopmental conditions
75
prevalence of comorbid conditions and ADHD (andrewes et al., 2002)
21% of persons with ADHD have three or more other neurodevelopmental conditions
76
comorbiditoy of developmental language disorder and dyslexia symptoms
25-90% (tomblin et al., 2000)
77
comorbidity of underlying symptoms
unclear whether underlying symptoms are: - causally related to the core symptoms of the syndrome - the result of a common cause - outcomes of the syndrome
78
examples of common additional symptoms in developmental disorders:
1. visual stress 2. auditory processing disorder 3. atypical executive functions
79
what is visual stress?
visual stress in response to bright, contracting stimuli - common in ASD - cooccuring in dyslexia
80
visual stress and the grid illusion
people with dyslexia perceive illusory effects more strongly than non-dyslexics this is because the lateral inhibition is stronger or they experience more glocal intergration of the contrast response
81
coping strategies for visual stress
avoiding strong light reducing contrast
82
auditory processing definition
central/auditory processing disorder (C/APD) normal hearing pure tone sensitivity but experience auditory processing difficulties in everyday life that are indexed by reduced performance in other more sophisticated audiometric tests such as speech audiometry in noise or complex non-speech sound perception difficulty processing brief, rapidly presented stimuli and/or making frequency discriminations
83
auditory processing symptoms
* difficulty following verbal instructions * need instructions to be repeated * slow to process verbal information * easily overloaded with auditory information -> daydreaming, distracted * difficulty sustaining attention on speech
84
APD and ASD (lau et al., 2023)
70% of children diagnosed with autism show CAPD
85
APD and dyslexia (king et al., 2003)
50% of children with dyslexia show CAPD
86
APD And language impairment (sharma et al., 2009)
76% of children with CAPD have language impairment
87
APD and ADHD (ricco, 1994)
50% of children with ADHD have CAPD
88
executive functions examples
planning, monitoring, correcting and executing associated with prefrontal cortex slow maturation
89
what is dyschronia?
condition of cerebellar dysfunction in which an individual cannot accurately estimate the amount of time that has passed
90
dyschronia and dyslexia
time management problems difficulties in visual/auditory processing of transient stimuli (llinas, 1993)
91
problems with single deficit theories of developmental disorders
theory of mind deficit provides a good explanation of the problems in social interaction and communication in autism, but - does not explain the third autism core symptom: repetitive behaviours and restricted interests; - does not explain some of the cognitive strengths found in autism (e.g. in visual perception)
92
multiple cognitive deficit model of developemental disorders
in multifactorial causation, more than one causal factor is required to yield a given outcome e.g phonological deficit theory in dyslexia and an inhibition deficit theory in ADHD - dyslexia is defined by cognitive tests whereas ADHD is defined by behaviour ratings (usually from teachers and parents), the comorbidity is not due to definitional overlap
93
MCDM and atypicality
* traditional boundaries between typical and atypical are arbitrary (based on standard deviation) * neurodiversity paradigm and Multiple Cognitive Deficit Model suggests diffused boundaries between typical and atypical)
94
cultural relativism and single deficit theories
single deficit theory of dyslexia may be restricted to the english language and thus lack generalizability phonological deficits is observed in only 15% of chinese readers with dyslexia (ho et al., 2002).
95
risk and protective factors in multiple cognitive deficit models
etiology of complex behavioural disorders is multifactorial and involves the interaction of multiple risk and protective factors factors alter the development of cognitive functions necessary for typical development no single etiological factor is sufficient for a disorder comorbidity among complex behavioural disorders is to be expected because of shared etiologic and cognitive risk factors vulnerability is often continuous and quantitative, rather than being discrete and categorical
96
benefits of MCDM
- helps explain changes of pattern (sub-types) with age - implicatiosn for treatment
97
challenges of MCDM
- theory is diffcult to falsify - currect cross sectional studies cannot establish causality
98
what does the neurodiversity paradigm reject?
rejects the assumption that typical brains function correctly while atypical brains function incorrectly since people with typical development are more numerous, the world is organised according to their needs
99
what is an IPSP?
hyperpolarises a postsyanptic neuron so decreases the rate of action potentials
100
what is an EPSP?
depolarises a neuron so increases firing rate of action potentials
101
process of synaptic transmission
1. action potential in presynaptic neuron 2. vesicle fuse with neuron and releases neurotransmitters to syanptic cleft 3. neurotransmitters bind to receptors and opens channels in postsynaptic neurons membrane 4. movement of ions causes potential in postsyanptic
102
when an action potential reaches the end of an axon, depolarisation opens...
voltage gated calcium ion channels in the presynaptic membrane
103
how long does the transmission of information in the synapse take?
2ms (0.0000001cm/ms)
104
what is the speed of conduction along an axon?
4cm/ms
105
the quantity of neurotransmitters released impacts...
the robustness of changes in the postsynaptic membrane
106
what is the role of a synapse?
send chemical information through the gap and opens ions' gates in the postsynaptic neuron
107
how many neurotransmitters do humans have?
around 100
108
excitatory synapse- Na+
sodium gates open and sodium ions enter the postsynaptic neuron = EPSP
109
inhibitory synapse- Cl-
chloride gates open and enter the postsynaptic neuron = IPSP
110
inhibitory synapse- K+
potassium gates open and potassium ions leave the postsynaptic neuron = IPSP
111
examples of excitatory neurotransmitters
glutamate, epinephrine, norepinephyrne
112
examples of inhibitory neurotransmitters
GABA and glycine
113
examples of excitatory and inhibitory neurotransmitters
acetylcholine, dopamine and serotonin
114
what are receptors?
chemicals specific to a given type of neurotransmitter
115
what are the two types of receptors?
ionotropic (fast) and metabotropic (slow)
116
example of an excitatory ionotropic receptor
glutamate
117
example of an inhibitory ionotropic receptor
GABA
118
ionotropic effects on postsynaptic membrane
as soon as the neurotransmitter binds to a receptor on the membrane, the ion gates open the process starts in 1ms and lasts for 20ms
119
metabotropic effets on postsyanptic membrane
a sequence of metabolic changes in a larger area of the cell the process starts in 30ms and lasts for seconds, minutes or longer
120
what senses use ionotropic synapses?
vision and hearing
121
what senses use metabotropic synapses?
taste, hunger and fear
122
what are neuromodulators?
is a chemical in the brain that changes (modulates) how neurons communicate with each other — but in a more general and long-lasting way than a normal neurotransmitter.
123
what chemicals may activate metabotropic receptors?
dopamine, norepinephrine, serotonin, neuropeptides and sometimes glutamate and GABA
124
what is synaptic strength?
the strength of a synapse is defined by the size of postsynaptic potential
125
synaptic strength may very over time:
* short-term changes (seconds, minutes) * long-term changes (memory and learning effects, brain plasticity)
126
what is long-term potentiation?
intensive use of a synapse may lead to its potentiation -> stronger effects on postsynaptic membrane this is a mechanism behind memory and learning
127
what is synaptogenesis?
formation of synapses
128
what is synaptic pruning?
very intensive in 2-16 years old humans elimination of unnecessary synapses is beneficial learning - > pruning
129
how are used neurotransmitters terminated?
1. reuptake- brings neurotransmitters back to the presynaptic neuron (by chemicals called transporters) 2. broken down- e.g acetylcholine 3. diffusion- big neurotransmitters (peptide) do this
130
wha does reuptake of neurotransmitters concern?
recycling process that concerns serotonin and the catecholamines (dopamine, nerepinephryne, epinephrine)
131
what is acetylcholine broken down into?
acetylcholinesterase breaks down ach into acetate and choline via enzymatic degradation
132
glial cells and reabsorption
astrocyte encloses the synapse where it absorbs the neurotransmitter glutamate from the cleft and recycles glutamate into its precursor glutamine glutamine returns to the presynaptic terminal for re-use this can influence synaptic activity by granting or witholding such absorption
133
syanpses and medication
facilitation of transmission- agonist inhibition of transmission- anatagonist
134
risks of amphetamines to synapses
block reuptake of dopamine and other transmitters
135
risks of cocaine to syanspes
block reuptake of dopamine and other transmitters
136
risks of methylphenidate (ritalin) to synapses
blocks reuptake of dopamine and others, but gradually
137
risks of MDMA to synapses
releases dopamine, serotonin and norepinephrine
138
risks of nicotine to synapses
stimulates nicotinic-type acetylcholine receptors which increase dopamine release
139
risks of opiates (heroin, morphine) to synapses
stimulates endorphin receptors
140
risks of cannabinoids to synapses
excites negative-feedback receptors on presynaptic cells
141
risks of hallucinogens (LSD) to synapsess
stimulates serotonin type 2A receptors
142
mood disorder treatment
SSRIs=reuptake of serotonin from the synaptic cleft is reduced
143
alcoholism and dopamine
in healthy people alcohol increases dopamine release but in alcoholics there is reduced number of dopamine receptors leading to reduced dopamine release this leads to alcohol craving as dopamine leads to feelings of reward
144
functions of the the nervous system
1. control of vital functions (breathing, heart rate and digestion) 2. control of movement 3. reaction to external events for survival 4. cognitive/emotional processes
145
definition and types of nerves
set of axons (fibres) in the periphery 1. descending (efferent nerves) from CNS to effectors 2. ascending (afferent nerves) from receptors to the CNS
146
what is the role of the somatic nervous system?
convey information from sense organs to CNS, and from CNS to muscles
147
what is the role of the autonomic nervous system?
controls internal organs like heart, intestines, etc
148
what is the dorsolateral (pyramidal tract) of the SNS?
primarily involved in fine, precise, voluntary movements, especially of the distal limbs (e.g., fingers, hands) = lateral corticospinal and rubrospinal control contralateral movement
149
what is the ventromedial tract of the SNS?
esponsible for posture, balance, and gross motor control, especially involving the trunk and proximal muscles (e.g., shoulders, hips) = anterior corticospinal, reticulospinal, vestibulospinal and tectospinal bilateral and ipsilateral control
150
what is the dorsal column medial lemniscal pathway?
carries information about touch, vibration and proprioception
151
what is the spinothalamic tract?
carries information about pain and temperature
152
what is the symapthetic divion of the ANS?
prepares the body for action during times of threat and prepares the body for muscular exertion or stressful activities ("fight or flight") uses norepinephrine
153
what is the parasympathetic division of the ANS?
is active during times of relaxation and rest and dominates in controlling the body for metabolic "business as usual" uses acetylcholine
154
what is homeostasis?
stability of biological processes inside the body: - body temperature - chemical characteristic (ph) of body fluids - osmotic solution of body fluids - blood volume - glucose concentration in blood
155
what is negative feedback?
if discrepancy from the set point is detected, the remedial action is maintained until the homeostasis is regained this can be neurohormonal or behavioural
156
where is the centre for homeostatic regulation?
hypothalamuc
157
pratical uses of the nervous system
“lie detector” - deceptive answers produce physiological responses that can be differentiated from those associated with nondeceptive answers skin conductivity varies with its moisture level meditation- respiratory technic to calm the ANS
158
examples of interhemispheric brain connections
corpus callosum and anterior commissure
159
what do cortico-sucortical pathways connect?
cortex to subcortical areas, motor areas in brainstem and spinal cord (up-down)
160
what do subcortical-cortical pathways connect?
from brainstem, sensory areas in thalamus to the cortex (down-up)
161
what is the corpus callosum?
wide bundle of neural fibres, connecting right and left hemispheres
162
nervous system development
a neural tube undergoes cephalisation to form initially three, then five vesicles phylogenesis - the sequence of events involved in the evolutionary development of a species. ontogenesis - the process of an individual organism grow
163
what is included in the forebrain?
hemispheres limbic system thalamus hypothalamus
164
what is included in the hindbrain?
cerebellum pons medulla
165
weightings of the brain
hemispheres = 85% brainstem = 4.5 % cerebellum = 10.5%
166
functions of the brainstem
transmits information from and to the brain responsible for simple reflexive behaviour physiological states
167
functions of the medulla
controls vital reflexes (heart rate, circulation, respiration, salivation, coughing and sneezing)
168
functions of the pons
axonal projections cross sides (contralateral) takes part in body balance, vision and auditory processing contains centres related to sleep and arousal
169
functions of the cerebellum
controls fine motor skills, coordination and balance
170
role of the superior colliculi
helps guide eye movements and fixation of gaze
171
role of the inferior colliculi
helps sound localisation
172
role of the substantia nigra
plays a role in reward, addiction projects to the basal ganglia to intergate movements (a dopamine-containing pathway implicated in parkinsons disease)
173
role of the thalamus
relays and processes information from sensory organs (expect olfaction) and transmits it to the cortex
174
role of the hypothalamus
regulates body temperature, hunger, thirst and sexual behaviour (autonomic NS)
175
role of the mamillary bodies
a relay for impulses coming from the amygdala and hippocampus
176
what is a gyrus?
a protuberance on a surface of the brain
177
what is a sulcus?
a fold that separates one gyrus from another
178
what is a fissure?
a long, deep sulcus
179
what is the primary cortex?
area of the cortex responsible for the first stage of sensory processing receives inputs from lower structures (mainly thalamus) sends projections to higher level areas.
180
brodmann's map of the cortex
distinguished 52 cortical areas via a cytoarchitectural analysis
181
what are brodmann areas 1, 2 and 3?
primary somatosensory cortex
182
what is brodmann area 17?
primary visual cortex
183
what is brodmann area 41?
primary auditory cortex
184
what is the secondary cortex?
area of the cortex responsible for the second stage of sensory processing receives inputs from primary cortex
185
what is the associative cortex?
advanced stages of sensory information processing, multisensory integration, or sensorimotor integration
186
what are the 3 functions of the cortex?
1. analysis of perceptual inputs 2. organisation of movements 3. higher cognitive functions
187
main functions of the frontal lobe
- contains the primary motor cortex and broca's area for speech production - prefronal cortex for planning, decision making and impulse control - prefrontal cortex adjusts behaviours in response to rewards and punishments
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issues associated with prefrontal lobe dysfunction
impaired ability to learn from consequences and to control impulses often found in depression and schizophrenia
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prefrontal cortex damage: phineas gage
- gage was left with no speech, movement, intelligence or learning impairment - te injury changed his personality and behaviour
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main functions of the parietal lobe
- important for body sensations and spatial localisation - postcentral gyrus receives infor about the senses, body position and movement and maps these functions as a sensory homunculus
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what are the parietal association areas?
inferior and superior parietal lobules and precuneus
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functions of the parietal association areas
- combines information from body sense and vision - identifies objects by touch, determine the location of the limbs and locate objects in space - complex language processing
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functions of the occipital lobe
- hosts the primary visual cortex (V1) aka the striate cortex - destruction in the sitriate cortex causes cortical blindness in the related part of the visual field - other visual areas that process individua components of a scene, including colour, movement and form
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functions of the temporal lobe
the auditory cortex which receives information from the ear and contains the language and auditory and visual association areas
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function of wernicke's area
language comprehension and production damage results in meaningless speech and poor written and spoken comprehension
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function of the inferior temporal cortex
visual identification damage causes difficulty in recognises objects and familiar faces (prosopagnosia)
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what subcortical areas make up the basal ganglia?
the caudate nucleus, putamen and globus pallidus
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role of the basal ganglia
participates in planning behaviour and emotional expression, abundant connections with prefrontal cortex direct inentional movements
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what does an undersupply of dopamine in the basal ganglia lead to?
parkinsons disease
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role of the hippocampus
creation of new memories (learning) and intergration of new memories into stable knowledge
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role of the amygdala
emotional behvaiour and formation of emotional memories
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role of the cingulate cortex
linking behvaioural outcomes to motivation and learning (critical in depression and schizophrenia)
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what is locked-in syndrome?
condition in which patient is aware and awake but cannot make any voluntary movement
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what is the cause of locked-in syndrome?
brainstem lesions in which the anterior part of the pons is damaged
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what might result in locked-in syndrome?
traumatic brain injury neurodegenerative diseases strokes
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cause of encephalitis lethargica
provoked by injury of basal ganglia and midbrain structures due to an immune recation to bacterial infection
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what is akinetic mutism?
medical condition where patients tend neither to move (akinesia) nor speak (mutism)
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what is the hindbrain called?
rhombencephalon
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what is the midbrain called?
mesencephalon
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what is the forebrain called?
prosencephalon
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what are the 4 theories of emotion?
james-lange (1880s) cannon-bard (1920s) scahcter and singer (1960s) lazarus (1990s)
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what is an emotion?
an internal process that modifies the way an organism responds to certain kinds of external stimul (numan and woodside 2010)
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what area of the NS do emotional situations arouse?
autonomic nervous system
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what is the james-lange theory of emotion?
we feel emotion because we experience phsyiological reactions to stimuli predicts that: 1. people with weak autonomic or musculo-skeletal responses will feel less emotion 2. causing or increasing someone’s action/response should enhance an emotion
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what is pure autonomic failure?
failure of output from autonomic nervous system to the body – ANS no longer regulates heart rate and other organs.TF stressful situations do not lead to autonomic changes (raised blood pressure, sweating) patients have little difficulty identifying emotions others might experience but FEEL their emotions less intensively than before – this is consistent with the J-L Theory
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paralysis and the J-L theory
people with paralysis through damage to the spinal cord are unable to instigate fight or flight behaviours. HE most report experiencing emotion at the same level as before their injury (cobos et al., 2004).
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davis et al (2010)- botox and J-L
botox used to paralyze the whole face and people reported reduced emotional responses when watching short positive videos compared to those receiving a cosmetic filler that did not paralyze the facial muscles
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somatosensory cortex and J-L theory
people with somatosensory cortex damage had normal autonomic physiological response to emotional music but little subjective experience
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pre-frontal cortex and J-L theory
patients with damage to the PFC had weak autonomic (physiological) responses but normal subjective response (johnson et al., 2009)
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spotaneous rapid breathing and J-L theory
spontaneous rapid breathing leads to worry about suffocation and panic attacks (kein, 1993)
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smiling and J-L theory
A: holding pen in lips uses the frown muscles B: holding pen in the teeth uses the smile muscles subjects rated a comic strip as funnier when holding the pen in their teeth (strack et al., 1988)
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suggestion of the cannon-bard theory
emotional stimulus simultaneously triggers autonomic response AND emotional experience in the brain
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reasons for the cannon-bard theory
1. ANS responds too slowly for a rapid onsent of emotion, e.g blushing takes 15-30 seconds to occur 2. people have problems detecting changings in ANS activity (e,g HR) 3. if non-emotional stimuli (temp rise) cause the same pattern of the autonomic activitythrn why do we not feel afraid when we have a fever?
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bard (1934)
severed the connection between the visceral organs and the brain in animals and this did not abolish emotional behaviour meaning emotion can still occur even without physiological feedback
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what is sham rage and how can we induce it?
sham rage is an intense undirection aggressive behvaiour that occurs without an emotional trigger this can be caused by removing the cortex in cats
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shame rage in cats with no cortex
sensory information is relayed to the thalamus where it bifurcates - one route goes to the cortex - one route to the hypothalamus (controls bodily responses) sham rage suggests that the cortex has a role in inhibiting emotional responses and controlling rage response – top down theory of emotion (cog processes generate emotion)
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schacter and singer (1962) theory
J-L right to equate emotion with bodily states and C-B right to note there are not enough distsinct bodily reactions to account for the variety of emotions we experience TF two-factor theory of emotion suggests emotion arises from a combo of physiological arousal and cogntive interpretation of that arousal
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schacter and singer study
one group informed they were getting injected with adrenaline, other werent and there was a control saline group in informed adrenaline injection group they had a mild emotional response to pictures of happy/angry faces uninformed group had strong emotionnal responses
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findings of schacter and singer study
participants given an adrenaline shot but not informed of this “interpreted” their change in physiological state differently this theory increased the importance of brain processes in experienced emotion cognitive interpretation important with pereptual context!
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suggestions of lazarus' theory
it is the cognitive interpretation which mediates emotional experience (cognitive appraisal theory) thinking shapes feeling
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lazarus model and memory
to determine emotional response we have to interpret a frightening stimuli to arouse a general physiological state which is shaped by memory
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feldman-barrett suggestion
emotions are under our control to some extent they are also subject to our previous experience creating new experiences to events could change our emotional responses this is a basis for CBT
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the amygdala and fear
- recieves input from pain, vision and hearing centres (conditioned responses) - projects to hypothalamus (autonomic) and prefrontal cortex (behaviour) - also projects to pons (startle response)
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the moro reflex
a normal reflex for an infant when he or she is startled or feels like they are falling
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moro reflex and rats
animal is presented with a loud noise and a startle response recorded –usually within 5-8ms a light is then paired with a shock repeatedly finally light precedes the loud noise and increases the startle response in rats with amygdala damage there is still a startle reflex but no increase from the light stimulus
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does damage to the amygdala destroy fear?
no- suggestions that these animals may have difficulty interpreting signals with emotional consequences
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toxoplasma gondii and fear
TG is a parasite that lives and breeds in feline hosts the host cat excretes the parasite’s eggs and these are released into the ground which infects rats parasite attacks and damages the amygdala such that the rat shows no fear when approaching cats (perhaps because it fails to interpret the emotional significance of a cat)
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kluver-bucy syndrome
rare neurological disorder resulting from bilateral damage to the amygdala caused by HSV encephailitis, brain injury, neurosurgery etc leads to hypersexuality, docility, change to eating and psychic blindness
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what is psychic blindness?
aka visual agnosia is an inability to recognize "the emotional importance of events" so the can see an object but cant understand what it is or what is represents
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psychic blindness and animals
monkeys with amygdala damage attempt to pick up lighted matches and other objects they would normally avoid they are also less fearful of snakes and more dominant monkeys
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whalen et al (2001)
comparing fearful faces with neutral faces shows bi-lateral amgydala activation comparing angry with neutral faces also shows amygdala activation but so do happy and neutral faces (somerville et al 2004)
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whalen et al (2001) findings
argue that the pattern of activation found for the amygdala may not reflect the processing of negative emotion/threat per se, but more about detecting ambiguity in the face and how that relates to predictability of the other persons actions both fearful and angry faces convey perceived threat but ANGRY face conveys information about the source of the threat FEARFUL face conveys ambiguous threat
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gaze and ambiguity- adams et al (2003)
angry face with direct gaze and fearful face with averted gaze are unambiguous ambigious gazes create greater activation in the amygdala
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urbach-wiethe disease
individuals with this disease accumulate calcium in the amygdala and it atrophies mutation in the ECM1 gene
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patient SM- urbach wiethe
viewed 10 clips from scariest movies and only reports excitement stated she hates snakes but was happy to hold a snake in a haunted house instead of screaming at monsters she laughed was held at gun point, at knife point and was physically abused- expresses anger but not fear in these situations when a male confederate stood nose-to-nose with her she showed and reported no discomfort SM fails to recognise FEAR expressed by others she can draw most facial emotions with the exception of fear fails to look at eyes for interpretation
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whalen et al (2004)
amygdala responds more to fearful than happy eye whites so perhaps the amygdala is responsible for detecting the presence of emotional information and directing other brain areas to pay attention to it
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what is sound?
periodic compressions of air, water or another medium an object (e.g a tree) vibrates the air and sets up sound waves that hit the ear hearing is a mechanical sense
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lateral line in fish
- prey makes vibrations - lateral line transduces signal activating afferent nerve (glutamate) and brain detects prey - fish swims to prey creating vibrations and lateral line transduces mass of noise - brain fails to detect prey - brain of swimming fish silences lateral line to match own muscle movements using efferent nerves (ACh) which supress lateral line
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noisy environments and sound detection
sounds overlap in time so the brain needs to use incoming sensnory input and prior knowledge about sounds to understand them
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what is the outer ear called?
the pinna
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what is the role of the pinna?
captures sound and amplifies it by funneling it into the smaller auditory canal
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what is the role of the middle ear?
eardrum collects vibrations which transmits to the ossicles (hammer, anvil and stirrup) which sens vibration to cochlea
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wilska (1935) sound detection
we can detect sound when the eardrum vibrates as little as the diameter of the hydrogen atom
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what is the role of the inner ear?
cochlea translates pressure to bioelecttical activity and sends to upper structures in the nervous system
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what is balance controlled by?
vestibular system
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role of semicircular canals
detect rotation
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role of otolith organ
detects acceleration
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what are the otolith organs?
hair cells in the utricle and ear stones
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how do semiciricular canals detect rotation?
with each rotation, with the movement of endolymph, the hair cells undergo either depolarization or hyperpolarization, depending on whether the endolymph moves them toward or away
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role of the organ of corti
contains specialized sensory cells called hair cells, which are arranged in rows along the cochlear membrane these hair cells are embedded in the endolymph and their cilia extend into the overlying fluid
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auditory pathway: from cochlea to cortex
1. first relay- ipsilateral cochlear nuclei in the brain stem, which receive input from the auditory nerve; some decoding of the signal duration, intensity and frequency occurs here 2. second relay in the brain stem - in the superior olivary nucleus (pons). majority (but not all!) of the auditory fibres are contralateral 3. third relay takes place in the inferior colliculus of the midbrain 4. final relay, before the cortex, occurs in the medial geniculate body 5. projection from the thalamus to the auditory cortex
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what is heschl's gyrus?
located in the primary auditory cortex (superior temporal gyrus) and plays a critical role in processing sound brodmann's area 41 and 42
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sound physical property: intensity
how much air fluctuation (compression/rarefaction) the sound creates, i.e the energy in the sound loudness is a subjective value which correlates with the objective intensity this is measure in decibles above 90dB=sustained exposure resulting in hearing loss there is a non-linear correspondence between intensity and loudness
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how is sound intensity encoded by the brain?
encoded via neuron firing rate neurons fire more frequently as sound intensity grows the higher the neuron firing rate, the louder the sound
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sound physical property: frequency
number of air compression/rarefaction cycles per second that the object creates - 10 cycles per second = 10 Hz (can’t be heard by humans) – 100 cycles per second = 100 Hz (bass guitar) – 1000 cycles = 1kHz (speech)
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what is pitch?
perceptual correlate of frequency
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how is frequency encoded by the brain?
in basilar membrane: high frequencies cause vibrations near the base (narrow and stiff part) low frequencies cause vibrations near the apex (wider and more flexible end) this is the place code
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tonotopic organisation in the PAC
the more anterior the firing neuron, the lower the pitch
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most sounds (200-20000Hz)
– frequency is encoded in accordance with the Place code – intensity is encoded via the neurons’ firing rate
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special patten for encoding sounds <200 Hz
– frequency is encoded via the firing rate of individual neurons (aka temporal code) – intensity is encoded via the number of firing neurons
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determining sound location
listeners can identify where the sound source is: in front/behind, left/right 3 main binaural (involve the use of both ears) cues for sound localization: – difference in intensity between the ears – difference in time of arrival at two ears – phase difference between ears
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role of the inferior colliculus
integrates sound information from both ears, playing a critical role in processing spatial auditory information and coordinating reflexive responses to sound localisation
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wernicke's area
understanding spoken language superior temporal gyrus
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broca's area
speaking inferior frontal gyrus
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voice onset time
the release of a stop consonant (like /p/, /t/, /k/) the start of vocal cord vibration (voicing) it’s the main acoustic cue that helps us tell the difference between voiced and voiceless stop consonants e.g difference between b and p is 40ms
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brain lateralisation and audition
the cochlear nucleus receives input from the ipsilateral ear only all later stages have input from both ears
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dichotic listening tasks
different syllables presented simultaneously, each to a different ear the ear contralateral to brain hemisphere dominant for speech gives more responses
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lateralised processing and audition
right ear dominance for speech recognition – more connections to the left brain hemisphere speech = left hemisphere music = right hemisphere male participants show more asymmetry in performance of tasks related to language and speech processing than their female counterparts prosodic aspect of speech - intonation, expression, emotional aspect of speech (right) vocabulary and grammar (left)
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where is conductive hearing loss associated with?
outer/middle ear
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where is sensorineural hearing loss associated with?
inner ear (cochlea)
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what is conductive hearing loss?
results from damage to the eardrum or ossicles in the middle ear → failure to transmit sound waves to the (intact) cochlea therefore sounds are muffled or quieter, but not necessarily distorted corrected by medication, surgery or by sound amplification from hearing aids, or by using bone conduction
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bone conduction hearing aids
the sound is used to vibrate the mastoid bone → the cochlea receives the vibrations, turns them into the electric signals & passes to the auditory nerve
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what is sensorineural hearing loss?
damage to (part of) the cochlea/hair cells in the inner ear congenital, result of a disease or repeated exposure to loud noises sounds may be distorted or unclear, even if loud enough corrceted by cochlear implants
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cochlear implants
surgically implanted electronic device which receives a sound signal via a microphone and conducts s via thin wires to directly stimulate the auditory nerve
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main visual pathway
90% of axons in optic nerve connect the retina to the lateral geniculate nucleus (LGN) of the thalamus this region then connects with the primary visual cortex (V1)
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what are 3 neurons of the LGN?
magnocellular (layer 1 and 2) parvocellular (layer 3 and 6) koinocellular (thin layers between mago and parvo)
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what are magnocellular neurons?
large receptive fields that respond to motion, low contrast and temporal resoultion black and white
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what are parvocellular neurons?
small receptive fields that detect colour (red-green), fine detail and high spatial resolution
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what are koinocellular neurons?
mostly small fields but varies, blue-yellow colour processing
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secondary visual pathway
remaining 10% of axons connect to the pulvinae nucleus of the thalamus and the superior colliculus (SC) - more axons in this 10% than in all the auditory pathway connections SC important in visual attention and may have direct connection area V5/MT
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visual perception
posterior-anterior organisation cells respond stimuli of increasing complexity receptive fields become increasingly larger 2 pathways- ventral and dorsal
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what is V1 (striate cortex)?
- located in calcarine sulcus on medial occipital - process edges and lines, light/dark boundaries, basic colour processing and binocular disparity - lays the foundation of sight through edges, motion and depth
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what are simple cells?
layer 4 of V1 that respond best to a bar or edge of a specific orientation these combine input from centre-surround concentric cells
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what are complex cells?
layers 2/3 of area V1 large receptive fields respond to a bar edge anywhere in the receptive field and are often sensitive to motion or direction
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what is the best way to cell if a cell is simple or complex?
a cell that respons to a stimulus in only one location is a simple cell and one that responds equally throughout a large area is a complex cell
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what are end-stopped/hypercomplex cells?
sensitive to edges, corner or angles oriented lines of a specific length if a line extends a length then the cell stops responding
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V2 and V3
- V1 has reciprocal connections with V2 and V2 has reciprocal connections with V3 - in V2 and V3 many complex and hypercomplex cells, but also cells that respond to even more complicated patterns (e.g., circles, lines that meet at a right angle etc.) - from V2/3 visual information passed on to several additional regions across the occipital cortex - these regions analyse additional visual attributes such as colour, motion, shape, location (V4 & V5)
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what is a receptive field?
area of the visual field that when stimulated by light causes action potentials
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private W case study
fragment of shell entered in the middle line of the skull, and passed forwards and to the left, produced a considerable injury of the left visual area, and consequently right hemianopia (loss of vision in half the visual field)
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what does damage to the visual cortex cause?
blindsight- someone can perceive the location of an object despite being cortically blind
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patient DB case study (weiskrantz 1974)
right primary visual cortex (V1) removed by surgical ablation to remove tumour left visual hemifield “blind" patient had no awareness of any visual stimuli presented to the ”blind hemifield but could * point quite accurately to the location of the light source * report whether a stick was angled vertically or horizontally * discriminate between Xs and Os he reported sometimes having the feeling of ‘smoothness’ or ‘jaggedness’ but denied that these feelings were ssociated with any visual experience
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cowey (2010)
why can people detect motion stimuli? suggestion that SC (to pulvinar) or LGN (koniocellular) pathway to V5 intact and thus motion processing preserved
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aljina et al (2015)
DTI on patients with and without blindsight suggests that the presence of strong LGN-V5 (hMT) pathways better predicts blindsight than SC-V5 (hMT) pathway LGN-V5 (hMT) pathway also predicts other shape and location discrimination abilities
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extra striate visual pathways
areas V4= greyscale contrast hMT/V5= static contrast
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damage to area V4 (verrey 1888)
early case of cerebral achromatopsia patient suffered a left sided stroke and reported she had lost the ability to perceive colours in her right visual field. after her death verrey performed an autopsy and identified a region across the lingual and fusiform gyrus as being the “centre for chromatic sense”
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where are lesions in patients with cerebral achromatopsia?
V4A (anterior)
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extra issues of V4 damage
in addition to deficits in colour perception they also have some issues with form perception this may be due to the proximity of V4 with further processing areas in the ventro-temporal cortex or to the importance of colour in shape processing
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bouvier and engel (2005)
analysed the lesion locations of a 46 patients with cerebral achromatopsia and noted whether these patients had other visual processing deficits A. lesion overlap in patients with cerebral achromatopsia AND prosopagnosia B. lesion overlap in patients presenting only with cerebral achromatopsia. lesions more focal in the group with the unitary disorder
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damage to area V5/hMT (draganski et al 2004)
juggling induced changes in grey matter volume in area V5/hMT area involved in perception and spatial anticipation of moving objects
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what does damage to V5 result in?
cerebral akinetopsia
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stevens et al (2009)
TMS to V5 significantly impaired global motion direction detection
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what are the areas of the brain associated with memory?
medial temporal lobe structures
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case of HM
- removal of bilateral hippocampus and medial temporal lobes - anterograde amnesia - impairment independent of the sensory modality involved (unable to remember verbal and non-verbal material) - issue with declarative memory
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what is anterograde amnesia?
cannot form new memories
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what is retrograde amnesia?
unable to retrieve memories prior to damage (initially thought to be 1-3 years)
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HM and working memory
milner asked him to remember 584. he recalled it 15 minutes later. a moment later after his attention had been distracted, he had forgotten the number and his explanation of how he remembered it doesnt show any recency effect but show primacy effect
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what does the case of HM tell us about the medial temporal lobe?
1. important for long-term memory, but less so for working memory functions 2. more important for remembering recent life events than remote life events. 3. important for explicit memory regardless of the encoding or retrieval modality 4. important for transferring events and facts into long-term memory 5. NOT IMPORTANT for retaining information “online” (e.g., for working memory) 6. NOT IMPORTANT for memories linked to non-declartaive memory
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MTL damage and memory impairment is an example of a...
single dissociation- might only reflect differences in impact of brain lesion. they may not reflect unique brain-behavior associations.
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double dissociations in STM and LTM
KF – damage to Left temporo-parietal area. does not show a recency effect in memory. MH – damage to bilateral temporal lobe. KF: impaired STM and preserved LTM MH: preserved STM and impaired LTM evidence that medial temporal lobes and temporo-parietal cortex support different types of memory
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skaggs, mcnaughton, wilson and barnes (1996)
recordings from seven cells from a single electrode in the hippocampus of a rat as it moves several hundred times around a triangular maze. fifferent colours represent the firing of different cells. - hippocampus of the rat builds up a spatial representation of the maze.
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morris water maze
rat is placed in the maze and swims until it finds the submerged platform A) random swim-path after 5 trials. B) more efficient after 35 trials. C) after 71 perfect.
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clark, broadbent and squire (2007)
if the hippocampus is damaged in the rat that has learned the location of the platform it reverts to random patterns of searching – in fact it forgets that there is a platform at all right hippocampus appears more important in spatial memory
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maguire et al (2000)
a study of London taxi drivers trained to memorize a spatial map of the city streets. there was greater hippocampal activity when answering questions about routes through the city than when answering non-spatial questions. Ttxi drivers also had a larger than average posterior portion of the hippocampus - the size of which correlated with their experience as a driver
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cognitive map theory (o'keefe and nadel 1978)
in humans, similar hippocampal responses were evoked for photographs of buildings that were near one another suggesting a role in spatial memory. evidence from rodents and from humans suggests that the hippocampus mediates memory for spatial relations among objects in the environment.
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relational memory theory (eichenbaum et al 1999)
hippocampus supports the formation and retrieval of associations (or relations) among multiple items, events, or features in memory. its not just about remembering things — it’s about remembering how things are connected e.g the red coffee cup was on the table next to the book when you walked into the kitchen on sunday morning (instead of coffee cup)
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eichenbaum et al 1999 study
rats learn the relative rewards associated with pairs of odours placed into cups of sand. in reward terms: A>B B>C C>D D>E
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RMT and the fornix (eichenbaum)
rats with a lesion to the fornix disrupting hippocampal output can remember the outcomes of individual odour pairs. but they are impaired at relationships among different elements such as B-D whereas control rats are able to locate the reward in these trials. that’s is disruption of hippocampal function in lesioned rats leads to problems in memory for overlapping relations. particularly linked to left hippocampus
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episodic memory theory (tulving and moscovitch)
postulates that the hippocampus is critical for episodic but not semantic memory
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episodic memory theory- retrograde amnesia evidence
patient KC damaged a number of brain structures, including the hippocampus in a motorcycle accident. lifelong retrograde amnesia in episodic memory. preserved intellectual abilities. could still play chess at the same level as before the accident. in contrast, he was able to retrieve semantic memories acquired before the accident. for example, he could retrieve the meaning of technical terms from his work as a machinist but could not recall any events that happened in the factory. his factual knowledge and vocabulary are also equivalent to others with similar educational background
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epsiodic memory theory- evidence from anterograde amnesia
HM was able to learn a few new names (in his dense anterograde amnesic period). when given first names of people who became famous after his injury he was able to provide the correct surname on some occasions. e.g elvis presley fidel castro MLK lyndon johnson
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episodic memory theory- evidence from developmental amnesia
due to anoxic lesions in the hippocampal region following birth complications individuals perform poorly on tests of episodic but not working memory and learn normally in school (semantic)
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episodic memory theory- evidence from double dissociations
left lateralized damage to the anterior temporal lobe tends to affect semantic more than episodic memory – SEMANTIC DEMENTIA
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graham and hodges (2001)
patient AM had been referred to hospital with difficulty with naming things (anomia). episodic memory for holidays was good (preserved event detail). normal performance in copying and drawing from memory in the rey-ostereich test of non-verbal episodic memory severely impaired in semantic processing tests like the pyramids and palm trees test
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integrating theories of hippocampal memory function
1. spatial memory appears to be linked to right hippocampal processing whereas relational functions are associated with left hippocampal processes. 2. spatial memory appears to be linked to posterior hippocampal processing (taxi drivers) whereas relational functions are associated with anterior hippocampal processes 3. lesions in rat hippocampus have a significant effect on recollection (episodic memory) but not familiarity.
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mental time travel and the hippocampus
hassabis, kumaran, vann & maguire (2007) discovered that patients with hippocampal lesions not only had problems remembering the past but could not imagine new experiences in the future
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delayed response task and working memory
cells in prefrontal cortex continue to respond in the delay interval suggesting a role for PFC in the maintenance of information in working memory
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phonological loop (chein and fiez, 2001)
participants performed delayed serial recall tasks (remembering and repeating back sequences of words) phonological store was linked to activation in the left inferior parietal cortex (particularly the supramarginal gyrus)
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visuo-spatial working memory (sala et al 2003)
- faces or house presented - participants either had to remember the object or remember the locations presented - faces and houses activate the fusiform face area and parahippocampal place area respectively - faces and houses activate the left inferior frontal gyrus location more dorsal and caudal area - location seems to activate inferior and superior parietal lobe bilaterally also
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working memory- building blocks
for WM we need: selective attention, rehearsal, patterns, retrieval, updates, sustained attention and inhibition
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working memory- maintenance
various processes and representations interact during a task that requires maintenance of visual information, e.g., a delayedmatch-to-sample (DMS) task, and how the involvement of different processes change dynamically throughout task performance are exemplified
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working memory- manipulation
interactions and dynamics during performance of a manipulation task, e.g., multiplying forty-two by twelve, are exemplified. here, procedural long-term memory representations may also support solving the task, e.g., by recollecting procedures for how the multiplication of two-digit numbers can be done efficiently.
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summary of WM brain regions
1. regions of prefrontal cortex and parietal cortex are involved with executive/attentional functions in working memory 2. areas of association cortex appear important in the storage of specific material during working memory delay 3. temporal cortex more associated with visual working memory but less in spatial working memory. 4. parietal lesions likely to have greater effect on spatial working memory than visual working memory
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link between age and working memory
aged monkeys have fewer neurons and reduced input connections to PFC. older humans have impaired working memory abilities. decline in memory performance linked to reduced PFC activity in older adults. older people with intact working memory ability show even greater PFC activation than younger controls – PFC working harder to maintain performance levels and to compensate.
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drugs and memory
stimulant drugs linked to dopamine receptors improve memory performance in aged monkeys some evidence that these help in the case of ADHD also WM deficits also observed in Schizophrenia
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what are the two visual processing streams? (ungerleider and mishkin, 1982)
dorsal (pareital lobe) ventral (temporal lobe)
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what is the role of the dorsal pathway?
"where" stream - invovled in spatial vision, including judgements of spatial attributed of objects and the use of spatial information to guide movement V1-posterior parietal
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what is the role of the ventral pathway?
"what" stream - involved in processing the characteristics of objects V1-V2-V4-inferotemporal cortex
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milner and goodale (1992) refinement of visual pathways
dorsal="how stream" and how we use visually guided actions
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what input does the dorsal stream receive?
input only from magnocellular cells (therefore cannot see in colour)
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what input does the ventral stream receive?
input from magnocellular, parvocellular and koinocellular cells (can see in colour)
351
what brodmann area is the primary visual cortex?
BA17
352
what brodmann area is the secondary visual cortex?
BA18
353
what brodmann area is V4?
BA18/19
354
what brodmann are is V5/middle temporal?
BA18/19/39
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what gyrus is included in the inferior temporal cortex?
fusiform gyrus (supports visual recognition)
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what is the primary pathway of ventral information?
information from V1 through visual association areas V2 (involved in the processing of simple properties such as orientation), V4 (tuned for properties such as orientation, spatial frequency, colour, and simpler geometric shapes) as we get further out, responsive fields become larger and cells respond to different types of objects
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kelley et al (1998)- ventral stream
- people in fMRI and presented words, pictures of objects and faces - words activates left fusiform gyrus - objects ativates bilateral fusiform - faces cativate bilateral fusiform but more on the right
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kanwisher et al (1997)- ventral stream
- perfected facial study by ruling out differences in low level properties, stimuli and animation - localiser task - in faces>objects= activation of right fusiform gyrus - intact faces>scrambled,houses,hands=activation higher for intact face in right hemi of FG TF=fusiform face area
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why do you have bilateral activation of the fusiform when responding to objects?
can be processed in two different ways (language and visual)
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kalanit grill-spector (2003)- ventral stream
common areas of activation=parahippocampal place area for scenes and fusiform face area for faces lateral occipital and V4 respond to objects, faces and scenes (lower activation)- early in processing stream TF we have unique and common activation sites
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damage to the lateral occipital cortex
linked to apperceptive agnosia
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damage to anterior structures in inferior temporal cortex (right)
associative agnosia
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what is apperceptive agnosia?
struggle with the ability to perceive or form a clear mental image of objects, shapes, or scenes, making it hard for them to recognize objects by sight and copy images
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what is associative agnosia?
person can perceive and recognize objects and shapes in terms of their basic visual features, but they cannot link these perceptions to their meanings or function (semantic)
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what is intergrative agnosia?
can often recognize individual components of an object, but they struggle to perceive the object as a unified entity (e.g square, roof and door but cant say its a house) lateral occipital complex
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category specificty in visual agnosia
e.g living vs non-living (wallice and sharrington 1984) JBR- when shown pictures of common objects (scissors) his memory was much better (90% accurate) than when shown images of living things where he was accurate to on less than 10% of trials
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damasio (1990) criticism of category specific agnosia
inanimate objects like scissors also activate kinesthetic and motor representations that might be a clue to identity (remember the agnostic’s hands identifying the combination lock) when participants are presented graspable objects (i.e., tools, things with handles) additional motor affordance areas are indeed activated automatically (handy et al., 2005) and these may support identification
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damage to the fusiform gyrus
results in prosopagnosia (category specific)
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what is prosopagnosia?
impairement at recognising human faces vs other living things
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mcneill and warrington (1993)- prosopagnosia
report the case of WJ who was impaired at recognizing human faces (prosopagnosic) but had no difficulty recognizing and naming his sheep
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gauthier et al (2000)- is there a difference in face and object processing?
same person (subordinate) vs model vs species if you were a bird expert you would say the species of the bird not just 'its a bird' - recruited car experts and bird experts - showed faces, cards and birds - car experts shown faces=FG, shown cars=FG, shown birds= no FG (double dissociationed) results suggest that expert subordinate-level recognition for any category may be mediated in the same regions
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gauthier et al (1997) subordinate vs basic judgements
participants scanned while taking part in basiclevel (BIRD) versus subordinate-level (PELICAN) judgment about objects region of right and left FG more active for subordinate than basic level judgments greebles=novel face like after training can identify at subordinate e.g glorp-type greeble and this increase activation in FFA TF FFA tuned for expert-level visual categorisation
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turk et al (2005) person identification and categorical processing
john malkovich vs actor percept is same (same picture) but category differs FG responds to occupation and identity judgment but favours identity quicker to say name rather than that he is an actor not due to perceptual differences
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do faces activate other brain regions? (haxby et al 2001)
inferior occipital (eearly face processing to features) and fusiform gyrus (invariant for indentification) (ventral) posterior superior temporal sulcus processes dynamic features of facial gestures (dorsal)
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amgydala/insula/striatum and prosopagnosia
sweating increases when there is autonomic arousal following recognition of a face a prosopagnosic will sweat when they recognise someone but this is unconscious and will not help remember others (emotion but no recognition)
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what is capgras delusion?
individuals have damage to emotion system and you have an unconsious feeling that something is wrong with a family member/spouse/friend's face you therefore believe they have been replaced by an imposter the minute they talk (different modality) you can properly recognsie them (recognition but no emotion)
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what is optic ataxia?
affects a person's ability to visually guide their hand movements to reach or grasp object damage= posterior parietal cortex, typically in the dorsal stream
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patient WF (holmes and horrax 1919)
wounded by a machine gun bullet when he was asked to take hold of or point to, any object, he projected his hand out vaguely, generally in a wrong direction, and had obviously no accurate idea of its distance from him a pencil was held up at various distances from him; when it was 24 inches he estimated it at 12 inches, when 5 feet he said 18 inches, when at 2 feet he said it was about 7 feet away he underestimated or overestimated distances indiscriminately
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what damage causes optic ataxia?
damage to the inferior and superior parietal cortex
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double dissociations in toptic ataxia and visual agnosia
optic ataxic-recognise but no direction visual agnosic- mo recognition but direction
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what is hemispatial negelct?
person fails to be aware of or respond to stimuli on one side of their body or in their environment caused by stroke in middle cerebral artery causing damage to parietal lobe generally to left
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theories for hemispatial neglect: hemisphereic rivalry and communication
damage to one hemisphere leads to hyper-exitation of the intact hemisphere damage to the right hemisphere leads to hyper-exitation of the left hemisphere due to release of inhibition from the damaged, hypoactive right side of the brain subsequent damage to the left hemisphere can sometimes remove the neglect – due to rebalancing this leads to a focus on right hemispace
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problems with the theory of hemispheric rivalry
1. does not explain why neglect is almost always due to RH damage 2. damage to the corpus callosum, affecting the balance in communication between the hemispheres does not lead to neglect
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theories for hemispatial neglect: right hemisphere dominance theory
right hemisphere controls attention to both sides of space left hemisphere, however, mainly attends to the right side if the right hemisphere is damaged, the left side of space gets no attention at all (since the left hemisphere isn’t wired to cover it) if the left hemisphere is damaged, the right hemisphere can compensate — so right-side neglect is rare or mild
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what is non-declarative memory?
a collection of various forms of memory that operate automatically and accumulate information that is nont accessible to conscious recollection = skill learning and priming
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what is skill learning?
depends on extensive training (e.g playing an instrument) that takes place over a long period of time this ciuld include perceptual skill. motor skill or cognitive skull
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where is the basal ganglia and what are its interconnections?
situated at base of the forebrain - interconnected with cerebral cortex, thalamus and brainstem
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what diease has significant impacts on the basal nuclei?
parkinsons
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what is the weather task?
probabilistic learning - ppts given symbols and are required to predict the weather (sun/rain) and none of the images allow total accuracy - participants must build up a probabilistic model of dofferent combinations of information that best predict the weather
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the basal ganglia and the weather task
after 30 trials, both amnesics and parkinsons patients show impaired results in weather task compared to control but after 40 trials, the amnesic group show better performance than the parkinsons patients
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why are parkinsons patients bad at the weather task? (knowlton 1996)
normal ppts focus on one image- use declarative, episodic (hippocampal) memory after many repitions ppts approach 100% accuracy but appear unable to declare their strategy the basal ganglia lean these probabilistic relations implicitly so parkisnons patients continue to adopt the declaratie memory strategy so dont learn effectively
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patient JK- parkinsons
engineer who started to show signs of parkinsons agd 78 he began to show signs of memory distrubance for highly practiced procedural tasks recalled explicit events demonstrating to LTM deficit (declarative) shows double dissociation
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why can amnesics become good at the weather task?
unable to use their declarative memory strategy initially as they have damage to the hippocampus but if they continue they show gradual improvements through the use of the intact basal ganglia
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what is priming?
a change in the efficacy of stimulus processing arising from a previous encounter with the same or a related stimulus, in the absence of conscious awareness of the first encounter
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what are the two types of direct (repition) priming?
perceptual and conceptual
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what is an example of indirect priming?
semantic priming
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perceptual priming example
LIST A (read by ppts): element, corduroy, pleasant, techncial LIST B (not read): pendant, crocodile, pillow, terrain then give a stem completion task and they are more likey to complete the words they saw (e.g ter, pen, cor)
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neural activity and perceptual priming
brain acitivation reduces during repitition suppression (when a stimulus is repeated, neurons in sensory cortex (like visual cortex) show reduced activity — even though behavioral performance improves e.g in left lateral preforntal cortex and left occipito-temporal lobe
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what is neural sharpening? (henson and rugg 2003)
when a stimulus is repeated non-essential neurons respond less and less which leads to reduced hemodynamic response function sharepened representation is smaller (fewer and only critical neurons) and more selective we can therefore examine brain areas show this repitition suppression
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what happens to preceptual priming if the percept is different? (koutstaal et al 2001)
left fusiform gyrus shows a repitition suppression effect for same and different exemplars right fusiform gyrus shows a repitition suppression effect for same exemplars only
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why does the left fusiform gyrus respond to both same and different exemplars?
as it encodes verbally
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what happens to preceptual priming if the WORD percept is different? (dehane et al 2001)
primes are masked and targets are either the same or in a different font/case left fusiform cortex shoes a repition suppression effect for same adn different case right occipital cortex shows a repition suppression effect for case specific priming effects only
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what do priming studies show about the two hemispheres?
the left hemisphere is perhaps focusing on the language elements (known to be left lateralized in most humans) right hemisphere appears to be governed by more perceptual/visual aspects of the stimulus
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conceptual priming (wagner et al 2000)
task is to determine if word is concrete/abstract or upper/lowercase in left anterior inferior frontal gyrus (IPFC) there is suppression within task only (coneceputal priming) in the left posterior inferior frontal gyrus (IPFC) there is suppression within and across task (non-semantic)
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coneceptual priming exploration
reflects prior processing of conceptual aspects sensitive to conceptual manipulation conceptual processing is presernved in medial temporal lobe amnesia under implicit/unconscious testing
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perceptual vs conceptual priming and alzheimers
dissociation between P vs C priming and brain processing in AD AD characterised by deterioration in MTL but also lateral temporal lobe and pre-forntal cortex AD impaired in declarative memory (like amnesics due to MTL) AD spared in perceptual priming (like amnesics due to intact visual cortex) AD impaired at conceptual priming due to lateral temporal and pFC damage
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semantic priming (rossell et al 2003)
3 conditions, ppts have to decide if the item presented was a word or a pseduo word prime for 150ms and target for 150ms when there is a real word that is semantically related there is repitition suppression effects in the left anterior temporal lobe this links to semantic dementia
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summary of repitition suppression and perceptual priming
- posterior sensory regions important (visual cortex) for words: left lateral PFC, left occipito-temporal cortex shows repitition suppression pictures: left temporal love for same and different exemplars, right temporal lobe only for some expemplars
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summary of repitition suppression and conceptual priming
appears to be frontal lobe distinction anterior left inferior frontal gyrus = semantic processing posterior left inferior frontal gyrus = non-semantic aspects
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summary of repitition suppression and semantic priming
left anterior temporal lobe- consistent with semantic dementia
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not all repitition leads to suppression of neural responses...(henson et al 2000)
participants required to detect an inverted face target between repititions of familiar vs unfamiliar faces in the right fusiform gyrus you have a repitition suppression effect when there is a familiar face but enhancement for the unfamiliar faces
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explanation of repitition enhancement in the rigth fusiform gyrus
familiar faces can activate a representation in LTM and allows for a “sharper” representation on the second presentation for unfamiliar faces, we need to create a new representation leading to greater cortical activity in perceptual areas and the need to invoke episodic memory retrieval which is associated with greater levels of activation
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what are morals/ethics?
pertaining to the consensus of manners and customs within a social group, or to an inclination to behave in some ways but not in others these sets of customs and values therefore guide social conduct but this is without the need for an absoulte moral value
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what is morality to byproduct of?
evolutionary pressures that shape social behvaiour human morality can be observed in primates e.g caring for prres, striving for dominance and stability to social groups derived from a sense of justice
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what is deontology?
moral rules pertain to absoulte rights
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what is consequentialism?
the moral value of an action is in one way or another function of its consequence alone
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what is utilitarianism?
endorising harmful actions for the greater good
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kohlberg (1969) morality
morality is a by product of reason (cognitive evaluation)
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moral versus non-moral decisions (moll et al 2002)
fMRI (block design) make a judgement on whether a statement is right or wrong no response was made in scanner but subjects again viewed the statements outside the scanner and asked what they thought and the emotional impact of the statement asked to rate the degree of moral content e.g criminals should go to jail
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behavioural data of moral versus moral study (moll et al 2002)
moral statements rated as higher moral content than non-moral and neural statements moral sentences were also rated as having higher impact than non-moral sentences both were rated as more emotional than neutral
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neurological data of moral versus non-moral study (moll et al 2002)
moral>neutral= greater activation in left medial OFC, left STS and left temporal pole non-moral>neutral=greater activation in the lateral OFC, left amygdala and bilateral visual cortex moral>non-moral= greater activation in left medial OFC non-moral (emotional)>moral= greater activation in left lateral OFC and left amygdala
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conclusions of moll et al (2002)
- moral judgments associated with negative emotions activate a distinct region in medial OFC. - nonmoral (social) judgments associated with negative emotions activate lateral OFC. - these networks (and other areas) probably work in tandem on social judgments that combine moral, social and emotional demands. - suggestion: that one can separate out cognitive and emotional factors in moral judgments. also that there is a MORAL brain area.
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what does the dual-process theory of moral judgement criticise (greene)
greene explores philosophy there is a rationalist tradition in moral psychology emphasising the role of reason but is there really just a cognitive basis?
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suggestion of the dual-process theory of moral judgement
distinguish between personal and impersonal moral dilemmas both will ultimately lead to harm to another, but the harm is inflicted in different ways evolutionarily, up close and personal harm looms large in our past however, in order to survive it was necessary ro restrain primitaive urges ro violence thus we develop a negative emotional response to interpresonal violence impersonal harm fails to trigger alarming response TF answer in more cognitive (utilitarian way) when harmful actions are impersonal we can detach ourselves this distinction makes a prediction regarding diffeent neural activity for personal and impersonal moral dilemmas
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what reactions are involved in personal moral dilemmas?
driven by emotional reactions (fast, intuitive) linked to areas like the amygdala and vmPFC
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what reactions are involved in impersonal moral dilemmas?
driven by slower cognitive reactions linked to areas like the dlPFC and parietal cortex
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greene et al (2001) trolley vs footbridge dilemma
argues that the crucial difference in the tasks lies in the tendency for the footbridge task to engage peoples emotions (having to push someone off a bridge rather than pulling a lever)
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what are the predictions of the dual-process theory?
1. personal moral dilemmas lead to greater activity in brain regions associated with emotion 2. as these are automatic there would be a decrease in cognitive control brain areas 3. response time for yes in personal dilemmes is slower than no 4. impersonal scenarios would show no reaction time effect
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neural basis of trolley vs footbridge dilemma
personal>impersonal=activation increase in medial frontal gyrus, posterior cingulate and STST inferior parietal lobe impersonal>personal= greater activation in DLPFC and parietal lobe (BA 7/40)- 40=supramarginal gyrus for WM
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reaction times for personal and impersonal dilemmas
- for personal moral dilemmas it takes significantly longer to make “appropriate” judgments, than to make “inappropriate” judgments. - also there is less consensus of opinion between subjects for some personal moral judgments
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the crying baby and infanticide dilemma
baby crying in warmtime= if you remove your hand your baby cries and soldiers here and they will kill you, your baby and your fellow villagers if you dont remove your hand, your baby will suffocate infanticide= youre a 15 year old girl who doesnt want the baby and puts it in a bin
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greene explanation of crying baby vs infanticide dilemma
argue that in both cases there is a pre-potent (automatic) negative response to the dilemma. however, in the crying baby scenario a cost-benefit (utilitarian) analysis strongly favours smothering the baby (who would be killed by soldiers anyway). in this case the “cognitive” analysis wins – but this takes time – hence the longer response latency.
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hypothesis 1 for the crying baby and infanticide dilemma
in personal moral dilemmas where subjects take a long time to respond (e.g., crying baby) a strong pre-potent emotional response associated with the thought of killing one’s own child competes with a more abstract, “cognitive” utilitarian response (the baby will die anyway and killing it will save lives) - this conflict will be reflected in brain areas associated with cognitive conflict such as the anterior cingulate cortex (e.g., stroop test). - it was also predicted that brain regions associated with abstract reasoning and cognitive control would also exhibit increased activation on high-RT compared to low-RT trials
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hypothesis 2 for crying baby and infanticide dilemma
high-RT trials in which actions were deemed “appropriate” would be characterized by judgments based upon utilitarian “cognitive” processes and thus should show higher activity in cognitive brain areas (e.g. DLPFC) than high-RT trials in which actions were deemed inappropriate. that is that DLPFC activity would track with utilitarian decisions.
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neural explanation of crying baby dilemma
anterior cingulate (BA 32) and DLPFC (BA 10/46) more active for high-RT personal moral dilemmas than low-RT personal moral dilemmas also activation in parietal cortex (BA7) related to working memory. evidence for conflict monitoring and cognitive control processes.
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what brain region is activated when we make utilitarian responses?
DLPFC
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what can we conclude from the crying baby vs the infanticide dilemma?
- these results show that emotion may be a significant driving force in moral judgments – based perhaps on an automatic sense of what is right. - however, cognition also plays an important role in impersonal moral judgments, and in personal moral judgments where reason and emotion are in conflict (crying baby). - these same interactions between emotional and cognitive mechanisms also subserve aspects of social cognition (e.g. ToM). - there is no specifically moral part of the brain (opposite to moll et al earlier). - morality refers to a variety of more fine-grained and disparate processes, both “cognitive” and “affective”.
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damasio (1990) 'somatic marker hypothesis'
reflects the importance of emotional information to social moral judgements when we face a decision, we don’t just think logically — we also use “somatic markers”, which are emotional bodily responses (like a gut feeling, tight chest, or increased heart rate)
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brain damage and the somatic marker hypothesis
patients with damage to the ventromedial PFC can detect the implications of a social situation but are unable to make appropriate decisions in real life situations patients are unable to make such implications with advantageous actions the model explians why lesion patients can still reason about social problems but still fail in naturalistic settings e.g elliott lost job, savings and marriage folowing tumour in vmPFC, could artiuclate what the right thing to do was but could not act on it
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IOWA gambling task (damasio et al 1994)
each card has either win value for financial gain or loss value. the losses are unevenly distributed acorss the decks so that some decks would lead to a net gain and others to a net loss.
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how do normal individuals respond to the IOWA gambling task?
show anticipatory autonomic responses (GSR) when making risky choices (sweating) they also choose advantageously before being consciously aware of the best strategy
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how do vMPFC patients respond to the IOWA gambling task?s
show no anticipatory response so they behave as if unaware of the future consequences as they are guided by immediate prospects so take risky choices
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koenigs et al (2007), VMPFC damage and moral judgement
six patients with bilateral, adult onset damage to VMPFC patients responsed to 50 sceanrios (greene): non-moral, impersonal moral, personal moral subidivded into high and low conflict
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findings of VMPFC damage (koenigs et al 2007) (personal/impesonal)
non-moral judgemets and impersonal judgements are similar VMPFC patients are more likley to endorse personal judements
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findings of VMPFC damage (koenigs et al 2007) (low/high conflict)
LC- immediately say yes or no LC generally cog function and similar results between patients and controls HC patients with VMPFC are more likely to endorse them because they can do the maths= strategy for aggregation of welfare (utilitarian)
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conclusion from koenigs et al (2007) study
VMPFC data illustrate the dual roles that intuitive affective processing mechanisms (lacking in these patients) and evaluative (utilitarian) cognitive mechanisms play in making moral decisions
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deontology and emotion
result of moral behvaiour being driven by intuitive emotional responses to situations (moral alarm bells- greene)
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haidt (2001) and morality
talks about the relative importance of unconscious emotional processes in making moral judgments he argues that for the most part moral reasoning is a post-hoc affair that we decide what is right and wrong based upon emotionally driven intuitions, and then make up reasons for these responses
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deontology has a what basis of morality?
emotional
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consequentialism and utilitarinsim have a what basis?
cognitive
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consequentialism and cognition
cognitive in the way it uses CBA this can be seen in terms of lateral PFC