biological Flashcards
what is cephalisation?
occurs in bilaterians where nervous tissue is concentrated toward one end of an organism
80% water
what is the CNS?
brain and spinal cord
what is the PNS?
NS other than brain and spinal cord
what are the two main types of cells in the NS?
neurons and glia
what are the functions of glia?
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
multiple sclerosis
common symptoms: vision problems, fatigue, difficulties with
walking
cause: demyelination of axons in the brain and spinal cord
neuron structure: soma
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
neuron structure: axon
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
neuron structure: dendrites
branching fibres reciving information from other neurons
neuron structure: myelin sheath
insulating layer that speeds up electrical transmission
how did myelin sheath form?
an ancient virus helped to form a myelin sheath around
nerve fibres
afferent neurons
sensory neurons that carry information from receptors
efferent neurons
carry signals away to the effectors (muscles/glands)
interneurons
connect other neurons
what is resting potential?
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)
what are the two stages of excitation of neurons?
- transmission of information from
the exterior through dendrites to the cell
body - transmission from the cell body through the axon out of the neuron
excitatory synapses
EPSP is a change in polarisation moving along dendrites toward the cell’s body
EPSP is positive -> provokes depolarisation
inhibitory synapses
IPSP is a change in polarisation moving along dendrites toward the cell’s body
IPSP is negative -> provokes hyperpolarisation
what is summation?
postsynaptic potentials sum up when meet
other postsynaptic potentials or if followed by others
what are the two types of summation?
over space (spatial) – from different dendrites
over time (temporal) – from the same dendrites
all or nothing principle
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
propagation of action potentials
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
postmortem studies (19th and 20th century)
relationship between brain damage and loss of function
damage to broca’s area in the left frontal lobe found via PM
microscopic analysis of neural tissue
brodmann areas
6 layers of brain cortex (neocortex)
4 layers of hypothalamus (archicortex)
postmortem microscopic anaylsis of tissue
5 brains of people previously diagnosed with dyslexia- smaller neurons in magnocellular layers of LGN in thalamus
structural imaging- in vivo examples
computerised tomography (CT)
magentic resonance imaging (MRI)
computerised tomography
X-ray machine rotates around the head taking multiple X-ray images from different angles.
X-rays pass through the brain and are absorbed in different amounts by
different types of tissue.
detectors measure the X-rays: after passing through the brain, the X-rays are detected by sensors on the other
side of the head.
computer processes all the data from
the detectors and combines it to create
a detailed, cross-sectional image (or
“slice”) of the brain (can be put together
to form a 3D image).
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
CT evaluation
fast and cost effective
x-ray exposure
less detailed than other methods (MRI)
CT scan example- hier (1978)2
24 people with dyslexia
atypical anatomical asymmetry in brains of some people with dyslexia
magnetic resonance imaging
magnetic field:
- the MRI machine generates a very strong magnetic field that causes the protons
(hydrogen atoms in H2O) to align with the magnetic field.
radio waves:
- the MRI machine sends a pulse of radio waves, they disturb the alignment of the
protons in the tissues of the brain. when the radio pulse stops, the protons return to
their original alignment.
signal detection:
- as the protons realign themselves, they send out signals, which are detected by the
MRI machine. the way they realign (and the strength of the signals) depends on the
type of tissue.
image creation:
- a computer processes these signals and creates a detailed, cross-sectional image of the brain.
magnetic field of MRI
25000 times the magentic field of the earth
MRI evaluation
no x-ray exposure
great spatial resolution
expensive
time consuming
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%
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)
investigation of nervous system activity
bioelectric activity
- EEG
- evoked potentials
energy consumption (indirectly)
- fMRI
- PET
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
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)
abnormal discharge on an EEG
spike and wave pattern
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
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)
animal studies- single cell recordings
neurons behvaiour can be examined through microelectrodes but does not stimulate it
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
single cell recording example- quiroga et al (2005)
single-cell recording of cells in the hippocampus that recognise sepcific people
jennifer aniston neuron
magentoencephalography (MEG)
recording of magnetic fields produced by
electrical currents in the brain using arrays of SQUIDs (superconducting quantum interference devices)
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
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.
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
fMRI evalution
excellent spatial resolution
poor temporal resolutiom
very expensive
discomfort
susceptible to artifacts (head shape, movement)
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.
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).
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
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.
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
examining the effects of brain damage: informal tasks
drawings of different
emotional states by a
patient with amygdala
dysfunction in limbic system
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
animal studies- Hunsperger, R.W. & Bucher, V.M. (1967).
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
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
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
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
dated dyselxia definition (morgan 1896)
originally used to describe the loss of the ability to read as the result of brain damage
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
medical model to neurodiversity paradigm
clincial classifications (categorical) to neurodiversity spectrum
comorbidity of symptoms and syndromes is the rule rather than the
exception
prevalence of developmental language disorder
7%
prevalence of ASD
2%
prevalence of dyslexia
15%
prevalence of dyscalculia
6%
prevalence of dyspraxia
6%
prevalence of ADHD
4%
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
single cognitive deficit model of dyslexia
phonological deficit
single cognitive deficit model of ADHD
inhibition deficit
single cognitive deficit model of autism
theory of mind deficit
prevalence of comorbid conditions and ADHD (kadesjö and gillberg, 2001)
87% of persons with ADHD have one or two other neurodevelopmental conditions
prevalence of comorbid conditions and ADHD (andrewes et al., 2002)
21% of persons with ADHD have three or more other neurodevelopmental conditions
comorbiditoy of developmental language disorder and dyslexia symptoms
25-90% (tomblin et al., 2000)
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
examples of common additional symptoms in developmental disorders:
- visual stress
- auditory processing disorder
- atypical executive functions
what is visual stress?
visual stress in response to bright, contracting stimuli
- common in ASD
- cooccuring in dyslexia
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
coping strategies for visual stress
avoiding strong light
reducing contrast
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
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
APD and ASD (lau et al., 2023)
70% of children diagnosed with autism show CAPD
APD and dyslexia (king et al., 2003)
50% of children with dyslexia show CAPD
APD And language impairment (sharma et al., 2009)
76% of children with CAPD have language impairment
APD and ADHD (ricco, 1994)
50% of children with ADHD have CAPD
executive functions examples
planning, monitoring, correcting and executing associated with prefrontal cortex slow maturation
what is dyschronia?
condition of cerebellar dysfunction in which an individual cannot accurately estimate the amount of time that has passed
dyschronia and dyslexia
time management problems
difficulties in visual/auditory processing of transient stimuli
(llinas, 1993)
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)
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
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)
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).
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
benefits of MCDM
- helps explain changes of pattern (sub-types) with age
- implicatiosn for treatment
challenges of MCDM
- theory is diffcult to falsify
- currect cross sectional studies cannot establish causality
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
what is an IPSP?
hyperpolarises a postsyanptic neuron so decreases the rate of action potentials
what is an EPSP?
depolarises a neuron so increases firing rate of action potentials
process of synaptic transmission
- action potential in presynaptic neuron
- vesicle fuse with neuron and releases neurotransmitters to syanptic cleft
- neurotransmitters bind to receptors and opens channels in postsynaptic neurons membrane
- movement of ions causes potential in postsyanptic
when an action potential reaches the end of an axon, depolarisation opens…
voltage gated calcium ion channels in the presynaptic membrane
how long does the transmission of information in the synapse take?
2ms (0.0000001cm/ms)
what is the speed of conduction along an axon?
4cm/ms
the quantity of neurotransmitters released impacts…
the robustness of changes in the postsynaptic membrane
what is the role of a synapse?
send chemical information through the gap and opens ions’ gates in the postsynaptic neuron
how many neurotransmitters do humans have?
around 100
excitatory synapse- Na+
sodium gates open and sodium ions enter the postsynaptic neuron = EPSP
inhibitory synapse- Cl-
chloride gates open and enter the postsynaptic neuron = IPSP
inhibitory synapse- K+
potassium gates open and potassium ions leave the postsynaptic neuron = IPSP
examples of excitatory neurotransmitters
glutamate, epinephrine, norepinephyrne
examples of inhibitory neurotransmitters
GABA and glycine
examples of excitatory and inhibitory neurotransmitters
acetylcholine, dopamine and serotonin
what are receptors?
chemicals specific to a given type of neurotransmitter
what are the two types of receptors?
ionotropic (fast) and metabotropic (slow)
example of an excitatory ionotropic receptor
glutamate
example of an inhibitory ionotropic receptor
GABA
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
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
what senses use ionotropic synapses?
vision and hearing
what senses use metabotropic synapses?
taste, hunger and fear
what are neuromodulators?
chemicals that affect metabotropic receptors
they may affect multiple synapses
what chemicals may activate metabotropic receptors?
dopamine, norepinephrine, serotonin, neuropeptides and sometimes glutamate and GABA
what is synaptic strength?
the strength of a synapse is defined by the size of postsynaptic potential
synaptic strength may very over time:
- short-term changes (seconds, minutes)
- long-term changes (memory and learning
effects, brain plasticity)
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
what is synaptogenesis?
formation of synapses
what is synaptic pruning?
very intensive in 2-16 years old humans
elimination of unnecessary synapses is beneficial
learning - > pruning
how are used neurotransmitters terminated?
- reuptake- brings
neurotransmitters back to the presynaptic
neuron (by chemicals called transporters) - broken down- e.g acetylcholine
- diffusion- big neurotransmitters (peptide) do this
wha does reuptake of neurotransmitters concern?
recycling process that concerns serotonin and the catecholamines (dopamine, nerepinephryne, epinephrine)
what is acetylcholine broken down into?
acetylcholinesterase breaks down ach into acetate and choline via enzymatic degradation
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
syanpses and medication
facilitation of transmission- agonist
inhibition of transmission- anatagonist
risks of amphetamines to synapses
block reuptake of dopamine and other transmitters
risks of cocaine to syanspes
block reuptake of dopamine and other transmitters
risks of methylphenidate (ritalin) to synapses
blocks reuptake of dopamine and others, but gradually
risks of MDMA to synapses
releases dopamine, serotonin and norepinephrine
risks of nicotine to synapses
stimulates nicotinic-type acetylcholine receptors which increase dopamine release
risks of opiates (heroin, morphine) to synapses
stimulates endorphin receptors
risks of cannabinoids to synapses
excites negative-feedback receptors on presynaptic cells
risks of hallucinogens (LSD) to synapsess
stimulates serotonin type 2A receptors
mood disorder treatment
SSRIs=reuptake of serotonin from the synaptic cleft is reduced
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
functions of the the nervous system
- control of vital functions (breathing, heart rate and digestion)
- control of movement
- reaction to external events for survival
- cognitive/emotional processes
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
what is the role of the somatic nervous system?
convey information from sense organs to CNS, and from CNS to
muscles
what is the role of the autonomic nervous system?
controls internal organs like heart,
intestines, etc
what is the dorsolateral (pyramidal tract) of the SNS?
controls movements in peripheral parts such as hands, fingers, and
toes
controls the contralateral part of the body
what is the ventromedial tract of the SNS?
controls more proximal parts of the body: muscles of neck,
shoulders, and trunk
responsible for bilateral movements like walking
controls both (left and right) sides of the body
what is the dorsal column medial lemniscal pathway?
carries information about touch, vibration and proprioception
what is the spinothalamic tract?
carries information about pain and temperature
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
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
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
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
where is the centre for homeostatic regulation?
hypothalamuc
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
examples of interhemispheric brain connections
corpus callosum and anterior commissure
what do cortico-sucortical pathways connect?
cortex to subcortical areas, motor areas in brainstem and
spinal cord (up-down)
what do subcortical-cortical pathways connect?
from brainstem,
sensory areas in thalamus to the cortex (down-up)
what is the corpus callosum?
wide bundle of neural fibres, connecting right and left hemispheres
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
what is included in the forebrain?
hemispheres
limbic system
thalamus
hypothalamus
what is included in the hindbrain?
cerebellum
pons
medulla
weightings of the brain
hemispheres = 85%
brainstem = 4.5 %
cerebellum = 10.5%
functions of the brainstem
transmits information from and to the brain
responsible for simple reflexive behaviour
physiological states
functions of the medulla
controls vital reflexes (heart rate, circulation, respiration, salivation, coughing and sneezing)
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
functions of the cerebellum
controls fine motor skills, coordination and balance
role of the superior colliculi
helps guide eye movements and fixation of gaze
role of the inferior colliculi
helps sound localisation
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)
role of the thalamus
relays and processes information from sensory organs (expect olfaction) and transmits it to the cortex
role of the hypothalamus
regulates body temperature, hunger, thirst and sexual behaviour (autonomic NS)
role of the mamillary bodies
a relay for impulses coming from the amygdala and hippocampus
what is a gyrus?
a protuberance on a surface of the brain
what is a sulcus?
a fold that separates one gyrus from another
what is a fissure?
a long, deep sulcus
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.
brodmann’s map of the cortex
distinguished 52 cortical areas via a cytoarchitectural analysis
what are brodmann areas 1, 2 and 3?
primary somatosensory cortex
what is brodmann area 17?
primary visual cortex
what is brodmann area 41?
primary auditory cortex
what is the secondary cortex?
area of the cortex responsible for the second stage of sensory processing
receives inputs
from primary cortex
what is the associative cortex?
advanced stages of sensory information
processing, multisensory integration, or
sensorimotor integration
what are the 3 functions of the cortex?
- analysis of perceptual inputs
- organisation of movements
- higher cognitive functions
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
issues associated with prefrontal lobe dysfunction
impaired ability to learn from consequences and to control impulses
often found in depression and schizophrenia
prefrontal cortex damage: phineas gage
- gage was left with no speech, movement, intelligence or learning
impairment - te injury changed his personality and
behaviour
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
what are the parietal association areas?
inferior and superior parietal lobules and precuneus
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
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
functions of the temporal lobe
the auditory cortex which receives information from the ear and contains the language and auditory and visual association areas
function of wernicke’s area
language comprehension and production
damage results in meaningless speech and poor written and spoken comprehension
function of the inferior temporal cortex
visual identification
damage causes difficulty in recognises objects and familiar faces (prosopagnosia)
what subcortical areas make up the basal ganglia?
the caudate nucleus, putamen and globus pallidus
role of the basal ganglia
participates in planning behaviour and emotional expression, abundant connections with prefrontal cortex
direct inentional movements
what does an undersupply of dopamine in the basal ganglia lead to?
parkinsons disease
role of the hippocampus
creation of new memories (learning) and intergration of new memories into stable knowledge
role of the amygdala
emotional behvaiour and formation of emotional memories
role of the cingulate cortex
linking behvaioural outcomes to motivation and learning (critical in depression and schizophrenia)
what is locked-in syndrome?
condition in which patient is aware and awake but cannot make any voluntary movement
what is the cause of locked-in syndrome?
brainstem lesions in which the anterior part of the pons is damaged
what might result in locked-in syndrome?
traumatic brain injury
neurodegenerative diseases
strokes
cause of encephalitis lethargica
provoked by injury of basal ganglia and midbrain structures due to an immune recation to bacterial infection
what is akinetic mutism?
medical condition where patients tend neither to move (akinesia) nor speak (mutism)
what is the hindbrain called?
rhombencephalon
what is the midbrain called?
mesencephalon
what is the forebrain called?
prosencephalon
what are the 4 theories of emotion?
james-lange (1880s)
cannon-bard (1920s)
scahcter and singer (1960s)
lazarus (1990s)
what is an emotion?
an internal process that modifies the way an organism responds to certain kinds of external stimul (numan and woodside 2010)
what area of the NS do emotional situations arouse?
autonomic nervous system
what is pure anatomic 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
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).
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
somatosensory cortex and J-L theory
people with somatosensory cortex damage had normal autonomic physiological response to emotional music but little subjective
experience
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)
spotaneous rapid breathing and J-L theory
spontaneous rapid breathing leads to worry about suffocation and panic
attacks (kein, 1993)
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)
suggestion of the cannon-bard theory
emotional stimulus simultaneously triggers autonomic response AND emotional experience in the brain
reasons for the cannon-bard theory
- ANS responds too slowly for a rapid onsent of emotion, e.g blushing takes 15-30 seconds to occur
- people have problems detecting changings in ANS activity (e,g HR)
- 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?
bard (1934)
severed the connection between the visceral organs and the brain did not abolish emotional behaviour
what is sham rage and how can we induce it>
spotaneous fight or flight responses
can be caused by removing the cortex in cats
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 – top down theory of emotion.
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
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
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!
suggestions of lazarus’ theory
it is the cognitive interpretation which mediates emotional experience
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
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
the amygdala and fear
- recieves input from pain, vision and hearing centres
- projects to hypothalamus and prefrontal cortex
- also projects to pons (startle response)
the moro reflex
a normal reflex for an infant when he or she is startled or feels like they are falling
moro reflex and rats
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
does damage to the amygdala destroy fear?
no- suggestions that these animals may have difficulty interpreting signals with emotional consequences
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)
kluver-bucy syndrome
bucy surgically removed the temporal
lobes and some of the limbic system (including amygdala)
this lead to psychic blindness
what is psychic blindness?
an inability to recognize “the emotional importance
of events”
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
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)
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
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
urbach-wiethe disease
individuals with this disease accumulate calcium in the amygdala and it atrophies
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
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
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
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
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
what is the outer ear called?
the pinna
what is the role of the pinna?
captures sound and amplifies it by funneling it into the smaller auditory canal
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
wilska (1935) sound detection
we can detect sound when the eardrum vibrates as little as the diameter of the hydrogen atom
what is the role of the inner ear?
cochlea translates pressure to bioelecttical activity and sends to upper structures in the nervous system
what is balance controlled by?
vestibular system
role of semicircular canals
detect rotation
role of otolith organ
detects acceleration
what are the otolith organs?
hair cells in the utricle and ear stones
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
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
auditory pathway: from cochlea to cortex
- 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
- second relay in the brain stem -
in the superior olivary nucleus (pons). majority (but not all!) of the auditory fibres are contralateral - third relay takes place in the inferior colliculus of the midbrain
- final relay, before the cortex, occurs in the medial geniculate body
- projection from the thalamus to the auditory cortex
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
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
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
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)
what is pitch?
perceptual correlate of frequency
how is frequency encoded by the brain?
the place code (von bekesy)
- different places along the cochlear respond to different sound frequencies because of differences in stiffness/elasticity of the cochlear membrane= tonotopic organisation
- each frequency has its designated path from the cochlear to the brain
tonotopic organisation in the PAC
the more anterior the firing neuron, the lower the pitch
most sounds (200-20000Hz)
– frequency is encoded in accordance with the Place code
– intensity is encoded via the neurons’ firing rate
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
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
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
wernicke’s area
understanding spoken language
superior temporal gyrus
broca’s area
speaking
inferior frontal gyrus
voice onset time
a small difference in the time it takes for the vocal cords to start
vibrating after releasing a consonant makes the difference
between a “b” and a “p” sound.
even though the VOT is on a continuous scale, we perceive these sounds categorically as “b” or “p”
brain lateralisation and audition
the cochlear nucleus receives input from the ipsilateral ear only
all later stages have input from both ears
dichotic listening tasks
different syllables presented simultaneously, each to a different ear
the ear contralateral to brain hemisphere dominant for speech gives more responses
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)
where is conductive hearing loss associated with?
outer/middle ear
where is sensorimotor hearing loss associated with?
inner ear (cochlea)
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
corrected by medication, surgery or by sound amplification
from hearing aids, or by using bone conduction
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
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
corrceted by cochlear implants
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
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)
what are magnocellular neurons?
large receptive field, movement and large patterns
tend to be black and white
what are parvocellular neurons?
small receptive field, detect visual details and colour
what are koinocellular neurons?
mostly small fields but varies, multiple functions
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
visual perception
posterior-anterior organisation
cells respond stimuli of increasing complexity
receptive fields become increasingly larger
2 pathways- ventral and dorsal
what is V1 (striate cortex)?
- contains many cells (i.e., neurons) tuned to bars in different positions of the visual field
- based on combination of many neurons with simple, complex and hypercomplex receptive fields we are able to detect basic features in images- edges
concentric cells in LGN
on-centre or off-centre
what happens when you sum 3 concentric cells?
create simple cells to detect straight lines (primary visual cortex)
what are complex cells?
- collection of concentric cells
- receptive field of medium size
- bar/edge shaped but without fixed excitatory or inhibitory zones
- cells respond to moving light patterns
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
end-stopped/hypercomplex cells
receptive field of large size
bar/edge shaped
strong onhibitory area on one end
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)
what is a receptive field?
describes the spatial pattern of light to which a cell responds
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)
what does damage to the visual cortex cause?
blindsight- someone can perceive the location of an object despite being cortically blind
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
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
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
extra striate visual pathways
areas V4= greyscale contrast
hMT/V5= static contrast
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”
where are lesions in patients with cerebral achromatopsia?
V4A (anterior)
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
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
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
what does damage to V5 result in?
cerebral akinetopsia
stevens et al (2009)
TMS to V5 significantly
impaired global motion
direction detection
what are the areas of the brain associated with memory?
medial temporal lobe structures
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
what is anterograde amnesia?
cannot form new memories
what is retrograde amnesia?
unable to retrieve memories prior to damage (initially thought to be 1-3 years)
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
what does the case of HM tell us about the medial temporal lobe?
- important for long-term memory, but less so for working memory functions
- more important for remembering recent life events than remote life events.
- important for explicit memory regardless of the encoding or retrieval modality
- important for transferring events and facts into long-term memory
- NOT IMPORTANT for retaining information “online” (e.g., for working memory)
- NOT IMPORTANT for memories linked to non-declartaive memory
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.
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
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.
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.
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
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
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.
relational memory theory (eichenbaum et al 1999)
the hippocampus does not represent
space as such, but more the relationships among overlapping cues in the environment.
this can include spatial maps but may
also include other overlapping
associations that may not be primarily
spatial in nature (reward cues, temporal
cues etc)
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
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
episodic memory theory (tulving and moscovitch)
postulates that the hippocampus is critical for episodic but not semantic memory
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
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
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)
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
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
integrating theories of hippocampal memory function
- spatial memory appears to be linked to
right hippocampal processing whereas
relational functions are associated with left hippocampal processes. - spatial memory appears to be linked to
posterior hippocampal processing (taxi drivers) whereas relational functions are associated with anterior hippocampal processes - lesions in rat
hippocampus have a significant effect on recollection (episodic memory) but not familiarity.
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
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
phonological loop (chein and fiez, 2001)
supramarginal gyrus
increased activation with increased verbal memory load
(more syllables) – increased rehearsal/maintenance
suggestion that phonological
WM sub-served by these key regions
increased activation
with increased verbal
similarity – increased
demand on store
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 FFA and PPA respectively
- faces and houses activate the left IFG
location more dorsal and caudal area
-l ocation seems to activate inferior and
superior parietal lobe bilaterally also
working memory- building blocks
for WM we need: selective attention, rehearsal, patterns, retrieval, updates, sustained attention and inhibition
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
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.
summary of WM brain regions
- regions of prefrontal cortex and parietal cortex are involved with executive/attentional functions in
working memory - areas of association cortex appear important in the
storage of specific material during working memory
delay - temporal cortex more associated with visual working memory but less in spatial working memory.
- parietal lesions likely to have greater effect on spatial working memory than visual working memory
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.
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
what are the two visual processing streams? (ungerleider and mishkin, 1982)
dorsal (pareital lobe)
ventral (temporal lobe)
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-M2
what is the role of the ventral pathway?
“what” stream
- involved in processing the characteristics of objects
V1-V2-V4
milner and goodale (1992) refinement of visual pathways
dorsal=”how stream” and how we use visually guided actions
what input does the dorsal stream receive?
input only from magnocellular cells (therefore cannot see in colour)
what input does the ventral stream receive?
input from magnocellular, parvocellular and koinocellular cells (can see in colour)
what brodmann area is the primary visual cortex?
BA17
what brodmann area is the secondary visual cortex?
BA18
what brodmann area is V4?
BA18/19
what brodmann are is V5/middle temporal?
BA18/19/39
what gyrus is included in the inferior temporal cortex?
fusiform gyrus (supports visual recognition)
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
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
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
why do you have bilateral activation of the fusiform when responding to objects?
can be processed in two different ways (language and visual)
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
damage to the lateral occipital cortex
linked to apperceptive agnosia
damage to anterior structures in inferior temporal cortex (right)
associative agnosia
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
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)
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)
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
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
damage to the fusiform gyrus
results in prosopagnosia (category specific)
what is prosopagnosia?
impairement at recognising human faces vs other living things
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
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
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
may reflect differences in perceptual processing across
these types of judgment
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
do faces activate other brain regions? (haxby et al 2001)
inferior occipital and fusiform gyrus process invariant features for indentification (ventral)
posterior superior temporal sulcus processes dynamic features of facial gestures (dorsal)
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)
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)
what is optic ataxia?
affects a person’s ability to visually guide their hand movements to reach or grasp object
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
what damage causes optic ataxia?
damage to the inferior and superior parietal cortex
double dissociations in toptic ataxia and visual agnosia
optic ataxic-recognise but no direction
visual agnosic- mo recognition but direction
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
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
problems with the theory of hemispheric rivalry
- does not explain why neglect is almost always due to RH damage
- damage to the corpus callosum, affecting the balance in communication between the
hemispheres does not lead to neglect
theories for hemispatial neglect: right hemisphere dominance theory
left hemisphere attends to right
hemispace
right hemisphere attends to both
left and right hemifields
this better explains the prevalence of
left hemispatial neglect symptoms observed
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
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
where is the basal ganglia and what are its interconnections?
situated at base of the forebrain
- interconnected with cerebral cortex, thalamus and brainstem
what diease has significant impacts on the basal nuclei?
parkinsons
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
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
why are parkinsons patients bad at the weather task?
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
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
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
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
what are the two types of direct (repition) priming?
perceptual and conceptual
what is an example of indirect priming?
semantic priming
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)
neural activity and perceptual priming
brain acitivation reduces during repitition suppression
e.g in left lateral preforntal cortex and left occipito-temporal lobe
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
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
why does the left fusiform gyrus respond to both same and different exemplars?
as it encodes verbally
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
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
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)
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
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
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
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
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
summary of repitition suppression and semantic priming
left anterior temporal lobe- consistent with semantic dementia
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
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
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
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
what is deontology?
moral rules pertain to absoulte rights
what is consequentialism?
the moral value of an action is in one way or another function of its consequence alone
what is utilitarianism?
endorising harmful actions for the greater good
kohlberg (1969) morality
morality is a by product of reason (cognitive evaluation)
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
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
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
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.
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?
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
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)
what are the predictions of the dual-process theory?
- personal moral dilemmas lead to greater activity in brain regions associated with emotion
- as these are automatic there would be a decrease in cognitive control brain areas
- response time for yes in personal dilemmes is slower than no
- impersonal scenarios would show no reaction time effect
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
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
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
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.
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
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.
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.
what brain region is activated when we make utilitarian responses?
DLPFC
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”.
damasio (1990) ‘somatic marker hypothesis’
reflects the importance of emotional information to social moral judgements
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
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.
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
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
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
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
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)
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
deontology and emotion
result of moral behvaiour being driven by intuitive emotional responses to situations (moral alarm bells- greene)
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
deontology has a what basis of morality?
emotional
consequentialism and utilitarinsim have a what basis?
cognitive
consequentialism and cognition
cognitive in the way it uses CBA
this can be seen in terms of lateral PFC
