BIOPSYCHOLOGY 2.0 Flashcards

1
Q

what is the holistic theory of brain function?

A

any partof brain could carry out any function

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2
Q

when was the holistic theory of brain function challenegd?

A

when it was found that ppl who suffered trauma in pat part of brain
-> thru illness or accidents lost spec function

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3
Q

what are the early studies? (3)

A

case of phineas gage
work of broca and wernicke
on role of brain in speech + lang

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4
Q

who was phinea gage? waht was he known for?

A

1823-1860
american railroad construction foreman
being the victim of an accident in 1848 that greatly contributed
to our understanding of cognitive neuroscience
and localisation of brain function

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5
Q

waht was the cause of the acc+ the subsequent injury he received?

A

tamping iron went through his frontal lobe
… damaging it
when he was compacting gun powder
-> that was when the gun powder ignited

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6
Q

after the accident what skills did gage retain?

A

could still walk + talk

brain could still regulate

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7
Q

desc gage p before accident

A

smart
energetic
determined
thoughtful

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8
Q

after acc?

A

rude and vulgar

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9
Q

what can we concl about br func from case of phineas gage?

A

brain made of diff parts
each w diff funct
-> frontal lobe controls the personality

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10
Q

who was Paul Broca?

A

1824- 1880

french surgeon + studied in uni of paris

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11
Q

when did Broca discover brocas area?

A

when Tan died at 51 (1860s)

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12
Q

where is Brocas area located?

A

in frontal lobe in left hemisphere of brain

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13
Q

how did Broca make his discovery

A

Tan suffered w epilepsy + lsot ability to speak at 30
10yrs later he met Tan in surgery 1861
broca found tans underst of speech seemed rel in tact
broca was curious about y this should be
-> tan died 51 Broca perf post mortem
.. found damage in brocas area

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14
Q

what is the role of brocas area?

A

controls speech
-> ability to prod meaningful sounds
allows us to haev good control over tongue/mouth muslces
in order to prod speech

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15
Q

what happens if brocas area damaged?

A

could lose ability to prod meaningful sounds
.. affect ability to communicate
however inteliigence + lang comprehension still remains in tact
.. can still underst language
difficulty rpoducing connective “and”

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16
Q

waht is it called if brocas area is damaged?

A

Broca aphasia

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17
Q

who is carl wernicke?

A

1848 - 1905
german physician
known fro disc wernickes area shortly after broca 1874

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18
Q

wehre is wernickes area located?

A

in dominant cerebral hemisphere

-> left hemisphere and further back in temporal lobe

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19
Q

how did wernicke make his disc?

A

w noticed not all lang deficits were resutl of damaged to brocas area
obs patients w brain damage as result of stroke
-> noted all beh + conducted post mortem autopsies to locate brain damage

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20
Q

what is the role of wernickes area?

A

controls comprehension of language

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21
Q

what happens if wernickes area is damaged?

A

results in receptive or fluent aphasia (wernicke aphasia)
.. unable to understand lang in neither written or spoken form
-> but speaks w normal grammar, syntax, innotation
however cannot express themselves meaningfully using language

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22
Q

what do all of these early studes give rise to ?

A

gives rise to theory of localisation of brain function

.. each part of brain carries out a pat func

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23
Q

desc str of brain

A

divided into 2 hemispheres
left and right
-> connected by thin band of tissue called the corpus collosum

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24
Q

desc func of brain?

A

for most funct 2 hemispheres are symmetrical
altho some processes controlled by 1 side of br only
-> most of body ocntrolled by opp hemisphere of br
e.g picking up smth w right hand would be controlled by left hemsphere
-> this is called lateralisation

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25
Q

waht is the outermost layer of the brain called?

A

cerebral cortex
is highly folded + much more dev in humans than in other mammals
.. allows huamans to ahve a much higehr cog function
-> eg h can appreciate and eval artworks
-> eg cant do further planning of future
but animals cant
-> due to having a larger cerebral cortex

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26
Q

how is cerebral cortex divided?

A

cerebral cortex in both left and right hemispher divided into lobes
-> each lobe is subdivided into areas that control diff functions

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27
Q

motor cortex descp

A

in each hemisphere area controls the voluntary muscle movements in opp sides of body
if area damaged muscles may be paralysed + fine motor control can be lost
-> eg writing, using a knife etc
this cortex is at back of frontal lobe

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28
Q

brocas area descr

A

located in frontal lobe

most ppl its found only in left hemisphere

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29
Q

auditory cortex descr?

A

damage to this cortex may produce hearing loss or reduce ability to understand lang
areais found in each hemisphere in temporal lobe

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30
Q

somatosensory cortex descr?

A

front of the parietal lobes
recieves sensory info
from receptors in skin about temp, pressure etc
skin areas of high sens e.g face are represented by larger areas within this cortex

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31
Q

visual cortex descr?

A

area processes info from eyes
crotex is in the occipital lobe
each eye send sends info from right visual field to the part of the cortex in left hemisphere
.. damage to only 1 half of occipital lobe can affect vision in both eyes

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32
Q

wernickes area descr?

A

in temporal lobe

most ppl found in left hemisphere only

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33
Q

support for theory of localisation of brain function

-> supprots brain ahs diff parts to do diff functions (3)

A

work of broca supports idea of pat brain areas performing sepc functions
.. sugg brocas area controlls production of speech
work of wernicke supprots -> wernickes area
-> damage to w area caused fluent aphasia
both studies highly scientific -> post mortems .. empirical evidence

brain scans have shown lang proesses are localised in brain - Petersen 1988
-> conducted br scans showed w area active when lsitening to lang being spoken + brocas area active whilst reading aloud

Dougherty 2002 reported on 44 OCD patients who ahd undergone cingulotomy.
at psot surgical follow up after 32 weeks
a third of p met criteria for succ resp to surgery
14% of p were partial resp to srgery
-> shows symptoms or beh assoc w serios mental disorders are localised

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34
Q

whats cingulotomy

A

neurological proc
involved isolating part of the brain
which thought to be involved w OCD

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35
Q

contradiction to localisation o brain function? (2)

A

the brain can show plasticity
-> Draganski et all 2006
imaged the brains of med students 3 months b4 + after final exams
-> learning induced changes have occured to posterior hippocampus and parietal cprtex
as a reuslt of exam
… shows brain can adapt and change in resp to certain experiences
… shows 1 part on brain does not have only 1 specific function

some brain function may be holistic rather than localised
lashley 1950 studied learning in rats by removing 10-50% of their cerebral cortex that were learning a maze
rats ability to learn was not affected by removal of any pat part of brain
.. supports the fact that learning maze req every part of brain
-> learning is not a localised function

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36
Q

what is another phrase for plasticity?

A

cortical remapping

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37
Q

what does plasticity mean?

A

refers to the brains ability to change + adapt in resp to exp and learning

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38
Q

when did plasticity used to be thought it ocuured?

A

plasticity thought to be occured only in childhood

  • > has been known for a long time that brain incr no of synaptic connections
  • > peaks around 3 yr old
  • > as we get older connections we use freq stregnthen and those we dont get lost
  • > this is called synaptic pruning
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39
Q

waht else about plasticity?

A

used to be thought inadolesence critical period
once passed brain showed no furhter plasticity
-> recent studies showed that plasticity can occur in adulthood
-> examples are Maguire et all 2000

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40
Q

what was procedure of maguire et al 2000?

A

16 healthy right handed male licenesd London taxi drivers participants have to pass test of knowlegde
-> mean age 44
taxi drivers brain scans compared with scans of 50 healthy right handed males who did not drive taxis
the r used MRI scans + controlled v
->e.g no. of years of taxi dr, age, sex and handedness
data collected using MRI
MRI scanner exposes a p’s br to a strong mag field + radio waves
.. producing detailed pics of brain
+ used VBM to measure density of grey matter in brain

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41
Q

findings of maguire et al 2000?

A

posterior hippocampus of taxi drivers sig larger relative to those of control subj
anterior hippocampal region was larger in control subj than in taxi drivers
second main findings was hippocamal vol correlated with amount of taxi driving years
-> positively in the right posterior and neg in the right anterior hippocampus
-> the VBM analysis found taht sign incr grey matter vol was found in brains of taxi dr
compared w thoes of controls in only 2 brain regions, namely the right and the left hippocampi
no diff were observed elsewhere in brain

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42
Q

concl?

A

maguire et al argue that this study demonstrates that plasticity of hippocampus in resp to environmental demands
they argue that posterior hippocampus stores a spatialrepresentation of the envi + in london taxi drivers the vol of posterior hippocampus expanded bc of their dependance on navigation skills

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43
Q

pos of maguire? (3)

A

normally diff to make concl from natural/quasi exp as any diff found between 2 grps (e.g vol of grey matter) may not have occured bc of IV -> if they r taxi driver
however r carried out orrelational analysis which clearly demonstr theres a strong pos correlation betwe legnth of time p driving taxis + their posterior hippocalpul vol
.. sugg legnth of time driving taxi in london assoc w grey matter within hippocampus
MRI scans highly scientifiv + empirical methods of inv providied vast amount of quantitive data
-> relating to vol + size of hipoocampus
.. enabling them to carry out statistical analysis + make direct comparisons
-> employed many controls, eg samples amtched for age, sex and handedness
also r analysing brain scans were “blind”
-> they did not kno if brain scan belonged to a taxi driver or non taxi driver
.. incr the internal validity of results
.. can be more confident when drawing conlc

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44
Q

neg of maguire et al 2000

A
all p were male
.. not a repr sample
-> may be differences betw males+ females in terms of spatial memory 
... resukts diff to gen onto women
-> .. lacks population validity
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45
Q

name 2 other r into plasticity?

A

mechelli 2004 -> bilingual ppl had a larger parietal cortex comp to matched participants who had spoken one lang
draganski et al 2006

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46
Q

waht is functional recovery?

A

is the typeof plasticity shown after brain damage or trauma
in many casesbrain can rtansfer functions from damaged parts to undamaged parts of the brain so function can be recovered
it may be that the function is transferred to the homologous area (same area) in the other hemisphere
thought that functional recovery occurs quickest after trauma is expierienced + slows down later
.. rehabilitive theraphy most effective if used straigth after trauma if patient can
-> in order to assist functional recovery

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47
Q

waht is rehabilitive theraphy

A

physiotheraphy, speech therapy

48
Q

how does functional recovery occur?

A

brain can reorganise itself by forming new synaptic pathways
close to area of damage
neural connections that wouldnt normally be used are activated
-> allowing function to continue
-> this is helped by 4 things

49
Q

what 4 things help function to continue?

A

Repairing and growing new blood vessels
Axonal sprouting -> the growth of new nerve endings which connect w undamaged neurones to form new oathways
Recruitment of the homologous area on the other hemisphere of brain
-> eg if brocas area (in left hemi) damaged the equivalent area on right hemisphere may carry out funciton
Denervation supersensitivity may occur-> when undamaged neuronees near area of damage become more sens .. compensating for loss of neuronees in area
RARD

50
Q

research into functional recoevry?

A

taijiri et al 2013
found stem cells provided to rats after br trauma
-> showed clear dev of neurone like cells in area of injury
.. demonstrating the ability of brain to create new connections using neurones manufactured from stem cells

51
Q

pos of func recovery?

A

strength of r examing func recovery is the application of findings to field of neurorehabilitation
understanding processes of func rec led to dev of neurorehabilitation
-> use motor therapy + electrical stimulation of brain to counter neg effects + deficits in motor adn cog functions following accidents injuries and or strokes
.. demonstrates pos application of r in thisn area to improve the cog function of ppl suffering from inj

52
Q

neg of research into func recovery

A

it is possible this abiltiy can deteriorate with age
Elbert et al concl that capacity for neural reorg is much greater in children than in adults
… neural regeneration less effective in older brains
-> may explain why adults find change moredemanding than young ppl do
.. we msut consider the indiv diff when assessing the likelihood of cun recovery in brain after trauma

53
Q

adv of plasticity and func recovery 3

A

has important practical applications, field of neurorehabilitation befinitted from findings of r into plasticity
-> the br may show a high degree of spontaneous recovery straightafter trauma but tend sto slow down or stop unless supported by relavent therapies. incl speech, physiotherpahy etc
knowledge of palsticirty hadled to better applications of these therapies

PLasticity thru life-> while plasticity does reduce w age, research has shown it can continue through to adult hood
Bezzola 2012 gave p aged 40-60 yrs old 40hrs of gold training
brain scans showed reduced motor cortex activity int his grp compared to a control grp.. sugg more efficient neural connections
Evdience for plasticity comes from nonhuman animal studies
eg Hubel adn Wiesal 1963 took kittens and sewed one eye shut
-> found the part of visual cortex that would receive info from closed eye was still active + processed info form that open eye

54
Q

disadv of plasticity and func recovery2

A

negative plasticity descr changes in the brain that hinder rather than help recovery
-> 60-80% of amputees develop phantom limb syndrome where patients have unpleasant or painful sensations as if their limb were still there
this thought is due to changes in the somatosensory cortex after amputation
Functional recovery may be due to factors other than plasticity
-> may be educational lvls
Schneider 2014 found greater time patients spent in education, greater chance of disability free recovery after brain injury
40% of disability free patients had more than 16yrs of education in their hisotry comp to 10% disability free patients who had less than 12yrs of education
-> also been found womean show greater recovery than men following braintrauma

55
Q

waht is lateralisation

A

idea that the 2 hemispheres of brain function differetly
-> each hemisphere has functional specialisations
.. meaning some functions are mainly controlled by one hemisphere only
->e.g left hemi controls right side of body incl right hand-> dominant for language
-> right hemisphere controls oeft side of body incl left hand -> dominant for processes facial recog, analysis by touch and visual adn spatial tasks

56
Q

what are the 2 hemisphere connected by?

A

connected thru nerve fibres called corpus callosum

  • > which facilitate interhemispheric communication
  • > eg allowing left and right hemisphere to “tlak to each other”
57
Q

where is evidence for theory of lateralisation from?

A

from split brain patients
in normal brain 2 hemisphers communicate + share info via corpus callosum
some ppl haev forms of epilepsy that dont resp to usual treatments + cause life threatenning seiures
-> for these patietns a last resort treatment wouldnt be haviong corpus callosum severed
.. reduces seizures but means they have split brain
-> meaning communication betw 2 hemispheres impossible

58
Q

both left eye and right eye have..

A

both elft and right eye have a left visual field and right visual field

59
Q

descr how info seen in left visual field is processed

A

info from left visual field is processed in the rigth hemisphere
-> which contains spatial functions, face recognition adn controls the left hand

60
Q

descr how info seen in right visul field is processed

A

info from rigth visual field is processed in the left hemi

-> which contains language functions and controls the rigth hadn

61
Q

what are eg of spatial visualisationa dn analysis?

A

recognsiing ppl

62
Q

sperry 1968 proc

A

sperry studied 11 split-brain patients
-> had theior corpus callosum severed bc of epilepsy
-> inv either giving patient smth to hold in one hand (with out seeing it), or smth they could only see from either the left or right visual field of vision
-> eg a word or part of a face
these stimuli would be processed by opp hemisphere only as info could not pass across the CC
-> control comaprison grp of 11 patients whp had no inter-hemi disconnection

63
Q

waht were 4 findings of sperry?

A

sperry 1968
1)
when p saw smth in rigth VF they could say waht they seen but couldnt do this if it was seen in left visual field
-> bc info from rigt VF processed by visual cortex inleft hemisphere which also has language and speech functions.
if info presented in LVF it wouldve been processed by visual cortex in rigth hemi.. unable to say what they ahd seen as right hemi no lang func

64
Q

another findingsperry 1968?

A

2) wehn a p saw smth in LVF (e.g Key)
they would selecta corresponding item with their left hand without looking
->bc info from LVF processed by visual cortex in rigth hemi + right hemi motor cortex controls left hand .. enabling p to select correct item.
they would be unable to select correct item using rigth hadn bc left hemi which controls right hand does not kno what item was presented as it only enters left hemisphere

65
Q

finding 3?

A

if 2 diff words oresented to each VF the p could write with left hadn the words from VF but couldnt say it
-> bc ijnfo from left visual field processed by VC in rigth hemi+ rigth hemi has n lang functions .. could not say it
they could ay words presented to rigth VF and write it down witht heir rigt hadn
->bc info from RVF proc by VC in left hemi
->motor cortex in left hemi controls rigth hand + has lang function.. could say words + could write it down

66
Q

finding 4?

A

rigth hemi dominant in facial recog

  • > when diff faces presented to each VF
  • > the p asked to select which face they had seen from a line-up
  • > they consistently chose face that was presentd to left visual field
  • > which face would split brain patient pick out of a selection of face pics as the one which matched face they could see?
  • > could see women bc in left visual f
  • > infofrom LVF processed by visual cortex in rigth hemi
  • > functions of spatial recog .. could recognise
67
Q

adv of theory of hemispheric lateralisation 2

A

sperrys research provides a large body of supprot for the thoery of lateralisation
studied split br patients + presented info
-> eg word to only one hemisphere
found that if word presented in LVF -> proc rigt hemi
-> no lang func .. p unable to say it.
-> r supportsidea that language is lateralised
-> controlled by left hemi

Sperrys r strong scientific methodology
-> p told to stare at fixed points + r looked at their eyes to check this
-> 1 eye was sometimes covered
images flashed up fro 0.1 seconds
-> too little time for eyes to move to focus
.. meant sperry could be sure only 1 hemisphere was receiving sitmuli

68
Q

3 disadv of hemispheruc lateralisation

A

some r do not agree with theory of lateralistion
2 hemi do not work in isolation
+ are both involved in most eveyrday tasks
-> soem r feel theory over-simplifies brain function + distinction betwe left and right is unhelpful
-> what one side of brain can do can also be done by other -> plasticity and functional recovery

Some r suggests degree of lateralistion of brain cahnges with ages + lateralised func in younger ppl can become bilateral in healthy older adults
Szarflarski 2006 found lang to be incr lateralised to left hemi until age 25
then lateralisation slowly decreased
-> cause is unknown but may be de to both hemi being needed to perform tasks to compensate for age related declines in func
ISSUES with sample sperry used
-> 11 patients
-> small sample size… cannot be generalised to eveyr one who has a brain
-> split brain patients cannot infrom us how the normal brain works
+ some of 11 patients had a more severe disconnection than others after surgery
..changing more than 1 variable
.. lowers the internal validity

69
Q

what are 4 ways the brain can be studied?

A

Post motrtem examinations (autopsies)
fMRI
EEGs
ERPs

70
Q

waht is a post mortem examination?

A

physical examination that occurs after death
-> performed since time of ancient egyptians
-> brains removed from body + visually examined for any differences or abnormalities
-> any abnormalities are then related to any particular problems of differences the p exhibited when alive
a post mortem may inv comparing brain of p with a neurotypical brain (normal brain)
-> may involve dissections where brain cut into thin slices and investigated under icroscope
.. allowing abnormalities or difference at cellular lvls to be observed

71
Q

stregtnh post mortem 2

A

allow links to be made betwe symptoms experienced + phy abnormalities in brain
Broca + Wernicke could draw concl abouit cause of lang difficulties using these examinations long before imaging of living brain possible
.. leading to fruther research
Can be considered a strong scientific method of inv as it inv empiricism
->reffering to gaining info by direct sensory observations
since brain as a psychical structure can easily be seen it can be measured reliably

72
Q

weaknesses of psot morterm

A

cause and effect may be an issue
-> assumption may be that symptoms experienced by p when alive were caused by brain abnormalities seen at psot mortem
-> hpwever brain abnormalities could be unrelated problems experienced
-> in addition could be that the problem first occured adn then causes less info to pass thru brain area which leads to area becoming damaged rather than the damage causing problem
Neuronal changes during + after death may weaken valdiity of any conclusions made from post mortem examination
Patietns suffering from ill ness of abno may be unable to give fully informed consetn for a psot mortem examination after death
-> fmaily may feel pressured to agreeing if this is only possibility to gain rare medical insights

73
Q

stages of fMRI?

A

person is put in an fMRI scanner
person is usually given a stimulus to see, hear or feel
may be asked to imagine smth or given a mental task to perform
more active parts of brain req more o2 .. have an increased blood flow
the magnets detect where more haemoglobin is
due to its iron content
Images are produced which show which parts of brain more active during tasks
links are established betw pat br areas and functions

74
Q

strength so fMRI 2

A

fMRI does not use radiation to produce the images .. is low risk to patients
-> also non-invasive .. doesnt req long recovery times
Very high spatial resolution - images are produced that give a clear indication of exactly where brain activity is occuring
.. allows r to pinpoint beh and problems exactly
-> which would possibly lead to better patient outcomes as if they kno exactly what problme is
.. do not need to trial and error
-> recommending best treatment or course of action immediately

75
Q

weakness fMRI 3

A

fMRI is an expensive technique
->req highly exp specialist equipment
-> ina ddition staff using fmri machinery have to undergo specialist training which incr costs further
… fmri facilities are not available at all hospitals meaning patients have to travel much further to access it
.. as compared with more inexp ways of studying brain eg EEG
-> cheap enough to be available at hospitals
-> also means that any concl made are absed in small sample sizes
Clear images only produced if p being scanned is compeltely still for duration of scan
-> 45-1hr 30minsbut can even be longer
.. ppl find it difficultto remain compl still for such long legnth of time
->resulting in lower quality, less clear images which are less useful
An assumption had to be made that the incr blood flow is related to br activity
fMRI scanner cannot directly detect brain activity itself

76
Q

what is the EEG?

A

EEGs measure general activity of brain via electrodes placed on scalp
-> usually as part of an elasticated cap
->electrodes pick up tiny signals omitted as nuerones send impulses
-> these signals are amplified
-> each electrode detects brain activity directly below where they are placed on scalp
.. resulting scan shows the brainwave patterns produced by the brain
EEGs used to study general brain activity such as during sleep
can also be used to diagnose a variety of conditions incl sleep disorders and epilepsy

77
Q

strengths of EEG 3

A

EEG priamry way of disagnosing ppl appropriately
->haev proved invaluable in diagnosis of conditions such as epilepy
->random bursts of activity in br easily be detected on screen
-> this can be helped to identify ppl who need treatment quickly + reliably
since eeg non-invasive + recovery time is minimal
Another stregnth is that eeg have also helped us to gain an in depth understanding of whats happening in br
as we exp diff stages of sleep
-> have learnt that dreams occur in rem stage +eegs can help us to understand sleep disorders such as somnambulism (sleep walking)
An adv of eegs is they have extremely high temporal resolution
-> precision of a measurement with respect to time
meaning thye can detect brain activity at a resolution of a single millisecond or less ins ome cases

78
Q

weakness of eeg 1

A

poor spatial resolution
can only indicate the general lcoation of acvitiy
.. deso not allow r to pinpoint precise lcoations where activity is taking place
-> veyr difficult to distinguish betw activities originating in different but adjacent locations

79
Q

waht is ERP?

A

small electrical charges elicited by a spec task or stimuli
when eeg is taken in resp to a pat stimulus the resulting scan shows all brain actvity happning at that time
-> that in resp to stimuli and “bacground activity”
however using an ERP the extraneous activity can be removed from the EEG leaving only the brainwaves that have occured in resp to pat stimuli being investigated
brainwaves on erp can then be related to cog processes being oerformed at time -> eg memory, recall

80
Q

strengths erp? 3

A

erps combine high temporal resolution of eegs with ability to indicate some areas of brain activity more precisly than eeg
r .. able to identify areas suchas P300 component which is involved in attention + working memory
.. erps have useful real life application
Different types of erps have been identified + researchers can now descr role these brainwaves have in cog functioning
->E.g wave called p300 thought to be involved in wroking memory
this evry precise knowledge can be used in order to identify + help treat ppl who suffering w problems in working memeory
ERPS does not use radiation to produce the brainwave patterns
.. low risk to patients
-> non invasive.. doesnt req long recovery times

81
Q

weakness of erp 3?

A

no standardised methology yet for erp
.. making comparisons betw diff studies difficult
.. reduces usefullness of erps as harder to make firm conclusions due to inconsistencies in carrying out technoque
.. decr reliability
Incr spatial resolution compared to EEGs
altho still veyr low when compared to fMRI
this could reduce the validity of conclusions as r may be less sure exactly which parts of brain involved
In order to prod good qual erps all other stimuli apart from that being investigated msut be removed
-> background noise, changes in temp etc
this is very difficult to achieve which emans that there may be soem extr variables
.. make it harder to interpret the info
-> reducing validity of concl
-> r less sure of what they,easured

82
Q

waht is a biological rhythm?

A

huamsn have no. of biological rhythms
-> hepl us to function in line w the physical worlds cycle
a biological rhythm is any change in biological acitivity which repeats periodically
it occurs regularly in cycles with regular intervals between cycles
eg menstrual cycle, sleep wake cycle etc

83
Q

what are the 3 main types of biological rhythm?

A

circadian rhythms -> around 24 hrs to complete
infradian rhythms -> more than 24 hrs to compl e.g several days or several months
ultradian rhythms -> take less than 24 hrs to complete

84
Q

what controls our biological rhtysm?

A

biological triggers

environmental triggers

85
Q

give 3 biological triggers

A

neurological structures eg brain
hormones eg melatonin
biological processes ie digestion

86
Q

3 environkental triggers

A

noises
ligth intensity
clocks

87
Q

name a cricadian rhythm

A

sleep-wake cycle

88
Q

waht is an endogenous pacemaker?

A

internal, biological mechanisms or body clocks which regulate our biological rhythm
eg incl the SCN
pineal gland
hormones eg melatonin

89
Q

waht deso the SCN to be an endogenouse pacemaker?

A

scn is main endogenous pacemaker in all mammals
it is a nucleus located in the hypothalamus just above the optic chiasm
-> where the optic nerves cross over
-> its made up of photoreceptor cells which resp to intensity of light

90
Q

what is an exogenous zeigeiber?

A

external environemtnal cues which interact w endogenous pacemakers in order to adjust our biological rhytms so they are in line w our environment
-> process of adjustment known as entrainemnt eg jet lag

91
Q

waht are exmapeks of exogenous zeitgebeirs

A

light including natural patterns of light and dark and artificial room lighting
social cues eg meal times
outside temp

92
Q

waht are the interactions between endogenous pacemakers and exogenous zeitgebers in the running of the sleep- wake cycle?

A

info regarding lvls of ligth and dark enters the retina + travels along optic nerve to SCN
->containing neurones made up of photoreceptor cells
.. sens to light
.. when low lvls of light detected the SCN sedns message to pineal gland
-> producing hormone melatonin
.. causing us to feel drowsy + shuts down brain mechanisms for wakefulness causing us to fall asleep
when incr lvls of ligth detected scn instr pineal gland cease production of melatonin
-> p feels more alert + wake up
-> cycle repeats once eveyr 24hrs
.. a circadian rhythm

93
Q

waht are research into circadian rhythms sleep wake cycle, endogeous pacemakers and exogenous zeitgebeirs

A

siffre 1979

morgan 1995

94
Q

siffre 1979

A

siffre 1979supports role of endogenous pacemakers + exogenous zeitgebers in sleep wake cycle
-> spent 2 months in cave with no natural light
-> slept when he felt and got up when he felt ready
his sleep waking pattern became totally desyncrhronised from the world above
.. suggesting exogenous zeitgebers have an important role to keep our sleep wake cycle line w envi patterns of ligth and dark
-> altho circadian rhythm initally disrupted he eventually settled into regular 25hr slepe wake cycle
.. shpwing endogenous pacemakers have an important role to ensure that circadian rhyth, of sleep wake cycle continues to run around 24hrs of legnth

95
Q

moragn 1995?

A

morgan 1995
supports idea SCN is main endogenous pacemaker in mammls
-> he removed scn in hamsters
-> cricadian rhythms disapperared
m transplanted scn cells from foetal hamsters + circadian rhythm re-established
-> suggests scn has main control of circadian rhtyhms
+ without the scn exocgenous zeitgebers have no infl
m also bred mutant hamsters so they ahd circadian rhythms of 20hrs instead of 24
transplanted their scn into normal hamsters
-> normal hamsters then displayed mutant hamsters 20hr rhythm
.. suggesting scn has key role in determining the legnth og circadian rhythms

96
Q

what is a weakness of morgan 1995?

A

extrapolation is an issue
->can non human animals be applied onto humans
altho all mammals share a similar physiology
hamsters are veyr diff on the phylogenetic scale
.. brain anatomy + functions different when comparing humans to hamsters
-> hamsters are nocturnal.. cant be confident that scn plays same role in human circadian rhthyms

97
Q

folkard et al 1985

A

1985 supports the role of exogenous zeitgebers in sleep wake cycle
-> he artificially shortened the legnth of day by manipualting clock in envi to see if exogenous zeitgebers eg clocks have any effect on slep wake cycle
they put 12 p in an undergroundncave fro 3 weeks + isolated from natural light but did have a clock
p agreed to go bed + wake up at set times
-> at first clock ran normally but gradually sped up
p cycle did speed up to match clock at beginning of exp
.. shows that exogenous zeitgebers do infl the speed of cycle
however as day shortened to 22hrs the maj of p reverted back to their normal 24hrs cycle
this shows that exogenous zeitgebers only have limited control over the cycle
however 1 p did adpat to 22hr cycle
-> which suggests there are indiv diff in role of exogenous zeitgebers
-> they have more infl over some ppl rhythms than others

98
Q

what is a strength for folklard rsearch

A

practical application to shift work

-> some ppl going against bodys natural bodyclokc gives us a better quality life

99
Q

2 common disruptions to biological rhythm?

A

shift work
jetlag
-> when body is out of synch
-> examples of entrainemnt

100
Q

waht are some negative effects of entrainment or disrupting biological rhythms? 6

A

insomnia
nausea
loss of appetite
fatigue
illness (heart disease 3x more liekly w long terms shift work 15yrs or more)
increase in accidents
all due to disruption of biological rhtyms

101
Q

waht was bovin et al1996?

A

bovin et al 1996
studied shift workers working night shifts
-> alertness lowest betw midnight and 4am
-> cortisol lvls lowest
-> an alertness hormone
-> high lvls at 7am .. help us stay alert
-> 12M low lvls make it harder for us to cocnentrate .. incr risk of accidents

102
Q

2 infradian rhytm

A

menstrual cycle

seasonaL AFFECTIVE DISORDER

103
Q

waht is the menstrual cycle

A

driven by fluctuating lvls of hormones whereby the utreus is prepared for pregnancy
fsh secreted by pituatry gland.. causing egg to matur ein ovary
-> also stimulates ovaries to release hormone oestrogen
oestrogen secreted by ovaries.. inhibits fsh production
.. only egg matures in a cycle
-> causing uterus lining to thicken + stimulates PG release LH
LH causes mature egg to be released from ovary
progesterone another horome secreted by pvarie-> incr lvls maintain blood lining
-> 2 weeks after ovulation if no preg progesterone lvls fall causing lining of womb to shed
-> takes 28 days
repeats monelthy

104
Q

mcclintock and stern 1998

A

supports idea hormones/chemicals control cycle
10yr longitudinal study invl 29 women
->20-35yrs of agehistory of irregular spontaneous ovulation
-> pheromones gathered from 9 women at diff stages in menstr cycle via cotton pad placed in armpit worn for 8hrs
pads were treated w alcohol + frozen then rubbed on upper lip of other p
mcclintok 68% of w exp changes to timing of mestr cycle… brought them closer to cycle of their phernomone donor

105
Q

pos mcclintok + sterns r 1

A

evolutionary adv
menstr synchrony thougt to have evolutionary selective adv
may have been adv in women to menstr simialr times as other women .. fall pregnant at similar times
-> newborns cared fro collectively incr chances of offsprings survival

106
Q

weakness mcclintok + stern 1

A

methodology limitatins
-> syncrhronisaition studes hard to control the many factors known to affect timing of menstr cycle
eg stress, diet, excerise all act as confounding v
.. synchronisation of mesntr cycle may not be controlled by pheronome lvls
but other factors
+ sample sizes small .. cant generalise findings to all women

107
Q

give another infradian rhythm

A

Seasonal affective disorder SAD
a type of depression triggered by seasons
-> most common type -> winter-onset depression
-> symptoms beg in later autumn or early winter go away by summer
much lesscommon type is summer-onset depression
-> sympt begin later springs or early summer goes away by winter
SAD may be related to changes in amount of daylight during diff times of yr
psych hypothesised melatonin is cause of sad
in p of darkness PG produces melatonin
-> incr melatonin production in darker months reduces production of seratonin
.. low lvls seratonin linked to depressive symptoms

108
Q

research into SAD

A

useful real life applicarion + treatments
-> an effective therapy inv use of strong lights in early morning of early evening
->aka phototherapy
-> 6000-10000 lux equiv to daylight
Eastman et al 1998 compared to phototherapy with palcebo condition a fake neg ion generator
he found that phototheraphy was sig more successful in improving symp of SAD comp to placebo condition
however 32% of placebo condition did impr

109
Q

give 2 ultradian rhythms

A

sub-stages of sleep cycle

basic rest activity cylcle

110
Q

waht are substages of sleep cycle

A

sub stages of SC take around 90mins to compl 1 cycle
-> when we go to sleep we may have around 5 cycles per night
->each cycle starts stage 1 and stage 2 which are ligth sleep
in ligth satges of sleep brain activity is characterised by alpha waves
..which slow to theta waves
in S2 occasional bursts of activity known as sleep spindles and K complexes can occur
S3 and S4 known as deep sleep
br activity characterised by large slow delta waves
a p extr diff wake up from s4 sleep if awoken they may exp sleep inertia
-> final stage of sleep is knwon as REM
->here brain is extre active + characterise by beta waves
-> muscles of body paralysed (except eye whhich mpve rapidly)
-> in this stage dreams occur
-> the first 90 mins cycle follows the order 123432rem then cycle begins again

111
Q

research into substages of sleep cycle proc

A

dement + kleitman 1957
supports idea of distinct stages in sleep
-> and the link betw REM and dreaming
PROC- monitoredthe sleep patterns of 9adult p in sleep lab
brainwave activity recorded on eeg + r controlled the effects of caffeine and alcohol

112
Q

findings

A

REM sleep is predominantly though not exclusively associated with dreaming
nearly all dream recall in nonrem awakenings occured within 8 mins of rem ep.. suggesting dreams may have been remembered from previous rem eps
A relationship betw dream content and type of eye movement
-> when p woken up from a series of verticle eye movements they reported dreams such as standing at bottom of cliff operating a climebrs hoist
or dreamer watching 2 pppl throw tomatos at each other -> horizontal

113
Q

neg of sub stages of sleep cycle research 2

A

small sample -> 9 p + only adults
.. lowers generalisabitly to whole pop
as not veyr repr .. findings cant be appleid to everyone
Done inlab .. low ecological v
-> findings may not be valid
cant be confident all 9 p had best qaulity of sleeep compared to at home in bedrooms

114
Q

2 pos of sub stages of sleep cycle research

A

lab exp .. high control over variables -> caffeine or alcohol
.. high internal validity as can be more confid whne drawing concl
limits extr v
+ lab can be repli use of standardised proc + instr
… if same concl we knwo its reliable
Recorded on eeg
.. highly scientific + empirical evid
as cannot fake a eeg
-> no p bias
eeg has high temporal resolution
.. know exactly what stage of sleep cycle ppl are in + veyr objective

115
Q

waht is another ultradian rhtym

A

basic rest activity cycle
investigated using eeg
in sme way that there is to a 90 min cylce during sleep, kletiman suggests that there is also a 90min cycle which continues during walking hrs
aka basic rest activity cycle
cycle characterised by period of alterness follwoed by period of rel fatigue
->importance of 90min rhythm is probs to ensure biological processes keep timing + work in unison

116
Q

evaluating basic rest activity cylce

A

anecdotal evidence supprots existance of basic rest activity cycles such as students find it diff to concentrate for periodslonger than 90 mins at a time
simialrly most workers will req coffee break in order to fivide up working morning + afternoon
Ericsson et al 1993 studied violinists + found best performers tended to practise for 3 sesh during day
-> each no loner than 90mins
+ break between each to “re-charge”