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Psychology 2A > Psychobiology > Flashcards

Psychobiology Flashcards

0
Q

What is the definition of psycholobiology?

A

1) the study of the effects of cognition, emotions and experience on animal psychology
2) the school of psychology that interprets personality, behaviour and mental illness in terms of responses to interrelated biological, social, cultural and environmental factors
3) attempt to understand the psychology of organisms in terms of their biological functions and structures

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1
Q

What are psychobiologists aims?

A
  • to understand the human mind and how it affects our behaviours
  • ability to predict - want to have this underlying knowledge to predict how people behave and help treat them
  • want to understand the relationships between things, in particular the brain and behaviour
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2
Q

Where has psychobiology come from?

1800’s

A

Freud (functional) vs Kraeplin (somatic)

F - initially a physiologist, then branched off to start psychoanalysis

K - understanding through the physiological - there must be a
physiological event or reason for exhibiting certain behaviours

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3
Q

Describe the case of Anna O

A
  • diagnosed with hysteria, caring for her dying father
  • symptoms: partial paralysis, blurred vision, headaches, hallucinations

F view - psychoanalytic view

  • ‘hysteria’
  • Pappenheim - dubbed it as the ‘talking cure’
  • caring for her dying father - kind of obvious why she may have some of these symptoms

K view - wanted a more somatic view of what was going on

  • must be something in her physiology causing the symptoms
  • connections between brain biology and mental illness
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4
Q

Who was Adolf Meyer?

A
  • ‘dean’ of American psychiatry
  • first to really do psychobiology
  • took on Kraeplin’s work and ran with it
  • saw that people were being locked away if they had a mental illness - stigma attached to mental illness, people did not want to deal with it
  • first to conduct autopsies in an attempt to correlate brain lesions with psychiatric diagnoses
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5
Q

What was general paresis?

A
  • a functional disorder
  • what you were diagnosed with if something appeared to be wrong
  • ‘mental strain of a life of excess’
  • reason - didn’t go to church enough
  • 1911-1919 - 20% of male admissions into NY mental hospitals had this disorder
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6
Q

What used to be the treatment for disorders such as general paresis?

A

Kellogg (1897) country retreats for people

  • general paresis - caused by living in the city and its conduct a
  • go to these country, agricultural settings to get better
  • eat fine food and wine etc to cure the disorder
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7
Q

ECT - Bickerton et Al (2009) and Rose et al (2005)

A

ECT still used as a treatment, for severe depression

Bickerton - investigated the total estimations of ECT as treatment
- did decrease over time as a result of differnt treatments being developed, such as drug treatments (Prozac)

Rose - ECT in BJP

  • investigate the information people received before getting treatment
  • people did not know what the treatment was - more info needed!
  • issue still occurring today - are people able to make their own decisions about their treatment? At what point is the line crossed?
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8
Q

Henry A Cotton - Focal Infection Theory

A
  • reason for a lot maladaptive behaviours - bacteria
  • took people’s teeth out
  • 1990’s - personal hygiene was not the best

Previously laughed at - why would bacteria cause mental illness?
Coming back into fashion, research has been done into the area

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9
Q

Pizzo et al (2010) - Focal Infection

A
  • periodontal infection may influence systematic health by:
    1. bacteria getting into the bloodstream by cuts or lesions in the mouth
    2. metastatic injury such as lesions from the effects of circulating toxins
    3. metastatic inflammation due to the immunological response to the pathogens and their toxins

Poor oral health is linked to:
Cardiovascular disease, respiratory diseases, diabetes, osteoporosis, preterm low birth weight, pancreatic cancer

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10
Q

Lobotomy - Moniz and Freeman

A
  • surgical operation involving incision into the prefrontal lobe of the brain
  • basically entered the brain through the eye sockets
  • 52% of the first 623 surgeries yielded good results but did not offer a clinical yardstick for what constituted an improvement
  • P’s often had to be re-taught certain skills - how to eat or use the bathroom
  • not often successful
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11
Q

Examples of Lobotomy cases

A

Mrs Hammat - agitated depression and sleeplessness

  • drilled 6 holes into the top of her skull
  • able to go to the theatre and enjoy the play
  • lived for another 5 years

Rosemary Kennedy - JFK’s sister

  • needed full time care for 64 years
  • stigma - don’t want to show her off due to the popular name?
  • just say its learning difficulties instead?
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12
Q

How did we previously find out about the link between brain and behaviour, before we had scanning techniques?

A

Through autopsies

  • Broca and Wernicke discovered their respective types of aphasia
  • Phineas Gage?
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13
Q

What do damaged brains tell us about normal brain function?

A
  • can tell us where in the brain certain functions are processed and how these functions get processed
  • can gets lots of information

Problems?

  • relations may be differnt?
  • spatial issue - brain damage does not always affect the same area?
  • individual differences in brains too
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14
Q

What is Prosopagnosia?

A
  • the inability to recognise individuals faces
  • usually follows after brain damage
  • intact intellectual and cognitive function
  • preserved low-level visual processing

Damage - to the visual cortex as seeing a face is a visual process

  • context becomes very important - since they cannot recognise faces, pathways need to be established so that when you see a face you can say that this is my daughter / wife / sister etc
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15
Q

De Haan et al (2011) - covert and over recognition in Prosopganosia

A

Presented with a photo of a familiar face - given 2 possible names, one of which was the correct name

PH - could select the appropriate name with above chance accuracy

When asked how he performed this task, he consistently reported that he was just guessing and didn’t experience any confidence in his decisions

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16
Q

Nishimura et al (2009) - Prosopagnosia and face space

A

Face space = where you can look at and recognise faces

  • congenital and acquired Prosopagnosia (as a result of trauma)

Congential:

  • did not significantly differ from controls on their ability to say it was a face and recognise a face
  • there is face space there but they just aren’t aware of it?
  • cannot consciously say they recognise the face
  • behavioural outcome is not there - oh I recognise blah-blah

Acquired - displayed the significant difference from the controls

Difference between the two - an inability to recognise faces

  • has the face area acquired damage?
  • C - already have the tools as they have never know the difference so the brain has re-wired itself
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17
Q

What is face space and what are of the brain is it associated with?

A

Fusiform gyrus
- part in the middle that says this is a face (eyes, nose etc)

  • as you move away from this, you get more and more distinctive
  • distinctive faces - further away from the middle
  • recognise distinctive faces faster
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18
Q

What is Capgras syndrome?

A
  • converse of Prosopagnosia
  • where you can recognise people but you think they are imposters
  • this is my mum - no it’s not, it’s an imposter

Ramachandran:

  • student from the University of California in a car accident
  • several weeks in a coma and then regained consciousness
  • mother came to visit - claimed she was another person pretending to be his mother!
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19
Q

Ellis and Lewis (2001) - Capgras Syndrome and skin conductance

A
  • skin conductance - measures emotional responses - sweat!
  • SC is higher for recognising familiar faces
  • because of the emotional response when you see a familiar face
  • significant differences found in normal controls & psychiatric patients
  • NO significant difference in the Capgras patients!
  • no objective physiological response to people they are familiar with compared to people they are not familiar with
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20
Q

What can Capgras Syndrome and Prosopagnosia give evidence for?

A

A DOUBLE DISSOCIATION!!!!!

P - inability to recognise faces until more information is given
- feel separate from people until they get more information as they cannot immediately recognise the face

CS - recognise the face but have no emotional response

  • evidence for two different pathways that feed into this recognition, processing and understanding of ‘well this is a person’ and whether you can recognise if you like them / if they are a familiar face
  • strong evidence for independent mechanisms in the brain?

P - recognising faces = impaired, emotional response = not impaired
CS - recognising faces = not impaired, emotional response = impaired

Dual route of recognition?
P - OFA lesion whilst a Capgras lesion can be found in the dorsal route

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21
Q

What is Blindsight?

A
  • refers to people who had damage to their visual cortex but when presented with stimuli, they are still able to accurately / above chance level to say that a stimulus was present
  • eg can accurately point to a small spot of light flashed in their blind field when forced to guess even though they deny seeing it (can’t consciously see it)
  • can detect differences in line orientation, colour, direction of motion, basic shapes and facial expressions in their blind field
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22
Q

Santhouse et al (2002) - damage to the corpus callosum

A
  • looked at P’s with damage to the CC
  • competed an auditory task
  • presentation to right ear crosses the subcortical LH then colossal transfer to the RH for timbre discrimination processing
  • damaged CC - difference in reaction times due to bilateral and unilateral lesion placement
  • plasticity had taken place - re-wiring of the brain
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23
Q

Gable et al (2013) - global and local targets with the two hemispheres

A
  • global target - is an H presented here (H made up of F’s)
  • local target - is there a T presented here (F made up of T’s)

Local - more RH activation
Global - more LH activation.

  • difference in processing jobs between the two hemispheres
  • ERP’s also demonstrated differences in electrical activity
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24
Q

What does damage to Broca’s area result in?

A
  • left frontal area of the brain
  • an expressive aphasia

Deficits:

  • Agrammatism - impaired use of grammatical construction
  • Anomia - word-finding difficulties
  • Articulation difficulties - eg lipstick = lickstip
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25
Q

What does damage to Wernicke’s area are result in?

A
  • left temporal area of the brain
  • a receptive aphasia

Deficits:

  • poor speech comprehension
  • fluent but meaningless speech
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26
Q

Describe Geschwind theory

A

Do we have isolated parts of the brain that are specialised for specific behaviours?

  • damage to one bit - is only one thing affected?
  • not just about these area - about the pathways connecting the areas!
  • recent studies using spohiscayed brain-imaging techniques have questioned the model
  • damage to Broca’s and Wernicke’s area often has no lasting effect on language
  • but damage outside the classic areas of the model (especially in the frontal lobes) can cause aphasia
  • the extent of language areas varies considerably between individuals
  • moving away from the classic, isolated views
  • double dissociation???
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27
Q

What is developmental dyslexia?

A
  • specific disability in learning to read despite normal intelligence
  • no obvious sensory deficits
  • adequate educational or socio-cultural resources
    (APA 2000)
  • main part - phonological processing deficit
  • present in 5-17% of the population.
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28
Q

Dual system in dyslexia?

A
  • evidence comes from the existence of two kinds of acquired dyslexia; surface dyslexia and phonological dyslexia
  • left side route - allows us to read familiar words - regular and irregular such as dough, bough and trough
  • right side route - allows us to sound out regular unfamiliar words or pronounceable non words - anodyne, chint, glab, trisk, asculobatory
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29
Q

What is disrupted in Phonological Dyslexia?

A
  • the letter-sound rule application
  • cannot read out pronounceable non-words
  • but can read familiar words - not affected!
  • damage to the right side route!
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30
Q

What is disrupted in Surface Dyslexia?

A
  • interruption to the meaning
  • pronunciation errors
  • can accurately read words and non words that comply with the letter-sound rules
  • mistakenly pronounce exception words
  • damage to the left side route!
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31
Q

What is sleep?

A
  • condition of the body and mind
  • typically recurs for several hours every night
  • the nervous system is inactive, the eyes are closed, the postural muscles are relaxed and consciousness is practically suspended
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32
Q

What is the purpose of sleep since it constitutes such a large amount of human lifetime?

A
  • ancient humans - the soul left the body during sleep?
    > why we may experience fear before we surrender to unconsciousness every night?

Many reasons, still not sure as to why:
Homeostatic regulation, thermoregualtion, tissue repair, immune control, memory processing

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33
Q

What happens to us when we sleep?

A
  • it’s a behaviour
  • an altered state of consciousness
  • associated with the urge to lie down for several hours in a quiet environment
  • few movements occur during sleep (eye movements???)
  • nature of consciousness changes
  • may experience dreaming and may recall very little of it (the mental activity)
  • we speak about a third of our lives in sleep - so there must be an important function to it!
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34
Q

What kind of measures can we use to measure sleep?

A

Electrophysiological instruments can be used in a sleep lab to assess the physiological changes that occur during an episode of sleep

Electromyogram - EMG - muscle tone
Electroencephalogram - EEG - summated brain wave activity
Electro-oculogram - EOG - eye movements
Blood flow to the genitals

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35
Q

Describe the sleep stages

A

Found that that we move through these stages of sleep

Wakefulness, non-REM 1, 2,3 and REM sleep

  • can see how much time is spent in all these different stages and how this can change due to the influence of different things (eg alcohol)
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36
Q

What is the difference between alpha and beta activity in sleep?

A

Alpha activity = wakefulness (13-30 Hz)
- desynchrony - low amplitude, high frequency waveforms

Beta activity = eyes closed (8-12 Hz)
- synchrony - high amplitude, low frequency waveforms

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37
Q

How do you conduct a sleep study?

A
  • prepare the sleeper for the electrophysiological measurements
  • set up electrode cap to monitor EEG - measured electrical activity across the scalp
  • attach electrodes to the chin - EMG - muscle activity
  • attach electrodes around the eyes - EOG - monitor eye movements
  • other electrodes and transducting devices can be used to monitor heart rate and respiration
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38
Q

What are the two basic patterns of activity from an EEG?

A

Beta - 13/30 Hz

  • rapid fire kind of, irregular, mostly low amplitude
  • lots of different processes of the brain are awake and working
  • alert to the environment

Alpha - 8/12 Hz

  • regular, medium frequency waves
  • brain produces this activity when a person is resting quietly
  • not particularly aroused, excited or engaged in strenuous mental activity
  • can occur when a person’s eyes are open but are much more prevelent when the eyes are closed
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39
Q

Describe Stage 1 of sleep

A
  • transition between sleep and wakefulness
  • presence of theta activity
  • sharp vertex waves - high amplitude but slow frequency
  • brief periods of alpha activity
  • slow rolling eye movements, little muscle activity
  • hypnagogic hallucinations
  • myoclonic jerks
  • lasts only a few minutes
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40
Q

Describe Stage 2 of sleep

A
  • EEG is generally irregular
  • periods of theta activity, sleep spindles and K complexes
  • no eye movements

Sleep spindles - shorts bursts of waves (12/14 Hz)

  • occur between 2 and 5 times a minuted during stages 1-4
  • play a role in the consolidation of memories
  • increased scores of sleep spindles are correlated with increased scores on tests of intelligence (Fogel and Smith, 2011)

K complex

  • sudden, sharp waveforms
  • usually only found in stage 2
  • occur approx 1 per minute
  • often triggered by noises
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41
Q

Describe Stages 3 and 4 of sleep

A
  • marked by high amplitude delta activity
  • slow-wave sleep
  • associated with maladaptive behaviours, particularly in Stage 4; bed wetting, sleep walking and night terrors
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42
Q

Describe REM Sleep

A
  • EEG displays theta activity
  • increased brain activity
  • looks like wakefulness
  • EOG shows the characteristic eye movement
  • other physiological changes - increased respiration rate
  • no muscle activity - paralysis of voluntary muscles
  • stage in which most vivid dreams occur
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43
Q

Riemann et al (2012) - Sleep Structure differences

A
  • different in polysomnographic profiles of a good sleeper & patient with primary insomnia

Insomniac

  • more frequent periods of wakefulness and more periods of arousal
  • lots of time in stage 2, not as much in the others
  • same sleep opportunity and onset
  • completely different sleep structures
  • too aroused?
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44
Q

Link between sleep and poor mental health

A

National Statistics (2011) - sleep disturbance is foremost of all primary mental health complaints

Insomnia:

  • most widely reported psychological symptom in Britain
  • main reason for Benzodiazepine prescribing in primary care
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45
Q

Research into Insomnia and poor mental health

A

Doctor visits in the US

  • increase of insomnia visits from 4.9 million to 5.5 million - 13% increase!
  • prescriptions increased from 1999 to 2010 by a 293% increase!
  • now recognised as disorder in itself - not something that will just go away
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46
Q

Walker et al (2002) - Insomnia

A
  • sleep dependent motor memory enhancement
  • finger tap task where they had to learn a sequence
  • different conditions to see where their training was and performance was in relation to sleep

Group b - training at 10 am then pm and then performed after
- significant improvement after the opportunity to sleep

  • where the sleep was significantly improved performance on the task
  • purpose of sleep - motor memory enhancement
  • stage 2 - important in processing and consolidation of sleep
  • significant correlations between stage 2 and performance on task
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47
Q

Walker and Stickgold (2006) - Insomnia

A
  • presented P with positive, negative and neutral stimuli
  • group had been deprived of sleep
  • is there a difference between the sleep deprived and non-sleep deprived group in recall?
  • no significant difference for negative and neutral stimul
  • significant difference on the positive stimuli
  • important - lack of positive stimuli processed - more likely to develop depression?
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48
Q

Baglioni et al (2011) - Insomnia and Depression

A
  • non-depressed + insomnia = 2x risk of depression
  • incidence of depression in the insomnia group at baseline (13.1%> significantly higher than no sleep difficulties group
  • population incidence of depression is 9.9%
  • similar for children, adolescents, working age individuals and older adults
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49
Q

Yoo et al (2007) - sleep and amygdala

A
  • 35 hours total sleep deprivation
  • 60% increased activation in the amygdala in the SD group
  • 3x increased volume in SD group
  • enhanced reaction to negative stimuli
  • connection with the medial section of the prefrontal cortex (higher planning) was diminished in the sleep deprivation group
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50
Q

Woods et al (2011) - Insomniacs and what happened during the day

A
  • relationship between sleep quality and impairment in daytime domains
  • Posner paradigm - sleep and day times
  • predicted that the Insomniacs would have longer reaction times on the night times, more focused on sleep
  • found the opposite - longer reactions on the day times
  • sleep quality and daytime impairment produce different response patterns
  • sleep quality and daytime impairment with the view of insomnia as a 24 hours disorder?
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51
Q

Dixon et al (2006) - Insomnia and health quality

A
  • measured on health and well-being
  • how would the poor sleepers fair on this?
  • not very well indeed
  • co-morbidities with chronic illness and pain interference
  • not a long term solution for just giving them drugs - need to do something more?
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52
Q

Biello (2009) age and sleep

A
  • wanted to look at the effects of age and the neuro-chemicals involved in sleep
  • typical view of older people - go to bed earlier, wake up earlier, afternoon naps etc
  • no difference in timing but there was less of them - Glutamate, NMDA, GRP and HA
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53
Q

How is sleep regulated?

A
  • loss of SWS or REM sleep is made up somewhat on following nights
  • not controlled by chemicals
  • Siamese twins - same circulatory system but sleep at different times
  • bottle nose Dolphins - two hemispheres sleep independently
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54
Q

Neural control of arousal

A

Stimulate the reticular activating system - wake them up

Stimulate the thalamus - sleep

(experiments done in cats)

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55
Q

What substances are vigilance promoting?

A

Amphetamine - enhances monoaminergic neurotransmission

Caffeine - blocks adenosine receptors

Nicotine - stimulates cholinergic receptors

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56
Q

What substances are sleep promoting?

A

Alcohol, barbiturates
Benzodiazepines stimulate GABAa receptors

Antihistamines block H1 receptors that are involved in cortical and subcortical arousal

57
Q

Neural Control of SWS - Hypothalamus

A

Constantin von Economo

  • studied brains of those who had died from the virus encephalitis lethargica
  • most victims - difficulties staying awake
  • damage to the posterior region at the junction between the brain stem and forebrain
  • victims with difficulty sleeping - damage to the anterior region ventral streak preoptic area
58
Q

Neural control of SWS - Saper et al (2001)

A
  • confirmed it in mice
  • lesions of the pre-optic area produce total insomnia leading to death - - electrical stimulation of the pre-optic area - induced signs of drowsiness

VLPA sends inhibitory GABA projections to regions that promotes arousal and it receives inhibitory inputs from the same regions
- certain point of arousal - need something to de-arouse you
- certain point of de-arousal - need something to arouse you
FLIP-FLOP mechanism!

  • activation of orexin systems tips the flip-flop towards wakefulness!
59
Q

What is the Flip-Flop switch?

A
  • these circuits avoid transitional States because when either side begins to overcome the other, the switch flips into an alternative state
  • explains why sleep transitions are abrupt
  • dangerous for animals to have impaired alertness when they are awake and it’s useless to spend sleep periods half awake
  • small perturbation can give one side advantage - turn off alternative state abruptly
    Eg falling asleep while driving
60
Q

What are the arousal centres in the brain?

A

Tuberomammilary Nucleus (TMN) - histamine

Orexin - narcolepsy and cataplexy
Substance secreted from the lateral hypothalamus

61
Q

What is narcolepsy?

A

When sleep appears at odd times

62
Q

What is a sleep attack?

A

An uncontrollable urge to sleep during the day

63
Q

What is cataplexy?

A

REM paralysis occurs whilst the person is still conscious

64
Q

What is sleep paralysis?

A

REM paralysis that occurs just before or after sleep

  • often go directly into REM sleep, skipping the first period of slow-wave sleep
  • fragmented sleep, disrupted by periods of wakefulness
  • treatment - stimulants
  • management of the the flip-flop mechanism is implemented in this disorder
65
Q

What are biological rhythms?

A
  • many of of behaviours display rhythmic variation
  • SWS/REM cycles last about 90 minutes
  • circadian rhythms - one cycle lasts about 24 hours
  • monthly rhythms - menstrual cycle
  • seasonal rhythms - aggression, sexual activity in deer and hibernation
66
Q

What are zeitgebers?

A

External factors that resets the endogenous rhythm (internal clock)

67
Q

Biological rhythms - experiments with humans

A
  • humans locked in caves or bunkers with no clocks or day/night cues have shown that human circadian rhythms free dun with a period of just over 24 hours
  • these rhythms do persist in the absence of external cues under the influence of an internal biological clock
  • clock is however normally regulated or revert by regular external cues (zeitgebers) such as light and dark
68
Q

1972 - SCN and biological clocks

A

Researchers found 2 clusters of neurones in the hypothalamus called the suprachiasmatic uncles (SCN)

Contained a biological clock that governs some circadian rhythms

Lesions of the SCN in rats - disrupt normal rhythms of activity, body temperature and sleeping/waking

69
Q

SCN

A
  • receives input from the amacrine / ganglion cells in the retina and parts of the thalamus that mediate the ability of other environmental stimuli to reset circadian rhythms
  • projects to adjacent endocrine regions to the VLPO and to orexin neurons
  • well positioned to control endocrine and alertness cycles
70
Q

SCN clock cells

A
  • SCN glucose metabolism - higher during the day than night

- each SCN seems to have its own clock

71
Q

What can effect our circadian rhythms / SCN?

A

JET LAG

  • disturbance of sleep rhythms due to different time zones
  • sleep disturbance, fatigue, physical and cognitive deficits
  • CR are accepted during eastern flight and decelerated in western flights

SHIFT WORK
- sudden changes to a new pattern before adaptation can cause desynchronisation of rhythms

SUBSTANCES
- that act on SCN functioning eg ecstasy

DRUG THERAPY

  • certain illnesses who symptoms show a circadian rhythm respond when drugs are coordinated with that rhythm
  • eg asthma, epilepsy, cancer and heart disease - all show better effects and fewer side-effects when given at particular times of the day
72
Q

What is Transcranial Magnetic Stimulation (TMS)?

A
  • method of brain stimulation
  • a large coil that can be placed at the scalp
  • interferes with brain functions at the areas which you place it on the scalp
  • non-invasive, pain free technique
  • wherever you place it on the head - disrupts the functions going on there
73
Q

How does TMS work?

A
  • creates a rapidly changing magnetic field
  • place it against your head, near the moratorium cortex - arm twitches
  • placed on the visual cortex - see flashes of flight
  • creates a temporary lesion
  • depending on where you put the coil, it will interfere with different functions
  • not only causes behavioural or perceptual changes, it also causes neurophysiological and metabolic changes
74
Q

What is single pulse TMS?

A
  • where TMS is applied briefly at a certain time
  • eg to interfere with a certain response
  • positive or disruptive effect
  • eg muscle twitch or longer reaction time
  • usually time locked within a task - apply a pulse to interfere with a response after seeing a certain stimulus?
75
Q

Prime, Vesia & Douglas (2009) - Single pulse TMS

A

Trans-saccadic memory and TMS over frontal eye field

  • T-S memory - memory for eye movements / saccades across a scene
  • frontal eye field - area involved in visual mapping

TMS over the frontal eye field and disrupt it at certain points in time
Look at fixation point and then look at certain target stimuli
Had to remap the target
Baseline - no differences
TMS application:
- Right FEF - RH is crucial in spatial memory, larger % of errors
- Left FEF - involved in attentional orientation

76
Q

What is repetitive TMS?

A
  • applied during a task
  • basically creating an artificial lesion
  • done over a longer time
  • over a certain task constantly, test then apply then test
  • can be done to compare performance before and after
77
Q

Basso et al (2006) - Repetitive TMS - Prefrontal cortex in visuo-spatial planning

A
  • planning - automatic
  • usually involves imaginary visualisation with all the steps, heuristics
  • sometimes have to come up with alternative stare goes
  • planning - an executive function processed in the prefrontal cortex
  • lesions here - difficulties with planning, stick to the same plans

Gave P’s different problems (travelling salesman problem)

  • start point and end, need to go through all the stations in between
  • Interfered planning with TMS - stimulated both L and R PFC’s
  • stuck with original strategies
  • stuck to the same, identical heuristics
  • applied to other areas - was just TMS in the PFC that affected planning
78
Q

What are the advantages and disadvantages of TMS?

A

Advantages:

  • precise timing
  • relatively good localisation

Disadvantages:

  • cannot stimulate deep structures directly
  • magnetic field decays quickly
  • P’s tend to move their heads about - can’t hold them down and as soon as they move, the coil has no effect anymore
  • need previous evidence to say that an effect may be produced
  • background detail is needed
  • have to control location
  • sharp noise and feeling associated with it too
79
Q

Measuring electrical activity in the brain - intracelluar

A
  • measuring within single cells - the primary current, action potentials

Hubel and Wiesel - single cells in cat’s brains

  • certain neurones responded to certain directions (vertical, horizontal or diagonal lines)
  • came up with a layout of what cells respond to
  • mapped out the visual cortex

Monkeys and amygdala

  • face detector neurones in the temporal cortex
  • identify selected neurones and expression-selective neurones
  • some were selective whilst others were overlapping for objects and faces
80
Q

Electroencephalogram (EEG)

A
  • electrodes on the scalp surface, all over the head
  • measure electrical activity generated by the brain
  • not painful
  • all electrodes have certain labels for certain areas in the brain
  • can calculate differences between electrodes - need a reference electrode!
81
Q

Event Related Potentials (ERPs)

A
  • want to see what happens during a task
  • EEG - average score of the wavelengths?
  • need to where a stimulus was presented and then average the scores
  • N = negative chance of voltage
  • P = positive chance of voltage
  • average get a characteristic curve
82
Q

Magentoencephalogram (MEG)

A
  • measure the magnetic field on the surface of the scalp with detectors
  • electric activity creates a magnetic field
  • want to measure this tiny magnetic field in the brain
  • need a shielded room as lots of other magnetic fields are around that could interfere with your measure,net
  • sensitive detectors - SQUIDS
  • Superconducting Quantum Interference Device
  • placed over different areas of the head
  • similar to EEG, labelled electrodes
83
Q

MEG - word and pseudo-words

A
  • when subjects paid attention to the stimuli, the brain response to pseudo-words was larger than it was for words
  • maximum response occurred 410ms post stimulus-onset and wa s larger on the left side
84
Q

ERP’s - Rossion and Jacques (2011) and Rossion and Caharel (2011)

A
  • seeing faces - very large, characteristic negative peak when a face is presented to us

R & C (2011)

  • is it just for faces or for other objects too?
  • faces and cars but also scrambled faces and cars
  • large negative peak for intact faces and cars but not for the meaningless stimuli
  • very large peak for faces, not so much cars
  • scrambled images - no peaks
85
Q

What do structural brain imaging techniques tell you about the brain?

A

The structure of the brain, what it looks like

86
Q

What do functional brain imaging techniques tell you about the brain?

A

Tells you about the activity of the brain

87
Q

What brain imaging techniques are structural techniques?

A

CT and MRI

88
Q

Computer Tomography (CT)

A
  • very common procedure
  • also known as CAT
  • like an x-Ray of the brain
  • scanner rotates around the brain and takes images whilst you lie in it
  • can see different slices of the brain
  • different tissues absorb different amounts of radiation
  • can do angiograms too to see vessels, if they are blocked or not
89
Q

Magnetic Resonance Imaging (MRI)

A
  • better resolution that CT
  • can see slices of the brain at different orientations
  • see all the details and locations of the brain
  • the higher the magnetic field, the better quality the image / scan / details
  • on all the time - banging noise = coils that are vibrating
  • big magnet around at the side
  • have H atoms in our brains that are spinning around randomly in different directions
  • they are magnetic so when in the scanner they align themselves up
  • radio frequency coils - produce a radio frequency wave that disrupts the alignment of these atoms
  • measure when these waves are being transmitted back
  • different tissues in the body take different times to realign
90
Q

Different Types of MRI

A
  • small changes in radio waves and magnetic fields can change the image

Proton Density, T1-weighted, T2-weighted and MR angiography

T1 - best scan resolution, often used for localisation of structures
T2 - often used for lesion detection

91
Q

CT vs MRI

A

Big differences between the two!

CT = resolution is not the best, can see structures okay 
MRI = resolution is much clearer, can see much more detail

Can’t scan everyone with an MRI - need 10/20 mins to lie still
CT scans are much quicker
Some stroke patients are highly restless - can’t put them in the MRI
Tattoos or pacemakers - can’t use the MRI

92
Q

Precautions with MRIs

A
  • very strong magnet so have to remove all metal items before entering the scanner
  • metal on you - can get very hot, could get third degree burns if you are not careful
93
Q

What can structural brain scans show you?

A

Localisation of brain structure (eg for TMS and PET)

Localisation of lesions or tumours

Can investigate correlation between brain structures and behavioural parameters

94
Q

Describe lesion mapping

A
  • get a scan from the patient
  • every brain is different so have to map it onto a template so you can compare between patients
  • draw it on all the slices to see where the lesion is in the brain
  • lesion studies - lesions are often very large
  • can’t really see which part is responsible for the neglect of behaviour
  • usually test lots of patients to investigate
  • do an overlay to see if the patients have anything in common - can see if they have an areas of neglect in common
95
Q

Structural Brain Scans - Spatial Awareness in the Temporal Lobe

Kamath, Ferber & Himmelbach (2001)

A
  • often difficult to study patients with the same lesions - finding the and studying them so have to do it over a long period of time
  • done over 20-30 years in this study
  • right superior temporal cortex processes spatial awareness in humans
  • compared lesions of neglect patients (with no visual deficits) to stroke patients without neglect
  • area in common - temporal lobe
  • this area is involved in neglect and therefore spatial awareness
  • superior temporal gyrus - lesion here, P’s show spatial neglect
96
Q

Structural brain scans - Maguire et al (2000)

A
  • navigation related structural change in the hippocampus of taxi drivers
  • can see if structures in healthy people differ
  • conducted MRI scans to see if there were any differences
  • hippocampi - responsible for spatial memory
  • taxi drivers who are licensed need a very good spatial memory
  • eg London cab drivers - the ‘Knowledge’ test
  • compared sizes of the hippocampi in licensed London cab drivers to controls to see if there were any differences
  • volume of grey matter in the right posterior hippocampus was larger in the taxi drivers compared to the controls
  • volume also correlated with the amount of time spent as a taxi driver
  • demonstrates plasticity in the brain
97
Q

What functional brain imaging techniques are there?

A

fMRI and PET scans

98
Q

functional Magnetic Resonance Imaging (fMRI)

A
  • like an MRI, but functional
  • same underlying technique but measures the activity of the brain
  • brain activity requires blood - more activity = more blood flow to brain
  • measures the Blood Oxygenation Level Dependent (BOLD) signal
  • measures the oxygenation level of the blood which will then transfer into how active a certain area of the brain is
  • in blood - haemoglobin that carries oxygen
  • have to measure blood oxygen levels indirectly
  • increased blood flow = when the haemoglobin is oxygenated
  • so we measure the haemoglobin which is magnetic (what we measure with the scanner)
  • increase of neural activity results in an increase of cerebral blood volume
  • known as the hemodynamic response (HDR)
99
Q

fMRI research - Fusiform Face Area (FFA)

A
  • area for processing faces
  • is there a particular difference in this area for certain tasks?
  • comparing in tact and scrambled faces or objects
  • more active for intact vs shambled faces and faces vs objects
  • greater FFA activation for emotional faces vs neutral faces
  • decreased activation here for autistic participants!
100
Q

Positron Emission Tomography (PET)

A
  • blood flows to the brain area that is most active
  • inject P with a radioactive tracer that goes into their blood
  • tracer has radioactive positrons that follow blood flow to the active sites
  • the positrons collide with electrons and in doing so release gamma rays which go in different directions
  • scanner detects these gamma rays
  • draw lines to see where the Rays come from
  • blood to most active areas - most of the gamma rays will be traced back to here
  • have different options to measure - can have different radio tracers
  • depending on the different tracers, you can measure different functions eg can measure dopamine functions
101
Q

PET research - Shigemune et al (2010)

Effects of emotion and reward motivation on neural correlates of episodic memory

A
  • emotional items are better recalled that neutral items (amygdala)
  • rewards motivate learning

Previous:
- reward enhances memory only under positive emotional conditions and not under neutral or negative conditions

Behavioural results:
- negative emotion and high reward enhanced memory, no interaction

Brain imaging results

1) left amygdala - main effect of emotion (neg vs neutral)
2) orbitofrontal cortex - main effect of reward (high vs low)
3) right hippocampus - region that was commonly activated

102
Q

What is Addiction?

A
  • the compulsive seeking of substance despite negative consequences
  • is a primary, chronic, neurobiological disease
  • an important social, health and scientific problem

In the UK:

  • 35.9% have used drugs in their lifetime (ever)
  • 8.7% have used drugs in the last year (recent use)
  • 5.0% have used drugs in the last month (current use)
103
Q

Give examples of abused substances

A

Alcohol, Nicotine, Cannabis, Opiates, Ketamine, Cocaine, Amphetamine, Heroine and Medication

104
Q

Give examples of behavioural addictions

A

Sex/Pornography, Gambling, Food, Work, Social Networking

105
Q

What is addiction? How does it work?

A
  • drugs enter the blood stream
  • are then carried to the central nervous system and the brain

Concentration of drug in brain and time after drug administration alters:

  • inhalation - nicotine - quick rush, quickly into the CNS and brain
  • injection - heroin - again a fairly quick rush
  • snorting / snuffing - cocaine - takes a while, then picks up
  • ingestion - mushrooms - takes the longest, lasts for a good while
106
Q

Cocaine and Methampetamine - Disorder / Effects

A

Schizophrenia
Paranoia
Compulsive Behaviour
Anhedonia (find less pleasure in doing things)

107
Q

Stimulant - Disorder / Effects

A

Anxiety
Panic attacks
Mania
Sleep disorders

108
Q

LSD, Ecstasy, Psychedelics - Disorder / Effects

A

Delusions and Hallucinations

109
Q

Alcohol, Sedatives, Sleep Aids, Narcotics - Disorder / Effects

A

Depression and mood disturbances

110
Q

Ketamine - Disorder / Effects

A

Antisocial behaviour

111
Q

Why are some people more likely to become addicted?

A

Risks for addiction are associated by a combination of factors:

1) Biological - genes people are born with in combination with environmental influences
2) Environmental - social environment, socio-economic status, quality of life
3) Developmental - can develop at any age but is more likely to start during adolescence

112
Q

Difficulties in quitting addiction - Physical Dependence Theories

A
  • many detoxified adults return to drugs if treatment is based on physical dependence because:
  1. Many drugs don’t have severe withdrawal symptoms - eg cocaine
    - think oh I can do that again, it didn’t effect me too much
  2. Drug taking habits
    - weekend binges, weekday toxifications
113
Q

What are causes for relapses?

A
  1. Stress - more likely to take drugs
  2. Priming - just come out of rehab, oh just one glass of wine is enough and then you start all over again
  3. Environmental Causes - being around people who take them
114
Q

Difficulties in quitting addiction - Insensitive-sensitisation theory

A
  • the anticipated pleasure of drug taking (the positive incentive value) is the basis of addiction
  • drug tolerance makes addicts crave more and more
115
Q

Addiction - Positive reinforcement

A
  • pleasurable effect of taking the drugs
116
Q

Addiction - Tolerance

A

After a while, you need to take more and more to feel the same effect

117
Q

Addiction - Physical dependence

A

The body needs the drugs to function normally

118
Q

Addiction - Withdrawal Effects

A

Negative side effects that you get if you don’t take the drugs

119
Q

Addiction - Craving

A

you have this to get to normal functioning

120
Q

Tolerance

A
  • the more drugs you take, the higher the effect
  • after a while, you need to take more
  • taking the drug for the first time - effect is very high
  • after a while, the initial dose does not have the same effect
  • receptors in your body are adjusting to this overstimulation; they have become used to the effects, they have become desensitised
121
Q

Metabolic tolerance

A

Drug produces less of an effect that when it used to before

122
Q

Functional tolerance

A

Caused by the reduced reactivity of the sites of action

Not as sensitive as they were before

123
Q

Cross tolerance

A

One drug can produce tolerance to other drugs

Eg nicotine tolerance can develop a tolerance for caffeine which has a much higher effect

124
Q

Drug sensitisation

A

Drug tolerance to some effects of a certain drug but still not sensitive to the other effects

Eg alcohol - don’t feel the nausea but still have longer reaction times

125
Q

Contingent Drug Tolerance research

A
  • tested the effect of drug tolerance to alcohol
  • rats were stimulated to have a seizure and got measured to see how long it was
  • treatment - alcohol before or after seizure
  • afterwards = no effect on the duration of the seizure
  • beforehand = effect on the seizure, almost non-existing
  • developed a tolerance - had less and less effect on seizures
126
Q

Conditioned Drug tolerance research

A
  • again alcohol used - has the effect of lowering body temperature
  • room 1 in both groups - alcohol given, body temperatures lowered
  • done 20x in room 1 and then did it again
  • no effect in lowering temperature once tolerance has been built
  • take to a different room - no tolerance due to new situation!
  • tolerance is linked to the certain place where the alcohol was given
127
Q

Addiction - Reward Circuit

Intracranial Self-Stimulation (ICSS)

A
  • electrode in certain areas in the brain
  • lever that can stimulate the certain areas in the brain
  • over the days - press the lever more and more, craving for the effect
  • wants and probably needs more and more to get the same effects
  • humans, rats and other species will administer weak electrical stimulation to specific areas of the brain
  • specific brain sites that mediate self-stimulation are those thought normally to mediate the pleasurable effects of natural rewards (food, water, sex etc)
  • not just any location - pleasure centres
  • drugs have pleasure inducing effects - cerebral “pleasure circuits” play a role in addiction
  • spicing
128
Q

Addiction - Reinforcement

A
  1. Detect the presence of the reinforcing stimulus
  2. Strengthen the connections between neurones that detect the stimulus and the neurones producing the instrumental response
129
Q

Addiction - Reinforcement: Strengthening neural connections

A

Need the discriminative stimulus and response which is then followed by a reinforcing stimuli

Eg:
Sight of level - presses the lever - Dopamine being released into the region where synaptic change takes place

130
Q

What brain circuits are involved in addiction?

A

VTA - reward

Amygdala and Hippocampus - memory, learning and motivation

Prefrontal Cortex, OFC and AFC - inhibition and motivation

131
Q

Addiction - Dopamine

A
  • a neuro-transmitter
  • functions - attention, learning and reinforcing the effects of drugs
  • nigrostriatal pathway - projects to dorsal striatum
  • mesolimbic pathway - projectes to various cortical and limbical sites
132
Q

Reward circuits involved in Addiction - Dopamine and NAcc in drug addiction

A
  • injecting drugs (cocaine, morphine etc) into the Nucleus Accubens (NAcc)
  • produce conditioned place preference
  • no craving / reward felt when these areas are damaged
  • associated with higher levels of dopamine in the NAcc

Dopamine agonists - increase self-stimulation
Dopamine antagonists - decrease self-stimulation

133
Q

Link between drugs and dopamine

A
  • addictive drugs tend to increase the dopamine release in the mesolimbic pathway and flood the circuit with dopamine
  • if the reward circuit is continuously overstimualted, the brain adapts to the overwhelming surges in dopamine
  • drugs impact is lessened as receptors sensitivity is reduced as the numbers of them
134
Q

Drugs - Effects of cocaine

A
  • removes dopamine from the synaptic cleft
  • subsequently degraded by monoamine oxidase
  • binds to dopamine re-uptake transporters
  • inhibits the removal and creates an overflow
  • over-stimulation - lots of dopamine so feel happy
135
Q

Drugs - Effects of Heroin

A
  • works on GABA
  • GABA would normally inhibit dopamine
  • works on the receptors so more and more dopamine can be released
  • so dopamine does not get blocked by the GABA receptors
136
Q

Drugs - Effects of Alcohol

A
  • inhibits the GABA terminals in the VTA
  • leads to a disinhibition of dopamine neurones in the VTA
  • results in an increased release of dopamine in the NAcc
137
Q

Drugs - Effects of Nicotine

A
  • works on acetylcholin
  • chronic smoker - lots of nicotine in synaptic cleft, hasn’t been removed
  • constant over-stimulation so reduced activity
  • activity of neurones goes down
138
Q

Drugs and Individual Differences

A
  • studies indicated that younger people report less effects of stimulants compared to adults - feeling tired or different instead of euphoria
  • brain still developing?
  • less hallucinations with ketamine compared to adults
  • more joints in daily cannabis user
  • brain doesn’t show as strong effects - why they take more drugs and become more addicted?
139
Q

Drugs and Individual Differences - Animal Studies

Levine et al (2007) and Markwiese et al (1998)

A
  • younger rats vs older rats
  • larger self administration of nicotine for younger rats
  • more disruption of LTP in young rats than older rats

Alcohol effects

  • younger rats were more sensitive to the memory impairing effects of alcohol
  • more disruption to LTP in younger rats compared to the adult rats
140
Q

Summary of addiction

A
  • it is a primary, chronic and neurobiological disease
  • characterised by the alteration of the reward system
  • changes in the dopamine pathway
  • some people are more likely to become addicted that others

Psychology 2A (4 decks)

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