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Psychology A level > Biopsychology > Flashcards

Biopsychology Flashcards

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1
Q

How can the nervous system be divided?

A

Central nervous system (CNS) and peripheral nervous system (PNS)

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2
Q

What is the endocrine system?

A

hormone system; is much slower to communicate but much longer lasting than the nervous system

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3
Q

What is the nervous system?

A

The body’s fast and short lived system of communication

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4
Q

What does the peripheral nervous system consist of?

A

Somatic nervous system (controls voluntary movements)

Automatic/Autonomic nervous system (controls involuntary responses/actions)

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5
Q

How can the Automatic nervous system be divided?

A

Sympathetic division: fight or flight

Parasympathetic division: rest or digest

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6
Q

What are the key sections of the brain (general)?

A

Frontal lobe (problem solving), Parietal lobe (sensory processing), temporal lobe (language and auditory processing), occipital lobe (visual processing), cerebellum (fine motor movements)

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7
Q

What are the key sections of the inner brain?

A

Hypothalamus (regulating endocrine system), Limbic system (animal instincts), thalamus (processing sensory info), hippocampus (memory), pituatary gland (master gland in endocrine system), cerebellum

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8
Q

What is a neuron?

A

neurons are cells that process and transmit messages through electrical and chemical signals

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9
Q

What are the parts of the neuron?

A

Cell body, dendrites, axon, myelin sheath, nodes of Ranvier, terminal buttons

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10
Q

What is the cell body?

A

Includes nucleus, containing the genetic material of the cell

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11
Q

What are the dendrites and terminal buttons?

A

Dendrites- protrude from cell body. carry nerve impulses from neighbouring neurons towards the cell body
Terminal buttons: communicate with the dendrites of the next neuron

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12
Q

What is the axon and myelin sheath?

A

Axon- carries impulses away from cell body

Myelin sheath- protects axon and speeds up electrical transmission

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13
Q

What are the nodes of Ranvier?

A

They are segmented gaps in the myelin sheath that speed up the impulse by forcing it to ‘jump’ across gaps down the axon

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14
Q

What are sensory neurons?

A

Internal and external receptor cells around the body take in information from the 5 senses. Information is then carried from the PNS to the CNS (brain)
Unipolar- one protrusion from cell body, Long dendrites

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15
Q

What are relay neurons?

A

Carry messages from one part of the CNS to another
Connect sensory and motor neurons or between relay neurons
Multipolar

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16
Q

What are motor neurons?

A

Carry messages from CNS
Connect the CNS to ‘effectors’ (such as muscles, organs and glands)
Short dendrites, long axons

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17
Q

What is a synapse?

A

Neurons do not touch, between each is a tiny gap called a synapse or synaptic gap

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18
Q

How are signals within neurons transmitted?

A

electrically

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19
Q

How do signals travel across synapses?

A

chemically

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20
Q

What is the first stage of synaptic transmission?

A

Electrical impulse reaches the pre-synaptic nerve terminal and triggers synaptic vesicles to move to the pre-synaptic cell membrane

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21
Q

What is the second stage of synaptic transition?

A

Synaptic vesicles fuse with the pre-synaptic cell membrane and release neuro-transmitters into the synaptic gap

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22
Q

What is the third stage of synaptic transition?

A

These neuro-transmitters enter the synaptic fluid and diffuses across the synaptic gap. If the neuro-transmitter fits the receptor sites of the post-synaptic neuron, it is taken up

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23
Q

What is the final stage of synaptic transmission?

A

Once enough receptors have neuro-transmitters bound to them, the chemical message is converted back into an electrical impulse

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24
Q

What is the lock and key mechanism?

A

when the right neurotransmitter (key) meets the right receptor (lock) a specific ion channel in the membrane is opened up
ions flow through the membrane into the neuron along their pathway. The flooding of ions cause a potential in the dendrites

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25
Q

What are the two actions of neuro-transmitters?

A

Excitatory and inhibitory

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26
Q

What do excitatory neuro-transmitters do?

A

(E.g. Adrenaline) are ‘on’ switches, these make it more likely that the next neuron will fire

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27
Q

What do inhibitory neurotransmitters do?

A

(e.g. GABA) are ‘off’ switches, these make it less likely that the next neuron will fire

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28
Q

How does the next neuron ‘assess’ whether or not to fire?

A

Post-synaptic neuron ‘sums up’ the total of excitatory and inhibitory signals (summations) and whichever signal the neuron receive most of will determine whether the neuron fires or not

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29
Q

What is temporal summation?

A

A large number of EPSPs at the same synapse by a series of high frequency action potentials on the pre-synaptic neuron. The rate at which a particular cell fires is determined by what goes on in the synapses (so if IPSPs are higher frequency the signal will fire at a slower rate)

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30
Q

What is spacial summation?

A

A large no. of EPSPs are generated at many different synapses on the same post-synaptic neuron, so it will fire at a faster rate (lower if large no. of IPSPs)

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31
Q

What are the key endocrine glands?

A

Hypothalamus, pituitary, thyroid, parathyroid, adrenal glands, pancreas, testes (male)/ovaries (female)

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32
Q

What does the adrenal gland do?

A

location: above kidneys (back), secretes: adrenaline, function: to initiate fight or flight

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33
Q

What does the testes gland do?

A

secretes: testosterone, function: linked to agression

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34
Q

What do the ovaries do?

A

location: pelvis, secretes: progesterone and oestrogen, function: regulates female menstrual cycle

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35
Q

What does the Hypothalamus do?

A

Location: in limbic system, secretes: various, function: acts as a thermostat- measuring hormone levels

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36
Q

What does the pituitary gland do?

A

Location: in limbic system, secretes: various, function: “master gland” - tells other glands what to release

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37
Q

What is the endocrine system?

A

Acts much slower than nervous system (but more widespread effects), made up of multiple glands around the body. Each gland releases different hormones into the blood which regulate activity of various organs/tissues

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38
Q

What happens as hormones travel around the body?

A

As hormones travel in the blood, they contact most cells, but they only affect a smaller no. of target cells with the right receptors for that hormone (cell can’t be affected if no receptor for that hormone)

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39
Q

What happens after hormones contact target cells?

A

When enough receptor sites on the organ are stimulated by the hormone there is a physiological reaction in the target cell

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40
Q

How are hormone levels regulated?

A

Hypothalamus sends message to pituitary gland in form of a releasing hormone; pituitary gland releases hormone into the blood. This stimulating hormone targets a specific gland to release melatonin

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41
Q

How does the release of melatonin regulate hormone levels?

A

Levels of melatonin in blood rise, when they reach a certain level the hypothalamus shuts down secretion of the releasing hormone and pituitary gland stops releasing stimulating hormone. This slows down secretion of target gland’s hormone production = stable concentrations in the bloodstream

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42
Q

What triggers the fight or flight response?

A

In stressful/threatening situation body reacts biologically- preparing you to fight the threat or run away

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43
Q

What systems are involved in the fight or flight response?

A

Both the endocrine and nervous system are involved

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44
Q

What is the fight or flight response?

A

Started by the autonomic nervous system (specifically the sympathetic branch) as an unconscious reflex response. However this response also requires the secretion of hormones

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45
Q

Why do we have the fight or flight response?

A

Evolved survival mechanism to allow people to act in life threatening situations but can be activated in non-useful situations

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46
Q

What biologically starts the fight or flight response?

A

Sympathomedullary pathway: the fight or flight response
Our amygdala associates sensory signals with emotions such as fear/anger.
When we’re faced with a threat our amygdala identifies this and sends a distress call to our hypothalamus

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47
Q

What occurs in the hypothalamus during the fight or flight response?

A

When hypothalamus identifies a stressor it activates the sympathetic nervous system (via the brain stem)
The SNS sends a signal to adrenal medulla causing release of adrenaline and noradrenaline into the blood

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48
Q

What happens in fight or flight response when adrenaline is released into the blood?

A

As adrenaline circulates it causes physiological changes

heart rate rises, digestion slows down, pupils dilate

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49
Q

What happens during fight or flight when the threat has passed?

A

The parasympathetic branch of the autonomic nervous system is activated. This returns the body to its normal resting state.

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50
Q

What happens during fight or flight if stressful situation continues?

A

HPA axis (pituitary-adrenal system) is activated as initial adrenaline subsides, release of cortisol, emphasis on energy production and stamina (long term response)

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51
Q

How do reactions of females differ from males? (evaluation point)

A

Tend and Befriend- it isn’t advantageous to run away and leave children behind so they befriend competitors

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52
Q

What are the negatives of the fight or flight response?

A

Outdated: we do not need to fight or run- modern stressors need a different response
negative consequences- Sympathomedullary= wear/tear on body and Pituitary/adrenal= cortisol=less white blood cells = more illness

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53
Q

What are ultradian rythms?

A

Repeated more than once every 24 hrs e.g 90min sleep cycle/sleep stages, BRAC cycle (basic rest activity cycle)

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54
Q

What are the fundamentals of sleep stages?

A

They follow a pattern of NREM (non-REM) (stages 1-4) and REM (stage 5) alternation + repeats approx every 90 mins
Stages vary in duration

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55
Q

Where does our information come from on sleep cycles?

A

Recording electrical activity of the brain with an EEG.
The EEG shows a distinct pattern at each stage
(EOG= optic movement EMG= muscle tension)

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56
Q

What are the features of sleep stages 1 and 2?

A

Lighter sleep (1= approx 4-5% of total sleep) (2= approx 45-50%)
Brain activity slows, breathing+heart rate slow, alpha (awake) waves slow and become more rhythmic theta waves
(occasional muscle twitching)

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57
Q

What are the features of sleep stages 3 and 4?

A 
Deeper sleep (3= 4-6% of total sleep) (4= 12-15%) 
deep sleep, not easily woken, slower delta waves, slowing down.
(only little eye movement/muscle activity)
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58
Q

What are the features of sleep stage 5?

A

REM (20-25% of total sleep) Brain is active as when awake: alpha + beta waves
eyes are active, muscle paralysis, breathing + heart rate increase
(70-75% report dreaming when woken in REM)

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59
Q

Who suggested the BRAC cycle?

A

Kleitman suggested we have a 90min waking cycle too- BRAC. Characterised by period of physiological alertness and fatigue every 90mins.
(we can focus our mind for 90mins approx and towards the end run out of resources- results in loss of concentration and hunger) (e.g. ppl often start work at 9 and break at 10.30)

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60
Q

What are infradian rhythms?

A

Occur less than once every 24hrs. e.g. monthly menstrual cycle and SAD (seasonal affective disorder)

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61
Q

What is an example of a monthly infradian rhythm?

A

Menstrual cycle: regulated by hormones- rising levels of oestrogen cause ovary to develop an egg + release it.
After ovulation progesterone helps thicken womb lining for pregnancy
If not pregnant womb lining comes away and leaves body.

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62
Q

How is the menstrual cycle governed?

A

By both endogenous and exogenous factors:

endogenous= hormones, exogenous = pheremones

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63
Q

How do pheremones affect the menstrual cycle?

A

When several women (of childbearing age) live together (and don’t take oral contraceptives) their cycles tend to synchronise.
This is due to secretion of pheremones which act on the body in a similar way to hormones but affect people close by to the person producing them

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64
Q

What is an example of a yearly infradian rhythm?

A

SAD: depressive disorder (onset in winter), darker for longer =, pineal gland produces more melatonin at this time of year, more melatonin requires serotonin o be produced. Can cause serotonin levels to be low linking to depression.

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65
Q

What support is there for the role of pheremones (in the menstrual cycle)?

A

Russell: took sweat from one woman (donor) Rubbed it onto upper lip of 5 pps every day for 5 months. control group given placebo. Single blind. 4/5 pps (sweat condition) synchronised to donor
None of control group synchronised
Demonstrates role of airborne hormones as exogenous factors

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66
Q

What is the evaluation of Russell’s study into pheremones?

A

+ well controlled (standardised procedure, placebo control group, single blind) measured what it intended to measure
-small sample & other studies have failed to replicate any sign of menstrual synchrony.
…So evidence for pheremones influencing menstrual cycle is weak

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67
Q

What does Penton-Voak et al’s research into the menstrual cycle show? (AO3)

A

Suggest human mate choices vary across menstrual cycle: fertile stage (ovulation) picked ‘masculine faces’
(sign of good genes for offspring)
Rest of the time women picked more feminine faces
(sign of good LT partnership/parenting)
Suggests evolutionary basis for mate preference is linked to menstrual cycle

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68
Q

What is the real life application produced from the study of the disorder SAD? (AO3 infradian)

A

Understanding role of darkness in SAD has led to effective therapies e.g. phototherapy (light boxes)
Uses very strong light in the evening and/or early morning to change levels of melatonin and serotonin.
SAD sufferers report feeling less tired + depressed when used daily.
BUT placebo effect? 32% pps improved with placebo alone.

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69
Q

What are the evaluation points for ultradian rythms?

A

Strengths: support for different sleep stages, objectve measures and support for BRAC
Weaknesses: low ecological validity and individual differences in sleep stages

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70
Q

What support is there for the different sleep stages? (AO3 ultradian)

A

Dement and Kleitman (1957):
Monitored sleep patterns in 9 adults in sleep lab + recorded brain activity using EEG, while controlling for caffeine and alcohol.
Found strong correlation between REM activity & dreaming. Brain activity varied according to how vivid dreaming was & found eye movement corresponded to dream content.
But- researchers have criticised small sample.
But further research has replicated such findings supporting validity of D + K’s study.

71
Q

What support is there for BRAC? (AO3 ultradian)

A

Ericsson et al (2006): Found that best violinists tended to practice 3 sessions during the day, each session lasting no more than 90 minutes.
Supports Kleitman’s argument of fatigue after 90 mins
Same pattern has been found among other musicians, athletes, writers etc.

72
Q

Why do many studies into ultradian ryhtms have low ecological validity? (AO3 ultradian)

A

Data gathered in sleep labs: pps wired up to machines; not sleeping in own bed + env. not natural
May affect their sleep- instead of measuring normal sleep, possibility that measurements reflect artificiality.
However, technology is becoming more sophisticated, enabling ppl to use smaller equipment in own homes

73
Q

How are individual differences in sleep stages a possible weakness? (AO3 ultradian)

A

Tucker et al suggests differences in sleep stages may be genetic, not external factors like room temp. (Studied pps for 11 days in strict lab env. assessed sleep duration, time to fall asleep + duration of stages. Lg indv. differences, particularly in deep sleep. Concluded differences down to biology not env.)
BUT there’re universal characteristics everyone shares e.g. regardless of stage length, ppl have more SWS at start of the night, + REM sleep towards end of night

74
Q

What are the different biological rhythms?

A

circadian, infradian and ultradian

75
Q

What are circadian rhythms?

A

Rhythm repeated approx. once every 24 hrs

76
Q

What is the sleep wake cycle?

A 
24 hr cycle: controlled by indogenous pacemakers (SCN, internal clock)
exogenous zeitgebers (light)
Homeostasis
77
Q

What is the core body temperature cycle?

A

Temp. also fluctuates in a circadian rhythm.
Lowest (36C) about 4:30 am + highest (38C) about 6pm. Sleep occurs when temp. begin to drop. Temp. rises during last few hours of sleep promoting alertness in morning. Also small drop in temp between 2-4pm – post lunch dip in alertness

78
Q

How are human circadian rhythms governed?

A

Our circadian rhythms are driven by our body clocks.
These clocks found in all cells + are synchronised by SCN in hypothalamus.

SCN must be constantly reset so we are in synchrony with outside world. Often governed by interactions between (Internal) Endogenous Pacemakers & (External) Exogenous Zeitgebers

79
Q

What is the link between the SCN and the sleep-wake cycle?

A 
Suprachiasmatic nucleus (SCN) keeps sleep wake rhythm fairly constant.
There are two peaks to this cycle, most likely to want to sleep 2-4 am and 1-3pm. 
(But cycle can vary around 24 hours naturally)
80
Q

How does light contribute to the sleep wake cycle?

A

Rhythm of light/darkness dictates when we should be sleeping/awake + takes 24 hours
So, light = external zeitgeber & provides primary input to SCN, setting body clock to correct time (process known as photoentrainment)

81
Q

How is the sleep-wake cycle affected by homeostatic control?

A

Need to sleep also under homeostatic control
If sleep deprived homeostasis tells us need for sleep is increasing as we energy is depleting more.
Homeostatic drive for sleep increases throughout day reaching maximum in the evening.

82
Q

How can an internal clock cause issues?

A

If not exposed to any external cues internal clock ‘free runs’ maintaining a rough 24/25 hr cycle. Then reset by light.
Causes problems when major alterations in sleep wake schedules (jet lag/shift work) as the biological clock is out of balance to the external cues.

83
Q

What was Siffre’s research into the sleep wake cycle?

A

Did many studies isolating himself in caves for long periods. No external cues guiding his rhythm (no daylight, clocks etc)
Woke, ate, slept etc as he wanted to. (this way only influence is internal circadian ‘free running’ clock)
Developed approx 25 hr sleep-wake rhythm, despite no knowledge of time of day

84
Q

What did Siffre conclude from his studies into the sleep wake cycle?

A

He had a rhythm = evidence of internal biological clock
But rhythm became longer, in absence of light (external factor) entraining 24 hr rhythm
But Siffre’s study was case study- he may be unique, therefore hard to generalise findings
But his findings replicated repeatedly by others, adding support + validity to role of internal control

85
Q

What research supports the idea of a strong internal clock that is hard to overcome?

A

Folkard et al: asked 12 pps to live in cave for 3 weeks.
No natural light, no normal time cues. Asked to sleep when clock said 11:45pm + wake at 7:45 am. Researchers sped up clock so pps (unknowingly) followed a 22 hr cycle.
11/12 pps couldn’t keep pace with 22-hr cycle.
Suggests a strong internal free-running circadian rhythm not easily overridden.

86
Q

What are the evaluation points for circadian rhythms?

A

Strengths: real life application to drug treatments (and shift workers), support for body temp cycle
Weaknesses: use of case studies + small samples, individual differences, flaws in methodology of early research

87
Q

What real life application for drug treatments has resulted from circadian rhythm research? (AO3)

A

Chronotherapeutics: study of how timing can affect drug treatments.Time patient takes medication can have significantly impact effectiveness.
E.g. risk of heart attack is greatest in morning so Chronotherapeutic medication taken 10pm, but released between 6am-noon. Shows how knowledge of bodily rhythms improve effectiveness of medication.

88
Q

What real life application for shift workers has resulted from circadian rhythm research? (AO3)

A

Knowledge of our circadian rhythm gives better understanding of consequences of disrupting it.
Bovin et al: Night workers experience reduced concentration around 6am (a circadian trough).
Accidents/mistakes more likely at this time – employers to be aware

89
Q

What support is there for the bodily temperature cycle? (circadian AO3)

A

Research found link between temp change in day & cognitive ability Folkard: studied 12-13 year old’s learning ability at 9am & 3pm.
Found superior recall & comprehension at 3pm.
Shows higher body temp may link to cognitive ability

90
Q

How is use of case studies and small samples a weakness? (circadian AO3)

A

Studies into it tend to use few pps or individuals. May not represent wider pop. so limits extent we can make real generalisations from them. Siffre’s later study showed his sleep cycle lengthened showing even one pps score can vary
(But other support for Siffre E.g. Folkard + Aschoff & Wever)

91
Q

How are individual differences a weakness for research into circadian rhythms? (AO3)

A

2 key individual differences in circadian rhythms:
Cycle length - can vary from 13-65 hrs
Cycle onset - ppl differ in when rhythms peak
‘Morning people’ prefer rise early/sleep early. Others prefer wake later/sleep later.
Such variations make it difficult to generalise findings from research into sleep/wake cycle

92
Q

What flaws are there in the methodology of early research into circadian rhythms? (AO3)

A

Pps in early studies (e.g. Siffre) deprived of natural light, but still had artificial light
Was assumed artificial light wouldn’t affect free-running biological rhythm.
However Czeisler able to adjust pps’ circadian rhythms from 22 to 28 hrs using dim artificial light.
Artificial light therefore acted as extraneous variable so poor control and therefore validity of findings.

93
Q

What is the localisation of function?

A

The principle that specific functions (e.g. forming & understanding language or storing memories) have specific locations in brain where they occur

(Also known as cortical specialisation)

94
Q

What is phrenology and why is it outdated?

A

phrenology: looking at the structure of the skull to determine a persons character- discredited by modern brain scans and theory of localisation.

95
Q

How are the two hemispheres of the brain connected?

A

By a bundle of fibres called the corpus callosum

96
Q

What is the cerebral cortex?

A

Outermost layer of brain, covers both hemispheres
Regulates our higher intellectual processes
Four lobes send and receive messages to/from it

97
Q

What are the four lobes?

A

Frontal lobe, parietal lobe, occipital lobe and temporal lobe

98
Q

What is the function of the parietal lobe?

A

Location for sensory info from skin (related to touch, heat, pressure) located in the somatosensory cortex within this lobe.

99
Q

What is the function of the occipital lobe?

A

Location for visual info – located in the visual cortex in this lobe.

100
Q

What is the function of the frontal lobe?

A

Location for awareness of what we’re doing within our environment (our consciousness). Motor cortex is located here- responsible for generation of voluntary motor movements

101
Q

What is the function of the temporal lobe?

A

Location for Auditory cortex (for auditory ability which analyses speech based info)
Also important in memory

102
Q

What are the four key structures in the limbic system?

A

Amygdala, pituitary gland, hypothalamus and hippocampus

103
Q

What are the functions of the four key structures in the limbic system?

A

Amygdala - Controls our emotions.
Hypothalamus and pituitary gland – control stress response & hormone release by homeostasis (process by which body maintains constant physiological state)
Hippocampus – Important in memory.

104
Q

What affects the size of sensory and motor areas?

A

The size of the sensory and motor areas is related to the number of receptors in that area of the body.

105
Q

How does the motor cortex function?

A

Located posterior of frontal lobe, spans both hemispheres & is contralateral.
Motor areas transmit impulses to effectors & therefore responsible for generation of voluntary motor movements.
Different parts of motor cortex control different parts of the body (arranged logically – region controlling foot next to region for leg)

106
Q

How does the somatosensory cortex function?

A

Situated in anterior of parietal lobe. Both hemispheres have a somatosensory cortex. (& cortex is contralateral)
Detects sensory info from body to produce sensations e.g. pain, which it then localises to specific body regions
It transmits info to the association areas to interpret it & to compare sensory input with previous experience, & make decisions

107
Q

Where are the visual cortices located?

A

One located in each hemisphere’s occipital lobe

108
Q

How do the visual cortices function?

A

Right hemisphere receiving input from left-hand side of visual field & vice versa
Visual cortex contains different areas, processing different types visual info e.g. colour/shape/movement
The 2 hemispheres see slightly different images from opposite of the visual field, & differences used to judge distance

109
Q

How do the auditory cortices function?

A

Two auditory cortices, one in temporal lobe of each hemisphere
Sound has already been largely decoded by this point, in auditory cortex its recognised & may result in appropriate response

110
Q

What did Broca find?

A

Broca treated patient ‘Tan’ – could understand spoken language but unable to speak/write. Could only say “tan”. Studied 8 others with similar language difficulties- they had lesions in left frontal hemisphere.
Lead him to identify language production centre in posterior (back) of frontal lobe, left hemisphere.

111
Q

What are the problems with Broca’s area as ‘language production area?

A

Neuro-scientists have found when ppl perform cognitive tasks (nothing to do with language) Broca area is active

112
Q

What did Wernicke discover?

A

Another area of brain involved in understanding language. Posterior (back) portion of left temporal lobe.
Patients with lesions on Wernicke’s area could speak but unable to understand language.

113
Q

What is the difference between Broca’s and Wernicke’s area?

A

Broca’s area – responsible for production of language

Wernicke’ area – responsible for understanding of spoken language

114
Q

What are the strengths of the localisation of function? (AO3)

A

Support for language centres from aphasia studies
Support form brain scanning studies
Support from case studies - Phineas Gage

115
Q

What are the weaknesses of the localisation of function theory? (AO3)

A

Individual differences in language areas
Communication may be more inmportant than localisation
Localisation is an oversimplification- locations can change
Research challenges localisation of function

116
Q

What support is there from aphasia studies for the localisation of function? (AO3)

A 
Evidence for functions of Broca’s + Wernicke’s from discovery that damage to 2 areas results in different  aphasia types. 
Expressive aphasia (Broca’s aphasia):  impaired language production. Mostly caused by damaged Broca’s area.
Receptive aphasia (Wernicke’s aphasia): impaired language understanding/extracting meaning from spoken or written words. Usually result of damaged Wernicke’s area.
(BUT.. case study nature of this study & limited technology at the time.)
117
Q

What is aphasia?

A

Aphasia refers to an ability (or impaired ability) to understand or produce speech as a result of brain damage.

118
Q

What support is there for the localisation of function from brain scanning studies? (AO3)

A

There is a wealth of evidence that supports that neurological functions are localised.
Peterson (1988): used brain scans to demonstrate how Wernicke’s area active during listening task + Broca’s area active during reading task

119
Q

What support is there for the localisation of function from case studies (Phineas Gage)? (AO3)

A

Working on railroad, Gage was preparing to blast rock using explosives, misfired & explosion caused 1m iron pole, point first through left cheek, behind left eye, + exited his brain & skull from top of head.
Before: capable/well balanced efficient foreman. After: personality changed- boisterous/rude & blasphemous. “No longer Gage.“
BUT must be careful generalising these findings- based on one very rare case.

120
Q

How are individual differences in languae areas a weakness for the localisation of function (AO3)?

A

Pattern of activity in various language centres can vary from person to person.
Studies have found significant gender differences in language areas, with women having larger Broca’s & Wernicke’s areas (Harasty, 1997). Some explain this as because women use language more than men.

121
Q

How may communication be more important than localisation? (AO3)

A

Research suggests how brain areas communicate with each other, more important than which regions control what. Dejerine: described case- patient couldn’t read due to damage to connection between visual cortex & Wernicke’s area. Damaged connection results in impairments resembling damage to localised region associated with that function. SO although specific parts of brain do specific jobs they must work together to meaningfully function. Localisation of functions can only provide partial answer… should also be looking at how processes utilise multiple areas.

122
Q

How is localisation an over simplification (locations can change) a weakness of localisation of function (AO3)?

A

Healthy areas of the brain can, sometimes, take on responsibility for function of a damaged area.
Therefore effects of damage will be down to extent of the damage not location.
Would mean standard idea of function of differing areas not always fixed.

123
Q

What is hemispheric lateralisation?

A

When a function is specialised in one hemisphere, it’s called lateralisation.
Sometimes hemispheres differ in functions- are said to have ‘functional specialisations’.
Hemisphere that does a function the most is ‘dominant hemisphere’ (cerebral dominance).

124
Q

What two functions are lateralised?

A

left hemisphere : language

right hemisphere: visual- motor tasks

125
Q

How can we study lateralisation?

A

Wada test:
Anaesthetic injected into carotid artery on one side of head. Anaesthetises one hemisphere.
Pps then read aloud. When left hemisphere anaesthetised, reading aloud disrupted in over 90%
Split brain research

126
Q

What is split brain research?

A

Study of split-brain patients.
Treatment for severe epilepsy, surgeons (do a commissurotomy) cut through ‘corpus callosum’ to prevent violent electrical activity in epileptic seizures crossing hemispheres.
Psychologists can study pps with split brain to see how hemispheres now work independently.

127
Q

What was Sperry’s research?

A

As Corpus Callosum split in split-brain patients, info presented to one hemisphere can only be processed there- no way of transferring to other hemisphere, allowing him to test each independently.
Pps asked to fixate on dot in screen’s centre. Info flashed up to right or left visual field. Then asked to respond with either: left hand (right hemisphere)
Or verbally (left hemisphere)
(11 pps, natural experiment)

128
Q

What were Sperry’s results?

A

If pps shown dog in their right visual field: Verbal response – “Dog”, Drawn response - nothing.
If pps shown cat in left visual field: Verbal response – “nothing”, Drawn response – picture of cat
Right hemisphere can process picture of the cat but cannot respond verbally. Left hemisphere (which could respond) does not see the cat.

129
Q

What were Sperry’s additional results?

A

Recognition by touch: Although patients could not say what shown to left visual field they could select matching object from grab-bag (hidden by a screen) of different objects with right hand. Left hand also able to select an object most closely associated with the object presented.

130
Q

What did Sperry conclude?

A

Sperry concluded that the two hemispheres have different functions.

131
Q

What support is there for Sperry’s research?

A

Heller and Levy showed faces with two emotions.

The face on the left is the emotion recognised (by the right hemisphere)

132
Q

What are the strengths of Sperry’s study? (AO3)

A

Useful to highlight differences between hemispheres

Used standardised procedures & he flashed images extremely quickly to control which hemisphere was receiving image.

133
Q

What are the weaknesses of Sperry’s study? (AO3) (about 4-5 points)

A

Natural experiment: Sperry couldn’t manipulate what groups pps in, pps also had various levels of disconnection.
Ppl with corpus callosum severed for severe epilepsy are rare. Only 11 pps - small sample.
Limited generalisation as study used mainly right-handers & split-brain patients are rare
Patients suffered severe epilepsy & on long-term drug treatments- may not be valid to generalise or compare their brains with ‘normal’ brains. Control group: ppl without epilepsy -may have been inappropriate

134
Q

What are the strengths and weaknesses of lateralisation? (AO3)

A

Support from Rogers

Weakness: lateralisation changes with age, language may not be restricted to left hemisphere

135
Q

What support is there for lateralisation from Rogers? (AO3)

A

Generally assumed benefit of lateralisation: ability to carry out multiple tasks more easily. (If one hemisphere can work on a task, leaves other free for another function)……. (But there is little evidence for this.)
Support from: Rogers et al: found chickens’ brain lateralisation associated with better ability to do two tasks – (finding food & being vigilant for predators) Thus, evidence for lateralisation increasing efficiency in cognitive tasks requiring different hemispheres

136
Q

How is the change of lateralisation with age a weakness for lateralisation? (AO3)

A

Across many tasks & brain areas, lateralised patterns found in younger individuals tend to switch to bilateral patterns in healthy older adults.
Szaflarski et al: found lang. became more lateralised to left hemisphere with increased age in children /adolescents, but after 25, lateralisation decrease each decade.
Implies lateralised brain only a feature of young adults, not true for everyone.

137
Q

How is the finding that language may not be restricted to the left hemisphere a weakness for lateralisation? (AO3)

A

Case studies have demonstrated language not completely lateralised to left hemisphere.
J.W.: developed capacity to speak out of right hemisphere, with result that J.W. can now speak about info presented to left or right brain (Turk et al 2002).

138
Q

What is plasticity?

A

The brains tendency to change & adapt (functionally + physically) due to experience & new learning.
Brain continues to create new neural pathways & alter existing ones to adapt to new experiences as a result of learning even in adulthood.

139
Q

What is cognitive pruning?

A

During infancy, brain experiences rapid growth in no. of synaptic connections. Rarely used connections deleted, frequently used connections strengthened. Brain is continually changing.

140
Q

What is an example of real life experience leading to plasticity?

A

Maguire’s taxi drivers study: studied brains of London taxi drivers using MRI. Measured amount of grey matter in brains of taxi drivers + control group of similar men. Significantly more grey matter in posterior hippocampus (associated with development of spatial & navigational skills) for TDs.
Significant positive correlation between size of posterior hippocampus volume + length of time as TD

141
Q

What did Macguire’s second taxi driver study show?

A

79pps, 39 passed the knowledge. Studied them pre-TDs, found no structural differences in brain.
3-4 yrs later found larger posterior hippocampus volumes in 39 passed + no changes in failed or control

142
Q

How can plasticity result from video games?

A

Kuhn et al (2014) : compared control group with ‘video game training group’ - played Super Mario 30 mins a day for 2 months. Significantly increased grey matter in various brain areas including cortex, hippocampus + cerebellum. (not in control). Concluded playing video games resulted in new synaptic connections in brain areas involved with spatial navigation, strategic planning, working memory & motor skills.

143
Q

What are the evaluation points for plasticity? (AO3)

A

Support from animal research, support from human research, evaluation of Maguire’s research, real life application- could be useful.

144
Q

What support is there for plasticity from animal research? (AO3)

A

Kempermann et al: Found evidence of increased number of new neurons in brains of rats housed in complex environments (compared to non-complex)
In particular, rats housed in complex env.s showed increased neurons in hippocampus, associated with forming new memories, & ability to navigate

145
Q

What support is there for plasticity from human research? (AO3)

A

Draganski et al (2006): imaged brains of medical students 3 months before & after final exams. Learning induced changes occurred in posterior hippocampus & parietal cortex, presumably due to exam.
Michelli et al (2004) also found larger parietal cortex in brains of ppl who were bilingual compared to matched monolingual controls.

146
Q

Evaluate Maguire’s research? (AO3 plasticity)

A

+ Control group allows us to say there’s significant difference between taxi drivers + others. (Therefore good design)
+Use of scientific, objective measurements (MRI)
-1st study: unsure if difference due to the ‘knowledge’, as weren’t tested before. Could have been TDs because of pre-existing spatial awareness skills. (solved by 2nd study)
-Lacks pop. validity - are women’s brains the same?

147
Q

How could knowledge of plasticity have real life application? (AO3)

A

Neurorehabilitation studies show that following damage movement therapy and electrical stimulation can counter deficits in movement and cognitive functioning.

148
Q

What is functional recovery?

A

Following physical injury or trauma e.g. infection or stroke, areas of brain can be damaged.
However, unaffected areas sometimes able to adapt or compensate for areas damaged.
Recovery of abilities & mental processes known as functional recovery.

149
Q

How does functional recovery happen? (2 ways)

A

Neural unmasking

Stem cells

150
Q

What is neural unmasking?

A

‘Dormant synapses’: synaptic connections that exist anatomically but function is blocked.
Increasing rate of input to these synapses (as would happen when surrounding area damaged) can open up/‘unmask’ dormant synaptic pathways.

151
Q

What structural changes is neural unmasking supported by?

A

Axon sprouting: new nerve endings grow & connect with undamaged areas.
Reformation of blood vessels.
Recruitment of similar areas on opposite hemisphere to do specific tasks. E.g if Brocas area damaged, an area on right might take over.

152
Q

What are stem cells?

A

Stem cells: unspecialised cells that have potential to give rise to different cell types

153
Q

How may stem cells contribute to functional recovery?

A

Number of views on how stem cells might work in functional recovery:
Stem cells implanted into brain directly replace dead/ dying cells
Stem cells secrete growth factor that rescues dying cells.
Stem cells form a neural network linking uninjured brains sites (where new stem cells made) to damaged region.

154
Q

How may educational attainment affect functional recovery? (AO3) (limitation?)

A

Schneider et al: Patients with college education 7x more likely to be disability-free 1 yr after moderate/ severe traumatic brain injury. ‘Cognitive reserve’ (associated with greater educational attainment) could be factor in neural adaptation during recovery from brain injury.

155
Q

What research support is there from animal studies for functional recovery? (AO3) (strength)

A

Tajiri et al: randomly assigned rats with traumatic brain injury to one of 2 groups. One received transplants of stem cells. 3 months after, stem cell rats showed clear development of neuron-like cells in the area of injury
Hubel and Wiesel: (1960s) if left eye of kitten sewn shut, right visual processing area just began processing info from right eye.

156
Q

What is the evaluation of animal research into functional recovery?

A

+ Animal studies: only way to monitor function of brain before & after trauma that we cause. Ethically can’t in humans & unlikely we would have measured their function before natural event.
- Study only involved rats- brains of rats very different to human so hard to generalise results to humans.

157
Q

How may functional recovery be easier at some stages than others? (AO3) (limitation?)

A

Functional plasticity reduces with age.
The capacity for neural reorganization is much greater in children than in adults
…However, studies have suggested that even abilities commonly thought to be fixed in childhood can still be modified in adults with intense retraining.

158
Q

How may the findings of functional recovery and plasticity be applied to the field of neurorehabilitation? (AO3) (strength)

A

understanding process of plasticity + functional recovery led to development of neurorehabilitation.
It uses motor therapy + electrical stimulation to counter negative effects/deficits in motor/cognitive functions after accidents/injuries/strokes. (positive application)

159
Q

How is human echolocation an example of functional recovery? (AO3?)

A

Human echolocation- learned ability to sense env. from echoes, used by someblind people to navigate their env./sense surroundings
Using fMRItechniques found parts of brain associated with visual processing adapted for echolocation.
But human evidence restricted to small scale of ppl who already have issues.

160
Q

What are the 4 main ways of studying the brain?

A

fMRI, EEGs, ERPs and post-mortem examinations

161
Q

How do fMRIs work?

A

Same as standard MRI but show activity as it occurs.
fMRI uses same principle as MRI, but instead of measuring energy emitted from water, measures energy released by haemoglobin
When haemoglobin has oxygen it reacts differently to when it doesn’t- so when area of brain active it uses more oxygen.
Difference in amount of energy released by haemoglobin detected by scanner + change measured.
Gives dynamic (moving) picture, shows activity about 1 second after. Accurate to 1-2 mm in the brain.

162
Q

Strengths of fMRI? (AO3)

A

+Produces moving pictures of activity, this means patterns can be compared rather than just looking at locations, this is important when studying how areas communicate.
+Produces high resolution images accurate to mm so provides clear image of where functions localised.

163
Q

Limitations of fMRI? (AO3)

A
  • Expensive compared to other techniques- requires expensive equipment + trained experts, so hard to organise research. Also makes large sample sizes difficult, so hard to generalise results.
  • Overlooks networked nature of brain activity, focusing too much on one localised function. So ignores communication between areas that can also be crucial to understanding abilities etc.
164
Q

How do EEGs work?

A
  • Electrodes put on scalp detect + measure changes in electrical activity, from activity of brain cells.
  • Anything from 2/3 to over 100 electrodes. EEG records brainwave patterns/activity generated by action of millions of neurons under each electrode. More electrodes provides overall account of brain activity.
  • EEG data can be used to detect various brain disorders (e.g. epilepsy) or diagnose other disorders influencing brain activity (e.g. Alzheimer’s) E.g. readings of patients with epilepsy show spikes of electrical activity.
165
Q

What are the strengths of EEGs?(AO3)

A
  • Provides a measure in real time, rather than a delay, and measuring activity directly not consequences of it like blood flow.
  • More widely available than other scanning techniques as cheaper.
166
Q

What are the limitations of EEGs? (AO3)

A
  • Can only detect activity in superficial regions of brain, cannot reveal deeper regions e.g. hypothalamus or hippocampus. (can implant electrodes into animals to test this but not ethically permitable in humans.)
  • General measure: signal from individual neuron not strong enough to detect, so only indicates area when many neurons firing.
  • Electrical signals can be picked up from neighbouring electrodes so not useful for exact source of activity- can’t distinguish between close areas. Researchers can’t differentiate when different but close areas firing.
167
Q

How do ERPs work?

A

ERPs use same apparatus as EEGs but record when there’s activity in response to stimulus.
All extraneous brain activity from original EEG filtered out leaving only ERPs - very small voltage changes triggered by specific events, tasks or stimuli.
Stimuli must be repeatedly presented to establish definite response.
ERPs can be divided into tow categories
Waves occurring in first 100milliseconds- ’sensory ERPs’. Reflect initial response to presentation of stimulus.
ERPs generated after first 100 milliseconds- ‘cognitive ERPs’. Reflect subject evaluating stimulus/ processing it.

168
Q

What are the strengths of ERPs? (AO3)

A

More widely available than other scanning techniques as cheaper.
Useful for testing the accuracy of self report (Costa) particularly when a topic is prone to social desirability bias.

169
Q

What are the limitations of ERPs? (AO3)

A

Large no. trials needed for meaningful data as hard to pick out ERPs from other electrical data. Large volume of trials needed limits types of topics can research
As with EEGs, cannot pick up responses deep in brain.

170
Q

How do post-mortems examinations work?

A

Post-mortem examinations can identify underlying neurobiology of a particular behaviour.
Researchers may study person who displays interesting behaviour while alive (suggesting possible brain damage).
When person dies, researchers can examine their brains for abnormalities that may explain behaviour.

171
Q

What are some examples of post -mortem examinations?

A

Early example: Broca’s patient ‘Tan’, who displayed speech problems when alive & was subsequently found with lesion in area of the brain now known as ‘Broca’s area’; area important for speech production.

172
Q

What are the strengths of post-mortem examinations?

A

Vital in early days of psychology before EEG,ERP,FMRIs developed.
Allow for more detailed study of brain anatomy than non invasive methods like scanning techniques. This is because it enables study of deeper brain regions such as the hypothalamus and hippocampus.

173
Q

What are the limitations of post-mortem examinations?

A

Cause & effect: differences we observe in dead brains may not have caused behaviours. Many confounding variables might affect brain after death e.g. time between death + post mortem, age of death, drug treatments, cause of death etc, all cause differences between cases & controls.
Approach is retrospective, researcher unable to follow up anything that arises from post mortem, also cannot see when it is activated.

Psychology A level (11 decks)

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