biopsych

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  • What is plasticity?
    brains tendency to change and adapt as a result of experiences and new learning. generally involves growth of new connections.
    during infancy brain experiences rapid growth in connection - 15,000 ages 2-3.
    synaptic pruning - rarely used synapses are deleted and frequently used are strengthened.
  • What research is there to support plasticity?
    1. Maguire found significantly more grey matter volume in posterior hippocampus of London taxi drivers than a control group. This area of the brain is linked with spatial and navigational skills. Shows how "the Knowledge" test appears to alter brain structure and the more experienced a person was the more pronounced the changes.
    2. Examined brains of med students 3 months ebfore and after final exams and observed changes in posterior hippocampus and parietal cortex.
  • What is negative plasticity? (W)
    Brains adaptation to prolonged drug use can leads to poorer cognitive functioning in later life which is associated with an increase risk of dementia. 60-80% of amputees develop phantom limb syndrome due to cortical reorganisation in somatosensory cortex. Brains ability to adapt in not always beneficial.
  • What research from Bezzola support lifelong plasticity?
    Plasticity may be a life long ability. Bezzola found how 40 hours of golf training produced changes in neural representation in participants aged between 40-60. fMRI scans observed increased activity in motor cortex of the novice golfers compared to control group suggesting that golfing had led to more efficient neural representations. Plasticity can continue throughout a life span.
  • Seasonal Plasticity?
    Research into SP shows that in response to environmental change in SCN which regulate sleeps shrinks in Spring and expands in Autumn.
    However - animal studies simply cannot be generalised.
  • What is Functional Recovery?
    A form of plasticity where following damage the brain has the ability to redistribute or transfer functions usually performed by damaged areas to undamaged ones.
    Spontaneous recovery - suggested to occur quickly and then slow down to the point where an individual requires rehab therapy.
    Brain rewires and reorganises itself by forming new synaptic connections close to damaged areas.
    Secondary Neural pathways - activated and unmasked to compensate.
  • What are the structural changes involved in FR?
    1. Axonal Sprouting - growth of new nerve endings to connect with undamaged cells and form new pathways .
    2. Denervation Supersensitivity - axons doing a similar job arise to compensate.
    3. Recruitment of Homologous Areas - opposite side of the brain takes over to compensate.
  • How does FR have RWA?
    Understanding of FR has led to field of neurorehabilitation - understanding of axonal growth has led to new therapies e.g. constraint induced muscle therapy is used with stroke patients and involves mass practice with the affected arm while the unaffected on is restrained. Helps medical professions know when to make interventions.
  • How is functional recovery linked with cognitive reserve?
    FR may be influenced by the level of education. Schneider examined brain injury patients time in education and chances of a disability free recovery. Those who spent 16 years in education had a 40% DFR whereas those who had spent less than 12 years had a 10% DFR. Shows cognitive reserve is crucial factor in determining adaptation after trauma.
    • means individual differences could affect results of research
  • Extra eval for FR?
    Research into treatments helping FR - Bankerjee showed total recovery from strokes using stem cells compared to 4% normal recovery.
    • only used a small sample of 5 pps with no control group which tends to be quite typical of FR research - may lack validity and generalisability.
  • Evaluate Maguire's taxi study?
    • all males - 16 male pps matched with control group.
    • matching helps to reduce cofounding variables but still research suffers from beta bias by assuming findings apply to women.
  • What are endogenous pacemakers?
    Internal body clocks that regulate many of our biological rhythms e.g. S/W cycle.
    SCN - suprachiasmatic nucleus
    • ting bundle of nerve cells in the hypothalamus above the optic chiasm - receives information from the eye about light.
  • What animal studies support EPs?
    1. Destroyed SCN connections in 30 chipmunks and returned them to the wild. Observed the animals for 80 days and found S/W cycle disappeared and many were killed by predators.
    2. Bred mutant hamsters to have 20 hour cycle. Transplanted then into normal hamsters which also developed a 20 cycle.
    + shows how SCN is crucial is determining typical rhythms.
    S - animal studies are useful because share similar mechanisms but they lack generalisability and studies often risky & unethical -unnecessary harm to animals.
  • What are exogenous zeitgebers?
    External factors that entrain & affect our biological rhythms e.g. light.
    Light can reset SCN, indirect influence on key processes in body such as hormone secretion & blood circulation.
    Campbell & Murphy woke 15 pps at in the night & shone lights on the back of their knees - produced deviation in S/W. Light is powerful EZ that doesn't necessarily rely on eyes to exert influence.
    Social cues - most babies entrained - 16 weeks, schedules imposed by parents are key influence e.g. bed times. Jet lag - adapt to local eating & sleeping patterns, entrains CR.
  • Evaluate EZ's?
    W - effects of EZs differ in different environments, they do not have the same effect on people who live in places of little summer lightness and little winter darkness. Innuits of Arctic circle have similar sleep patterns all year despite constant darkness. S/W cycle is primarily controlled by EPs which overide environmental light changes.
    W - case study evidence undermines EZs, man blind from birth had abnormal rhythm of 24.9 hours and despite exposure to social cues it couldn't be adjusted. Cues are not effective in resetting B clock - stronger.
    • lacks generalisability
  • Strength of EZs?

    Hood found insomnia in elderly people improved if they were more active and had exposure to natural light. Exogenous changes may just be as likely to cause changes as EPs.
  • What is localisation?
    Theory that different areas of the brain are responsible for specific behaviours, processes or activities.
    Lobe - part of an organ that is separate in some way from rest.
    Frontal Lobe - motor cortex controls voluntary movement in opposite side of the body, damage would result in loss of control over fine movement.
    Parietal - somatosensory areas which processes sensory info from the skin such as touch. Amount of area denotes relative sensitivity e.g. receptors for hands and face occupy over half.
  • Localisation cont?
    • Occipital - visual area receives and process visual info, LH controls RVF and RH controls LVF.
    • Temporal - auditory area that is concerned with the analysis of speech based info.
    • Broca's - frontal lobe in LH, speech production.
    • Wernicke's - temporal lobe of LH, language comprehension.
  • Strengths of localisation?
    S - neurosurgery evidence. Damage to certain areas has been linked to certain disorders e.g. a cingulotomy involves isolating a region known as cingulate gyrus which is thought to be involved in OCD. Dougherty reported on 44 patients with cingulotomy and after 32 weeks, 30% had a successful response and 14% had a partial response. Understanding can enable treatments.
    S - evidence from brain scans - Petersen found WA = listening and BA = reading. Semantic and episodic were on opposite sides of the brain. Scanning is objective method providing clear evidence.
  • Weakness of localisation?
    W - Lashley removed areas of cortex in rats leanring route through maze and found no area was more important than the other. Required every part of the cortex. Higher cognitive processes may be more holistic.
    W - questioned language loc, Dick and Tremblay found only 2% of modern research think language is controlled by BAs and WAs. Advances in technology have found it to be distributed more holistically including areas such as thalamus. Contradicts theory.
  • Evaluate Lateralisation?
    S - research showing connected brains hemispheres process differently. Fink used PET scans to identify active areas during visual processing task. Found RH was associated with global elements whereas LH was associated with finer details. As far as vision goes hemispheric lateralisation is a feature.
    W - Analyser and synthesiser may be wrong. Research suggests people do not have dominant side of the brain. Nielsen - 1000 brain scans from (7-29) certain hemispheres were responsible for certain tasks but there was no dominant hem. Notion of R vs L brain is wrong.
  • What is lateralisation?
    Idea that two halves of the brain are functionally different and so certain mental processes and behaviours and mainly controlled by 1 hemisphere rather than the other. Language is lateralised.
    • LH - analyser
    • RH - synthesiser
    Motor area is cross wired.
    Vision is contralateral and ipsilateral (opposite and same sided). LVF of both eyes goes to RH and RVF of both eyes goes to LH - allows comparison and different perspectives -aids depth perception.
  • What was Sperry's research?
    11 pps who had a corpus callostomy.
    • projected images to either LVF or RVF.
    • LVF - couldn't verbally describe what they saw as info went to RH but they could select the object with left hand.
    • RVF - could verbally describe what they saw.
    Shows that certain functions are lateralised supporting the idea the LH is verbal and RH is silent but emotional.
  • Evaluate split brain research?
    S - Gazzinga showed split brains perform better than connected control on certain tasks. They were faster at identifying odd ones out in array of similar objects. In normal brain the left hemispheres cognitive strategies are watered down by inferior right hemisphere. Suggests that two hemispheres can operate independently.
    W - generalisation issues. hard to establish causal relationships as CG didn't have epilepsy - major CV. Participants all have different med and severities of disorder. Differences may have been due to epilepsy and not split brain.