Human Memory and Learning Exam 3

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41 Terms

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false memories

  • memories that don’t correspond to events as they actually happened

  • experienced as a memory, not a lie/imagined events

  • not all false memories are equal

    • incorrect detail from real events

    • incorporation of second-hand experiences into own memory

    • inability to distinguish between imagined/real events

    • falsely remembering event that didn’t happen

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importance of false memories

  • high stakes situations → false/erroneous memories can cause an innocent person to be jailed or a guilty person to be freed

  • eyewitness testimony often considered gold standard in legal system/very compelling to juror’s perspective

  • about 70% of wrongful convictions overturned by DNA evidence involved in mistaken eyewitness testimony

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subtle wording manipulations

  • loftus/palmer (1974)

    • the degree of impact suggested by the question was linearly related to the speed participants estimated cars were traveling

    • clear implications for way which the police/lawyers question victims, eyewitnesses, those accused

  • mccloskey/zaragoza (1985)

    • participants in misleading group more likely to select misleading item when available; normal performance when it was a new word

  • loftus/zanni (1975)

    • the difference between “a/the” more than doubled the likelihood that the participant will report having seen something they didn't

  • important that researchers/people from legal world choose their words carefully

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misinformation effect

  • result of presenting post-event misinformation about a witnessed event that can obscure, change, degrade memory of original event

  • most robust findings un memory research

  • timing of misinformation is important:

    • significant increase in retrieval of misleading narrative information only when the narrative is closely followed encoding episode

    • demonstrates how powerful misinformation effect is and how important misinformation is delivered shortly after the target event takes place

  • self-generated misinformation (Zaragoza et al., 2001)

    • giving positive feedback to the incorrect information you yourself made led to more false memories

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trace impairment

  • explanation for misinformation effect

    • original memory traced altered by misinformation

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coexistence hypothesis

  • explanation for misinformation effect

    • one memory trace for real event, second for the misinformation event + another new trace for each retrieval of the real event

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imagination inflation

  • merely imagining an event increases the likelihood that you will falsely remember it happening to you

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false memory induction

  • loftus/pickrell (1995) and loftus et al. (1996)

    • false memories for events are induced in adults by repeatedly asking then about childhood events they never experienced

    • participants asked about a time they were lost in the mall as a child (didn’t happen)

      • if a participant couldn’t remember, experimenter pushed them into it

      • 25% of participants reported they remembered event/provided specific details

        • leading questions, imagination, social pressure

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weapon focus

  • focus on a weapon at the expense of other things in the environment/on the person

    • individuals who witness crimes necessarily experience high level of arousal

    • high arousal often combined with/ weapons focus

  • Maass/kohnken (1989)

    • presence of a dangerous object increased false recognition of confederate

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anatomy of a false memory

  • differences in brain activity associated w/ true vs. false memories

  • hippocampus, parahippocampal cortex, medial/lateral prefrontal cortex

  • false memories thought to be a failure to inhibit the misinforming memory

    • hippocampus/parahippocampus → recollection

    • prefrontal cortices → control over thoughts

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metacognition

  • thinking about thinking; knowing what you know and don’t know

    • our knowledge/awareness of our own memory processes, introspective awareness of our own memory abilities

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metamemory

  • our knowledge and awareness of our own cognitive processes

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metamemory: monitoring

  • part of metamemory

    • refers to our ability to reflect on and become aware of what we know/don’t know

    • confidence in our memory

    • knowledge about sources of our memory

    • judgements about whether we’ll be able to recall something from the past

    • judgements about whether we think we’ll remember something in the future

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metamemory: control

  • part of metamemory

    • refers to our ability to regulate our learning/retrieval (update, change, improve, etc.)

    • if output of metamemory minoring at the time of retrieval suggests you could access a memory, then you can control whether/how you engage in the active search

    • if monitoring suggests that you have not learned something well, you can exert control to study longer

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judgements of learning

  • metamemory at encoding

    • judging how well you’re learning it at time of encoding

    • predictions about future memory performance

    • can also be thought of as an important monitoring process that contributes to self-regulated learning

    • while learning, we make implicit judgments of learning that influence how we engage w/ a given item and where we dedicate additional time to encode it

      • cue-target learning and cue-only learning

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determining accuracy

  • dunlosky/nelson (1994)

    • participants encoded cue-target Paris using either imagery (deep) or rote rehearsal (shallow)

      • group 1: JOL immediately after ending

      • group 2: JOL after delay

    • results

      • immediate JOLs are not sensitive to levels of processing and are inaccurate (WM)

      • delayed JOLs are sensitive to levels of processing and accurate (LTM)

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neural basis of jols

  • kao et al. (2005)

    • subsequent memory paradigm w/ fMRI

    • scanned encoding

    • unscanned retrieval

    • JOLs for scenes

    • medial temporal lobe most active for scenes that were later remembered

      • MTL is what they actually remember

    • ventromedial/dorsomedial prefrontal cortex most active for scenes participants predicted they would remember vs. scenes they predicted they would forget

      • VM/DMPFC is what they’re predicting

  • participants who made more accurate JOL predictions showed greater activity in VMPFC than participants who made inaccurate predictions

    • suggests that VMPFC may support JOLs

  • activity in left lateral PFC is sensitive to both memory/JOL accuracy

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amnesia

  • pathological loss of memory, usually due to brain damage/dysfunction

  • often sudden onset (hypoxia, injury, surgery, infection, medications)

  • severe memory impairment (other cognitive function; language, intelligence, attention) negatively spared

  • daily functioning moderately preserved w/ support/external aids

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dementia

  • symptom of a disorder/disease (not a diagnosis on its own)

  • gradual, acquired cognitive decline

  • multi-domain cognitive deficits beyond memory (language, attention, executive function, visuospatial abilities, social cognition)

  • progression loss of independence in everyday activities

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anterograde amnesia

  • inability to form new memories (after damage)

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retrograde amnesia

  • inability to retrieve old memories (before damage)

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amnesic syndrome

  • characterized by anterograde amnesia that makes it difficult and impossible to encode new episodic and semantic memories

    • intact WM

    • intact implicit memory

    • intact procedural memory

    • impaired EM

    • impaired SM

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mtl/declarative memory system

  • all structures in medial temporal lobe (MTL) contribute to declarative memory, so damage to any structure in this system should produce a declarative memory deficit

  • role of hippocampus in EM consolidation is time limited, w/ these memories consolidated to cortex over time

  • system independent of other aspects of cognition including perception, WM, non-declarative memory

  • first aspect of this theory suggests that there is no way to dissociate EM/SM in individual w/ MTL damage

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E/S memory in amnesia

  • developmental amnesia (children w/ damage to MTL)

    • for a long time, it was thought that they would be unable to learn declarative information (E/S) and would therefore have profound developmental delays

    • vargha-khadem et al. (1997)

      • neuroanatomical specificity of brain damage remarkable in that their bilateral hippocampi are compromised but surrounding neocortical structures (perirhinal, entorhinal, parahippocampal) are intact

      • in line w/ academic achievements and general ability to get by in daily life, they have SM abilities that are within normal range

      • profound episodic deficits by intact SM

      • apparent division of labor in MTL, such that hippocampus is not required for all forms of declarative memory

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recollection

  • recognition memory that’s associated w/ retrieval of contextual details from previous encounters (“I remember”)

    • requires recovery of link between retrieval cue and specific past episode

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familiarity

  • recognition memory that is based on stimulus itself, i.e., not retrieval of contextual information (“I know”)

    • feeling that the cue is old but not the link to specific episodic

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recollection vs. familiarity

  • yonelinas et al. (2002)

    • c = controls

    • h+ = MTL damage that affects the hippocampus/MTL cortex

    • h = MTL damage that affects the hippocampus only

    • deficits limited to recollection

  • Eldridge et al. (2000): healthy adult fMRI study

    • hippocampus shows increased activity for “remember” responses but not “know”

    • MTL cortical areas show increased activity for “know” but not “remember”

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recall vs. recognition

  • mayes et al. (2002)

    • patient w/ selective hippocampal damage (Y.R.)

    • deficits on free-recall tests

    • intact performance on recognition-memory tests

    • findings relate to familiarity/recollection

      • recall tasks can be solved only by recollective processing,

      • recognition tasks (i.e. when you have the stimulus right in front of you) can be solved by either familiarity or recollection

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Korsakoff’s syndrome

  • primarily affects thalamic nuclei and mammillary bodies

  • severe amnesia caused by chronic alcoholism (vitamin B1 deficiency)

  • anterograde amnesia

  • retrograde amnesia

  • anosognosia → lack of awareness of memory problems

  • confabulation → believed lies due to source monitoring deficit

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electroconvulsive therapy

  • individuals w/ severe depression may be treated w/ ECT

  • powerful electric shock to the head

  • temporary retrograde amnesia is a side effect

  • loss of episodic and semantic memories from previous 1-2 years

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dementia types

  • alzheimer’s disease

  • vascular dementia

  • frontotemporal dementia (ftd)

  • lewy body dementia

  • mixed dementias

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alzheimer’s disease

  • most common cause of dementia

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vascular dementia

  • related to strokes, small vessel disease; often stepwise decline

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frontotemporal dementia (ftd)

  • early changes in personality, behavior, language

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Lewy body dementia

  • visual hallucinations, Parkinsonism, fluctuating cognition

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mixed dementias

  • combinations of pathology (ex: Alzheimers and vascular)

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amyloid plaque

  • accumulation of proteins in spaces between neurons

  • disrupt communication across neurons

  • trigger immune response that results in inflammation/death of surrounding neurons 

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neurofibrillary tangles

  • Tau proteins contribute to structural integrity of neurons and allow for the intracellular transport of essential compounds

  • in AD, Tau proteins collapse inside neurons and cause cell death

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progression of neuropathology in alzheimer’s

  • brain changes lead behavioral changes, often by several decades

  • makes it difficult to detect early-stage AD (post-mortem or CSF sampling w/ spinal tap)

  • pharmacological interventions have proven ineffective, but typically only administered after behavioral changes

  • early detection likely key to successful intervention

  • early-stage

    • earliest neuropathological changes affect the MTL/posterior cingulate (structure at the bottom of the frontal lobe)

    • thought that these changes begin to emerge as many as 20 years before meeting diagnostic criteria

    • complaints: mild forgetfulness

  • mild to moderate

    • may span 2-10 years

    • neuropathology extends to frontal lobes, posteriorly thorough temporal lobe, into medial parietal areas

    • more pronounced cognitive problems

      • EM, aggression, reasoning, word finding, inhibition, disorientation

  • late-stage

    • life expectancy 1-5 years

    • neuropathology extends throughout entire brain

    • profound and global cognitive declines

      • unable to recognize family

      • unable to care for self/communicate

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AD/identity

  • addis/tippett (2004)

    • 20 individuals w/ AD, 20 age-matched controls

    • autobiographical interview to assess E/S retrieval in autobiographical memory

    • questionnaire used to measure identity

    • results

      • patients w/ AD showed deficits in retrieving S/E details from their personal past

      • problem was most apparent for recent life events: graded retrograde amnesia

      • AD patients showed changes in several aspects of their identity (personal family, social, moral)

        • consistent w// reports from caregivers of patients

      • degree of impairment in recalling episodic details in the autobiographical interview was associated with/ magnitude of identity loss

        • not just about memories, but also sense of identity and the loss of it

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capgras syndrome

  • delusional misidentification: beliefs that a person, place, or thing has changed identity

  • delusional beliefs: unsubstantiated by reality, not shared by other people, resistant to counter-evidence and counterarguments

  • when in relation to well-known people (ex: loved ones) referred to as this

    • belief that a loved one is an imposter often deepens over time and these interactions become increasingly aggressive

  • historically thought to be a psychiatrist illness (ex: schizophrenia) but can be observed in other dementias

  • what usually happens in a typical human:

    • autonomic nervous system contributes to our affective (emotional) state

    • sympathetic branch induces an arousal response

    • cognitively, this arousal is interpreted as a “feeling of familiarity”

  • what happens here:

    • this system is not getting turned on

    • reduced autonomic responses in this

      • skin conductance response not that different between familiar and unfamiliar

      • face processing in brain is decoupled from autonomic system

      • no “feeling of familiarity”