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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
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
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
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
trace impairment
explanation for misinformation effect
original memory traced altered by misinformation
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
imagination inflation
merely imagining an event increases the likelihood that you will falsely remember it happening to you
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
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
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
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
metamemory
our knowledge and awareness of our own cognitive processes
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
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
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
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)
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
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
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
anterograde amnesia
inability to form new memories (after damage)
retrograde amnesia
inability to retrieve old memories (before damage)
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
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
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
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
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
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”
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
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
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
dementia types
alzheimer’s disease
vascular dementia
frontotemporal dementia (ftd)
lewy body dementia
mixed dementias
alzheimer’s disease
most common cause of dementia
vascular dementia
related to strokes, small vessel disease; often stepwise decline
frontotemporal dementia (ftd)
early changes in personality, behavior, language
Lewy body dementia
visual hallucinations, Parkinsonism, fluctuating cognition
mixed dementias
combinations of pathology (ex: Alzheimers and vascular)
amyloid plaque
accumulation of proteins in spaces between neurons
disrupt communication across neurons
trigger immune response that results in inflammation/death of surrounding neurons
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
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
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
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”