Lecture FOCUS-Learning objectives
Brain Changes
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EEG is a method of measuring brain activity-high temporal low spatial-detects electrical
signals within the brain
CT-high special, very specific about the where, not exactly good with time/temporal.
Computerized topography.
Fmri-high spatial, very specific, it’s a form of florescence medical imaging-low to moderate
temporal magnetic resonance.
DCBA-how a signal travels/composition of a neuron
Signal slows down, myelin becomes decreased-starts to break down signal is blocked.
We see white matter abnormalities, decrease in neurons, synapses, and myelination. Brain
volume loss is also observed-hippocampus.
The formation of new memories and fine muscle movement is affected, higher order
processes. Dopamine levels are seen to decrease, along with neuro-plasticity, the brain is
less fluid=loss of neurons, and the brain starts to compensate for these loss functions
making it less effective in certain areas.
STM
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The capacity to store small amounts of info-30 seconds
Passive storage-millers magic number=7
Memory span requires that we remember the order and the item, and memory digit span
task, you read the numbers and then try to write down as many as you remember and IN
ORDER.
The modal model states that STM is part of a process= of converting simple sensory
memories to LTM/ATKINSON
The phonological loop-is the idea that audio rehearsal is more effective in learning or
remembering something, so articulatory rehearsal/ Baddeley and hitch
The modal model states that there is no manipulation of STM, so there is no way you can
alter how to encode it.
WM
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Manipulation of information/memory for brief intervals. Holding and processing
information
The multicomponent model-states that there are different components to the encoding of
STM
Visuospatial sketchpad- visual-verbal tasks are easier to do, encode better than just verbalverbal. Has components of special tapping, and articulatory rehearsal is repressed/Pearson
Logie.
The central executive controls attention-what you should be doing-additional control is
frontal lobes.
If frontal lobe damage is present-often doing the same task, behavioral issues, attention
problems etc.
Chess players, random generation task was horrible, impaired performance/Robins et Al
Healthy changes in STM=not that much, little bit in lab tests, but in daily life not that significant
results. WM= seen a decline, but more significant than STM.
Why does this happen?
Interference
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Manipulation results in a large amount of interference, not great at multitasking, but as you
get older, much worse as they can’t ignore the interference.
CORSI TASK tests visual/spatial STM
Episodic and Semantic Memory
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Both part of LTM-part of the explicit-can explain declarative memory.
Episodic- allows to look back at certain events that happened, at a point in time
Semantic-a general knowledge, it is your world knowledge, facts. May arise through
consolidation of EM
Eating breakfast=episodic/what you eat/people you eat with=semantic
Dissociations associated with these two memories-retrograde and anterograde amnesia.
Retrograde=trouble forming either episodic or semantic memories=ONLY ONE
Anterograde=have trouble remembering/forming new episodic and semantic memories so
impairments in BOTH.
Source memory=is remembering the source of who/what or where the memory happenedseen to decline with age
Rivermead vs RAVLT- one is real life, one is clinical/ both test episodic memory/semantic,
subjective more is RAVLT, rivermead is more judgement. Both present interference.
What/when/where memory task-refer to article
Decline in episodic memory
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Capacity, brain is not fluid
Processing capacity affected, slower in older adults
Interference, attention
FREE RECALL is mostly affected, they need more environmental cues to remember
Associative deficit disorder-cannot make links between the info, have trouble contentcontext binding.
Overman and Becker did a test-showed a face matched with a word, older adults had no
problem remembering the face, had no context though=CONTENT/CONTEXT BINDING
issues.
Misplaced something, don’t know where, remember someone, don’t know how/examples
Remembering is recalling original learning and knowing is just familiarity.
Deficits small in STM, WM does decline, Episodic memory decline. But semantic, possibly
increase and well maintained.
Semantic Memory
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Cohort effects, exposed to more already since they are older.
Bias-cultural differences, different way to say things location matters
Variations in naming
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Uncertain prior knowledge-researcher does not know of prior knowledge of the older
adult so how can you know if they know it?
That is all maintaining old memories, how do we form new? This process is still stable.
Rahhal et Al-shown two images, one is bad and one good, content is okay, source is a
problem as stated before.
Autobiographical memory
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Memory related to self related info-across lifespan
Hard to test-self diary
Memory probe method-task is to write something down randomly by a prompt-write
something down memory related to it.
Positivity bias- we tend to remember more positive things than negative.
Reminiscence bump-participants over 40, tend to remember more stuff from their late
teens/20’s
Possibly remember the peak in their life
Difference between copy=what you remember and reconstructed-learned after the fact.
There are different perspectives in memory-observer and field.
Observer-observing the event for yourself/outsider
Field=first hand and less emotional and less self aware
Flashbulb memories
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Detailed and highly vivid memories of a dramatic experience
HIGH DETAIL HIGH VIVID
Flashbulb memories change lives, they are like 911/Talarico and Rubin, conducted a survey
to follow up for consistency,
But the quality of memories, is less specific and takes field perspective.
Positivity Bias in Aging
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Older people tend to view memories more positively-most semantic self images are seen as
more positive well-being.
Older adults have over general memories=frontal lobe impairment, the details are lost, lack
of rehearsal.
Affect is something that occurs in response to a stimulus or event, how you feel after it.
Valence is positive and negative effects/arousal=physiological activity.
Mood can last for months-feeling is an subjective experience, an emotion
What changes in autobiographical memory?
Decreased self-independence, function, decline in self-representation, since you don’t know who
you are, cannot remember your life.
Music=good for recall, takes you back
Prospective memory
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Remembering to carry out some intended action-in the future memory-time based, event
based.
Henry et Al-meta-analysis-Ret M- aging paradox
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Processing demands-martin and Schuman- varied task demands, older adults low with high
complexity-they outperform in naturalistic tasks.
Pro M hard to study, above study was conducted on PRO M, aging paradox, means that
older adults need more environmental cues, interference shows that it affected older adults
more.
Aging PARADOX
Eyewitness memory
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Leading questions, loftus and palmer- leading the witness
Retroactive interference-prevents learning of new info
Proactive interference-prevents recall of old memories.
Aging and the misinformation effect
Metacognition
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Is thinking about thinking
Monitoring and second is control strategies
Older adults show great loss in metacognition-prefrontal cortex
This affects planning, reasoning, and thinking.
Palmer et Al, metacognition efficiency
Selective attention-focus on a task orientated relevant info. This requires FILTERING
Bottom up attention is stimulus driven
Top down is task orientated and goal focused.
Bottom up is seen to decline, but the other is maintained.
There is general slowing of processing vs attention
Divided attention
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When there are 2 or more concurrent tasks
THIS IS MULTITASKING
Previous experience helps, if the task is related to something known prior, there is less of a
decline in older adults-multitasking is maintained.
Attention is a limited resource, as older adults have a hard time doing things fast, speed is
slow, and distractions are more common. Show decline as tasks get harder.
Metacognition AGAIN
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Ability to evaluate our critical thinking, and reflect on it.
Memory efficiency- is the ability to selectively encode important info, HIGH importance
info
[POST MIDTERM MATERIAL]
DISORDERS OF MEMORY
Dementia
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progressive loss
difficulty in everyday life
dementia- many areas affected
speech, spatial, visual, and verbal, attention, and memory
balance, walking, eating/swallowing, restlessness, forgetfulness, wandering. Changes in
sleep/eat/bathroom
Primary and secondary aging
Normal aging
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not remembering the details of a conversation, a year ago, not being able to remember the
name of an acquaintance, forgetting stuff occasionally. Self worried, and sometimes have a
problem finding words.
Dementia
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not remembering a conversation, but you cannot remember a family members name,
forgetting things a lot commonly, finding substitutions for words, pausing a lot, relatives are
worried.
Subtypes of Dementia
Mild cognitive impairment
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cognitive impairment, noticeable but doesn’t interfere with life and independence. Only 1020 percent of the 65 percent of dementias.
There are two subtypes, amnestic primarily affects memory and nonamnestic MCI- affects
thinking, ability to make decisions and judgements.
Can progress to other dementias
Signs to watch for: Memory, forgetting, attention-losing your train of thought, executive
function-lack of following simple directions, trouble finding your way around familiar
environments, bill paying tasks, overwhelmed in making simple decisions.
Side effects also found with this are anxiety, depression, apathy, and irritability.
Brain changes NONE
Genetic disposition-AOEP4 not a guarantee
Diagnosing MCI
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Medication and supplement interactions, neurological and memory tests.
Assessment of daily functions
How to treat it?
Drugs used for Alzheimer’, exercise and modification of environment.
Alzheimer’s disease
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Early onset Alzheimer’s
Contributed to stress
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Familial-genetic and passed down
3 divisions: cortical subcortical and vascular
Very strong family history
Less than 5 percent all cases
Sporadic
non-genetic cause
a lot of people don’t have AOEP4 so… it can decrease/possibly increase risk not definite.
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50-70 percent of all dementias
Progressive
Early clinical symptoms-forgetfulness, difficulty remembering, concentrating, following new
things, getting lost, communication difficulties, mood shifts depression
Middle stage clinical symptoms-wandering, pacing, restfulness, memory problems are more
pronounced. Repetitive behavior, difficulty making decisions, changes in behavior, appetite,
and mood. Delusions and hallucinations.
Late clinical symptoms-severe cognitive impairment, loss of recognizable speech, impaired
swallowing, loss of independence eating and bathroom.
What stage is what? How do you diagnose with what stage?
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Brain changes
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Plaques-clusters of protein fragments-build up between cells
Tangles-proteins aren’t properly regulated which are necessary for axon growth. This forms
tangles within neurons leads to cell death.
There are a lot of associated risk factors
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Modifiable
Smoking
High blood pressure
Diabetes
High cholesterol
Alcohol
Head injuries
Depression
Low formal education
Non-modifiable
Age-risk doubles after 65
Family history-genetics
Treatments
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Sun downing is a phenomenon-increased behavioral problem in the evening/ could be due
to upset internal clock, exhaustion, and disorientation.
Medications for the early stages:
Cholinesterase inhibitors- may prevent symptoms for worsening for 6-12 months, may
reduce behavioral symptoms. Early medications are helpful to less than half to the people
taking them
Medications middle to late stages:
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Allows daily function-memantine
Regulates glutamate
Sometimes other medications cause side effects, and discomfort. Treatment for behavioural
symptoms can be relived or reduced with antidepressants and antipsychotics.
Other weird natural promoted medicines do NOT DO ANYTHING, use cautiously are not
medically verified. Or tested.
Future medications- beta amyloid blocking- tau protein= prevents plaques- keeps it from tangling
Non-drug interventions
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3 models that explain behavioural symptoms
Non-drug is for behavioral symptoms
Identify the source ex: pain
Catch problems early- Unmet needs model
Problematic behaviors are due to unmet needs.
Environmental vulnerability, reducing and removing bothersome stimuli may help.
Dementia friendly communities- can wander freely, staff are caregivers it is a safe place to
feel inclusive and not lost and or confused.
The three types/other listed are
 Sensory intervention
 Social contact
 Behavioral therapy
 Activities
 Family/medical intervention-Marriott et Al to reduce distress, make it easier for
caregiver, educate on the problem. These guys improved behavior for the carers,
overall better general health and fewer symptoms.
Ethical Issues in Dementia
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driving? What age can they not drive anymore?
Electronic tracking? Ethical? Should it be allowed?
Lying-soft lies/ they tend to choose the last one
Assisted, late stages in their life feeding? Artificial feeding.
Advanced care planning about now and future care-who will make decisions? Spouse, kin
children?
1. Alzheimer’s is cortical dementia- along with frontotemporal- bvFTD and PPA and FTD
movement disorders.
2. Vascular Dementia is another section.
3. Subcortical is Parkinson’s and Huntington’s.
Vascular dementia
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Second most common cause of dementia 20 percent-30
Caused by brain injuries/stroke
Symptoms based on where the injury occurs.
Brain changes
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Imaging detects blood vessel problems
Symptoms
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Post stroke
Trouble speaking/understanding speech
Confusion and disorientation
Vision loss
Very different from Alzheimer’s disease, where the symptoms even early onset includes mostly
memory problems, and cognition. Trouble remembering people faces, and what happened.
Wandering, and repetition, lots of problems with cognition not with the brain damage and stroke
like symptoms post after.
These symptoms in Vascular dementia result in
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Impaired judgment
Decline in attention
Inability to plan and complete tasks
Develop plans
Unsteady walking, restlessness
MEMORY LOSS MAY OR MAY NOT BE PRESENT. NOT LIKE ALZHIMERS
Risk factors
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Still include smoking, weight gain, blood pressure, heart disease, kind of like risk factors of
dementia at large.
Diagnosing VD
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Medical history of stroke, heart disease and high blood pressure.
Neurocognitive tasks-imaging to see blood vessels
Distinguishing between VD and AD
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AD is slowly progressive, VD can be sudden onset or progress in stages
Memory loss is more in AD early
History of heart disease more prominent in VD
Executive function impaired more and earlier in VD than compared to AD
Damage to blood vessels compared to normal hippocampal images in AD
Frontotemporal lobe Dementia
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Range of different disorders
Speech and behavior affected the most
Subtypes of FTD
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Behavioral variant frontotemporal dementia-bvFTD
Changes in personality and behavior \may be mistaken for depression
Symptoms include-binge eating, no sympathy, impaired judgement, repetitive or
compulsive behavior.
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Primary progressive aphasia-PPA
AFFECTS language skills initially
Semantic dementia- cannot find words
Progressive non-fluent aphasia- having trouble speaking fluently
Behavior affected with progression
FTD movement disorders- can look like Parkinson’s-involuntary muscle movements
affected, no control
Falls in early stages, symmetry of motor signs, rapid progression but lack of tremors
Risk Factors
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Familial- about 20-50 percent have previous family history
Sporadic- about 50-80 percent are the first
Diagnosing FTD
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Can often look like and misdiagnosed as psychotic disorders-at least in early stages
Visible changes seen in MRI
Distinguishing between FTD and AD
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Memory loss is seen in AD
FTD is diagnosed earlier in life
Early behavior changes more prominent in FTD
Spatial orientation is declined in AD, but problems with speech more common in FTD
FTD increase appetite and AD decreases it.
Focusing on SUBCORTICAL dementias
Parkinson’s disease
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Affects motor control, and movement symptoms first noticed
Only 2>65 percent of all dementias
Affects L-DOPA inhibition-dopamine receptors blocked and such
Speech impairments, mumbled speech, hallucinations, and delusions
Lewy body dementia- cognitive symptoms seen first
Parkinson’s-movement symptoms seen first
DLB
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Third most common form of dementia