Explain the dual model of memory
info -> STM (rehersal) -> LTM (forgetting) or (consolidation)
What lobe controls STM?
forntal lobe
How many items can you keep stored in your short term memory?
7 (+/-) 2 for 30 seconds
Describe patient HM (Henry Molaison)
Had siezures so they removed amygdala, hippocampus, and medial temporal lobe
Had anterograde amnesia
Had no declarative memory
His procedural memory was okay (improved on mirror drawing task)
His STM and LTM (old) were intact
showed recency effect
Anterograde Amnesia
cannot remember events that occur after brain damage
Retrograde Amnesia
cannot remember events that occur before brain damage
Explain Match to sample test
Patient HM could recognize the difference between the CBT but could not with the ovals
Explain mirror drawing task
copy something by looking through a mirror
HM made less errors each day but doesnt remember doing it
explain incomplete picture test
little dots appear on the screen and get more and more and you have to say what the dots make up
HM didnt remember doing it but did better each time
Explain pursuit rotar test
Put the thing on the record player
HM didnt remember doing it but did better each time
Explain declarative memory and what part of the brain
things you know that you can tell others (i know its 2017)
Episodic- remember your 16th bday
semantic- know the capital of france
hippocampus
Explain procedural memory and what part of the brain
things you know that you can show by doing
(mirror drawing)
skill learning- ride a bike
priming- more likely to use a word you heard recently
conditioning- salivating when you see food
basal ganglia/ cerebellum
basic memory problems associated with Korsakoff’s disease and the part of the brain affected by the disease
Alcohol is not the complete cause, it’s the fact that they are not eating well, causing thiamine deficiency, which causes damage and degeneration to the diencephalon, causing anterograde and retrograde amnesia
What is a confabulation?
fill in memory gaps with inaccurate memories (I drove here, but really walked and don’t remember
When a patient has a head injury and begins to recover, what changes do you see in their retrograde memory impairment?
Their amnesia decreases in the amount of time that they forget (regain memory)
What is the serial position curve?
tend to remember things at the beginning and end of a list, not middle
asymptote- words in the middle
What are the primacy and recency effects?
primacy effect- people remember things at the beginning of a list
recency effect- tend to remember the last part of the list
What is the difference between semantic and episodic memory?
Semantic- facts about the world
EX: know the capital of France
Episodic- remembering specific memories from your life
EX: remember your 16th birthday
Both are hippocampus dependent (declarative)
Where do the plaques and tangle first appear? Which lobe of the brain is not as affected by AD? Which proteins are found in plaques and tangles?
Plaques and tangles are first appear in Entorhinal cortex –> hippocampus –> amygdala –> prefrontal cortex –> Inferior temporal cortex –> posterior parietal cortex
Occipital lobe is not affected
Beta amyloid proteins are in plaques, tau are found in tangles
basics symptoms of AD
Memory loss (amnesia both learning and recall) Disorientation (time and space) Personality changes Language problems (aphasia) Inability to carry out motor activities despite intact motor function (apraxia) the problem is executing it when youre asked Inability to recognize objects or faces (agnosia) Impaired executive functioning (problem solving, planning) Mood disturbances (depression/ anxiety)
Explain familial AD
5% of all cases
Chr 21- APP, Beta amyloid, Plaques
Chr 14- Presenilin 1: proteins, 50% chance of inheritance
Chr 1 – Presenilin 2: proteins, 50% chance of inheritance
Explain sporatic AD
95% of all cases
Chr 19- ApoE bind to beta-amyloid, a component of neuritic plaques and tangles
*ApoE is located on Chr 19
what are the 3 isoforms of ApoE
E4- highest risk, 15% inheritance, increases risk of AD (NOT a causal factor)
E3- 77% inheritance, does not elevate risk of AD
E2- 8% inheritance, does not elevate risk of AD
* 1 allele of E4 = 3 times increased risk for AD
*2 alleles of E4 = 8-12 times increased risk for AD
What changes in the brains of AD patients can you see on a MRI? Which changes cannot be seen on a MRI?
MRI can see bigger ventricles, wider sulci and grooves due to atrophy, and smaller gyri
MRI cannot see plaques and tangles
Which neurotransmitter has been shown to be particularly decreased in patients with AD?
Acetylcholine (AcH)
What changes do we see in the brains of healthy older adults who do not show signs of dementia?
Decreased connection in the neural pathways
a little bit of cell loss (not a significant amount)
Overall volume of brain gets smaller
memory impairment for certain things
What is mild cognitive impairment?
A risk state for AD
The potential impairment can be assessed through a report (usually from caregiver)
Not globally impaired like AD
Normal over all thinking and reasoning
Perform normal daily activities
* someone with MCI are more likely to develop AD
What are the symptoms of normal pressure hydrocephalus and how is this condition diagnosed?
Symptoms- Gait abnormality, dementia like symptoms, and incontinence
Diagnosis- MRI looking for enlarged ventricles
* case study #2
explain source memory
memory for where you learned something
explain item memory
memory of the fact
explain prospective memory
remembering to remember(at 2 pm do this)
explain emotional memory
putting emotion on to a memory (16th bday)
Can neuropsychological testing clearly determine the difference between AD and vascular dementia?
No, a neurological test alone cannot determine the difference between AD and vascular dementia. Profiles of vascular dementia and AD patients are really similar on a neurological test, so an MRI is necessary to rule in vascular dementia and rule out AD (infarcts)
What are some differences between the symptoms of AD and the Lewy body variant (LBV) of AD? What neuropathologies would you expect to see in the brains of patients with LBV?
LBV patients display less memory impairment than AD and 2 or more of the following:
Extrapyramidal symptoms (bradykinesia- slowness in motor movement, masked face, rigidity)
Visual Hallucinations (House and TV misidentitfication) Fluctuations in attention and concentration
More rapid cognitive decline than AD
LBV have similar pathology to AD along with Lewy Bodies, however, have a relative absence of tangles (a hallmark of AD)
What are the basic symptoms of Pick’s disease (frontotemporal dementia)?
Executive function deficit, disturbance in personality (behavioral control) and social awareness (socially inappropriate behavior)
Less impairment on language and memory than AD
Which cortical dementias can be differentiated by autopsy?
All can be differentiated by an autopsy, look for:
AD: plaques and tangles
FTD: pick bodies in frontal and temporal lobes
Vascular dementia- presence of infarcts on the cortex
LBV- Lewy-body formation in the brain stem and occipital lobe
Which cortical dementias can be differentiated using MRI and which cannot be differentiated?
MRI can differentiate FTD and Vascular dementia (you look for infarcts)
LBV cannot be differentiated by an MRI
AD cannot be differentiated by an MRI (cant see plaques and tangles)
What is the most common behavioral disorder affecting children?
ADHD most common- 2-9.5% of school age children diagnosed
Are there gender differences in the diagnosis of the developmental disorders (ADHD and autism) discussed in class?
ADHD- boys are more likely to be diagnosed, 1:2 ratio, girls 1:10 ratio
Autism- boys are 3-4 times more likely to be diagnosed than girls
1 in 42 boys are diagnosed, 1 in 189 girls are diagnosed
Review the effects of ADHD on IQ?
IQ tests are biased against ADHD
Usually score lower on verbal IQ
Overall IQ usually slightly lower, but falls under the normal curve
Review the effects of autism on IQ?
IQs at or below 70, but it is possible that it is because of the design of the IQ test
Do best on non-interactive tasks, such as puzzles, math, visual spatial skills
Some have exceptional skills/abilities
How do the symptoms of ADHD change in adulthood?
60% of ADHD children carry ADHD symptoms into adulthood
inattentiveness tends to persist into adulthood
40% of ADHD diagnosed children grow out of it
What are some of the problems with diagnosing ADHD?
It is overdiagnosed
Hard to determine whether it is something that is age related (active 7 year old boy) or if it is ADHD
You cant look at the brain and diagnose
Some doctors just give the child adderall to see if it helps
What are the triad primary symptoms of autism? Think about how some of these symptoms may manifest in behavior
social interaction, communication, and repetitive behaviors
child can manifest these symptoms by flapping their hands, head banging, echolalia (repetition of others), inability to recognize others perspectives and fixation
When are symptoms of autism first observed, when is a diagnosis typically made, and how do the symptoms change across the lifespan?
Symptoms can be observed in early infancy, as early as 6 months but normally by age 3. Symptoms across the lifespan are variable (it’s a spectrum), but not curable
What is theory of mind and how does it relate to autism?
Theory of mind- being able to put yourself in someone else’s shoes; understanding that each person has his own thoughts, beliefs, knowledge, desires, ect
Individuals with autisms have difficulties with understanding/ seeing the world from another individuals perspective or comprehending that other people may see the world differently
Explain the Sally- Anne test
anne takes sally’s marble when sally is away and puts it in her box
An autistic person would say sally would look for the marble in anne’s box but should have said sally’s basket
What are some hypothetical causes of autism
90% are genetics, 10% might be a mix of things
prenatal- identical twins- 60%
postnatal- theory of “refrigerator mother” and vaccines (thimerosal debate) were proven false
parental age (40s)
birth proximity (a child within one year)
what are they causes of vascular dementia
strokes, endocaritis, amyloid angiopathy
Describe REM Sleep Behavioral Disorder
95% have lewy bodies
may precede dementia by 6 months to 50 yrs
may be related to fluctuation in attention
risk factors for AD
age, positive family history, down syndrome, mental inactivity, head injury, low education, mutation on presenilin 1 and 2
ApoE gene
most common drug treatment for AD
Aricept and Namenda
Whata re the pathological chanfes between LBV and AD
relative absense of tangles
Etiology and development course of ADHD
genetic- majority of cases
enviornmental- prenatal- exposed to alc, stimulants, nicotine
postnatal- food additives
dopamines role in ADHD
34% of cases linked to DA-4 receptor
treatment for ADHD
adderall and ritalin
behavior intervention
treatment for autism
behavioral interventions
- teaching language
- modifying abnormal behaviors
- discrete trial teaching