Dementias And Memory

Front 1

What is the primary memory deficit in Alzheimer dementia?

Back 1

Anterograde amnesia

Front 2

Name the three subtypes of MCI.

Back 2

Amnestic,

Nonamnestic,

Multiple domain

Front 3

What is the isolated impairment usually observed in amnestic MCI?

Back 3

Verbal memory impairment.

Front 4

What percentage of MCI cases convert to dementia every year?

Back 4

10 to 14%

Front 5

What are the earliest pathological biomarkers for preclinical Alzheimer disease?

Back 5

1. PET amyloid imaging

2. Accumulation of a-beta-42 in the cerebrospinal fluid.

3. Hippocampal volume loss.

Front 6

What are the neurofibrillary tangles in Alzheimer disease made of?

Back 6

Tau protein abnormalities

Front 7

What causes the lesions of Alzheimer disease?

Back 7

Amyloid plaques that are diffuse

Neurofibrillary tangles made out of tau abnormalities.

Front 8

What neurotransmitters/chemicals does the brain produce less of, and become less sensitive to, in Alzheimer disease?

Back 8

1. Choline acetyltransferase

2. Norepinephrine

3. Serotonin

C.N.S.

Front 9

In what direction (i.e., from what lobe to what lobe) does Alzheimer disease progress?

Back 9

Temporal to frontal spread that eventually involves multiple brain systems.

Front 10

What are the earliest brain structures implicated in Alzheimer disease?

Back 10

The hippocampus and Enterothinal cortex

Front 11

What structures are relatively unaffected until late in the disease process of Alzheimer's disease?

Back 11

Subcortical structures, Primary motor, visual, auditory, and somatosensory cortices.

Front 12

What is the single strongest risk factor for Alzheimer disease?

Back 12

Age

Front 13

What genetic risk factor is predictive of late onset Alzheimer's disease?

Back 13

ApoE4

Front 14

Which chromosome that is also involved in Down syndrome is associated with Alzheimer's disease?

Back 14

Chromosome 21.

Which is why it is hypothesized that individuals with down syndrome typically develop plaques consistent with AD

Front 15

What are some general medical risk factors for Alzheimer disease?

Back 15

1. Poorly controlled diabetes (diabetes causes everything)

2. Moderate to severe TBI.

3. History of chronic major depression

4. Small vessel cerebrovascular disease

5. Low cognitive reserve.

Front 16

What percentage of people over 65 have AD?

Back 16

5%

Or, 5.4 million

Front 17

At what rate does the prevalence of AD develop after age 65?

Back 17

It doubles every 4-5 years.

Front 18

What is the average age of diagnosis for Alzheimer disease?

Back 18

75, with most being diagnosed in the 70s

Front 19

Are minorities more or less likely to get Alzheimer's disease?

Back 19

More likely.

African-Americans are twice as likely and Latin Americans are about 1.5 times more likely

Front 20

What percentage of AD patients have the family variant of the disease?

Back 20

5%

Front 21

How many people over age 85 meet criteria for AD?

Back 21

25-50%

Front 22

What percentage of all dementia patients have AD?

Back 22

70%

Front 23

What is the length of illness in AD?

Back 23

5-15 years.

Front 24

Does AD progress faster or slower with older age?

Back 24

Slower.

(It's the opposite of PD, where patients who are younger have a slower progression).

Front 25

What is the difference between early AD and pseudodementia?

Back 25

AD patients downplay their deficits; Pseudodementia patients complain a lot about their problems.

AD patients have less fluctuations in their battery.

Front 26

What behavioral challenges can be seen in early AD?

Back 26

Social withdrawal

Loss of interest

Trouble with sequencing and problem solving

(usually at work or home environment)

Front 27

How accurate is clinical diagnosis of AD based on a comprehensive evaluation?

Back 27

85 to 90%

Front 28

What does a comprehensive evaluation of AD include?

Back 28

MRI

Blood work

Neurologic Exam

Neuropsychological Exam

Front 29

What are 4 common sensory and motor declines in normal aging?

Back 29

Hearing loss

Decreased visual acuity, scanning, and adaptation to the dark

Reduced odor sensitivity

Decreased motor speed, coordination, and strength

Front 30

How do sleep patterns change in normal aging?

Back 30

Sleep is more fragmented with less at night and naps during the day

Sleep earlier and get up earlier

Front 31

Is reduced brain volume normal with aging?

Back 31

Yes.

Front 32

What cognitive abilities are resistant to aging?

Back 32

1. Vocabulary and verbal skills

2. Simple attention and concentration

3. Basic math

4. Recognition memory and remembering the gist of information

5. Remote memory

Front 33

What cognitive abilities decline with aging?

Back 33

1. Sustained attention

2. Divided attention

3. Slower learning and acquisition

4. Decreased cognitive flexibility

Front 34

What percentage of patients in their 70s are diagnosed with MCI? 80s?

Back 34

10%

25%

Front 35

What are the cognitive signs of Stage 1 AD?

Back 35

1. Worsening immediate memory and learning

2. Dysnomia

3. Anosodiaphoria (indifference to your condition)

Front 36

What are the behavioral signs of Stage 1AD?

Back 36

1. Shy away from new experiences

2. Favor familiar routines

3. Problems functioning in unfamiliar situations, but ok in familiar places.

4. Depression or anxiety if aware of problems.

Front 37

What are the cognitive signs of Stage 2 AD?

Back 37

1. Poor recent (episodic) memory and rapid forgetting with good remote memory.

2. Slower speech patterns

3. Word-finding deficits

4. Poor sustained attention

5. Losing train of thought

6. Visuospatial deficits possible in topographical disorientation and poor constructional ability.

7. Confusion with complex tasks, like bill pay.

Front 38

What are the behavioral signs of Stage 2 AD?

Back 38

1. Guardedness or suspiciousness

2. Irritation

3. Agitation from forgetfulness

4. Worsening functioning in all but the most familiar environments.

5. Possible behavioral problems.

Front 39

What are the imaging findings in Stage 2 AD?

Back 39

MRI = Sulcal Enlargement and Ventricular Dilation

SPECT/PET = Bilateral parietal hypoperfusion/meatabolism

EEG = Diffuse slowing of background rhythm

Front 40

What are the cognitive findings in Stage 3 AD?

Back 40

Profound global cognitive impairment

Global Aphasia and possible Mutism

Front 41

What are the possible behavioral findings in Stage 3 AD?

Back 41

1. Nighttime wandering

2. Hallucinations

3. Sleep disturbance

Front 42

What are the imaging findings in Stage 3 AD?

Back 42

MRI and CT show progressive atrophy

EEG shows diffuse global slowing

Front 43

What are the cognitive symptoms of Stage 4 and 5 AD?

Back 43

1. Disorientation

2. Unable to follow basic routines

3. Noncommunicative

Front 44

What are the behavioral symptoms of Stage 4 and 5 AD?

Back 44

Increasingly sedentary to the point of becoming bedridden.

May become incontinent

Front 45

How can the course of VaD differ from AD?

Back 45

VaD can have:

1. Rapid onset

2. Stepwise progression

3. Onset within 3 months of CVA.

Front 46

How do semantic and behavioral FTD present differently than AD?

Back 46

Behavioral Variant FTD presents as pronounced behavioral problems

Semantic variant FTD presents as primary declines in semantic knowledge and language.

Front 47

What is the most sensitive and specific method of detecting MCI and early AD?

Back 47

Neuropsychological Testing

Front 48

What is the classic triad of symptoms in early AD on neuropsychological testing?

Back 48

1. Declarative/Episodic Memory Impairment

2. Confrontation Naming and Semantic Fluency

3. Cognitive Felxibility (i.e., Trails B)

Front 49

What are the Intelligence findings in AD?

Back 49

Normal on crystallized knowledge (i.e., vocabulary, sight reading) early on.

Front 50

How are motor functions different in PD vs. AD?

Back 50

Rigidity is early in PD but late in AD

PD has prominent tremor much of the time.

Front 51

Characterize the memory deficits in AD.

Back 51

Explicit worse than implicit

Poor encoding, storage, and retrieval

Many intrusion errors

Recency effect

Anterograde far worse than retrograde

Front 52

What medications are used in AD, and when?

Back 52

Acetylcholinesterase inhibitors are used early on (e.g., Aricept)

NMDA receptor agonists are used for moderate disease (e.g., memantine)

Front 53

Name the tauopathies.

Back 53

1. Pick disease

2. PSP

3. Corticobasal degeneration

4. AD

Front 54

Why does Chromosome 21 matter in AD?

Back 54

It is associated with amyloid plaques

Front 55

Which chromosome is ApoE4 allele on?

Back 55

19

Front 56

What is the risk of AD if you do/don't have ApoE4?

Back 56

29% vs. 9% for late onset AD

Front 57

What structures show the earliest degeneration in AD?

Back 57

Temporal lobes

Upper Brainstem Nuclei (i.e., locus ceruleus & nucleus basilis of Meynert).

Front 58

What does the locus ceruleus produce?

Back 58

Norepinephrine, the loss of which is telling of AD

Front 59

What does the nucleus basilis of Meynert produce?

Back 59

Acetylcholine

Front 60

Where are neurofibrillary tangles found?

Back 60

1. Hippocampus

2. Amygdala

3. Nucleus basilis of Meynert

4. Raphe Nucleus

5. Locus ceruleus in anterior pons

Front 61

Alzheimer disease has been called a disease of the ________ cortices.

Back 61

Association corticies

Not primary or heteromodal cortex

Front 62

Describe Binswanger's Disease.

Back 62

Cognitive impairments co-occuring with:

1. Periventricular white matter loss

2. Lacunar infarcts in the subcortical structures (e.g., thalamus and basal ganglia).

3. BUT! sparing of subcortical U fibers

Front 63

What's wrong with Binswanger's as a diagnosis?

Back 63

Old people just have lots of white matter changes normally, so it may not be a valid diagnosis.

Front 64

Define Leukoariosis.

Back 64

Nonspecific loss of density in subcortical white matter.

A.K.A. White Matter Hyperintensities

Front 65

If someone has stepwise decline in cognitive functioning, with temporally related cerebral infarctions, then what is the diagnosis?

Back 65

Multi-infarct dementia

Front 66

Name 5 common strategic infarcts.

Back 66

1. Left Angular Gyrus- Gerstmann Syndrome

2. Caudate, globus pallidus, and thalamus- disrupted prefrontal-subcortical circuits and motor deficits.

3. Thalaums - Leads to a fresh hell of cognitive problems depending on which thalamic nuclei are affected

4. Single branch of the PCA- Memory impairments if the portions supplying mesial temporal lobe are hit.

5. Single branch of the ACA

Front 67

What are the most common cognitive deficits in VaD?

Back 67

1. Slowed processing speed (e.g., Trails A, Symbol Search) from white matter disruption

2. Letter fluency

3. Cognitive aspects of executive dysfunction (e.g., WCST, Trails B) due to disrupted fronto-subcortical loops in the white matter.

4. Sensorimotor, gait, and urinary incontinence

5. Poor attention

Front 68

What is small vessel disease?

Back 68

Microvascular infarcts and ischemia that may occur secondary to atherosclerosis (i.e., plaque in the blood vessel) or lipohyalinosis (i.e., thickening vessel wall shrinking diameter).

Front 69

What areas are most vulnerable to small vessel disease?

Back 69

Subcortical white matter

Lenticulostriate arteries

Thalamic arteries off the PCA

Front 70

What percentage of dementia cases have VaD pathology?

Back 70

18%

Third behind AD (70%) and Lewy Body Dementia (26%)

Front 71

What percentage of VaD cases are actually mixed dementia?

Back 71

77%

Front 72

What percentage of individuals labeled as "Cognitively Impaired Not Demented" VaD cases progress to dementia within 5 years?

Back 72

About half

Front 73

What are the three top cognitive deficits in VaD?

Back 73

1. Poor attention

2. Executive dysfunction

3. Slowed processing speed

Front 74

What is cerebral amyloid angiopathy?

Back 74

Pathophysiologic process involving amyloid deposition in blood vessels that result in repeated hemorrhages and ischemia. Usually starts after age 55.

Front 75

What are argyrophilic globular inclusions called?

Back 75

Pick bodies

Argyrophillic means having an affinity for silver

Front 76

What are swollen achromatic neurons called?

Back 76

Pick cells.

Front 77

What are the histological findings of bvFTD?

Back 77

Pick cells, Pick bodies, and neurofibillary tau protein that is STRAIGHT NOT TANGLED (like in Alzheimer disease).

There are NOT beta amyloid plaques or neurofibillary tangles.

Front 78

Where are Pick bodies and Pick cells commonly found in the brain?

Back 78

1. Amygdala

2. Dentate gyrus

3. Pyramidal Cells of CA 1 in hippocampus

4. Hypothalamus

5. Putamen

6. Globus Pallidus

7. Locus ceruleus

8. Mossy fibers of the cerebellum

9. FRONTOTEMPROAL NEOCORTEX

Front 79

How does bvFTD differentially affect the cerebral hemispheres?

Back 79

50% have greater left hemisphere involvement

20% have greater right hemisphere involvement

Front 80

What are MRI findings in bvFTD?

Back 80

Atrophy in the:

1. Orbitofrontal cortex

2. Mesial frontal cortex

3. Anterior insula

Front 81

What do SPECT and FDG-PET show in bvFTD?

Back 81

Frontal hypoperfusion and hypometabolism

Front 82

What neurotransmitters are affected in bvFTD?

Back 82

Serotonin

Dopamine in the CSF

Front 83

What neurotransmitter system is not affected in bvFTD, but is in AD?

Back 83

Cholinergic system

Front 84

What are the sex differences in bvFTD?

Back 84

Men are more affected

Front 85

What is the average age of onset for bvFTD?

Back 85

54

Age range is 40-65, and it becomes more RARE with age after 65

Front 86

What is the life expectancy for bvFTD?

Back 86

3-8 years from diagnosis

Front 87

What are the first indications of bvFTD?

Back 87

Behavioral changes without deficits on cognitive testing.

Hypometabolism on FDG-PET without structural changes.

Front 88

What are the behavioral changes in bvFTD?

Back 88

1. Poor social cognition/Loss of comportment

2. Apathy and Intertia

3. Perseverative/Ritualistic Behavior

4. Lack of insight

5. INCREASED DISINHIBITION

6. LOSS OF EMPATHY

7. Hyperorality/Dietary Changes

Front 89

What is the difference between possible, probable, and definite bvFTD?

Back 89

Possible = behavioral or cognitive symptoms

Probable = Behavioral/cognitive symptoms AND imaging findings

Definite = Behavioral/cognitive symptoms AND imaging findings AND histological evidence from biopsy or postmortem OR known genetic mutation

Front 90

What is the hallmark behavioral change in bvFTD?

Back 90

BEHAVIORAL DISINHIBITION as manifested by:

1. Loss of social grace

2. Impulsive and rash actions

3. Socially inappropriate behavior

Front 91

What is the most common symptom of bvFTD?

Back 91

Early apathy and inertia

Front 92

What percentage of bvFTD present with severe amnesia?

Back 92

10-15% but memory is usually preserved until late in the disease.

Front 93

Are aceytlcholinesterase inhibitors effective in bvFTD?

Back 93

NO! The cholinergic system is not affected.

Front 94

What is the pharmacological treatment of choice for bvFTD?

Back 94

SSRIs and SRNIs

Front 95

What is another name for language variant FTD?

Back 95

Primary progressive aphasia

Front 96

What are the three subtypes of language variant FTD?

Back 96

1. Logopenic

2. Non-fluent/Agrammatic

3. Semantic dementia

Front 97

What regions are involved in logopenic FTD?

Back 97

Left temporal parietal regions.

Front 98

What regions are involved in nonfluent/agrammatic FTD?

Back 98

Left posterior frontal and insula

Front 99

What regions are involved in semantic dementia?

Back 99

Anterior temporal regions

Front 100

What autosomal dominant genes can be involved in language variant FTD?

Back 100

GRN (Progranulin gene)

[MAPT (micro tubule-associated protein tau) can also be involved]

Front 101

What is life expectancy of language variant FTD?

Back 101

12 years

Front 102

What type of FTD is most prevalent and most rapidly progressive?

Back 102

bvFTD

Front 103

What is the general progression of language variant FTD (i.e., PPA)?

Back 103

Language deterioration that precede other cognitive declines that come later in the disease.

Front 104

What are the core features of Logopenic variant?

Back 104

1. Impaired single-word retrieval in naming AND spontaneous speech

2. Impaired repetition of sentences and phrases.

3. Phonological errors

Front 105

What are common spared language features of Logopenic variant?

Back 105

1. Spared grammar (for the most part)

2. Spared motor speech

3. Spared single word comprehension and object knowledge

Front 106

What are the common/core features of Semantic Dementia?

Back 106

1. Impaired object knowledge (key differentiating feature from other language variants).

2. Surface alexia or dysgraphia

3. Impaired confrontation naming

4. Impaired single word comprehension

Front 107

What is spared in Semantic Dementia?

Back 107

1. Spared Repetition

2. Spared grammar

3. Motor speech production

Front 108

What are common features of Nonfluent/Agramatic variant?

Back 108

1. Impaired comprehension of syntactically complex sentences.

2. Agrammatism (telegraphic speech, errors in tense, numbers, and gender). KEY DIFFERENTIATING FEATURE

3. Apraxia of speech (i.e., effortful halting speech).

Front 109

What are the three motor variant FTDs?

Back 109

1. Progressive supranuclear palsy

2. Corticobasal degeneration

3. FTD-Motor Neuron Disease

Front 110

What is the most common motor variant?

Back 110

PSP

Front 111

Where are astrocytic lesions and tau tangles found in PSP?

Back 111

Brain stem and basal ganglia

Front 112

Where is atrophy found in CBD?

Back 112

1. Bilateral Premotor cortex

2. Bilateral Superior Parietal Lobules

3. Striatum (the Basal part of the disease)

Front 113

Is FTD-Motor Neuron Disease a tauopathy?

Back 113

No. It is ubiquitin based disease affecting the frontal and temporal lobes.

Front 114

What is the life expectancy for PSP?

Back 114

5 years from diagnosis

Front 115

What is the average age of onset for FTD-Motor Neuron Disease? Life expectency?

Back 115

55

Death usually comes fast by the late 50s

Front 116

What is surface dyslexia?

Back 116

The inability to recognize words as a whole, which causes problems with irregularly spelled words (like half the friggin' English language).

Front 117

What are the common features of FTD-MND?

Back 117

Basically a combination of bvFTD with significant executive and memory impairment and motor problems that include:

1. Clumsiness and muscle atrophy

2. Hyperreflexia

3. Slowed vertical saccades

4. Fasiculations

5. Dysphagia and dysarthria

Front 118

What are common features of CBD?

Back 118

ASYMMETRICAL LIMB APRAXIA AND IDEOMOTOR APRAXIA, USUALLY STARTING WITH THE LEFT

Poor spatial organization, timing, sequencing

Stark behavioral and cognitve Executive dysfunction.

Resting tremor.

Front 119

What is retroactive interference?

Back 119

When newly learned information impedes the recall of previously learned information.

Front 120

What is proactive interference?

Back 120

Difficulty learning new information because of already existing information.

Think about when patients cannot learn List B on the CVLT-II because they recall the words from List A trials instead.

Front 121

What are the 4 components of the Information Processing Model of Memory?

Back 121

1. Encoding

2. Storage

3. Consolidation

4. Retrieval

Front 122

What are the 6 types of Memory?

Back 122

1. Declarative

2. Episodic

3. Semantic

4. Prospective

5. Non-Declarative (implicit)

6. Autobiographical

Front 123

What is declarative memory?

Back 123

System concerned with CONSCIOUS RETRIEVAL of information

Front 124

Define Semantic Memory

Back 124

Memory for facts

Not time dependent

Front 125

Define Episodic Memory

Back 125

Memory for EVENTS IN TIME

Front 126

What is prospective memory?

Back 126

The ability to remember how to do things in the future.

Front 127

What is implicit memory?

Back 127

Takes place without awareness and has to do with memory for procedures and habits.

Front 128

What is transient global amnesia?

Back 128

A complete loss of immediate memory.

Usually resolves in 2-8 hours.

Person can still recall personal information, but is disoriented to place and time

Does not have a known cause