• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/56

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

56 Cards in this Set

  • Front
  • Back

What plays the most significant role in causing dementia-related disorders?

Non-neuro degenerative, modifiable risk factors

Is amyloid-beta diagnostic of Alzheimer’s?

No!


It may not even be present in the disease




Required to diagnose AD, however




*A number of other pathologies mimic Alzheimer’s by presenting with amyloid-beta

Does normal aging lead to significant memory loss?

No




Only experience significant memory loss if another pathology is present




I.e. neuro degeneration or amyloid aggregation

Key pieces of history that indicate Lewy body disease

1. Loss of smell


2. Constipation


3. Parasomnias




Also:


-Parkinsonism


-Mental blocks


-Inattention


*Visual hallucinations


-REM sleep disorder

Do dementias affect level of consciousness?

No

What psychiatric illness is most likely to mimic dementia?

Depression

What drugs are most likely to cause treatable dementia? What is the clinical significance of this?

Anticholinergics:




Ex’s.


Amitryptaline (TCAs)


Trihexyphenidyl


Benadryl





*NEVER use these is a patient who is 65+


*NEVER diagnose Alzheimer’s in a patient taking these medications (may be mimics)

Multi-infarct Dementia is gradually progressive and requires multiple CNS hits:


-Multiple micro-strokes

...

Most common cause of infection-related dementia in older people

Neurosyphilis

How fast do Alzheimer’s disease and Creutzfeldt-Jakob progress?

Alzheimer’s: years (2-10)


CJD: months (much faster)

Dementia + startle myoclonus

CJD

What transplant may cause CJD?

Corneal transplant

Periodic triphasic sharp wave complexes

CJD

Is REM increased or decreased in depression?

INCREASED


*Also increased in PTSD




**Increases the retention of emotional memory (negative emotions, in these cases)

Distinguish the following: episodic, semantic, and procedural memory

Episodic- real experiences




Semantic- concepts, facts, and definitions




Procedural- Concrete, executable programs; can be combined into larger programs by “chunking”

Is memory loss required to diagnose dementia?

NO

Know what, know when, and know how

Know what: Impaired in Alzheimer’s disease


*Default network


Episodic memory and semantic knowledge




Know when: Impaired in frontotemporal dementia


*Salience network


Do the right thing at the right time


-Impulse control issues


-Apathy/loss of empathy


-Socially-inappropriate behavior






Know how: Impaired in Lewy body disease


*Executive network


Working memory impaired


Goal-directed behavior impaired


Motor and visual-spatial impaired



Compare the progress of Neurodegeneration in Alzheimer’s and frontotemporal dementia

Alzheimer’s:


*Begins in temporal lobe and angular gyrus


-Connected to a “default network”


*Spreads throughout this network in the dementia stage




FTD:


*Begins in right frontal insula and the anterior cingulate cortex


-Connected to “salience network”


*Spreads throughout this network

What is the #1 determining factor of Alzheimer’s disease onset and risk?

-Clearance rate of beta amyloid




Lower clearance = early age of onset

Describe the following for Alzheimer’s disease: clinical course, key clinical features

Clinical course:


-Insidious onset


*Slowly progressive (8-10 years; Amboss)




Key clinical features:


1. Amnestic- impaired learning AND recall


2. Language- word retrieval impaired


3. Visual- object agnosia, simultanagnosia, alexia, face recognition


4. Executive- impaired reasoning, judgment, and problem solving

Biomarkers for Alzheimer’s disease

CSF:


*LOW a-beta amyloid


-High tau




PET (FDG):


Hypoperfusion of bitemporal lobes and parietal lobe




MRI


Posterior temporal atrophy (MRI)

What drugs raise dementia risk?

1. Antihistamines




2. TCAs




3. Anti-muscarinics

What are the untreatable dementias?

1. Alzheimer’s disease




2. Prion disease




3. Any dementia-related neurodegenerative disease (ex. Parkinson’s and Huntington’s)

What is the least significant cause of dementia?

Cerebral infarction

Biomarkers required to be in the Alzheimer's continuum

A-beta amyloid

Decreased glucose uptake in occipital lobe on FDG-PET

Lewy body disease (executive network)

Cingulate island sign

Dementia with Lewy bodies spares the posterior cingulate cortex (shown on FDG-PET)




*Distinguishes DLB from AD!

What type of dementia has no amyloid beta present onPIB-PET?

Frontotemporal dementia (salience network)

“I went to the front door and range the bell” vs. “I went tothe place and did the thing”

Phonemic paraphasia




*Alzheimer’s disease

“John hit Mary” vs. “Mary hit John”

Semantic paraphasia




*Frontotemporal dementia (salience network)

Sleep apnea

Alzheimer’s disease (default mode network)

REM sleep disorder

Parkinson’s (Dementia with Lewy bodies)




*Executive network

Biomarkers required for Alzheimer’s

Amyloid and phosphorylated tau




*Don’t need to see Neurodegeneration (t-tau)

Three networks and their associations

Frontal executive




Default (Alzheimer’s disease)




Salience (fronto-temporal degeneration)

Clinical staging of dementia:

Cognitively unimpaired




Subjective cognitive impairment




Mild cognitive impairment




Dementia (mild, moderate, or severe)

All dementias are considered as a continuum

...

Alzheimer’s disease is a syndrome, NOT an etiology




*It is a clinical consequence of one or more diseases

...

What neurodegenerative and non-neurodegenerative pathologiesaffect the different brain networks?

Default


Neurodegenerative:


-Alzheimer’s



Non-ND:


Epilepsy


HSV



Salience


ND:


-Behavioral variant FTD


-PSP


-CBS



Non-ND:


-TBI


-Frontal stroke or tumors



Executive


ND: alpha-synuclein-opathies


-Lewy body dementia


-Multiple system atrophy


-Parkinson’s disease



Non-ND:


-External factors (alcohol, sleep disturbance, anticholinergic drugs, diabetes)

Is it possible for neurodegenerative pathologies to coexist?

YES




*Most autopsied brains show mixed pathologies

What disease pathologies cause the fastest and slowestchange in Neurodegeneration?

Most- Alzheimer’s disease




Least- vascular pathology

Does age cause neurodegeneration?

NO




*Only the pathologies associated with aging cause neurodegeneration

Key principal: amyloid burden -> increasedneurodegeneration




*Aging alone does not lead to cognitive impairment

...

What biomarkers are indicative of the Alzheimer’s continuum?

Amyloid




*Anything without amyloid (even tau and neurodegeneration) is a non-Alzheimer’s pathology

What categories are assessed to determine dementia severity?

CHOMP J




Community affairs




Home and Hobbies




Orientation




Memory




Personal care




Judgment and problem solving

What are the five fingers of dementia diagnosis?

1. History




2. Motor/Neuro exam




3. Cognition




4. Mood and behavior




5. Objective tests

Vertical and horizontal gaze disorder pathologies

Vertical- progressive supranuclear palsy




Horizontal- corticobasal syndrome




*Both effect the salience network

What pathologies affect episodic and working memory?

Episodic- Alzheimer’s disease




Working- Lewy body diseases and non-neurodegenerative dementias


Ex. blocks in the middle of thoughts


-Inconsistent task execution


-Forgetting the purpose of a task while performing it

What dementias are sleep apnea and REM sleep disorderassociated with?

Alzheimer’s disease- sleep apnea


*Reduced ability to clear amyloid through the glymphatic system




Parkinsonian disorders- REM sleep disorder

Memory deficit progression of Alzheimer’s

First- repetition


*Unable to form new memories (will often repeat themselves)




Second- reminiscence


*Start to forget most recent memories (will often reminisce about memories from long ago)




Third- reference


-Lose connections and associations?


(ex. may see their children and their siblings)

Describe the language deficits for the different types ofdementias

Default mode network: logopenia


-Semantics


-Sounds (phonemes)


-Nouns


-Phonemic paraphasias (words become jumbled; substitute words that don’t make sense)


-Nonspecific referents, circumlocutions




Salience network: semantic


-Semantics


-Loss of word knowledge


-Nouns


-Semantic paraphasias (lost the meaning of words)


-Social use of language--discourse




Executive- nonfluent


-Affects grammar and articulation


*Difficulty linking words into a sentence


-Can produce only short words and very short phrases


*Basically: Broca’s aphasia

Mild dementia- difficulty with instrumental ADLs




Moderate dementia- difficulty with personal ADLs

...

What senses are usually lost first in dementia?

Smell/taste




*Auditory, visual, and somatosensory are lost later

Describe the mood and behavior abnormalities with differenttypes of dementia

Alzheimer’s (default network)


-Irritable; anxious; depressed


-Apathy (present in ALL dementias)


-Restless pacing




Frontotemporal dementia (salience network)


-Euphoria


-SEVERE Apathy


-Rituals, obsessions, compulsions


-Impulsive




Dementia with Lewy bodies (executive network)


-High anxiety


-Depression


-Apathy (present in ALL dementias)


-Delusions


-Visual hallucinations

Can hippocampal volume used to predict Alzheimer’s?

NO




*LEAST SPECIFIC MARKER for AD (lots of overlap with other pathologies)

What is the most specific diagnostic procedure for Alzheimer’s?

Lumbar puncture


1. Decreased amyloid-beta


2. Increased phosphorylated tau (p-tau)


3. Increased total tau (t-tau; indicative of neuronal injury)

Greatest genetic risk factors for early onset and late onset Alzheimer’s disease

Late onset- Apolipoprotein E4 (chromosome 19)




Early onset:


APP gene (chromosome 21)


Presenilin 1 (chromosome 14)


Presenilin 2 (chromosome 1)


*All of these are autosomal dominant (not sure about Apo-E4)