Neurocognitive Disorders Flashcards

1
Q

What is the core feature in Neurocognitive Disorders?

A

Acquired Dysfunction in a cognitive domain that occurs after “early life”

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2
Q

What are the Domains of Cognition?

A
  1. Memory
  2. Language
  3. Executive function
  4. Visuospatial functioning
  5. Attention
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3
Q

Diagnostic Criteria for Delirium (AKA: acute confusional state, acute brain syndrome)

A
  1. Disturbance in awareness and attention
  2. Additional disturbance in a cognitive domain
  3. Sudden onset-symptoms typically fluctuate during the day
  4. Evidence for a direct physiological cause (ETOH withdrawal etc)
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4
Q

Risk Factors for Delirium
(modifiable, non modifiable)

A

Non-modifiable: poor health, old age, male
Modifiable: immobilization, sleep disturbance, ICU setting

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5
Q

Course of Delirium

A
  1. Symptoms persist until causal factors are treated
  2. Resolution typically within 3-7 days
  3. Amnesia common during delirium
  4. Poor prognostic sign for long-term survival in long ICU stays
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6
Q

Treatment for Delirium

A
  1. Treat underlying condition
  2. Antipsychotics-for associated symptomology
  3. Environmental Support measures (bed rails, lights)

Benzos are a risk factor for delirium-USED TO TX ETOH WITHDRAWAL

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7
Q

Dementia Diagnostic Criteria

A

Multiple and severe cognitive impairment without impaired consciousness
* progressive and irreversible
* more common in elderly (>65)

If no impairment in ADLs-Mild Cognitive Impairment

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8
Q

Alzheimer’s Dementia (AD)

A
  1. Significant memory impairment plus 1 other cognitive domain
  2. Gradual onset and steadily progressive decline
  3. Must exclude other symptoms (stroke)
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9
Q

3 Types of Alzheimers Dementia

A
  1. Early stage: memory deficits and word finding problems (anomia)-rapid forgetting
  2. Middle Stage: Agnosias (inability to identify/comprehend meaning of stimuli-mood changes, personality changes, psychosis
  3. End stage: Global cognitive impairment, motor deficits, and death from opportunistic infections

Middle Stage: ADL’s compromised. End Stage: round the clock asstance

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10
Q

Neuropathology of Alzheimers Disease

A
  1. Hippocampus atrophy
  2. Enlarged ventricles
  3. Cortical Atrophy
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11
Q

Neurochemistry of Alzheimers Disease

A
  1. Acetylcholine decreases (important for memory function
  2. Drugs try to increase ACH and decrease glutamate
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12
Q

Alzheimers Disease Neuropathology

Neurofunctional/Histopathological

A
  1. Reduced metabolism in posterior parts of brain (parietal and temporal lobes)
  2. Beta-Amyloid plaques and neurofibrillary tangles
  3. Detection of amyloid in brain by: CSF, PET imaging

Definitive Dx can only be made post-mortem by brain tissue sample

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13
Q

Genetics of Alzheimers Disease

A
  1. Early-Onset ( less than 65 years) strong genetic component
    3 genes (chromosome 1,14, 21)
    * If 1 copy of the gene is inherited-the person WILL develop early onset AD
  2. Late-Onset: Chromosome 19 -1 or 2 copies increase chance of developing

APOLIPOPROTEIN E (APOE) late-onset

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14
Q

Drugs that treat Alzheimers Disease

A

1.Increase Acetylcholine (cholinesterase inhibitors): Donepezil, Galantamine, Rivastigmine
2. Decrease glutamate (NMDA-receptor blockers): Memantine
3. Decrease amyloids (prevent plaque formation) Aducanumab

NO NEUROLEPTICS (ANTIPSYCHOTICS) INCREASED MORTALITY

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15
Q

Vascular Diagnosis

Alzheimer differential

A

Symptoms of vascular disease (HTN, elevated BMI)
Stepwise progression of dementia symptoms

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16
Q

Frontotemporal (Pick’s) Diagnosis

Alzheimers differential

A

Frontal signs predominate early
Dishinhibition & personality change (starts cussing)

17
Q

Lewy Body Dementia Diagnosis

Alzheimers Differential

A
  1. Fluctuating cognition
  2. Visual hallucinations
  3. Mild parkinsonism
    Severe neuroleptic sensitivity (extrapyramidal symptoms develop)

If dementia develops within 12 months then this is the diagnosis

18
Q

Huntington’s Disease Diagnosis

Alzheimers Differential

A

Motor disorder w/ choreiform and athetoid movements and often psychiatric disturbance

19
Q

Prion Disease (Creutzfedlt-Jakob)

Alzheimers Differential

A

Dementia progresses rapidly death under a year

20
Q

Neurocognitive Diagnoses

DSM-5-TR

A
  1. Delirium
  2. Major NCD: “Significant” decline in 1 or more cognitive domains-interferes w/ ADLs
  3. Minor NCD: “Modest” decline in 1 or more cognitive domains-does not interfere w/ ADLs
21
Q

Amnesia

A
  • Acquired significant memory impairment
    1. Retrograde: loss of memories for events prior to damage
    Information is forgotten in a temporal gradient
    2. Anterograde: loss of ability to store new memories of events after damage
22
Q

Paraphasias (3)

A
  1. Phonemic: sound substitution “I wear my red dat to church”
  2. Semantic: “Meet my son Mary”
  3. Neologistic: made up words

Dysarthria: slurred or slow speech

23
Q

Broca’s Aphasia

Non fluent

A
  1. Dysarthria, stuttering, effortful
  2. Speech is off-missed syllables
  3. Able to understand spoken language
24
Q

Wernicke’s Aphasia

Fluent Aphasia

A
  1. Speech is normal
  2. Word salad
  3. Unable to understand spoken language
25
Q

Normal Memory Systems (3)

A
  1. Short-term Memory (STM): brief duration (approx 30 seconds) small capacity
  2. Long-Term Memory (LTM): divided into “recent” vs “remote”
  3. Encoding & consolidation: process of turning STM into LTM (learning new info)
26
Q

What are the different types of Memory?

A
  1. Explicit (conscious)/ Implicit (unconscious)
  2. Declarative (facts, events)
  3. Procedural (skills, tasks)
  4. Episodic (experiences events)
  5. Semantic (facts, concepts)
27
Q

Where is memory stored?

A

Recalling pictures: R pre-frontal cortex
Recalling words: L pre-frontal cortex
LTM: storage occurs in the cortex

Consolidation of memory occurs in hippocampus but not stored

28
Q

Confabulation definition

A

Patient filling in memory gaps by unconsciously making up information

29
Q

What are the common causes of Amnesia?

A
  1. Direct damage to hippocampus
  2. Indirect damage to hippocampus: Korsakoff’s Syndrome- result of chronic alcoholism or thiamine deficiency
30
Q

Treatment of Amnesia

A
  1. Treat underlying cause
  2. Cognitive rehabilitation:
    * Restoration (memory exercises to strengthen memory systems
    * Training in use of mnemonic strategies as compensation
31
Q

2 Types of Mnemonics

A

External: lists, calendars, electronic schedulers
Internal:
1. Rhyme: saying that directly contains info to be remembered without needing to decode
2. Acrostic: a phrase that contains the first letter of each word as a cue to the information
3. Acronym: single word (SIGECAPS)
4. Clustering: group of similar information
5. Imagery: picturing information in a meaningful way

32
Q

Development of Language in Children

A
  1. 5-7 months: like sounds
  2. 7-8 months: well-formed syllables
  3. 1-2 years: first word ‘mama’-understands visual connection with acoustic appearance
  4. 2 years: speaking in rich phrase
  5. 3 years: most of the time correct use of words and grammar-but don’t understand rules
33
Q

Left Hemisphere

For Language

A
  1. DOMINANT 96%
  2. language processing
  3. Lexicon (dictionary of words)
  4. Phonetic assembly
  5. Phonetic procession
34
Q

Role of R hemisphere

A
  1. Communicative and emotion prosody (stress, timing, intonation). R Anterior damage-wrong intonation, R posterior damage: difficulty in interpretation
  2. Pragmatics of language: damage of Rt hemisphere-difficulty in construction of sentences into a story. Unable to understand jokes, sarcasm