Neurocognitive Disorders Flashcards

1
Q

What are Neurocognitive Disorders (NCDs)

A

Disorders in which the core feature is acquired dysfunction in a cognitive domain occurring after “early life.”

development went normally

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2
Q

What are common NCD conditions?

A

Delirium, Amnesia, Dementia

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3
Q

Delirium

AKA?

What are the cognitive domains?

A

Acute confusional state, acute brain syndrome, encephalopathy, ICU syndrome

•memory, language, executive functions, visuospatial functioning, etc.

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4
Q

What are the four things it involves?

A
1) A disturbance in awareness and
attention:
• Awareness is assessed by one’s
orientation to the environment.
• Attention is assessed by one’s ability to direct, focus, sustain, and shift attention.

2) An additional disturbance in a cognitive domain (e.g., memory, language, thoughts [delusions], and perceptions [incl. hallucinations, illusions]) Sensory misperception
3) Sudden onset of symptoms (over hrs to a few days) that typically fluctuate during the day.
4) Evidence for a direct physiological cause (e.g., a medical condition, drug intoxication/ withdrawal).

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5
Q

Pathology:

Where are the core deficits? (2 areas)

A

Core deficits in central cholinergic functioning

•Deficits in the Reticular Activating System and its ascending connections (important for attention and arousal)

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6
Q

What are the risk factors?

What is its course?

A

Risk Factors
• Non-modifiable (e.g., poor health, older age,
male gender)
• Modifiable (e.g., immobilization, poor sleep, and use of benzodiazepines in an ICU)

Course
• Symptoms persist until cause is reversed.
• Resolution typically occurs within 3-7 days.
• Amnesia for events during delirium is common.
• Delirium is a poor prognostic sign for long-term survival and results in longer ICU stays.

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7
Q

Treatments for Delirium?

There are 3

A

Treat underlying medical condition
•Manage associated symptoms (e.g., agitation, psychosis)
•Use antipsychotics to treat associated symptoms (e.g., agitation, psychosis) of most deliriums
•Use benzodiazepines to treat delirium caused by alcohol withdrawal
Utilize environmental supportive measures
▪regulate amount of environmental stimulation
▪provide orienting stimuli (e.g., lighting, personal effects, sensory aids)
▪provide for safety needs (e.g., attendant, bedrails, and possibly restraints)

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8
Q

What is an Amnesia

What area of the brain?

A
  • A significant acquired memory deficit
  • Caused by a medical condition or the effect of a substance (not from dissociation)
  • NOT diagnosed if it occurs in the context of general cognitive decline (i.e., a dementia).
  • Typically caused by damage to the mesial temporal lobe
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9
Q

What is a typical profile of someone with Amnesia?

A

Intact short-term (working) memory (STM)
•Short-duration retrograde amnesia
•If lengthy retrograde amnesia, there is often a temporal gradient to the memory loss with recent long-term memories (LTMs) more impaired than remote LTMs.
•Prominent anterograde amnesia

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10
Q

Treatment for Amnesia?

A

•Treat underlying cause (e.g., B1 deficiency in Korsakoff’s to stop amnesia progression)
•Cognitive rehabilitation
▪Restoration of Function: Memory exercises to strengthen memory through repetition.
▪Compensation (e.g., using mnemonics): ❖External strategies (non-mental activities
such as using lists, calendars)
❖Internal strategies (mental activities such as acronyms [e.g., RICE] and acrostics [e.g., “On Old Olympus Towering Tops…”])

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11
Q

What is a Dementia?

A

-Multiple and severe cognitive
impairment without impaired consciousness (is usually progressive and irreversible)
•most commonly occurs in the elderly
➢Note: “Mild Cognitive Impairment” (MCI) refers to cognitive decline that doesn’t cause impairment in activities of daily living.

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12
Q

What is Alzhemier’s Dementia?

A

Significant memory impairment plus impairment in at least 1 other cognitive domain
•A gradual onset with steadily progressive decline
•Exclusion of other causes of the symptoms
(e.g., stroke)

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13
Q

What is the general course of AD?

A
  • Onset in late 70’s with 10+ yr progression
  • Early Stages: Memory deficits (rapid forgetting) and anomia (labeling problem-but you know what it does)
  • Middle Stages:
  • further memory and language decline •visuospatial deficits
  • agnosias-you lose knowledge about the object (incl. anosognosia and prosopagnosia-can’t recognize yourself in the mirror
  • mood changes, personality changes
  • psychosis

•Late Stages: Global aphasia, motor dysfunction, death from opportunistic infections.

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14
Q
  1. Neuroanatomical pathology of AD
  2. Neurochemical?
  3. Neurofunctional?
  4. Histopathological?
  5. Markers?
A
  1. cortical atrophy, hippocampal atrophy, enlarged ventricles
  2. loss of cholingeric (ACH) neurons in the nucleus basalis of Meynert due to its role in memory formation
  3. Posterior
    hypometabolism (parietal/temporal
  4. ß-amyloid plaques and neurofibrillary tangles
  5. CSF amyloid & tau levels, PET imaging of amyloid plaques
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15
Q

What are the four FDA approved drugs?

Are these considered effective?

What are the side effects?

What is research on?

A
3 cholinesterase inhibitors
■ donepezil (“Aricept”)
■ galantamine (“Razadyne”) 
■ rivastigmine (“Exelon”)
*keep Ach in the cleft for longer

1 NMDA receptor blocker
■ memantine (“Namenda”)
*block glutamate release

No.

Side effects (e.g., hypotension, GI) have notable consequences for the elderly (e.g., risk of falls)

Efforts are on ↓ production and ↑ clearance of ß-amyloid through antibody drugs.

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16
Q

What are 7 other interventions for AD?

A

Treatment of neuropsychiatric symptoms (e.g., aggression, agitation)
•Non-pharm methods (e.g., music therapy)? •Antipsychotics
•used off-label for demented patients •FDA-black box warning of increased mortality
risk if used with this population •Anticonvulsants & antidepressants (select ones)
►Rule out non-dementia causes of behavioral
problems (e.g., pain) in AD patients.
•Use of external mnemonics in early AD stages
•Assessment and restriction of driving
•“Safe Return Program” for wanderers (Germany)

Risk of “Care Giver Syndrome” from psychological, social and financial sequelae of caregiving
•Resources through AD Assoc/AD Foundation:
■support groups
■caregiver tips (e.g., how to respond to psychosis)
■long-term care options
■legal and financial planning
■etc.

17
Q

Differential Diagnosis of AD
1. Vascular Dementia
Treatment?

A
  • Dementia results from multiple infarcts caused by cerebral vascular disease (CVD)
  • Typical patient history includes signs and symptoms of CVD
  • Sudden onset with stepwise progression
  • Usually focal neurological signs
  • Headache and seizure onset are more common in the early stages of vascular dementia than AD

•Treat underlying CVD to prevent further damage

18
Q

Differential Diagnosis of AD
2. Frontotemporal Dementia (FTD) (Pick’s disease)

“Lude, crude, disinhibited)

A
  • Earlier age of onset (40s-50s)
  • Similar to AD but “frontal” signs prominent early in the dementia (e.g., disinhibition & personality change)
  • Frontal lobe atrophy and hypometabolism
  • Histopathological changes (e.g., Pick bodies in Pick’s disease)
19
Q

Differential Diagnosis of AD
Lewy Body Dementia (LBD)

  1. Treatment for hallucination:
  2. Parkinsonism?
A

fluctuating cognition/alertness
■visual hallucinations
■mild parkinsonism (but usually not tremors)
•Histopathological changes (e.g., Lewy bodies)
•REM-sleep behavior disorder often precedes the onset of LBD (or Parkinson’s) by many years.

  1. “benign neglect”
  2. Parkinson’s drugs (l-dopa) are relatively ineffective in LBD and worsen psychosis.
20
Q

Differential Diagnosis of AD
Parkinson’s Disease Dementia (PDD)

How to differentiate between PDD and LBD?

A

Up to 50% of PD patients develop dementia •Similar pathology to LBD
•Use “1-year rule” for classifying PDD vs LBD: ■If dementia develops >12 months after well-
established PD → PDD
■If dementia develops first or within first 12 months of motor signs→ LBD

21
Q

Differential Diagnosis of AD

Huntington’s Disease Dementia (HDD)

A

Dementia develops AFTER the onset of choreoathetosis and psychiatric symptoms.

22
Q

Differential Diagnosis of AD
Prion Disease
(e.g., Creutzfeldt-Jakob)

A

Dementia progresses rapidly over a few months with death under a year.

23
Q

Differential Diagnosis of AD

►Reversible Dementias (e.g., infections)

A

Infections

24
Q

Differential Diagnosis of AD
“Pseudodementia”
(AKA “Dementia Syndrome of Depression” )

A

•Depressed elderly patients often show memory and other cognitive disturbances that resemble a dementia

25
Q

Differential Diagnosis of AD

►“Benign Senescent Forgetfulness”

A

Cognitive decline associated with normal aging.

•Neuropsych testing helps determine whether current cognition reflects a pathological process.

26
Q

What is neuropsychological testing and

A

A comprehensive evaluation of a person’s cognitive functions:

Performance on neuropsych tests reflects functioning of specific brain areas

Patterns of performance help to determine whether brain dysfunction (and which kind) is present

27
Q

What does it test?

For memory: if cue helps:
If cue doesn’t help:

7 things

What does asymmetry mean?

A

Intelligence: Assess for intellectual decline and look for hemispheric lateralizing and localizing signs

Attention: 
Visual attention (e.g., cancellation test)
Verbal attention (e.g., serial addition test)

Memory: Verbal vs visual memory tests: Immediate recall (STM) vs. delayed recall (LTM)

If cues help: Encoding occurred; thus, the problem is retrieval-based (prefrontal).
oIf cues don’t help: Encoding didn’t occur; thus, the problem is encoding-based (mesial temporal).

Language: Naming and verbal fluency

Visuospatial functions (rt. parietal): Copying and drawing tests (e.g., draw- a-clock)

Executive Functions:(prefrontal): Abstraction (proverb, interpretation, similarities)
•Concept formation and mental flexibility
(Wisconsin Card Sorting Test) •Inhibiting responses (Stroop Test

Motor Functions (looking for lateralizing signs)
•Dexterity and speed (finger tapping, pegboard test)

Vascular, lateralized

28
Q

Dementia vs benign senescent forgetfulness (BSF)?

A

If BSF, then the person’s cognitive performances will be at expected levels for one’s age, gender, and education

29
Q

2) Alzheimer’s Dementia vs Pseudodementia?

A

•Important distinctions are in:
▪the pattern of neuropsych deficits (esp. whether memory
deficits relate to memory encoding vs. retrieval)

The onset and course of problems:
Pseudodementia-Pinpointable, while Alz is indeterminant

Duration in Alz is long, pseudo is short

Cognitive impairment in Alz is consistent and pseudo is inconsistent

Memory: Cues don’t help in Alz and help in Pseudo

Answers to questions in Alz are filled with mistakes, but in Pseudo they pretend like they’re dumb and say “i don’t know” to everything

30
Q

Alzheimer’s vs Vascular Dementia?

A

Memory deficits:
■Alzheimer’s: Encoding problem-cues don’t help
■Vascular: Retrieval problem
•Motor functioning-cues help

■Vascular: Lt-Rt discrepancy
■Alzheimer’s: No Lt-Rt discrepancy

31
Q

What’s the difference between a Major and Mild Neurocognitive Disorder

A

Major: Significantdecline (deficits interfere with independence in daily activities)

Mild:“Modest”decline(deficits do NOT interfere with the capacity for independence in daily activities)