Neurocognitive disorders Flashcards

1
Q

Dementia - areas of impaired functioning

A
  • getting lost in familiar areas
  • difficulties with dressing
  • maintaining personal hygiene
  • food acquisition/intake
  • self-administration of meds
  • social interactions
  • operating common appliances
    • usually unaware of deficits, do not complain of memory loss

MMSE - (Sn for major NCD’s)
20-24: mild dementia
13-20: moderate
less than 12: severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

6 cognitive domains

A
Complex attention
Executive function
Learning and memory
Language
Perceptual-motor skills
Social cognition (interaction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Delirium

A

Medical emergency.
Cause: medical conditions, polypharmacy, pain, ICU and postop settings
MCC children: febrile illnesses, medications

Categories:

  1. Substance intoxication delirium
  2. Substance withdrawal delirium
  3. Medication induced delirium
  4. Delirium due to another medical condition
  5. Delirium due to multiple etiologies

Sx: Confusion Assessment Method: (1 + 2 + either 3/4)
1. Acute onset, fluctuating course
2. Inattention: digit span, serial 7’s, WORLD (sp - mundo)
(distractibility, diff maintaining focus)
3. Disorganized thinking
4. Altered consciousness (vigilant, alert, lethargic, stuporous, comatose)

Other:

  • Visual hallucinations
  • Impairment in recent memory

–> diffuse slowing on EEG (EXCEPT in DTs - hyperkinetic)

Mgmt:

  1. Treat underlying cause
  2. Reorient pt regularly
  3. D2 antags (haldol) to treat agitation PRN
    * use w caution in pts with parkinsonism

Do not use BZ’s!!! Unless in alc/BZ withdrawal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three types of delirium?

A
  1. Mixed type (most common)
    - stable psychomotor activity at baseline, or fluctuating
  2. Hypoactive (“quiet”) type
    - likely to go unnoticed, esp in elderly
  3. Hyperactive type (“ICU psychosis”)
    - more common in drug withdrawal or toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Difference between mild and major NCD?

A

Mild: IADLs preserved
Major: Impaired performance of IADLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some reversible causes of NCD?

A

1a. Hypothyroidism (fatigue, cold intolerance)
1b. Hyperthyroidism (“apathetic thyrotoxicosis” - depression, lethargy)
2. Vit B12 def
3. Wilson’s ds (?)
4. Normal pressure hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 2 screening tests for NCD?

A
  1. MMSE
    * Dysfunction: <25
  2. Mini-Cog (3 item recall + clock drawing)
    * Positive (aka need further w/u) screen:
    - no items recalled after 3 mins
    - only 1-2 items recalled with abn clock drawing

If positive screen –> need formal neuropsych testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Alzheimer’s disease

A

MCC; 2/3 are women, usually after age 65

Domains: Learning and memory, Language
[personality changes, mood swings, paranoia]
INSIDIOUS, GRADUAL
Pathophys:
*Extraneuronal B-amyloid plaques
*Intraneuronal tau protein tangles
*AD single gene mutation (APP, presenilin 1 or 2) –> early onset sx
*epsilon 4 variant of apolipoprotein gene –> RF for early onset

Mgmt:

  1. Mild-mod: Cholinesterase inhibitors
  2. Mod-severe: NMDA-R antag, memantine
  3. Agitation/aggression: antipsychotics
    * Black box warning of incr risk death in dementia pts. Use in low doses for short pds of time, monitor closely.
  4. Caregiver support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why do Down Syndrome pts have greater risk of early onset Alzheimer’s?

A

B-amyloid precursor protein (APP), gene is on chrom 21 –> B-amyloid peptide (A-beta) –> senile plaques

Trisomy 21 –> overexpression of APP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Vascular dementia

A

2nd MCC (~20%)

Cause:

  • lg vessel strokes (usually cortical)
  • small vessel strokes (lacunar, to subcortical structures)
  • microvascular disease affecting periventric white matter

RF: HTN, DM, smoking, obesity, HLD, afib, old age

Domains: Complex attention, Executive function

Dx: neuroimaging

Mgmt: Prevent future strokes, sx mgmt similar to AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lewy body dementia

pathophys
core features
suggestive features
how to make dx?
mgmt
A

Pathophys:

  • Lewy bodies (alpha-synuclein aggregates)
  • Lewy neurites (in brain, primarily in basal ganglia)

Core features:

  1. Waxing and waning cognition (Attention, Alertness –> resembles delirium)
  2. Visual hallucinations (animals, small ppl)
  3. EPS sx at least 1 YR AFTER cognitive decline becomes apparent (Parkinsonism)

Suggestive features:

  1. REM sleep behavior disorder (violent mvmts during sleep)
  2. Antipsychotic sensitivity

Possible dx: only 1 of the above
Probable dx: 2+ core, or 1 core and 1+ suggestive

Mgmt:

  1. Cog/behavioral sx: cholinesterase inhibitors
  2. Psychotic sx: Quetiapine (Seroquel) or clozapine
  3. Parkinsonism: Levodopa-carbidopa (can exac psychosis/REM sleep disorder)
  4. REM sleep disorder: melatonin, clonazepam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Frontotemporal dementia

A

Affects: Attention, Abstraction, Planning, Problem solving

  • Two variants: BEHAVIORAL, LANGUAGE
  • Increased Sn to adverse effects of antipsychotics
  • Common misdiagnosis: late onset bipolar disorder

Pathophys: frontal, temporal lobe atrophy

Mgmt:

  1. Sx-focused
  2. Serotonergic meds (SSRI’s, trazodone) - help w sx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Definitive dx made at autopsy for __, __, __

A

Alzheimer’s
LBD
FTD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the two variants of FTD.

A

BEHAVIORAL VARIANT:

  • disinhibited verbal, physical, sexual behavior
  • overeating or oral exploration of inanimate objects
  • lack of warmth, empathy
  • apathy or inertia
  • perseveration, repetitive speech, rituals, obsessions
  • decline in Social Cognition and Executive Abilities

LANGUAGE VARIANT (primary progressive aphasia):

  • difficulties w/ speech and comprehension
  • RELATIVE SPARING of learning/memory and perceptual-motor function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HIV infection

A

25% of those infected –> meet mild NCD criteria

RF: severe IC, high CSF viral loads, advanced infection

Sx: depends on part of brain affected
Dx: mild or major NCD attributed to confirmed HIV infec
Mgmt:
1. HAART
2. Fatigue, apathy, psychomotor retardation –> psychostimulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Huntington’s disease

A

Pathophys: CAG repeats ing ene encoding huntingtin (HTT) protein on chrom 4
Inheritance: AD
Avg age: 40 yrs

Sx:
TRIAD: motor, cognitive, psychiatric
Cognitive decline + behav changes -------> motor changes
DOMAIN: Executive function
Psych sx: depression, apathy, irritability, obsessions, impulsitivity
Motor sx: chorea, bradykinesia
*pts usually aware of deterioration
*incr rate suicide

Dx: look at family history / genetic testing

Mgmt: (sx directed)
1. Tetrabenazine (MOA unknown; anti-chorea; ? reversible depletion of monoamines)
or 2. Atypicals

17
Q

Parkinson disease

A

Cause: depletion of dopa in BG; idiopathic

Sx:
T - pill-rolling resting tremor
R - rigidity
A - a/brady kinesia
P - postural instability
S - shuffling gait

Also: mood changes, executive dysfxn, visuospatial impairments

Dx: BRADYKINESIA + [tremor or rigidity]
*MOTOR —–> COG DECLINE (occurs after)

Mgmt:

  1. Motor sx: Sinemet, dop ag’s (amantadine, etc)
  2. Cog/neuropsych sx: cholinesterase inhibitors
  3. Psychotic sx: reduce dose of dopa ag’s
  4. Psychotic med SE that don’t respond to dose reduction: quetiapine, clozapine
    * Avoid other antipsychotics, which can exacerbate motor sx!!!
18
Q

Cholinesterase inhibitors -

indicated in which types of dementia?

A

Alzheimer’s
LBD
Parkinson

Mild-mod: rivastigmine (PO, transderm), galantamine
All levels of dementia: donepezil

19
Q

Prion disease

A

Casue: prions —> subacute spongiform encephalopathy
MC type: Creutzfeldt-Jakob disease
*15% are familial (AD)

Sx:

  • Concentration, Memory, Judgment —-> early sx
  • Myoclonus
  • Apathy, hypersomnia
  • BG/cerebellar dysfxn –> ataxia, nystagmus, hypokinesia

Dx:

  1. Rapid progression of cognitive decline
  2. 2+ of clinical sx:
    - Myoclonus
    - Visual, cerebellar signs
    - Pyramidal or EPS
    - Akinetic mutism
  3. Supportive findings from at least one diagnostic modality:
    - periodic sharp wave complexes on EEG
    - CSF + for 14-3-3 proteins
    - MRI: lesions in putamen/caudate nucleus

Mgmt: no tx. die in 1 year.

20
Q

NPH

A

*potentially reversible

Pathophys:

  • enl’ged ventricles
  • localized CSF pressure elevation
  • BUT normal opening pressure on LP

Cause: idiopathic, or obstruction (hemorrhage, meningitis)

Sx: wet, wacky, wobbly
(wobbly is usually first; most responsive to tx)
(wacky - least likely to improve w/ tx)

Mgmt: VP shunt

21
Q

Pseudodementia

A
    • mostly “idk” answers (vs dementia: near miss answers)

- - “morning depression” - wake up bad, but feel better in evening

22
Q

Describe the course of HIV-assoc dementia

A

think of in a pt with: longstanding HIV + CD4 ct <200

  1. increasing apathy + impaired attention
  2. early on: subcortical dysfunction (slowed mvmt, slow limb mvmt)
  3. significant cortical neuron loss + memory decline