Neurocognitive DO - Collins

Question 1

What is Delirium

Answer 1

transient, reversible cognitive impairment
- acute onset; attention, awareness, cognitive and memory impacted
often fluctuating - 24 hour period

Question 2

who is at higher risk of delirium

Answer 2

anyone adding “insult to injury”
- polypharmacy
-multiple medical co-morbidities
- sensory impairment (vision, hearing)
substance or alcohol use

Question 3

What are the three likely causes of delirium

Answer 3

Drugs
Dehydration
Infection

Question 4

what are mental status exam findings in Delirium

Answer 4

Attention impairment
altered LOC
disorientation
delusions/hallucinations/paranoia
confusion
disordered thinking and/or speech
erratic or irregular behaviors
irritability/agitation
lethargy/withdrawn
poor insight and or judgement
irregular sleeping/eating

Question 5

What are the diagnostic criteria for Delirium

Answer 5

Disrupted attention/awareness
develops over a short period and fluctuates
acute change in cognition - memory, language, perception, thinking

Question 6

What is CAM

Answer 6

confusion assessment method
sensitivity: 94-100%
Specificity: 90-100%

Question 7

what is the difference between Delirium and dementia

Answer 7

delirium: acute, fluctuating, impaired awareness, disturbed attention, poor working memory, short lived or changing, fragmented sleep

Dementia: insidious onset, gradual deterioration, often clear awareness, often good attention, poor short-term memory, more fixed delusions, sleep-wake reversal

Question 8

what is the treatment of Delirium

Answer 8

treat the underling cause - prevention is the best medicine
remove/treat any exacerbating factors

agitation: Haloperidol IM/IV
high mortality rates
higher risk for long-term cognitive and functional decline

Question 9

What is Wernicke’s encephalopathy (WE)

Answer 9

first step on the continuum of Wernick-Korsakoff syndrome
acute neuropsychiatric disorder
reversible with appropriate treatment

Question 10

what are the cerebllar tests

Answer 10

1 rapid alternating movement
2 finger to nose
3 gait and balance
4 heel to shin
5 pronator drift

Question 11

If WE is left untreated what can happen

Answer 11

it can progress to Korsakoff’s syndrome - more often irreversible

Question 12

what is the pathophysiology of WE

Answer 12

inadequate thaimine (B1)
ETOH use leads to - GI inflammation -reduced absorption
Poor nutritional intake

Question 13

what is the classic presentation of WE

Answer 13

delirium
AMS
hypotension
+/- peripheral neuropathy
ataxia - broad based gait - inability to ambulate
Ocular: nystagmus, CN plasies, Sluggish pupils, ptosis, anisocoria

Question 14

what is the classic Triad of Symptoms for WE:

Answer 14

AMS
Gait ataxia
Ophthalmoplegia (weakness/paralysis)

Question 15

How is WE trated

Answer 15

Cessation of ETOH use
Thiamine replacement
MUST have thaimine prior to any glucose treatment in AUD patients

Question 16

what is Korsakoff Syndome (KS)

Answer 16

next step in Wernicke- Korsakoff syndrome - from untreated WE

Question 17

what is KS characterized

Answer 17

antero- and retrograde amnesia (short term)
Confabulation(fabricated memories or jumbled up old memories)
Apathy
preserved cognitive skills (attention/behavior)

Question 18

what is the treatment of KS

Answer 18

no specific treatment - nutritional support and ETOH cessation to prevent further insult

Question 19

What is CJD

Answer 19

Crutzfeldt-Jakob Disease
rapidly progressive prion disease

Question 20

what is CJD closely related to

Answer 20

Mad Cow disease “bovine spongiform encephalopathy

Question 21

What are the forms of CJD

Answer 21

sporadic - no known transmission
Hereditary
Acquired - exposure to disease tissue (sx equipment)

Question 22

what is the presentation of CJD

Answer 22

RAPIDLY PROGRESSIVE DEMENTIA
impaired coordination and cognition
personality change
insomnia
depression
sensory changes
myoclonic jerking
impaired vision
speech impairment
psychiatric distrubances
coma

Question 23

How do you work-up CJD

Answer 23

definitive diagnosis requires histology (biopsy or autopsy)
supportive lab findings (EEG abnormalities, Brain MRI abnormalities, CSF analysis)

Question 24

what is the likely diagnosis when Sharp wave complexes are seen on EEG

Answer 24

CJD

Question 25

what are CJD probable diagnosis criteria

Answer 25

neuropsychiatric disorder and positive CSF
rapidly progressive dementia AND 2+ of the following: myoclonus, visual or cerebellar signs, EPS/Pyramidal symptoms, Akinetic mutism
AND 1+ of the following + labs: Typical EEG, Positive CSF assay, MRI consistent with CJD

Question 26

what is the treatment of CJD

Answer 26

no curative treatments - 100% fatality
Treatment is palliative: sedatives for anxiety, antidepressants, antispasmodics, pain control