9/28 Dementia & Delirium - Schneider

Question 1

syndrome vs disease

Answer 1

syndrome: collection of symptoms, NOT necessarily identified as a specific disease/linked to a causative agent

ex. dementia, delirium

→ from there, think about the causes of dementia/delirium

Question 2

dementia vs delirium

Answer 2

both used to describe breakdown/failure of brain fx

old school definitions:

dementia: state of being out of mind

delirium: delusions and brain diseases (phrenitis)

Question 3

connectivity in the cerebral cortex

Answer 3

cortical units are connected by three fiber types:

1. association fibers: connection between different cortices in same hemisphere
   
   • ex. U-fibers, fasciculi
2. commisural fibers: connection between two cerebral hemispheres
3. projection fibers: corticocubcortical fibers

Question 4

delirium: DSM5 definition

Answer 4

• disturbance in attention (reduced ability to direct, focus, sustain, shift attn) and awareness (reduced orientation to environment)
• develops over a short period of time (hr-days), represents a change from baseline attn/awareness, and tends to fluctuate in severity over course of day
• addtl disturbance in cognition (memory deficit, disorientation, language, visuospatial ability, perception)

Question 5

key points on

Acute Confusional State

&

delirium

Answer 5

• disturbance of arousal and/or attention
• multiple systems affected : WHOLE BRAIN affected!
  
  • (DSM criteria only mention cognition and perception, but there is more)
• develops over a short period of time
• not clearly explained by another psych condition
• sx can fluctuate

Question 6

dementia

Answer 6

• significant cognitive decline (complex attn, executive fx, learning/memory, language, perceptual-motor, social cognition)
• weighted on concern of the individual or someone who knows them and impairment in cog performance
• deficits must interfere with independence in daily activities

now aka “major neurocognitive impairment”

summary of criteria:

1. change from baseline
2. evidence of cognitive impairment
3. significant functional impairment

Question 7

mild cognitive impairment

Answer 7

decline in fx from baseline that is not normal for age and that affects one or more cognitive domains

however,

not associated with significant functional impairment!

Question 8

delirium vs dementia

time course

primary sx

daily sx

reversible

treatment

mortality

Answer 8

overall:

delirium = acute brain failure

dementia = chronic brain failure

Question 9

etiology of delirium

Answer 9

delirium is the failure of cells of the brain to function appropriately (acute failure)

generally due to failure in cerebral metabolism

• failure in availability or distribution of fuel for metabolism (glucose, water, oxygen)
• failure of cells to utilize fuels due to impaired cellular integrity or toxic interference

Question 10

delirium routine assessment

&

specialized assessment

Answer 10

1. ABCs, vitals, finger stick glucose
   * glucose low? thiamine!
2. history and physical exam
   * looking for physical exam findings that point to an etiology
3. 5 routine labs/diagnostics
4. specialized assessment
   * brain imaging, LP, EEG, blood cultures, etc.

Question 11

delirium tx

Answer 11

medical emergency! → requires urgent care

step 1: identify and treat underlying cause

step 2: symptomatic treatment

• behavioral/environmental strategies first
• phama interventions as last resort

Question 12

dementia risk factors

Answer 12

• gender (F > M by 1.2-1.6x increase)
• family hx of early onset dementia
• cerebral-vascular disease
  
  • high chol, high bp, diabetes, smoking, obesity
• decreased daily activity/exercise
• decreased mental stim

Question 13

dementia: list of etiologies

Answer 13

1. potentially reversible

• functional, metabolic, infectious, paraneoplastic/autoimmune causes
• ex. thyroid disease, B12 def, syphilis, limbic encephalitis, sleep disorders, depression

2. arrestable, but non-reversible

• structural lesions
• ex. vascular lesions, tumors, MS, normal pressure hydrocephalus, head injury

3. noncurable, progressive - but able to slow progression

• neurodegen, but only: Alzeheimer’s and Lewy Body dementia

4. non-curable, progressive

• all other neurodegen
• ex. frontal temporal demential, cortical basal degen, CJD, Huntington’s

Question 14

dementia treatment

Answer 14

behavioral tx (dependent on target sx)

medications: cognitive enhancers

• AChE inhibitors: donepazil, rivastigmine, galantamine
• NMDA receptor antagonists: mementine

medications: symptomatic tx (dependent on target sx)

psych interventions

• advanced directives
• caregiver support
• comm resources

Question 15

case example

what specific etiology is suggested?

delirium, ataxia, eye-movement abnormality

Question 16

case example

what specific etiology is suggested?

delirium, ataxia, eye-movement abnormality

Answer 16

Wernicke’s!

Question 17

case example

what specific etiology is suggested?

delirium, ataxia, pupillary dilation, tachycardia, decr sweating, slurred speech, picking behavior

Answer 17

anticholinergic delirium

Question 18

case example

what specific etiology is suggested?

delirium, bradykinesia, rigidity, polyminimyoclonus, negative myoclonus

Answer 18

hepatic encephalopathy

Parkinsonism (syndrome)

negative myoclonus: decrease in muscle tone that makes you jerk

• aka asterixis

Question 19

case example

what specific etiology is suggested?

delirium, mostly postural/action tremor, autonomic instability, agitation, diarrhea, intense hallucination

Answer 19

delirium tremens (assoc with alcohol withdrawal)

Question 20

Lewy body dementia

Answer 20

Lewy bodies discovered in 1912

presence of dementia

2/3 of the following:

• fluctuating attention, concentration
• recurrent well-formed visual hallucinations
• spontaneous Parkinsonian motor signs

OR

1/3 of the above PLUS another one of the following:

• rapid eye movement sleep behavior disorder
• severe neuroleptic sensitivity
• low DA transporter uptake in basal ganglia

pathology

• Lewy bodies diffusely throughout entire brain or mostly in cortex
• amyloid plaques, neurofibrillary tangles (lower density than AD)
• loss of cholinergic neurons in nucleus basalis of Meynert, decreased cortical choline acetyltransferase, depletion of DA-containing neurons

Question 21

frontotemporal dementia

Pick’s disease

Answer 21

• characteristic patterns of atrophy
• absence of plaques and tangles
• characteristic inclusion bodies (Pick bodies)
  
  • involve either tau, TDP43 (TAR DNA-binding protein), FUS (fused in sarcoma) proteins

damage in this area can also present as:

semantic dementia

progressive non-fluent aphasia

Question 22

frontotemporal dementia (FTLD) genetics

Answer 22

40% of cases have genetic heritability pattern (10% auto dom)

mutations in 3 most common genes account for 60% of inherited cases:

1. tau: mutation to microtubual-assoc protein tau (MAPT, chr17) → FTDP-17
2. TDP-43: mutation to progranulin gene (PGRN, chr17) and C9orf72 (chr9) have high association
3. FUS: mutations to FUS (chr16)

Question 23

memory loss, “patchy” focal neuro findings, high bp, high cholesterol, diabetes

Answer 23

vascular dementia

Question 24

memory loss, wide-based gait with short stride length and step height, urinary incontinence

Answer 24

normal pressure hydrocephalus

Question 25

memory loss, poor attention/executive function, chorea, ataxia, dystonia, depression

Answer 25

Huntington’s

Question 26

significant memory loss over a few months, starte myoclonus, disinhibition, personality change

Answer 26

CJD