9/28 Dementia & Delirium - Schneider Flashcards Preview

M2 Neuron Brain Behavior > 9/28 Dementia & Delirium - Schneider > Flashcards

Flashcards in 9/28 Dementia & Delirium - Schneider Deck (26)

syndrome vs disease

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


dementia vs delirium

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)


connectivity in the cerebral cortex

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


delirium: DSM5 definition

  • 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)


key points on

Acute Confusional State



  • 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



  • 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


mild cognitive impairment

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


not associated with significant functional impairment!



delirium vs dementia


time course

primary sx

daily sx





delirium = acute brain failure

dementia = chronic brain failure


etiology of delirium

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


delirium routine assessment


specialized assessment

1. ABCs, vitals, finger stick glucose 

  • glucose low? thiamine!

2. history and physical exam

  • looking for physical exam findings that point to an etiology

2.5 routine labs/diagnostics

3. specialized assessment

  • brain imaging, LP, EEG, blood cultures, etc.


delirium tx

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


dementia risk factors

  • 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


dementia: list of etiologies

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


dementia treatment

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


case example

what specific etiology is suggested?


delirium, ataxia, eye-movement abnormality


case example

what specific etiology is suggested?


delirium, ataxia, eye-movement abnormality



case example

what specific etiology is suggested?


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

anticholinergic delirium


case example

what specific etiology is suggested?


delirium, bradykinesia, rigidity, polyminimyoclonus, negative myoclonus

hepatic encephalopathy

Parkinsonism (syndrome)


negative myoclonus: decrease in muscle tone that makes you jerk

  • aka asterixis


case example

what specific etiology is suggested?


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

delirium tremens (assoc with alcohol withdrawal)


Lewy body dementia

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


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



  • 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


frontotemporal dementia

Pick's disease

  • 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


frontotemporal dementia (FTLD) genetics

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)


memory loss, "patchy" focal neuro findings, high bp, high cholesterol, diabetes

vascular dementia


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

normal pressure hydrocephalus


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



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


Decks in M2 Neuron Brain Behavior Class (53):