9/28 Dementia & Delirium - Schneider Flashcards
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:
-
association fibers: connection between different cortices in same hemisphere
- ex. U-fibers, fasciculi
- commisural fibers: connection between two cerebral hemispheres
- 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
&
delirium
- 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
dementia
- 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:
- change from baseline
- evidence of cognitive impairment
- 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
however,
not associated with significant functional impairment!
delirium vs dementia
time course
primary sx
daily sx
reversible
treatment
mortality
overall:
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
- ABCs, vitals, finger stick glucose
* glucose low? thiamine! - history and physical exam
* looking for physical exam findings that point to an etiology - 5 routine labs/diagnostics
- 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
Wernicke’s!
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
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
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:
- tau: mutation to microtubual-assoc protein tau (MAPT, chr17) → FTDP-17
- TDP-43: mutation to progranulin gene (PGRN, chr17) and C9orf72 (chr9) have high association
- 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
Huntington’s
significant memory loss over a few months, starte myoclonus, disinhibition, personality change
CJD
