5- Delirium and Dementia Flashcards
other names of delirium syndrome
acute confusional state
Toxic metab encephalopathy
signs of delirium syndrome
rapid developing disorder of attention –> can’t maintain coherent line of thought (hyperaroused + agitation + restlessness)
1) fluctuating consciousness
2) impaired attention
3) incoherent speech
delirium syndrome
reversible or not?
more common form (hypo or hyper) and causes of ea
reversible
more common = hypoaroused with lethargy/somnolence
less common = hyperaroused = delirium tremens
common etiologies of delirium
drugs and toxins metab disorders infection/inflamm structural lesions seizure disorders
usu reversible or metabolic/toxic cause
what is a major drug cause of delirium
polypharmacy
20-30 meds not manageable esp older patients and disrupts normal brain homeostasis
ddx of delirium
1) dementia
2) amnesia
3) aphasia
4) schizo
5) mania
6) depression
evaluation of delium
1) H and P
2) mental status
3) blood chem
4) urinalysis
5) ECG
6) CXR
7) toxicology
8) CT/MRI, LP, EEG
describe dementia
acquired and persistent impairment in intellectual functions with deficits in
1) memory
2) language
3) visuospatial skills
4) complex cog
5) emotion or personality interfere with usu social/occup fxn
dementia
acute or chronic
level of consciousnesss
can causes include toxic or metab
chronic, not progressive
normal level of consciousness
not usu toxic and metab causes
reversible causes of dementia
1) drugs/toxins/alcohol
2) mass lesions
3) NPH
4) hypothyroid
5) vitamin B12
6) neurosyphilis/SLE
7) mild TBI
8) depression
irreversible causes of dementia
1) alzheimer’s
2) FTD
3) vascular
4) huntington’s
5) parkinson’s
6) lewy body
7) CJD
8) AIDS dementia
evaluation steps of dementia
1) H and P
2) CMP, CBC, TSH, B12, RPR for syphilis
3) MRI or CT
4) lumbar, eeg, hiv, esr
types of dementia
cortical
alzheimer’s
frontotemporal (pick’s)
types of dementia
subcortical
parkinson’s disease
huntington’s
types of dementia
white matter
NPH
binswangers
types of dementia
mixed
multi infarct dementia
CJD
stages of alzheimer’s disease
live 6-12 yrs after onset; decr 3 points on MMSE/yr
I = initial amnesia, anomia (can’t recall names of everyday objects), apathy
II = marked amnesia, fluent aphasia, visuospatial dysfunction, anosognosia, neuropsych features
III = severe dementia, global aphasia, or incontinence
causes of alzheimer’s disease
genetics
all down syndrome get AD (overexpressed amyloid plaque formation)
older folks susceptible because APOE gene on chrom 19
cholinergic hypothesis = loss of ACh
cholinergic hypothesis of alzheimer’s disease
early loss of cholinergic cells in basal forebrain so treat with
cholinesterase inhib (donepezil, rivastigmine, galantamine, memantine
guiding treatments of delirium
1) attention to etiology
2) environmental manipulations
3) adequate sleep (no nap/daytime)
4) treat agitation
drugs for adequate sleep in delirium
1) trazodone
2) zolpidem
drugs for agitation in delirium
atypical neuroleptics
benzodiazepines
understand principles guiding treatment of dementia
cholinergic hypothesis
informed counseling
avoid drugs that worsen
cautious of alternative treatments
drugs for AD
cholinesterase inhib (donepezil, rivastigmine, galantamine) memantine
easier to deal with __ compared to delusion or behavioral changes
major symptoms of dementia
memory loss
aggressiveness, delusions of fidelity
delirium vs dementia timing level of consciousness attention? speech difficulty? toxic metab causes? reversibility?
delirium vs. dementia acute vs. chronic fluctuating vs. normal impaired vs. normal incoherent speech vs. aphasia found vs. not reversible vs. not
underlying pathophys of delirium
diffuse brain dysfunction due to disruption of normal homeostasis
mostly cholinergic, dopaminergic, histamin, nroadrenergic, serotoninergic
define mild cognitive impairment
memory impaired for age/education
normal cognitive, no dementia
intermediate btwn normal aging and Alzheimer’s (incr risk for AD)
gross signs of Alzheimer’s
etiology of AD
1) cerebral atrophy
2) cortical neuron/synapse loss
2) major damage to limbic and assoc cortices
etiology = genetic + environment
microscopic path of AD
1) neuritic (amyloid) plaques
2) neurofibrill tangles in neocortex and hippocampus
mutations assoc with early onset AD
onset before age 65
APP on chrom 21
PSEN-1 on chrom 14
PSEN-2 on chrom 1
mutations assoc with late onset AD
APOE on chrom 19
E4 = higher risk
E2 = protective
FTD affects where?
what is spared until late dz
so symptoms?
affects frontal +/- temporal lobe
hippocampus spared
behavioral early before memory loss
FTD suggested by early features of
frontal lobe dysfunction (disinhib, apathy, exec dysfunction, aphasia
memory normal
many patients first dx with bipolar disorders
Parkinson’s disease
1) mechanism
2) what kind of deficit seen? and treatment?
1) loss of dopaminergic cells in midbrain SN
2) cholinergic deficit–> use cholinesterase inhibitor
Huntington’s disease
1) symtpoms
2) drugs to use?
AD
dementia and chorea; early personality changes –> disinhibition, poor judgment, antisocial
use neuroleptics and tetrabenazine for chorea
Binswanger’s disease
1) mechanism
2) symtpoms
1) vascular dmeentia with severe cerebral white matter ischemia
2) insidious behavioral and cognitive decline
acute focal onset (stroke) in 1/3
neuroimaging of binswanger’s disease
CT
MRI
CT = low density white matter lesions
2) MRI = patchy or confluent white matter; hyperintensities on T2, proton density, FLAIR
ventriculomegaly
neuropath of binswanger’s disease
white matter volume loss esp periventricular = hydrocephalus ex vacuo
thick and hyalinized small vessels
ischemic demyelination esp of association fibers (spare U fibers)
incomplete infarct of white matter
NPH
reversible?
clinical triad?
CT MRI signs?
treatment?
reversible
dementia, gait disorder, and urinary incontinence
ventriculomegaly and normal cortical gyri
high volume lumbar tap test improves gait and cognition
treatment of NPH
surgery = VP, VA, LP shunts
gait more likely to improve
Multi-infarct dementia
combination of ?
clinical course?
prevent and treatment =?
combo of cortical + subcortical strokes –> dementia from accum destruction of brain tissue
step wise course from new strokes
ASA, heparin, warfarin, tPA, carotid surgery
CJD
symptoms
progression
treatment?
rapid dementia with acute confusion, hallucinations, delusions, myoclonus
ends in 1 yr
no treatment
mechanism of CJD
diagnosis of CJD
what do you see on EEG and CSF
conformational change in prion –> neuronal loss, gliosis, spongiform changes
diffusion MRI = deep gray matter/cortical hyperintensity
EEG = periodic discharges
CSF = 14-3-3 protein
treatment of cognitive impairment in dementia
cholinesterase inhib
memantine = NMDA antagonist
delirium tremens symptoms
hallucinations
delusional
agitation/restlessness
from alcohol withdrawal
most common cause of Binswanger’s disease
uncontrolled HTN
