Neurocognitive Flashcards
dementia
slow onset, progressive, chronic
not better explained by different disease
how is delirium different from dementia
acute onset of reversible mental status
dementia is characterized by
significant and progressive decline in cognition involving one more more cognitive domains that affect independence in everyday activities
can’t be exclusively during delirium and not better explained by another disorder
symptoms of dementia
difficulty…
retaining new information
handling complex tasks
reasoning
spatial ability/orientation
language
behavior
behavioral disturbances
common in dementia
associated with adverse outcomes, increased disability, caregiver stress, earlier institutionalization
behavioral assessment should asses which disturbances
agitation/aggression
hallucinations
delusions/paranoia
sundowning
mCI
presence of memory difficulty and objective memory impairment BUT preserved ability to function in daily life
increased dementia risk
10 warning signs of dementia
- memory loss
- difficulty preforming everyday tasks
- problems with language
- disorientation to time and place
- poor or decreased judgement
- problems with abstract thinking
- misplacing things in unusual places
- changes in mood/behavior
- Changes in personality
- loss of initiative
dementia detection
minimental status exam
orientation, registration, language, recall
max score is 30, less than 24 Is abnormal
best if done serial
subtypes of dementia
- Alzheimer’s dz
- vascular multi infarct dementia
- dementia with Lewey bodies
- frontotemporal dementia
- Parkinson disease w/dementia
MC cause of all dementia
alzheimer
rare autosomal dominant but MAJORITY OF CASES are sporadic
histological findings of AD
extracellular amyloid plaques (senile plaques)
intraneuronal protein tau in neurofibrally tangles
AD pathophysiology
development of progressive atrophy and gloss
first to hippocampus then moves into areas of brain controlling thinking and decision making
AD risk factors
increasing age
family history
HTN, depression, insulin resistance, down’s head trauma
MC in women, African Americans
genetic disposition for AD
mutation accounts for <5% of AD but all early onset AD
when to consider AD
insidious and progressive memory loss
significant impairment in language, visuospatial dysfunction ,executive function and behavior changes
AD work up
should rule out other causes
physical exam, MME
Blood work (LFT, B12, TSH, CBC, RPR)
Imaging (non contrast CT)
staging of AD
pre clinical
no changes in judgment or impairment of daily activity
staging of AD
mild AD
pts get lost in familiar places, lose ability to handle money
increased dependence on the caregiver,
staging of AD
moderate AD
pt can’t make sense of world around and relies on caregivers
agitation, wandering, tearfulness (esp. @ night)
staging of AD
severe AD
completely unable to communicate
bed bound with loss of bowel/bladder = infection
mc cause of death in AD
infection (aspiration, PNA, UTI, skin infection)
general AD tx
symptomatic (cholinesterase, NMDA)
psychotropic drugs to change behavior and mood disturbance
cholinesterase inhibitors
benefit on cognitive fxn and ADLs, help non cognitive symptoms (personality changes)
used in all stages
cholinesterase inhibitors ADRs
weight loss, n/v/d and dizziness
bradycardia, AV block, syncope, falls
SJS
cholinesterase inhibitors used inAD
Donepezil (Aricept)
Rivastigmine (Exelon)
Galantmine (Razadyne)
Donepezil brand + indications + ADR+ formulation
(Aricept) AD tx
tablets or ODT
decreased drug interactions but cholinergic side effects common
OK in liver/renal
Rivastigmine brand + formulations + ADR + indication
(Exelon) mild-mod AD
tablet, patch
reiterate if d/c > 3 days
cholinergic SE, meals with food, no dose adjustment in CKD but in liver DZ
galantamine brand + indications + ADR+ formulation
Razadyne
suspension (can be mixed in non-EtOH)
mild - mod dementia
dose adjust in CKD + Liver dz
partial NMDA antagonist used in AD
Memantine (Namenda)
AD and NMDA receptor
excessive stimulation due excessive glutamate causing increased CA and disruption of information processing
memantine MOA
NMDA antagonist
improves glutamate transmission and lessening overstimulation = slowed death
Namenda indications
memantine/NMDA antagonist
mod-severe AD (+/- cholinesterase)
what can you do to slow progression or reduce risk of AD
reducing brain inflammation (I.e. NSAIDs)
Good diet and exercise (may slow progression, limited alcohol use)
vascular dementia
multi-vascular dz that causes dementia
Vascular dementia and AD often co exist
types of vascular dementia
multiple cortical infarcts
single infarct
small vessel disease
multiple infarct dementia
combined effects of different infarcts produces cognitive decline
single infarct dementia
one large infarct causes severe impairment
small vessel dementia is divided into two types
no big step off instead over time
subcortical leukoencepholopathy (white matter)
numerous lacunae (small vessel occlusions)
mild vascular cognitive impairment
cognitive decline worse than expected for age and edu. BUT effects don’t meet criteria for dementia
memory issue but functional skills are within normal limits
vascular dementia epidemiology
MC in men , asians
more rapidly fatal due to increased likelihood of other CV risks
HTN is main risk factor
vascular dementia presentation
acute cognitive impairment after a neurologic event (single infarct)
may develop subacute impairment of stepwise progression
progressive motor and cognitive, mood changes over years
depression and intellectual defects occur = disoriented with memory deficits inattention and vague inability to focus
how to differentiate vascular dementia and AD
vascular: greater deficits of frontal executive fxn (balancing check book), PATCHY* neuro deficits
AD: long term memory defects (what did I eat for breakfast?), global neuro deficits
apathy early on = VD
tx of vascular dementia
prevention of NEW strokes
Antiplatelet drugs, statins, controlling vascular risk factors
DLB
dementia that is 2/2 disruption of neuronal flow from frontal lobe to other areas of brain
DLB epidemiology
older age, more common in men, all ethnicities
may be with PD and AD
presenting clinical features of DLB
PRESENTS with dementia (AD -= memory loss)
early impairment in attention, executive and visuospatial fxn
severe sensitivity to neuroleptics, hypersomnia, orthostatic HoTN
4 core clinical features of DLB
Must have 2 of 4
- fluctuation in cognition and alertness (good days and bad days)
- visual hallucinations (v uncommon in AD)
- Parkinsonism (less severe than PD)
- REM sleep behavior disorder (dream enactment)
DLB testing
MMSE shows impaired figure copying, clock drawing, spelling world backwards (executive functioning)
AD pts have trouble with recall and orientation
clues to DLB diagnosis
fluctuations in cognitive functions, naps > 2 hrs, unresponsiveness, orthostatic HotN, hallucinations, delusions, parkonsonians
etc.
diagnostic work up of DLB + tx
neuropsychological testing
cholinesterase inhibitors (tx apathy, anxiety, hallucinations, delusions)
Parkinsonism meds
SSRI
atypical neuroleptics
what class of drugs is C/I’d in DLB
HALDOL (first gen antipsychotics)
dementia characterized by focal degeneration of frontal and temporal lobes
frontotemporal dementia
umbrella term for multiple different types
FTD epidemiology
patients in late 50s and early 60s
men > female
s/s FTD (9)
- personality/social behavior/language changes progressing to dementia affecting cognition
- extrapyramidal or motor neuron involvement
- difficulty with speech
- disinhibition, impulsiveness, giddiness, apathetic
- neglect of personal hygiene, mental rigidity, stereotyped behavior
- loss of social awareness, empathy
- hyperorality, inappropriate sexuality, binging, carb craving, EtOH and tobacco excess
- compulsions
- utilization behavior
FTD on exam
speech: non-fluent, difficulty finding words
behavior changes
visual and spatial functions and constructional tasks
memory is preserved
new artistic or musical talents
tx of FTD
symptomatic management
SSRI (Zoloft, Paxil)
trazodone (sleep and behavior changes)
neurotransmitter therapies don’t work
progresses more rapidly than AD (8-10 yr survival)
