Behav. Sci. Dementia Flashcards
what are age-associated cognitive changes?
- difficulty retrieving words and names
- slower processing speed
- difficulty sustaining attention when faced with competing environmental stimuli
- learning something new takes a bigger effort
- no functional impairment
how does dementia occur?
on a continuum (normal aging, followed by mild cognitive impairment, followed by dementia)
mild cognitive impairment definition
- memory complaint corroborated by an informant
- objective memory impairment for age and education
- preserved general cognition
- normal activities of daily living can still be done
- not demented
amnestic MCI
- memory loss not meeting the criteria for dementia
- progresses to AD at rate of 10%-15% per year vs. 1%-3% incidence in the general population
- may be the earliest phase of AD
- clinical diagnosis because no “MCI test”
DSM-IV diagnostic criteria for dementia
memory decline/impairment and at least one of the following:
aphasia (language decline)
impaired executive function
apraxia (inability to do certain actions)
agnosia (inability to interpret sensations)
-cognitive deficits must impact social/occupational function
early-onset AD
occurs btw 30-60
rare; familial in most cases
what are the gene mutations present in early-onset AD?
1,14,21
1 - presenilin 2 mutation
14- presenilin 1 mutation
21 - abnormal amyloid precursor protein
late-onset AD
MC
develops after 60
combination of factors
which gene is implicated in late-onset AD?
chromosome 19 - apolipoprotein E4 gene
what is present in the brain of someone with AD?
amyloid plaques (alpha beta) both extracellular and in arteries (amyloid angiopathy) neurofibrillary tangles (intracellular inclusions of tau)
what is disproportionately atrophied in AD?
hippocampus (memory!)
what does silver stain show?
neuritic plaques and neurofibrillary tangles in AD brain
congo red shows what?!
amyloid in plaques
what are the cleave sites on APP?
40 and 42 - 42 is worse
mutations in which gene is responsible for the large majority of cases of autosomal dominant alzheimer’s?
presenilin
how does a neuritic plaque appear?
dense central core of compact amyloid surrounded by a clear zone and a peripheral corona or halo
what is the patient at risk for when they have amyloid angiopathy?
hemorrhage
why does the body have difficulty clearing neurofibrillary tangles?
insoluble - body can’t clear
how do neurofibrillary tangles appear?
flame shape (form shape of neuron)
what are the neurofibrillary tangles?
hyperphosphorylated tau (microtubule-associated protein)
frontotemporal lobar degeneration gene
FTLD-tau (can also have TDP or FUS associated)
earlier onset than AD
affects anterior frontal and superior temporal lobes, spares occipital and parietal
knife edge
what protein is associated with frontotemporal lobar degeneration?
pick bodies (tau) - rounded
AD risk factors
increasing age, females, family history, less education, depression, head injury, low folate and vit B12, presence of apolipoprotein E4 allele, alcohol abuse
what are the 3 key features of AD?
impaired cognition, impaired function, and behavioral disturbances
how to tell the difference between depression vs dementia
- depression will demonstrate less motivation during cognitive testing
- express cognitive complaints that exceed measured deficits
- maintain language and motor skills
frontotemporal dementia (pick’s disease) vs alzheimer’s
Pick’s has insidious onset, gradual progression
early decline in social interpersonal conduct
early impairment in regulation of personal conduct with loss of insight
early emotional blunting
characterized by behavioral abnormalities
memory loss occurs later
treatment for frontotemporal dementia
no role for cholinesterase inhibitors
careful use of atypical antipsychotics (quetiapine, risperdol)
divalproex for behavior control
SSRIs for irritability, depression, impulsiveness
pharmacotherapy of alzheimer’s
cholinergic (donepazil - ACE inhibitor)
NMDA receptor antagonists
what is the most used class of drugs for AD right now?
neurotransmitter replacement
why do anticholinesterases work?
AD results in degeneration of basal nucleus causing acetylcholine deficiency which contributes to the memory deficits
what are the anticholinesterases used in AD?
donepezil, rivastigmine, galantamine
what is memantine?
glutamate NMDA receptor blocker used in AD
what are the options for treating neuropsychiatric disturbances in AD patients?
- counseling! look for the triggers - behavioral approach
- antipsychotics (risperidone and haloperidol)
- antidepressants (sertraline and venlafaxine)
- anxiolytics (buspirone and lorazepam)
vascular dementia
multi-infarct dementia
cerebral amyloid angiopathy (can be in association with alzheimer’s)
hypertension-related small vessel disease
what is present in the brain of vascular dementia?
lacunar infarcts subcortical dementia (cognitive slowing, impaired problem solving, visuospatial abnormalities, disturbances of mood/affect)
vascular dementia clinical appearance
“step wise progression” abrupt after CVA, seen with cardiovascular risks
“mixed” dementia with AD or Lewy Body not unusual
emotional lability
treatment of vascular dementia
focus on controlling cardiovascular risk factors
also: cholinesterase inhibitors (donepezil, galantamine, rivastigmine)
Lewy body dementia
characterized by intracellular, fibriller deposits of presynaptic terminal protein alpha-synuclein (lewy bodies)
what are the lewy body disorders
- parkinson’s
2. dementia with lewy bodies
parkinson’s disease
MCC parkinsonism (tremor, postural instability, impaired voluntary movement) dopaminergic deficit (responsive to L-dopa)
lewy body dementia vs parkinsons
lewy body: onset of dementia within 12 months of parkinsonism
parkinson’s: onset of dementia more than 12 months AFTER diagnosis of PD
what is needed to make diagnosis of parkinsons’
pallor of substantia nigra AND lewy bodies
dementia with Lewy bodies
- memory less affected than AD,
- frontal and subcortical features (deficits in attention and alertness),
- pronounced fluctuations and variations in symptoms
- have vivid visual hallucinations and delusions (including dreams - REM sleep disorder)
where are lewy bodies more present in dementia with lewy bodies?
cortical - amygdala and cingulate gyrus most common
how do lewy bodies appear?
dark core and pale corona - stain positive for alpha-synuclein
Mini Mental Status Exam
used for screening normal 30-27 mild 30-20 moderate 20-10 severe 10 or lower
MoCA (montreal cognitive assessment)
normal more than 26
mild 18-26
moderate 10-17
severe less than 10
functional assessment: ADLs
activities of daily living: DEATH
dressing, eating, ambulating, toilet, hygiene
functional assessment: IADLs
instrumental ADLs: SHAFT
Shopping, Housekeeping, Accounting, Food prep, Transport
