quiz 4 Flashcards
what are the criteria that define a major neurocognitive disorder (NCD)—and how is this differentiated from a minor NCD?
(from the diagnostic and statistical manual of mental disorders)
major NCD:evidence of a significant cognitive decline from a previous level of performance in 1 or more cognitive domainsª
-the cognitive deficits interfere with independence in everyday activities
-they don’t occcur exclusively in the context of delirium
-the cognitive deficits aren’t better explained by another mental disorder
minor NCD: cognitive decline is modest
-cognitive deficits do not interfere with independence
-but–greater effort, compensatory strategies or accommodation may be required
ª i.e. complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition
percent of american over age 65 and over age 85 that are estimated to have alzheimer’s disease
(in 2012–from the alzzheimer’s association)
13% of people over 65 yrs
45% of people over 85 yrs
alzheimer’s dementia
biological cause/markers, cognitive profile, & communication profile
biomarkers: [in vivo] amyloid metabolism or imaging abnormalities
- [neuropathologically] abundance of plaques & tangles
- [genetically] abnormalities in some patients
cognitive: deficits in memory & cognition
- no disturbance of consciousness
- impaired function in daily life
communication: aphasia is common (starting as F or NF)
- semantic system most affected—syntax & phonology later
- gradual progression to mutism
cognitive profile same as vascular
vascular dementia
biological cause/markers, cognitive profile, & communication profile
biomarkers: white matter ischemic necrosis w/ neuronal loss (leukoencephalopathy)
- multiple brain infarcts
cognitive: deficitis in memory & cognition
- no disturbance of consciousness
- impaired function in daily life
communication: motor speech disorder
- simplification of grammar & impaired writing
- slowness & reduced initiation
- abulic at later stages
lewy body dementia
biological cause/markers, cognitive profile, & communication profile
biomarkers: cortical & subcortical sites are affected
- daytime drowsiness in some & transient confusion on waking
cognitive: fluctuating attention (marked shifts in alertness)
- visual hallucinations
- parkinsonismª
communication: parkinsonian dysarthric features (e.g. hypophonia)
ªtremor and impaired muscular coordination
frontotemporal lobar dementia
biological cause/markers, cognitive profile, & communication profile
biomarkers: focal cortical atrophy (neuronal loss in particular cortical regions)
cognitive: depends on variant
- frontal lobe v: executive dysfunction
- temporal lobe v: semantic deficits
- NF aphasia v: NF progressive aphasia
communication: primary progressive aphasia [PPA] is no uncommon
- dysarthria unlikely
- progression may be very slow
genetic and biological markers for the likely conversion of mild cognitive impairment [MCI] to alzheimer’s disease
genetic: abnormality of the gene for apolipoprotein E [APOE]
biological: CSF analysis shows low levels of the beta-amyloid protein and/or the tau protein is elevated in CSF
- beta-amyloid and tau are biomarkers for amyloid plaques, neurofibrillary tangles, and loss of neuronal connections and cell death
cognitive stimulation
treatment for dementia patients
elicit active responses to increase memory, planning, and conversation
reality orientation
reinforce awareness by calling atention to upcoming events or current environment
simulated presence therapy
decrease social isolation, agitation, and verbal or physical aggression using tapes created by family members
reminiscence therapy
capitalize on preserved cognitive abilities to improve communication and discourse skills, memory, and recall of personal events
spaced retrieval
increase declarative memory using questions, while systematically lengthening the interval between stimulus and recall
