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positive impacts of aging
lifelong storage of semantic, procedural and episodic memories
brain experience specialization in areas of cognitive and linguistic strength
aging cognition
processing speed may slow
working memory ay decline in complex tasks
more effortful recall of episodic memory
semantic memory largely preserved or expanded
elderspeak
speaking to an elder as if they were a child
talk louder, slower and more motherly
is demeaning and can have negative influence on communication with patient
mild cognitive impairment (MCI)
condition of cognitive decline that is not consistent with normal aging (typically does not include aphasia)
impairment in at least one domain (memory, attention, language, executive functioning)
associated with neurodegenerative changes, not injury
often progresses into dementia but not always
3 subtypes
amnesic
single domain
multiple domain
MCI: amnesic
most likely associated with conversion to Alzheimer’s disease
episodic memory impairment
MCI: single domain
prominent deficits in a non-memory domain such as
executive function
language
visuospatial ability
only one domain impaired
MCI: multiple domain
involvement of multiple cognitive domains and may occur with or without memory impairments
dementia
major neurocognitive disorder (MND)
aquireed and persistent impairment of multiple cognitive domains of sufficient severity to limit competence
domains include
memory
language
attention
executive function
visuospatial abilities
DSM criteria for MND
significant decline in multiple domains
impairment in daily activities and independence
decline is not due to delirium
reversible symptoms
symptoms may be reversible if causes by issues like:
untreated depression
normal pressure hydrocephalus
vitamin or nutritional deficiency
some medications
thyroid disease
metabolic cause
assessments for dementia
cognitive screeners
informal cognitive screening tasks
caregiver report measures
formal assessment
dementia types
alzheimer’s disease (AD)
vascular dementia (VaD)
dementia with lewy bodies (DLB)
frontotemporal degeneration (FTD)
alzheimer’s criteria
an insidious onset (months to years)
clear history of worsening cognition
amnestic or non-amnestic cognitive deficits
alzheimer’s
severe memory loss, loss of control and mobility, aggressive or delusional behavior
most common type of dementia
progressive diffuse brain atrophy and neuritic plaque
start in medial and anterior temporal lobes
VaD criteria
decline in two ore more domains of cognitive functions
imaging evidence of cerebrovascular disease
temporal relationship between occurrence of vascular event and onset of cognitive deficits
no history of gradually progressive cognitive deficits
VaD
onset can be from vascular event
caused by problems of blood supply to the brain
progression of cogntive-communication symptoms either sudden spurts or slow and continuous
often have slow gait, poor balance, more frequent falls
DLB
presence of lewy bodies that balloon, clump of neuronal protein that build up in the cerebral cortex
sleep disturbances, hallucinations, fluctuating attention, reduced speech rate and fluency
symptoms occur in the absence of significant memory impairment
parkinson’s
DLB and parkinson’s biologically related, showing presence of lewy bodies
combo of cognitive impairments and extrapyramidal signs
dementia occurs only in some people with parkinson’s
FTD
umbrella term for neurodegenerative conditions caused by atrophy of the anterior frontal and temporal lobes
onset 45-60 years old
isolated speech and language impairments earliest symptoms
primary progressive aphasia used when speech and language deficits present for 2 years
3 types
behavioral
language
motor
dementia intervention
train compensatory strategies
direct treatment
incorporate loved ones
focus on social interaction
primary progressive aphasia
type of aphasia and considered form of dementia
first symptoms are linguistic in nature
onset is progressive with rapid progression
3 types
semantic (sv-PPA)
nonfluent (nfv- PPA)
logopenic (v-PPA)
assessments for PPA
SLPs do not diagnose on our own
not a single tests, but can use subtest from other tests
capture features on lexical retrieval, syntax and repetition
subtest
boston diagnostic aphasia exam (BDAE)
western aphasia battery (WAB)
hopkins action naming assessment
sv-PPA
bilateral anterior temporal lobe atrophy
prominent anomia (stems from loss of semantic knowledge)
verbal output includes intact syntax
frequent pauses, empty speech, numerous semantic paraphasias
word knowledge fades, understanding language becomes more difficult
sv-PPA intervention
people in all stages can learn new words, capitalize on
spared recognition memory
episodic memory
consistent rehearsal
using personally relevant stimuli
nfv-PPA
trouble repeating, difficulty with grammar
may have motor speech disorder
difficulty producing longer an more complex sentences
atrophy of left inferior frontal
“broca like aphasia”
nonfluent agrammatic
nfv-PPA interventions
using low and high tech AAC
script training
communication notebooks
lv-PPA
degeneration of frontal lobes
reduced output, reduced rate of speech with frequent pauses, grammatically simple but correct sentences
impaired auditory comprehension and word finding difficulty
impaired repetition, reading and spelling
lv-PPA intervention
phonological cuing repetition exercises
high and low tech aac
client-directed assessment and interventions
PPA intervention
maintaining language (SFA, script training, etc.)
training communication partners
considerations for proactive AAC
documentation
avoid documenting dementia inless high degree of certainty
inaccurate diagnosis may lead to unnecessary grief and stress
social stigma
may impact eligibility for coverage