1
Q
- evidence of substantial decline in one or more of the cognitive domains
- deficits are sufficient to interfere with independence
- test performance of >2 SDs below the mean
- problems cannot be attributed to another factor e.g. depression
A
Major neurocognitive disorder
1
Q
What is the name of the protein structures contained in neurites?
A
microtubules
1
Q
causes tau to unbind and form twisted filaments
A
hyperphosphorylation
1
Q
Treatment for Alzheimer’s disease (2)
A
- medication- act on neurotransmitter systems
- behavioral interventions- SLP
2
Q
- relatively rare
- neuropathology
- tau deposition in brain stem, including substantia nigra
- hypothesized causal agents include viruses, environmental exposures (via waer, air) random gene mutations, and free radicals
- symptoms
- similar to but different from Parkinson’s
- problems with balance
- cognitive changing, bradycognition, memory
A
Progressive supranuclear palsy (PSP)
3
Q
- cytoskeleton of the neurites
- also transport biomolecules (proteins, lipids, sugars) from the cell body to the axon end terminal
- MAP proteins bind to and stabilize the microtubles
- Tau is the axon’s MAP proteins
A
Microtubules
3
Q
Where does early cell loss often begin with Alzheimer’s?
A
medial temporal lobe
3
Q
- type of vascular dementia
- inherited
- mutation of Notch3 gene
- first symptoms can appear between 20 and 40 years
- often undiagnosed
A
CADASIL
4
Q
- modest decline in memory attention, language, orientation and/or perception
- noted by the individual, knowledgeable informant or the clinician
- test performance 1 to 2 SDs below the mean
- deficits do not interfere with independence
- problems cannot be attributed to antoher factor, e.g. depression
A
Minor neurocognitive disorder
5
Q
facility of a person in conversation; includes abilities such as turn-taking, type of initiation, and type of response
A
Conversational analysis
5
Q
- not everyone with PD will develop dementia, however majority will
- great individual variation in the time from initial diagnosis of PD to the development of dementia
A
Synucleinopathies- Parkinson’s Disease Dementia
6
Q
AD
no obvious signs or symptoms
A
preclinical stage
6
Q
- prevalence estimates vary from 2nd to 4th most common
- neuropathology
- several forms of FTD
- some forms of tauopathies
- some people with FTD have mutant gene for tau
- other forms of FTD involve mutant genes for other proteins- not tauopathies
- initially affects frontal and/or temporal obes
- two main types of FTD
- behavioral varient
- primary progreessive aphasia
- diagnosis
- imaging
- behavioral testing
- treatment
- medication
- antidepressants, antipsychotics
- Namenda for memory
- other drugs for memory used with AD may exacerbate symptoms
- speech-language therapy for the language varient
- medication
A
Tauopathies- frontotemoporal degeneration (FTD)
7
Q
- no specific gene that causes this
- certain alleles (forms) of the apolipoprotein E (APOE) gene increase risk for developing this
- presence of e4 allele increases risk
A
Late onset Alzheimer’s
8
Q
2 new terms that replace dementia
A
- minor neurocognitive disorder
- major neurocognitive disorder
9
Q
True or false
a definitive diagnosis of Alzheimer’s disease can only be made through autopsy
A
true
10
Q
what is the most common type of dementia?
A
Alzheimer’s Disease
11
Q
- most cases are familial Alzheimer’s disease (FAD)
- linked to a single gene mutation on chromososmes 21, 14, and 1
- gene mutation leads to cleaving problems of APP
- individuals with the mutation will develop AD
A
early onset Alzheimer’s disease
12
Q
- AD stage
- inability to communicate
- inability to self feed
- swallowing problems
- lack of bowel and bladder control
A
severe Alzheimer’s disease
14
Q
amount, quality, and efficiency of the discourse. Measures: correct information units; correct information units/minute; propositions
A
Informational content analysis
15
Q
- a common late onset disease
- tau deposits called argyrophillic grains found in limbic regions, including hippocampus
- signs and symptoms indistinguishable from late onset AD
A
Argyrophilic grain disease
16
Q
- Prion- misfolded form of PrPc protein (PrPsc)
- misfolded form was discovered before the normal form
- normal form plays a role in myelin formation and iron metabolism
- prions appear to cause the normal PrPc to misfold
A
Prion disease
17
Q
- relatively rare
- underlying neuropathology
- tau inclusions in neurons and glia
- may be tangles similar to AD
- swollen neurons
- affects frontoparietal regions and substantia nigra with relative sparing of temporal and occipital lobes
- signs and symptoms
- relatively young onset
- initial symptoms- movement disorder or cognitive problems
- initially, movement disorder affects on side of the body
- limb rigidity, or akinesia, limb myoclonus, limb dystonia
- orobuccal or limb apraxia
- as the disease progresses, both sides affected
- cognitive problems include memory loss, progressive difficulty with language, behavioral problems
- Slow progression 6-8 years
- diagnosis
- no definitive diagnosis until autopsy
- imaging, behavioral testing (including SLP)
- tx with levadopa (L-DOPA)- people with CBD do not respond
- Treatment
- medications to control movement problems
- SLP, PT, OT
A
Tauopathies- Corticobasal degeneration
17
Q
- type of vascular dementia
- caused by multiple small strokes
- more likely when the strokes occur bilaterally
- can be caused by single severe stroke
A
multi infarct dementia
18
* AD stage
* typically memory problems
* also may have word finding problems and poor judgement
very early signs Alzheimer's Disease
20
* AD stage
* brain damage continues to expand
* memory problems continue to decline
* problems recognizing family and friends
* problems learning new things
* difficulty with multi-step tasks (e.g. getting dressed)
* paranoia, delusions
* impulsive behavior
moderate Alzheimer's disease
21
relationship of verbalization to the general topic
global coherance
22
LBD 1 year rule
if cognitive symptoms preceed motor problems by a year, what dx?
Lewy Body Dementia
24
* be sensitive to the family's adjustment to disabilities
* different families need different types of education and intervention
* treat each family member uniquely
family/significant other involvement
25
* Autopsies have revealed that many individuals with dementia have more than one neuropathology
* the typical pattern is both AD and vascular pathologies
Mixed Dementia
27
* prevalence estimates vary from 2nd to 3rd most common type
* neuropathology
* alpha synuclein aggregates (collects) in nerve cells
* aggregates called Lewy bodies
* Lewy bodies ofund in hippocampus, substantia nigra, limbic cortex
* cause is unknown
* symptoms
* loss of smell
* sleep problems
* visual hallucinations
* may initially diagnosed as psychiatric disorder
* later course
* cognitive symptoms ismilar to AD
* motor problems similar to PD
* Diagnosis
* difficult due to similarities with AD and PD
* 1 year rule
* imaging, behavioral testing
* Treatment
* meidcation to control some symptoms
* speech, OT, PT
Synucleinopathies- Leroy Body Dementia (LBD)
29
the underlying framework of the discourse for the organization of the information into recognizable patterns; presentation of temporal and causal relationships between characters and events
Superstructural Analysis (story grammar)
30
What is the age for early oset Alzheimer's?
30-60 years
32
the effectiveness with which sentences are meaningfully linked in the discourse
cohesion
33
During life diagnosis of Alzheimer's disease is made based on what four factors?
* history
* behavioral measures (e.g., MMSE)
* medical tests to rule out other, remediable causes
* imaging (CT, MRI)
34
* play a role by influencing gene expression
* can have a positive or negative influence
* includes factors such as diet, exerciese, smoking, and chemical exposure
* explain why one family members develop the disease (express the phenotype) and others do not
* evidence suggests environmental factors play a role in this
environmental factors- epigenetics
Alzheimer's Disease
35
relationship of the or content of a verbalization to that immediately preceding;
local coherence
36
About how many people over age 65 have Alzheimer's disease?
about 5 million people
37
LBD 1 year rule
if motor symptoms preceed cognitive symptoms by a year, what dx?
Parkinson's Disease Dimentia
38
* type of vascular dementia
* rare
* microscopic damage to the small blood vessels and neurons
subcorticla vascular dementia (Binswanger's disease)
39
* AD stage
* memory problems get worse
* additional problems develop
* getting lost
* problems managing finances
* echolalia
* mood and personality changes
* losing or misplacing things in odd places
* taking longer to complete normal tasks
mild Alzheimer's disease
40
analyze the linguistic attributes of the sentences, regardless of their relationship to the rest of the discourse
sentence level analysis
41
damage to cerebral vasculature (3)
* hypertension
* diabetes
* hypercholesterolemia
42
* alpha synucleir= found in the brain
* function of alpha synulein is unknown
* synucleinopatnes- alpha synuclein accumulates in neurons
synucleinopathies
43
* Prion disease
* neuron pathology
* spngioform changes
* progressive empty spaces in the gray matter produced by abnormal PrPSc protein
* similar to mad cow disease
* symptoms
* changes in eating and sleeping
* cognitive deterioration memory, language
* visual disturbances
* speech problems
* occurs most often in 60's, but 16-82 years
Creutzfeldt-Jakob's Disease
45
* abnormal behavior of tau proteins in neurons
* causes
* hyperphosphorylation
* abnormal phosphorylation
* causes tangling of microtubles
* aggregation of tau
* affects cell function and cell dies
Tauopathies
46
* two underlying neuropathologies of Alzheimer's disease
* beta amyloid plaques
* found in the spaces between neurons
* not clear if they cause Alzheimer's disease or are a consequence
* plaques created by cleaiving problems of amyloid precurser protein (APP)
* Tauopathy- hyperphosphorylation of tau resulting in tangles in the axons
47
* prevalence estimates vary from 3rd or 4th most common
* caused by damage to the cerebral vasculature
* multiple types
* CADASIL
* Multi infarct dementia
* subcortical vascular dementia
* Symptoms
* can appear suddenly
* often a step wise deterioration
* multi-infarct- may be focal or more global depending on lesion site
* subcortical-psychomotor slowness, working memory, and executive function problems
vascular dementia
48
Nerve cell components (2)
* cell body or soma
* neurites
* axon
* dendrites
49
* variable age of onset
* about 60% aged 45-64 years
* as early as 21 years, as late as 80 years
* behavior and personality changes
* may behave impulsively - steal things, behave rudely
* overeating
* saying or doing inappropriate things
* production of repetitive behaviors, clapping, singing
Behavioral Variant- FTD
50
There is little empirical data about treating discourse deficits, but the data that does exist suggests (2)
* develop awareness
* develop strategies
51
* fluent speech
* grammatical spoken language, but grammatical and spelling errors in written language
* empty, tangential speech
* mild dysnomia with semantic paraphasias and indefinite references (it, thing)
* attention deficits
* ideational perseveration
* disoriented to time, ut not place or person
* good motor function and ability to perform ADLs
Cognitive Communication Disorders in Alzheimer's Disease- Early stage
52
* most dramatic changes
* loss of independence
* motor function remains good
* worsening of episodic memory and deterioration of semantic memory
* can perform basic ADLs with supervision
* speech is fluent, but slow and halting
* language structure remains intact but content is significantly impaired
* many errors in written language
* significant word finding problems
* literal interpretation of non-literal language
* disorientation to time and palce, but not person
Cognitive Comunication Disorders in Alzheimer's Disease- Middle Stage
53
* disoriented x3
* fluent, but halting speech
* grammatical spoken language
* significant semantic deficits in spoken language
* severe problems in reading comprehension
* inability to express themselves in writing
* Bayles et al. found 82% of late stage individuals produced some spoken language
Cognitive Communication Disorders in Alzheimer's Disease- Late Stage
54
* Executive dysfunction most prominent
* problems in communication vary among individuals depending on site of lesion
* mixed dementia (AD + Vascular Dementia) more common than vascular dementia alone
Cognitive Communication Disorders in Vascular Dementia
55
* slowing of information processing
* executive dysfunction-problems solving, planning, set shifting
Dementia and Parkinson's Disease
56
* almost 50% demonstrate fluctuation in cognitive symptoms
* hallucinations are common
* relative preservation of confrontation naming ability, but impairment in verbal fluency
Cognitive Communication Disorders in Lewy Body Dementia
57
* language is initially spared
* changes in personality and behavior are the most prominent symptoms
* executive dysfunction
* problems in social cognition
* inability to process facial emotion
* problems perceiving sarcasm
* lack of reaction to fearful or sad stimuli
* may, in part, reflect executive dysfunction
Cognitive Communication Disorders in Behavioral Variant FTD
58
Purposes of a cognitive communication assessment (5)
* detect the presence of dementia
* identify cognitive communication disorders
* identify retained abilities
* establish baseline function for planning intervention and measuring response to treatment
* counsel caregivers
59
What should you do prior to conducting a cognitive communication evaluation? (4)
* review the patient's chart
* look for information regarding sensory impairment
* be familiar with the instruments used to quantify dementia severity
* arrange for a good testing environment
60
What should you do during cognitive communication evaluation? (5)
* check vision
* check hearing
* check literacy
* try to reduce test-taking anxiety
* be alert to possible medication effects on testing
61
* Rozsa and Bourgeois' Screening Protocols
* Bourgeois' Safety Assessment
Functional assessments of cognitive communication disorders
62
* Arizona Battery for communication Disorders of Dementia (ABCD)
* Aphasia tests (WAB, CADL)
* Functional Linguistic Communication Inventory (FLCI)
* Ross Information Processing Assessment Geriatric-2 (RIPA-G:2)
Formal tests for cognitive communication disorders (4)
63
Role of SLP in management of communication problems (3)
* diagnosis
* tx planning and delivery
* training staff and family
64
* maintain independence as long as possible
* maintain quality of life through supported participation and engagement
* reduce demands on impaired systems
principles of treatment for management of communication problems
65
* communication with elderly nursing home residents constrained by sterotypes of aging and the sick role
* staff often have low expectations and a desire for residents to take on the sick role
* this results in decreased communication
communication predicament model (Orange, Ryan, et al., 1995)
Cognitive Communication Disorders
flashcards
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