Final Exam Flashcards

1
Q

Orientation Terms

A
  • Superior: top
  • Inferior: bottom
  • Anterior: front; towards nose/face
  • Posterior: back; towards back of head
  • Dorsal: top of the brain
  • Ventral: bottom of brain
  • Lateral: away from the middle
  • Medial: towards the middle
  • Rostral/anterior: front/toward the nose/anterior/front of the brain head end of the body
  • Caudal/posterior: back/toward the tail end of the body
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2
Q

Brain Lobes

A

Forehead/blue: Frontal
Back of skull/yellow: parietal
Side/temple/green: temporal
Back just above neck/red: occipital

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3
Q

Brain Planes

A

Coronal: divides into back and front
Horizontal: divides into top and bottom
Midsaggital: divides into right and left

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4
Q

Language Regions

A

Neuroanatomy: Language and regions
• Broca’s Area (frontal lobe)-Expressive Language
• Wernicke’s Area (temporal lobe)- Receptive Language
• Arcuate Fasiculus (bundle of white matter)-Connection between Broca’s and Wernicke’s
• Primary Auditory Cortex (temporal lobe)
• Primary Visual Cortex (occipital lobe)
• Primary Motor cortex (frontal lobe)
• Primary Somatosensory cortex (parietal lobe)
*****Motor is anterior/rostral to somatosensory

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5
Q

Language Lateralization/Dominance

A

Language tends to be left side dominant; only damage to left side of brain will cause an aphasia
• Right sided damage doesn’t tend to cause aphasia
o Can cause pragmatic problems (not always)
• Some people can have language on right
o Very rare
o More common in left-handed people
• Also bilateral language, also very rare

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6
Q

Hippocampus function

A

*episodic memory, especially long-term
*Spatial awareness and processing
*

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7
Q

The blood to the brain comes from two major arteries

A

o The carotid artery

o The vertebral artery

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8
Q

Circle of Willis

A

• Located on the ventral/inferior side of the brain
• Connects the carotid and vertebral arteries
• Creates the 3 major arteries of the brain
1. Anterior Cerebral Artery-
• Anterior communicating artery connects them
2. Middle Cerebral Artery: most important for sending blood to areas of brain imperative for language
3. Posterior Cerebral Artery- connects middle cerebral artery and posterior cerebral arteries
• Also contains the communicating arteries (Anterior and Posterior communicating arteries), which help compensate in case there is a blockage in one of the major cerebral arteries; if there is a blockage blood can go around

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9
Q

Cerebrovasculature and aphasia

A
  • Wernicke’s Aphasia (left), Broca’s Aphasia (right) IMPORTANT FOR LANGUAGE FUNCTIONING; left side of brain most important for language
  • Middle cerebral artery are inside of that area (profused by middle cerebral artery)
  • Wernicke’s area: posterior superior portion of temporal lobe
  • Broca’s area: inferior posterior portion of frontal lobe
  • To have broca’s aphasia- have to have blockage/rupture in left MCA, in the superior division
  • Inferior division damage to left MCA cause damage to wernicke’s area, causes wernicke’s aphasia
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10
Q

Brain imaging Techniques important for “Where” (spatial resolution)

A
  1. Postmortem correlations: Broca (1844): Leborgne: Lesion models (done through post-mortem correlation)
  2. Transcranial Magnetic Stimulation (TMS)
    • More Lesion Models
    o Intracarotid Sodium Amobarbital Procedure (ISAP)/WADA test- put it in carotid artery to find out which side of brain is dominant for language or memory- very invasive
    o Pre-surgical planning
    o Invasive- minimize damage to language and memory
    • Single pulse; Repetitive (rTMS) (transcranial magnetic stimulation) = lasting effects; no lasting effects from single procedure; creates a virtual lesion through magnetic stimulation (turn neurons off/stops them from firing for a second)
    o Migraine headaches
    o Nonfluent aphasia
    o Major depression
    o Electroconvulsive therapy popular for people with manic/major depression; put electric leads on temples and start a seizure
  3. SPECT
  4. Positron Emission Tomography (PET)
  5. Computed Tomography (CT)
    • Often used clinically – cheaper and faster than MRI
    • Radiation exposure significant (3D xray; can cause a lot of cancer; lead coat helps reduce exposure to xrays)
    • Left CVA/Infarct (loss of blood to area of brain) ; with imaging, left is right and right is left
    Vasculature/cerebral aneurism images
6. Magnetic Resonance Imaging (MRI)
o	Structural
o	Functional
o	Diffusion Tensor Imaging (DTI) (new)
Rely on facts that:
•	Every tissue of body has water in it
•	Hydrogen molecules
•	Huge magnet aligns them all
•	They all fall/relax at different rates (depending on what tissue they are in) 
Differing rates of relaxation produce
•	contrast in different tissue types
•	T1 relaxation produces a high resolution structural image of frontotemporal dementia
•	White matter, gray matter, bone
DTI: 
*       Way of imaging neural tracts (connect 2 different gray matter areas together); does not care about structure as much
•	Creates beautiful pictures of white matter (very colorful)
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11
Q

PET vs. SPECT

A

Both rely on fact that
o Metabolic activity requires glucose
o Useful for oncology as tumors have high glucose uptake

Uses gamma radiation and gamma cameras (nuclear), good for finding tumors

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12
Q

Brain imaging Techniques important for “When” (temporal resolution)

A
  1. Electroencephalography (EEG)/ERP
    • Real‐time neural activity- measures electrical signals in brain
    • Limited spatial sensitivity- not good at “where”
    • Messy movement artifact- will mess up if you blink move or wrinkle forehead
  2. Magnetoencephalography (MEG)
    • Electrical current produces a magnetic field
    • Close to real-time, but not quite
    • Better spatial resolution than EEG; where seizure activity is starting
    • Used for seizure; localize issue and remove that part of the brain
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13
Q

MRI vs. CT Scan

A

CT scan is better for stroke because MRI will not detect acute CVA (cerebro-vascular accident/stroke)

MRI is a lot slower and more expensive than CT

MRI has highest spatial resolution

CT scan best for muscle/bone issues, fractures, blod clots, bleeding from the brain; MRI for tendons, ligaments, spinal cord

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14
Q

Differential diagnosis for aphasia

A

Aphasia is a language difficulty worse than, NOT, and not due to a cognitive difficulty

Communication also shouldn’t be affected by
o Dysarthria- difficulties with articulating speech
o Apraxia- inability to perform purposive action
o Agnosia- inability to name things in a certain modality (disconnect between sensory system and semantic knowledge)- can still recall info when shown in a different modality
o Sensory Disorder
o Dementia

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15
Q

Problems in aphasia

A
  • Stereotypic Utterances
  • Anomia
  • Circumlocution
  • Paraphasia
  • Nonfluency
  • Jargon
  • Agrammatism
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16
Q

Stereotypic utterance

A
  • Usually seen in very severe aphasia
  • May not be able to say anything other than one utterance
  • Can be a real word or a non real word like “tono”
  • Prosody may be intact
  • Say the same word over and over again
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17
Q

Anomia

A
  • Word finding issues
  • Unable to come up with word
  • Can be perfectly fluent but may have difficult coming up with words in constrained situations
  • Does not mean you are fluent or non-fluent
  • May only occur in constrained/difficult situations
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18
Q

Circumlocution

A
  • Difficulty coming up with word
  • Circle around idea
  • Usually lengthy responses
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19
Q

Paraphasia

A
  • Semantic paraphasia- replace word with another of a similar semantic class
  • Phonemic paraphasia- replace word with another with similar phonology (do not have to be real words)
  • Mixed paraphasia- replace word with another of similar semantic class and phonology
  • Unrelated paraphasia- replace with completely unrelated real word
  • Neologistic paraphasia- replace with completely unrelated non real word
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20
Q

Nonfluency

A
  • Rate and naturalness of speech
  • Slow and labored speech
  • A lot of uhm’s, ah’s stops
  • Very effortful
  • Common with Broca’s aphasia
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21
Q

Jargon

A
  • Semantic jargon- producing real words but done in a manner which does not make sense
  • Neologistic jargon- same as semantic jargon but with the non real words as opposed to real words
  • Essentially meaningless speech that is spoken as if it had meaning
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22
Q

Agrammatism

A
  • Loss of grammar skills in speech
  • Telegraphic speech-mostly content words
  • Loss of complexity of sentences, not a lot of fillers
  • Can get point across, but words are very simplistic and do not follow grammar rules
  • This video does a nice job summing up agrammatism
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23
Q

Aphasia/stroke risk factors

A
  • High Blood Pressure
  • High Cholesterol
  • A-Fib (atrial fibrillation- abnormal beating of heart)
  • Diabetes
  • Atherosclerosis
  • Tobacco Use
  • Alcohol Use
  • Obesity
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24
Q

F.A.S.T.

A

o Face- drooping
o Arms – if one arm is lower than the other when you ask them to lift them above head
o Speech – slurred, nonsensical
o Time – the quicker you call 911 and get person to services the less possibility of disability

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25
Q

Ischemic stroke

A

• A block in the arteries either due to blood clot or more commonly the buildup of plaque
• About 87% of all strokes are ischemic
• The brain needs blood
o After only 10-15 seconds without blood you pass out
o 2-3 minutes without blood leads to permanent brain damage
Types of Ischemic Stroke:
1. Thrombosis- blood clot or blockage occurs locally
2. Embolism- blood clot forms elsewhere and travels to brain and causes blockage

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26
Q

Hemorrhagic stroke

A
  • 13% of all strokes are hemorrhagic strokes
  • Occur when a blood vessel in the brain breaks and blood begins to leak in the brain
  • Blood accumulates quickly and can put a dangerous amount of pressure on brain
  • More likely to cause death than ischemic stroke – because it so quickly causes brain loss to happen, pressure causes brain damage
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27
Q

Types of hemorrhagic stroke

A
  • Epidural hemorrhage- bleed occurs between the bone and the dura mater
  • Subdural hemorrhage- bleed that occurs between the dura and arachnoid
  • Subarachnoid hemorrhage- bleed that occurs between arachnoid and pia mater
  • Cerebral hemorrhage- any bleed that occurs in the brain
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28
Q

Ischemic stroke treatments (list)

A

Thrombolysis, Thrombectomy, other management/drugs

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29
Q

Hemorrhagic stroke treatments (list)

A

Surgery

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30
Q

Thrombolysis

A
  • Clot busting
  • rTPA
  • Must be administered close to the onset of the stroke (within three hours) (thrombolysis)
  • Better outcomes have been found although these are controversial (some studies found not much difference in outcomes with/without TPA)
  • Increase in chance of hemorrhage
  • At first a lot of people were in love with it, now seen to not do as much as they thought and point above
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31
Q

Thrombectomy

A
  • Surgical removal (ectomy) of the thrombi
  • Much more invasive and risky (than thrombolysis)
  • Really only done if there is significant threat of (impending) death
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32
Q

Other management/drugs

A
  • Antiplatelet drugs – reduce likelihood of clots forming (aspirin, Plavix)
  • Vasodilator – drugs that help arteries/blood vessels to open up wider
  • Anticoagulants – reduce coagulation/clotting of blood (coumadin, warfarin) – after stroke, higher incidence of embolism/thrombus, will knock blood clots loose, used as preventative measure
  • Blood pressure medications – reduce blood pressure
  • Beta blockers – reduce pulse rate
  • Reduce risk factors – improvements in diet, exercise, reduce tobacco/alcohol use, quitting tobacco use after just 1 year gives you same chance of stroke as someone who never smoked
  • Carotid Endarterectomy
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33
Q

Carotid Endarterectomy

A
  • Remember the carotid artery (main artery that sends blood to brain, along with vertebral artery)
  • Catch it early!
  • If it is very blocked this procedure will occur
  • Reduces risk of second stroke
  • Risky surgery so only done if a significant blockage is present
  • Invasive/dangerous- once you open up a vessel the strength and stability of that vessel are reduced
  • Can be scarring in the artery which leads to more narrowing
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34
Q

Surgery for hemorrhage

A
  • Closing off ruptured vessel (or dilate another vessel) to move blood to another area)
  • Draining pools of blood
  • Craniotomy
  • Very large brain compared to size of skull, not a lot of space for brain to move, pressure will build up if any liquid gets in the brain; if hemorrhages are epidural/subarachnoid/subdural, they can do craniotomy (removal of a portion of the cranium) to relieve pressure and pool of blood; if cranium is left off for a period of time they actually store the cranium in the gut; open the abdomen and but cranium in the stomach and keep it there until they have to put it back; relatively common but controversial
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35
Q

Areas of brain affected by each aphasia

A
  1. Broca’s Aphasia- Broca’s area (frontal lobe)
  2. Wernicke’s Aphasia- Wernicke’s area (border of parietal and temporal lobe)
  3. Global Aphasia- Wernicke’s area, Broca’s area, and arcuate fasciculus (white matter track that connects Wernicke’s area and Broca’s area)
  4. Conduction Aphasia- Arcuate fasciculus
  5. Transcortical Motor aphasia- ACA-MCA watershed areas
  6. Transcortical Sensory aphasia- MCA-PCA watershed areas
  7. Transcortical-mixed aphasia- both ACA-MCA and MCA-PCA watershed areas
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36
Q

Bilingual aphasia is an acquired language disorder that results in problems in both languages for:

A

Production/Speech, Comprehension/Listening, Reading, Writing

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37
Q

Bilingual aphasia affects all areas of language including

A
o	Phonology (Sounds)
o	Grammar (rules of language)
o	Morphology (sounds that carry meaning)
o	Semantics (meaning of words )
o	Pragmatics (rules of social discourse)
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38
Q

Impairment in bilingual aphasia occurs

A

in both languages in varying degrees; however, all of these areas are not necessarily impaired.

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39
Q

Pathological code switching

A

Difficulty staying in target language and code switching ; involuntary language mixing

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40
Q

Bilingual aphasia and proficiency

A

• Can occur even when there is minimal proficiency in the second language.
o For example, people who spend the summer in another country.
o Language is still disordered

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41
Q

Bilingual aphasia is not

A

a way to miraculously wake up speaking a new language from

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42
Q

Patterns of impairment for bilingual aphasia

A
Proficiency
•	Primary Language (L1)
•	Secondary Language (L2)
Age of Acquisition
•	Heritage Speakers
•	Second Language Learners
Use
•	L1 Dominance
•	L2 Dominance
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43
Q

Parallel vs. differential impairment

A

Parallel impairment
o Both languages are equally impaired

Differential impairment
o different degrees of impairment for each language (one language is more impaired than the other)
o Differential aphasia: aphasia symptoms differ across languages Example: Broca’s aphasia in one language and Wernicke’s in the other language.

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44
Q

Blended or mixed patterns

A

o mixed language patterns at any linguistic level (phonological, morphological, syntactic, lexical, or semantic)

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45
Q

Selective aphasia

A

o impairment of only ONE language

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46
Q

Example of mixed patterns

A

patient no longer recognizes what words or features belong to each language (not the same as code switching which is voluntary).

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47
Q

Patterns of bilingual aphasia recovery

A

• Parallel: Both improve together, same rate. (Most common.)
• Differential: one language recovers better than the other regardless of premorbid levels
• Selective: Only one language recovers.
• Blended: Inappropriate blending of languages.
• Successive: One improves, then the other. One language may plateau before the other can recover.
• Antagonistic: one language improves and the other regresses. Improvement in one language negatively affects the other language.
* Recovery can occur in both language or one more than the other.
• Language recovery can be either the L1 first or L2 first, no specific order regardless of native language, familiar language or language of the environment.

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48
Q

Relationship between aging and disease

A

• As age increases the incidence of disease increases as well

Why are so many diseases mostly seen in old age?
• We are copies of copies- you have none of cells you had 7 years past
• The selection shadow- diseases show up after 40 because it doesn’t matter if you die because you already had your children

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49
Q

Brain changes in normal aging

A

Normal aging is associated with structural and functional changes in the brain (between 18-25 brain volume begins to shrink)
o Global changes
o Regional changes
• Frontal (executive function, emotion, perception/behavior. judgment) and temporal (semantics, memory, content) regions are most affected
o Observable in neuroimaging studies

There are corresponding declines in cognitive functioning
o Executive functions and (processing) speed most affected
o Also changes in memory and other domains (multitasking not good)

Declines in gray and white matter (volume)

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50
Q

Normal vs. Abnormal aging

A

• The abnormal is dementia
• Not everyone is destined for dementia
• Please let people know this
o There are things they can do to help prevent dementia

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51
Q

MCI

A

Transitional zone between dementia and normal aging
o Aging → MCI → Dementia

Proposed Criteria (Winblad et al., 2004)
o Not normal, not demented by DSM-IV criteria
o Cognitive decline (self- and other-reported)
o Preserved ADLs (activities of daily living)

Can be difficult to tease apart form normal cognitive decline; executive functioning, memory, processing speed; not homogeneous diagnostic label- people are very different

Can improve, remain stable, or evolve to AD or another form of dementia (most commonly remains stable)

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52
Q

3 MCI categories

A
Amnestic 
o	Mostly memory 
o	Most likely to become AD 
Multiple Domain 
o	Spatial & Language, partially memory
Non-Memory Domain 
o	Language
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53
Q

Pseudodementias

A

normal pressure hydrocephalus, depression, polypharmacy

54
Q

Normal pressure hydrocephalus

A

Hydrocephalus- Blockage/increase of cerebrospinal fluid in brain
o Ventricles/empty spaces fill with CSF, sometimes blockages occur and pressure build up
• Slowly developing hydrocephalus
• Cerebrospinal fluid builds up if it cannot drain
o Pressure increases

Triad of symptoms are seen
o Confabulation- person tells a fictional story but they actually think it occurred/misremembering
o Gait disturbance – changes in walking movement/patterns
o Incontinence- inability to keep urine inside bladder voluntarily

55
Q

Depression

A

• Depression-related cognitive and brain changes have been linked with functional disability
o Memory and reasoning have been found to have an inverse relationship with level of depression.
• Depression is treatable and once treated cognitive deficits have been found to reverse

56
Q

Polypharmacy

A
  • Older adults are often taking a cocktail of drugs
  • These drugs can have negative consequences to cognitive health
  • Careful management of medications can reverse these cognitive deficits
57
Q

Dementia- an umbrella term

A

used to describe the symptoms of a group of more than 100 conditions that impair memory, behaviors, and thinking.

58
Q

Dementia definition

A

a decline in mental functioning that affects daily living

59
Q

Brain regions affected for each dementia

A
  1. Alzheimer’s disease- medial temporal lobe atrophy of hippocampus and cerebral cortex
  2. Vascular Dementia- subcortical and white matter damage
  3. Frontotemporal dementia (FTD)- frontal (Broca’s area leading up to motor strip) and temporal lobes
  4. Progressive non-fluent aphasia- atrophy of left posterior inferior frontal cortex
  5. Semantic dementia- atrophy of anterior, lateral, and ventral temporal lobe (will eventually bleed into frontal and parietal lobes)
  6. Parkinson’s disease- frontal and parietal lobes
60
Q

AD Language Profile

A

• Anomia – biggest noticeable change
Is it an access (get to knowledge) or a content (knowledge gone) problem?
• Mostly access at beginning, content problem as you progress
What does that mean?
• Worse at semantic fluency as compared to verbal fluency
• Sentence Comprehension can be impaired
Is that a memory or syntax problem
• No definitive answer
What does that mean?
• Some LD’s lead to short term memory problems

61
Q

VD Language Profile

A
  • Just as all over the place as cognitive symptoms
  • No true profile
  • Anomia common
62
Q

FTD Language Profile

A

• Language problems are less prominent than behavioral/social/personality problems
• Discourse often lacks thematic cohesion and had disjointed organization; trouble keeping themes together
o In part due to cognitive dysfunction (more-so than a true language problem

63
Q

PNFA Language Profle

A
Slow and gradual deterioration in the ability to produce speech:
o	Atrophy in/near Broca’s area 
o	Patients often become mute 
Characterized by: 
o	Non-fluent effortful speech 
o	Stuttering 
o	Apraxia and/or dysarthria 
o	Agrammatism 
o	Phonemic Paraphasias 
o	Impaired repetition 
o	Alexia and/or agraphia 
o	Late mutism 
Relatively Preserved: episodic memory, visuospatial abilities, orientation to time and place, word meaning preserved in beginning stages.
64
Q

SD Language Profile

A

• Characterized by:
o Empty speech (but with good syntax)
o Semantic paraphasias
o Severe anomia (degeneration of word meanings)
o Prosopagnosia and visual agnosia (bad recognition of faces)
o Comprehension difficulties (both single words and sentences)
* Relatively Preserved: Orientation, auditory perception, phonological knowledge (until latest stages), prosody, memory for recent events, syntax (until later stages), spatial skills
• Degenerative version of w\Wernicke’s aphasia

65
Q

Parkinson’s Disease hallmark symptoms

A

The hallmark symptoms in PD are motor in nature
o Bradykinesia- slowing of movement/energy of motion
o Rigidity
o Tremor- small rhythmic movement, resting tremor (only there when muscle has rest, goes away when they do an intentional action); intentional tremors possible but cause by cerebellar issues
o Postural Instability – fall easily

66
Q

PD leading cause of death, other complications

A
  • Get worse until wheelchair bound
  • Leading cause of death is aspiration pneumonia
  • Hunched over, shuffling steps w/tremor at the same time
  • Swallowing problems cause them to aspirate and then they get aspiration pneumonia
67
Q

PD cause

A
  • Lewy body deposits in the midbrain
  • Loss of dopamine secreting cells in the substantia nigra (lots of black substance in midbrain that goes away when you have parkinson’s disease)
  • Leads to dysfunction of the basal ganglia (BG important role in motor movement, gas and brake for movement; when not enough dopamine BG tends to be more of a brake, leads to bradykinesia or akinesia)
68
Q

PD treatment (list)

A

Levodopa (L-DOPA)

Deep brain stimulation

69
Q

Levodopa (L-DOPA)

A

o Have to be timed just right (slow release, takes an hour/an hour and a half before it works, must take at same time every day)
o Have to have the right dose (too little and you will still have motor symptoms, too much and will have jerky and all over place called dyskinesia)
o Effect wears off over time
• You need more and more over time in order to get the right effect
• Eventually you will not get a good effect, perfect window between tremor and dyskinesia becomes smaller and smaller

70
Q

Deep brain stimulation

A

o Basal ganglia is circuit, can use electrode that you stick into basal ganglia to reactivate parts that are not working
o Can be turned off and on (put battery in chest and use magnet to turn it off and on, tinker with amount/positivity or negativity of current; electrodes can cause damage and question whether it is worth it as compared to symptoms)
o Drawbacks: Doesn’t seem to improve speech, swallowing, language, cognition
o Not a “cure-all”

71
Q

PD other symptoms

A

Dysphagia – difficulty swallowing
o Aspiration Pneumonia the leading cause of death
o Dyskinetic, rigid, bradykinetic
o When things get into lungs you have increased likelihood for pneumonia
o Lose sensation; most people cough to get things out of airway

Dysarthria – difficulty with speech
o Hypokinetic dysarthria – not enough movement, will speak very softly, emotional changes in voice become less and less
o Movements too small

Cognitive changes
Language changes

72
Q

PD cognitive profile

A
  • Reduced processing speed – slower moving as well
  • Visuospatial deficits
  • Set shifting – difficulty smoothly moving between tasks
  • Attention
  • Working memory – difficulty with self-ordered working memory

All of this is not surprising why?
o Both Parkinson’s and ADHD patients have deficits in dopamine, not surprising that such deficits lead to cognitive issue because frontal lobes need dopamine to perform higher cortical functions

73
Q

PD language profile

A

(deficits pushed aside because motor, swallowing, cognitive issues more pressing)
• Deficits in sentence comprehension – difficulty understanding language
• Verb anomia – actions involve movement, Theory: people with PD have deficits in movement, if you have problems with movement/vision/hearing you have trouble coming up with words that rely heavily on these things because you do not have the experience

Deficits in discourse
o Less fluent
o Less syntax complexity
o Shorter MLU

Not sure if this is due to cognition or true language deficit?
o Working memory; longer sentences harder to understand for people with working memory deficits, discourse- when you talk in a conversation you have to remember what you said and practice in your head before you say it
o Deficits in working memory and discourse go hand in hand; more and more preponderance of evidence that difficulties have at least some true language deficit (not just cognitive deficit)

74
Q

PD dementia vs. LBD dementia

A

• Lewy bodies seen both in PDD and LBD (below not accepted by everybody)
o If first in midbrain=PDD
o If first in cortex=LBD
• Not too helpful because you can’t tell where it starts clinically until you look in their brain after they die

How do you tell where it starts?
o If dementia before motor symptoms=LBD
o If motor before dementia=PDD
• Biopsies very invasive; “probable” in record because not for sure until autopsy after death; which chemical are more predominant and where those things are found; “postmortem”

75
Q

Damage in TBI

A

Coup-Contrecoup
o Coup- (brain floating in fluid; sensitive and weak not a lot to it); skull continues to move forward because not attached to skull, hits front of skull
o Contrecoup- then rebounds back and hits back of skull
o Cause focal damage

Sheering – swerving (brain doesn’t just in one direction like front to back)

Rotation

76
Q

Areas of brain most susceptible to TBI

A

• Certain areas of the brain are most susceptible than others (because of the way brain sits in skull)
o Brain stem – sits at bottom of brain and eventually becomes spinal cord, twists/rotates because it face pressure of holding brain while locked in place with spinal cord
o Corpus callosum – big white matter track that connects left and right hemispheres; if each hemisphere rotates in opposite directions the connection will be frayed
o Frontal lobes – prominent and close to forehead
o Temporal lobes – floating out to side; the way that brain tortions/moves there is a lot of sheering there
• A lot of research on blast related injury effects/physics in comparison to TBI

77
Q

Diffuse Axonal Injury

A
  • Rotation sheering movement causes axons to break down (pull apart or injuries)
  • Axons break down
  • Release toxic levels of neurotransmitter
  • Other neurons start to die ; floats between neurons causing them to die bringing about a cascade of death, was once focal now spreading (damage grows)
  • Can spread across brain rapidly (must be controlled but not many good ways to control it)
  • Diffuse- not just in one place spreading all over brain
78
Q

TBI cognitive profile

A

(difficulties in cognition most long-lasting issues)
• TBI relatively heterogeneous because no injury the same: most common complaints are below
o Poor attention
o Poor multitasking skills
o Lack of insight – not aware of deficits/problems/issues (will not understand why you are doing what you are doing or why the need treatment)
o Poor impulse control
o Personality change
o Difficulties with learning and memory
o Also seem some dysarthria
• WHOLE PERSON- relatively impaired, can be very difficult for caregivers to deal with (rude, offensive, different person); must counsel people/caregivers to let them know personality changes/impulses are out of control
• Talkative can become passive or vice versa
• College students/young people- must integrate back into school life and get structures in place (very difficult with attention/impulse issues)

79
Q

TBI language profile

A

In acute stage
o Very confused/disoriented
o Empty
o Tangential (response has nothing to do with what you asked them)
o Confabulations – untrue story that they believe is true that they tell as if it is true
o Poor sequencing/ordering of language, thought, ideas

Aphasia tests wouldn’t catch them: do not have issues in isolation but you will see it when you put it all together

In chronic stage (out of hospital and into daily life)
o Biggest issues are with pragmatics (due to frontal lobe issues- social use of language, turn taking, sarcasm, appropriate jokes)
o Anomia also widely present (due to temporal lobe issues)
o Frontal lobe damage causes issues with cognitive attention, judgment, impulse control, personality

80
Q

Neglect

A

What Happens with Right Hemisphere Damage?
• Neglect- (most common) neglect the left side of body/visual space; will use left arm, will not notice is something is on their left, will not shave on left side, will only draw on right side of paper
• Right-sided neglect is very, very rare almost never happens but not impossible; most things in brain contralateral to body

81
Q

Types of agnosia (list)

A

Object agnosia, anosognosia, prosopagnosia, simultagnosia

82
Q

Object agnosia

A

inability to name an object (only when it is shown to you in certain domain; if shown visually you may not be able to name it but may name it after touching/hearing it)

83
Q

Anosognosia

A

poor insight to deficits that you have, not knowing you have an injury, not understanding that injury has caused you all these problems; be more wary/vigilant, will try to hop out of bed without realizing they have left-side paralysis which might lead to a fall (possibly fall on their head)

84
Q

Prosopagnosia

A

inability to recognize faces of familiar people; can’t look at a face and distinguish two people (man who mistook his wife for a hat)

85
Q

Simultagnosia

A

can’t put whole pieces together; only see specific objects in a picture but can’t put it together

86
Q

Right-sided stroke language profile

A

Pragmatic deficits (turn taking, sarcasm, jokes)

Discourse deficits (problems with natural back and forth of talking) 
o	Get lost in details – difficulty synthesizing what is important/what they should take away from the conversation
o	Difficulties with humor/sarcasm (good indicator of patient improvement)  
o	Confabulation (telling untrue story they think is real as if it is real) 
Affective/emotional communication deficits 
o	Flat affect  (complement/contradict what we say to make a point)
o	Reduced body language 
o	Aprosodia (difficulty with comprehending/expressing prosody- inflection of voice/emotional or linguistic meaning)
87
Q

Aprosodia

A
  • Difficulties with comprehending or expressing prosody during communication
  • Some argue that damage to Right Broca’s area (BA44) causes expressive aprosodia (biggest difficulty with Broca damage is expression/fluency of speech)
  • Right Wernicke’s (BA22) damage causes receptive aprosodia biggest difficulty with damage to Wernicke’s area is comprehension, understanding prosody)
  • Do not see this as one would expect, do not see this as same rate as you see receptive and expressive aphasia even though you should expect that because left and right side just as susceptible to stroke as any other area of brain
  • In theory it makes sense but in real world there are doubts
88
Q

Cognitive reserve

A

Cognitive reserve is influenced by
o Intellectual and lifestyle factors such as education, occupation and leisure activities
o Higher levels of cognitive reserve is associated with reduced risk of developing cognitive decline and a lower rate of memory loss
C.R. is your cushioning from inevitable cognitive decline

89
Q

Why study bilinguals?

A

Bilingual speakers the majority in countries throughout the world
Largely spanish or spanish/english bilingual speakers

90
Q

3 major bilingualism discoveries

A
  1. Both of the bilingual’s languages are always active (in brain).
  2. There are consequences of bilingualism that affect the native (L1) as well as the second (L2) language: The native language changes in response to second-language use.
  3. The consequences (to the brain) of bilingualism are not limited to language but reflect a reorganization of brain networks that hold implications for the ways in which bilinguals negotiate cognitive competition more generally. (negative effects)
    • Taken from Kroll, Bobb, & Hoshino (2014). Two languages in mind: Bilingualism as a tool to investigate language, cognition, and the brain. Current Directions in Psychological Science, 23(3), 159–163.
91
Q

Bilingualism definition

A
  • Individuals that use of two languages or more languages in their every day life
  • This definition suggests that bilinguals possess the ability switch languages or use both languages interchangeably for the purpose of communication
  • (Grosjean, 1982)
92
Q

Implications of bilingualism discoveries

A
  1. The two languages are always active
    o Bilingual speakers are not 2 monolinguals in one!
    o Bilingual speakers show slower response times or show lower scores on language tasks.
    • Faster at naming cognates (words that have same meaning and spelled the same, only pronounced differently) (e.g. Piano)
    o Norms for English speakers and Spanish speakers do not apply to bilingual English-Spanish speakers.
    • CLQT in English and Spanish- normed on monolingual English and monolingual Spanish, not bilingual
  2. The L2 changes the L1
    o Evidence of inhibition of the L1 to facilitate the L2.
    o Language of testing/Switch effects: Inhibition of the L1 when tested in the L2 first; but facilitation for the L2 tested in the L1 first.
    • Picture naming: Misra, Guo, Bobb, & Kroll (2012); Moriyasu (2014)
    • Verbal Fluency: Van Assche, E., Duyck, W., & Gollan, T. H. (2013)
    o Attrition of the L1 can impact performance on language tasks. (not deteriorate; L! impacted by L2)
    • More tip of the tongue states: Gollan & Acenas (2004)
    • Clause attachment (especially in ambiguities): Dussias & Sagarra (2007)
    • Sound/Word recognition (time/accuracy): Pallier et al. Cereb Cortex, 2003
    • Verbal Fluency: Linck et al. (2009)
  3. Bilingualism changes the brain
    o Constant inhibition and switching of languages creates stronger brain networks for cognitive control.
    • Competition and conflict resolution in non-linguistic tasks (Faster, but slower in linguistic tasks)
    o Cognitive reserve; neuro-protection
    • Bilinguals get symptoms of Alzheimer’s up to 5 years later Bialystok, E., Craik, F. I. M., and Freedman, M. (2007).
    o Changes to areas of the prefrontal cortex including the dorso-lateral prefrontal cortex (Area associated with code switching and conflict resolution). Luk et al., (2011)
    o Bilinguals are better language learners (easier for bilinguals to learn a third language than for a monolingual to learn a second language)
93
Q

Hypotheses of bilingual language

A

Extended system hypothesis
• Languages are represented in an undifferentiated way in the cortical language areas. One System!!
• The system then contains more elements. More phonemes, morphemes, syntactic constructions,
lexical items.
o L1 for L1 and L2 for L2.

Dual system hypothesis
• Elements of each language are stored SEPARATELY.
• The system then contains two sets of everything: phonemes, morphemes, syntactic constructions, and lexical items.

Tripartite system hypothesis
• Elements that are identical for each language are represented in one common area. Represented only once.
• Elements that are different are stored separately. Represented independently.
• Everything common represented once and everything different has different systems

Subset hypothesis
• We have one large cognitive system (language) and each language is a subsystem. Even that phonology and syntax, for example, can be subsystems.
• Each subsystem can be selectively impaired.
• Separate neuronal subsystems; part of larger linguistic system which can activate any part at any time

94
Q

Models of bilingual processing

A
  1. Revised Hierarchal Model (Kroll & Stewart, 1994)-there are connections between L1 and L2 and the central conceptual system which are influenced by fluency in L1 and L2. (translations)
  2. • Bilingual Interactive Activation Plus (BIA+) (Dijkstra & van Heuven, 2002) language nodes for a particular language are activated by lexical and phonological input. (input determines how we select nodes for a particular language)
  3. • De Groot’s distributed model (de Groot, 1992- word meanings represented by features (features may be shared) (e.g. dog can also activate cat, but can also activate gato because both are furry and have 4 legs)
95
Q

Bilingual Proficiency

A

• Proficiency may be different across languages AND across modalities.
o May be more proficient in speaking English but understands better in Spanish (or vice versa)
• In order to assess impairment, you must evaluate all areas in both languages.
o E.g., auditory comprehension, reading, verbal expression and written expression

96
Q

Bilingual Age of acquisition

A

Heritage Speakers vs Second Language Learners
o Heritage= of that culture, growing up with both languages, will learn native language of their culture at home even though not language of where they live
o Second language learners- learn a second language at school or through friends; can learn at an early or later age

Early vs Late Bilinguals
o Early: learned second language during early childhood; sometimes learned simultaneously (Simultaneous Bilinguals)
o Late: learned second language as older children and adults

97
Q

Bilingual Use

A
  • Balanced or equilingual: speak both languages with same or equivalent levels of proficiency
  • Dominant: dominant (sometimes more proficient) in once language versus the other. (Speaks one language better than the other)
  • “Perfect” bilinguals or ambilinguals: speak each of their languages with automaticity and accuracy with respect/response to the norm.
  • Semilingual: neither language is native-like and both languages are necessary to communicate.
98
Q

Code switching

A

Alternating uses between two languages
**Used with communicative intent
**
To add emphasis or emotional value
**Normal occurrence between bilinguals
**
May not be normal to a particular culture- get info from family; some instances of pathological code switching
**Voluntary, grammatical/syntactic event; will see pathological code switching in aphasia
Appropriate in some cultures and some contexts
**
Must interview family in order to determine what is appropriate
Code-switches are grammatical unless person is disordered (aphasia)
***Grammatical judgments on code-switches should be determined by bilingual speakers of that same community (or family); sometimes what you may think is inappropriate may be appropriate for that culture

99
Q

Bilingualism diagnostic considerations

A

Decreased eye contact
Different ways of greeting
Asking or not questions
Answering or not questions
Choice of topics for conversation
Being active or passive during the session (could be cultural)
Vocabulary differences (important to articulation assessment, naming tasks, dialect differences)
Differences in expressions (important for verbs; words may not have a one word translation)
Differences in grammatical patterns

100
Q

Why must both languages be assessed?

A

Use of interpreters
**They can alter the information
**
Their time is costly
**Should be trained
“Trained” family member
**
Sometimes is hard for them to see how impaired the patient is
**They can provide additional cues (help) to the patient
**
Fix patient’s errors to try to help them out

101
Q

Bilingualism informal assessments

A
  1. Language history questionnaires (correlate with outcomes)
    Examples: Leap-Q, Munoz
  2. Self-ratings: rate their abilities in each language
  3. Patterns of use- which language was used in which situation
  4. Ratings by family members- ask the family* (be very specific because they may not understand what you are looking for)
  5. Acquisition history- how was it learned (formal vs. informal), age of acquisition
102
Q

Bilingualism formal assessment: Test issues/complications

A

Limited number of tests compared to those available for monolinguals.
1. These tend to have cultural biases.
2. Validity and reliability are not equal among all cultures.
None are perfect- may have issues with validity and reliability depending on how you use them
Complications
1. Which language do you test first- will influence scores
2. Same assessment in language A and B will affect validity and reliability
Try to find assessments that have form A and B

103
Q

Bilingual child formal assessments

A

Spanish Articulation Measures (SAM)
Spanish Language Assessment Procedures (SLAP)
Bilingual English Spanish Assessment (BESA)
Bilingual English Spanish Oral Screeners (BESOS)

104
Q

Bilingual adult formal assessments

A

Functional Assessment of Communication Skills (FACS)- cognitive
Alzheimer’s Quick Test (AQT) (Many Languages)- cognitive
The Montreal Cognitive Assessment (MOCA) (Many Languages)- cognitive
Boston Diagnostic Aphasia Examination (BDAE)-Spanish Version
Multilingual Aphasia Examination
The Aachen Aphasia Test (German, Dutch, Italian)
Bilingual Aphasia Test (BAT) (Many Languages)

105
Q

Bilingual disorder diagnosis

A

Therapists use in-house developed tests in absence of appropriate standardized assessment
Cannot be used to provide a diagnosis (moderate Broca’s aphasia)
Can be used to describe characteristics of the patient’s impairment
Can be used to describe symptoms or provide a picture of the patients ability
7/10 accuracy for picture naming and 8/10 accuracy for Y/N questions
Presents symptoms of expressive aphasia

106
Q

Treatment of bilingual disorders

A
  1. Usually same treatment goals as monolinguals.
    E.g., Increase functional communication
  2. Work closely with the family to help determine goals.
  3. Goals should be realistic, meaningful to the patient, and tailored to the individual patient’s deficits.
  4. Modifications may be necessary to include linguistic differences of the other language (especially when using formal treatments)
    E.g., Lips program may need to be modified to include sounds of native language
  5. Can do this by including family; imitate sound and help patient imitate sound as well
107
Q

Which language to treat?

A

Use family interviews to determine premorbid use and proficiency, and what they think is best for the patient.
Alternating languages – can be done in blocks of sessions or weeks. Do regular probes to see if there is generalization from one language to the other.
With disorders like aphasia you can treat one language and both will improve. (Edmonds & Kiran, 2006; Holland & Penn, 1995; Penn & Beechman, 1992).
(Aphasia) Treat one language and the treated language will improve more than the untreated one (de Luca et.al. 1994; Laganaro & Overton Venet, 2001) especially for expressive language.
(Aphasia)Treat both languages and both improve (Kohnert, 2004). (Better generalization and maintenance using cognates)
Best way to make decisions: talk to family and review literature

108
Q

CETI

A

Communication from baseline to end of treatment, insurance companies love this; combination of patient, caregiver, your own input

109
Q

Different types of observation

A

• Different levels of observations
1. Unstructured observations
• As natural a setting as possible with familiar situation/people (but difficult)
• May be able to identify communication breakdowns
2. Moderately structured observations
• Story retell
• Describe pictures
• Procedural tasks (How do you change a tire?)
• Different types of discourse provide different types of information (try all of them)
3. Highly structured observations
• Bedside and screening assessment tools
• Aphasia batteries
• Other Standardized Assessments

110
Q

Problems with WAB and BDAE

A
  • In 25-70% of cases cannot definitively classify as aphasia type (people/diagnoses are very heterogeneous)
  • Even fluent OR nonfluent problematic
  • Aphasia type may differ depending on the battery used
  • Pt’s can have both receptive and expressive problems without having a global aphasia; even person’s brain anatomy is different
  • Type of aphasia can evolve
  • If using classifications (necessary to talk with physicians PT’s, OT’s, and other SLP’s), use clinical judgment in addition to test results!!

Severity
o WAB and BDAE provide indicators of severity
o But NOT indicators of how a person will do in various situations (ability to communicate may be better than is indicated by the batteries)

111
Q

Cultural considerations in assessment

A
  • Standardization group for tests. Is the patient a part of that group?
  • Language background (bilingual, first language, dialect, etc.)
  • Cultural norms for discourse and pragmatics – can vary
  • Pragmatic rules can vary by culture
  • Country of origin – some test items may not be familiar
  • Lots of other examples.
  • Be aware and be willing to learn!
112
Q

Things to control/consider in diagnosing the patient

A
  • Hearing screen – ask if they wear a hearing aid and USE IT
  • Vision – ask about visual field deficits, glasses, etc.
  • Apraxia of speech or limb apraxia – screens in the WAB and also Apraxia Battery for Adults -2
  • Dysarthria – motor exam
  • Depression (Beck Depression Index)
  • Fatigue – just woken up, just got into hospital, too long of an assessment
  • Motor limitations (limb apraxia)
113
Q

Evaluation: Aphasia vs. Dementia

A

• Assessment critical for development of informed therapy to have good assessment from beginning)

Other considerations:
o Neurodegenerative conditions present moving targets
o Know the clinical course of the disease
• Will the condition evolve to mutism? (e.g., PNFA)
• Is the condition “worse” now for a systemic reason?
o Goals might focus on maintenance and coping
o Family/psychosocial support
o Augmentative & Alternative Communication (will they be able to use it?)

Assess multiple domains of:
o Speech, Language, Memory (episodic, semantic), Pragmatics, Executive Function, Attention

114
Q

MOCA

A

Montreal Cognitive Assessment (MOCA) Nasreddine, 2005 (better than MMSE)
• Free alternative to the MMSE
• MOCA Test online: http://www.mocatest.org/

Advantages: 
o	Free 
o	Rapid (takes 10 minutes) gestalt measure of cognition 
o	Easily administered 
o	Less sensitive to aphasia 

Disadvantages
o Poor specificity
o Tasks are language-mediated and demand praxis
• Aphasia presents as a global cognitive impairment

115
Q

MMSE

A

Mini Mental State Examination (MMSE) (Folstein et al., 1975)

Advantages:
o Normative data and widely known
o Rapid (takes 10 minutes) gestalt measure of cognition
o Easily administered

Disadvantages:
o Poor specificity – can’t tell you about specific areas of cognition
o Tasks are language-mediated and demand praxis
• Aphasia presents as a global cognitive impairment

116
Q

CLQT areas assessed

A
General Areas: (w/ composite severity at center)
o	Attention
o	Memory
o	Executive functioning
o	Visuospatial functioning
o	Language
Tasks (in sequential order) 
o	Personal Facts 
o	Symbol Cancellation 
o	Confrontation Naming 
o	Clock Drawing (will always see this in cognitive tests)
o	Story Retelling 
o	Symbol Trails 
o	Generative Naming 
o	Design Memory 
o	Mazes 
o	Design Generation
117
Q

Semantic Feature Analysis (for aphasia)

A
(not as effective in dementia) 
Objects are composed of features 
o	Perceptual (e.g., tail) 
o	Categorical (e.g., animal) 
o	Functional (e.g., it fetches a bone) 
o	Action (e.g., it wags its tail) 
o	Associative (e.g., rawhide bones) 
o	Contextual (e.g., sleeps on the couch) 
Repeated engagement of a set of defining features ; solidifying concepts generalize to other concepts
How to structure the therapy… 
o	Generate a set of target items 
o	Repeated feature generation 
Category, use, action, properties, context, associations
118
Q

VNEST (for aphasia)

A

(verb network strengthening treatment)
SFA tends to not generalize outside of word level
o Doesn’t help with discourse

Training verbs has been shown to improve sentence level production
o We’re getting there

Who then What
• Then add where, when, why
• Shown to improve sentence production
• Edmonds, 2009

119
Q

Drugs in dementia

A

Learning/Memory
o ACH Inhibitors: All stages of AD
• Aricept/Exelon/Reminyl

Inhibition/Excitation 
o	Glutamate/GABA antagonist: Mod- Severe AD 
•	Toxic extracellular glutamate 
o	NMDA receptors blocked 
•	Namenda 
•
Movement/Reward 
o	Dopamine agonists 
o	Levodopa/Sinemet

Depression
o Serotonin Reuptake Inhibitors
• Paxil/Prozac
o MAO Inhibitor

Agitation/Sleep 
o	Dopamine antagonists (antipsychotics) 
•	Side effect is somnolence 
	Seroquel/Haldol 
o	Benzodiazepenes 
•	Ativan/Valium 
o	SSRI (old) 
•	Trazadone

Anti Beta-Amyloid Drugs
o Mixed results; likely vaccine before a cure (Dekoskey compared to unfrying an egg)

Tau Genetics (turning off tau) 
o	Methylthioninium chloride/Rember 
o	Tau aggregation in AD causes tangles in the cell, interferes with transport
120
Q

Dementia treatment continuum

A

• If you do decide to pursue treatment, therapy targets depend on your overarching goal
o Is the condition chronic or neurodegenerative? Stroke or dementia?
o Restorative tx is not always the best option for neurodegenerative
• Continuum of aims from:
o restitutive ←——————→ compensatory
/
maintenance
o restitutive- good for stroke but not for dementia
o Compensatory may be best goal for dementia

121
Q

Dementia treatment considerations

A

Progressive disease presents a moving target
o Difficult to show progress
o Limited treatment efficacy (efficacy is greater in aphasia than for dementia)
o Limited insurance reimbursement – if you do not see improvement insurance companies do not see purpose- be creative in showing improvement

What works for aphasia is LIMITED for dementia
o e.g., Semantic Feature Analysis (great for re-teaching concepts in aphasia, not so great in dementia)

122
Q

Errorless Learning (for dementia)

A
  • Rationale prevent encoding of errors (limited cognitive functioning so let’s not have them make errors and encode those errors)
  • Attain flawless production (e.g., repetition) prior to shifting to more difficult tasks
  • “Give” people the answer rather than permitting flawed retrieval
  • Paradigm can be applied/added to almost any conventional aphasia tx approach ; improves ability to work in dementia
  • Results of errorless vs. errorful for treatment of anomia equivocal
  • Important effects in aphasia as well
123
Q

Group Reminiscence Therapy- general info

A

• Communication is reduced in dementia
• Patients often show advantages for remote memories
o e.g., “the great depression”
• Session format:
o Facilitator (e.g., SLP, Psychologist, Age Exchange in UK)
o Session props by decade

124
Q

GRT- guidelines for implementation

A

• Guidelines for Implementation:
o Homogenize groups by cognitive level (close in cognitive level)
o Keep small staff-to-patient ratio
o Group facilitators should be knowledgeable about dementia
o Focus session around central theme
o Use personally relevant props/photos (based on decade)

Expected Outcomes:
• Small improvement in global cognition
• Greater number of conversational exchanges
• Improved narrative discourse
• Improved recall about specific topic
• Improved happiness, interacting more with others and more social engagement they didn’t have previously

125
Q

Multimodal Semantic TRaining (for maintenance treatment of dementia)

A

show an item, perform a feature matrix (just like in semantic feature analysis), has more multi-modal semantic training that improves outcomes

126
Q

Atypicality training

A

(good for both dementia and aphasia) (training atypical categories helps with typical category knowledge)
• We are fastest and most accurate to name category prototypes
• Prototype is the central tendency of a category
• One approach is to train on typical exemplars
• A different approach is to train on atypical exemplars
• Several surrounding (atypical) rings around a central (typical) planet

127
Q

Restitutive Ttreatment: Brute Force Paired Associate Learning

A
  • Case studies of FTD patients learning face-name associations through repeated exposure up to 12 hours a day
  • Patients learn pairings rapidly

Disadvantages:
o Shallow learning with poor retention (next day they lost it)
o Poor structure of targets
• Why relearn low frequency targets?

128
Q

Maintenance treatment for dementia

A

• Our Tx for Alzheimer’s Disease and FTD
o Focus on retention of known words rather than re-acquisition of forgotten words
o Start EARLY after disease diagnosis
o Craft a finite set of highly salient target items that combine very well
• Your goal is NOT generalization; it is maintenance
o Use Errorless Learning (Repeat then move to naming)

129
Q

FOCUSED

A
•	One effective tx is called FOCUSED. Acronym for: 
o	Functional (no “talking about nothing” because that leads to confusion and tension; patient will want to talk about things and will try but will just get cofused) 
o	Orient to Topic (do not bring up a topic that is completely out of their realm)
o	Continuity / Concrete Topics (do not jump between topics)
o	Unstick Communication Blocks (find a way to help them come up with word- do not let them get stuck on that error) 
o	Structure (yes/no and forced choice questions only) 
o	Exchange Conversation – do not just speak out to them, let them respond back to have a more fluid/normal conversation
o	Direct, short simple sentences
130
Q

ANCDS Evidence Based Practice Guidelines Caregiver Structured Environment

A

• Clinically applicable trends in educating caregivers:
o 1. Caregiver education may promote greater success in conversational exchanges
o 2. May either relieve (improves conversational exchanges) or increase caregiver burden (changes in communication move to caregiver)
o 3. May improve quality of life
o 4. May contribute to maintenance of language in AD
o 5 Increased understanding and coping for breakdown of language in AD

131
Q

Compensatory/environmental treatment: Caregiver structured environment

A

(level between where patient is at and where functional behavior is at; use compensatory strategies to bridge gap)
• Caregiver communication style when communicating with patient
• External memory aids/technology to organize us
o Smartphone
o Calendars
o Pagers
o Photo Cues
• Structured environmental factors; highly structured environment improves outcomes massively
Caregiver Structured Environment
• Few Systematic Studies of Caregiver Communication
o Intervention aimed toward caregivers (not toward patient)