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COGS 154 Final Flashcards

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1
Q

What are motor speech disorders

A

difficulty with properly planning and executing motor movements for speech

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2
Q

Motor planning

A

Processes that define and sequence articulatory goals -prior to initiation of movement `

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3
Q

Motor Programming

A

processes that establish and prepare the flow of motor info across muscle, as well as control timing and force of movement -prior to initiation of movement

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4
Q

Motor Execution

A

processes that activate relevant muscles -during and after initiation of movement

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5
Q

Motor planning/programming disorders:

A

inability to group and sequence the relevant muscle with respect to each other (apraxia)

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6
Q

apraxia of speech (AOS)

A

speech disorder due to dysfunctional motor planning and programming -the messages from the brain to the mouth are disrupted -severity of apraxia depends on the nature of the brain damage -can occur in conjunction with dysarthria or aphasia acquired and developmental

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7
Q

Motor Execution Disorders:

A

deficits in physiology and movement abilities of muscles (dysarthria)

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8
Q

dysarthria

A

-speech disorder due to dysfunctional motor execution resulting in incoordinated, weak, and slow articulatory movements -impaired movement for the muscles used for speech production -lips, tongue, vocal folds and/or disphragm acquired and developmental

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9
Q

signs of apraxia of speech

A

difficulty coordinating the muscle movements necessary to say all the sounds in the words -often say something completely different or make up words (bipem or chicken for kitchen) -quite frustrating for the person

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10
Q

causes of apraxia

A

in adults, damage is often to the left frontal cortex surrounding Broca’s Area -In kids, no known specific cause –theories suggest disruption of messages form brain to muscles to produce speech

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11
Q

apraxia treatment

A

focus of intervention is on improving the planning, sequencing, and coordination of muscle movements for speech production -retraining with repetition -AAC

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12
Q

Auditory habilitation (Aud Hab)

A

Subspecialty of SLP

-Primary Goal: Learning through listening

Concern is communication development

Make speech louder, deliver a better speech signal, provides a language through another modality (sign language)

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13
Q

Aural Rehabilitation (Aural Rehab)

A

Subspecialty of SLP or audiologist Primary Goal: Make the signal louder and teach the client compensatory strategies (Speechreading, preferential seating, environmental modifications, conversational strategies)

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14
Q

Candidates for Aud Hab or Aural Rehab

A

congenital or pre-lingual hearing loss (genetic, disease, trauma, cancer drugs) Acquired Hearing Loss (presbycusis-old ear-disease, trauma, cancer drugs, noise induced[ipods])

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15
Q

Hearing loss is measured in terms of:

A

pitch loudness discrimination (how clear is what you hear)

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16
Q

The Audiogram

A
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17
Q

How does a cochlear implant work?

A
  • sound waves enter through microphone
  • the sound processor converts the sound into a distinctive digital code
  • the electrically coded signal is transmitted across the skin through the headpiece to the internal portion of the device
  • the internal device delivers the sound to the electrodes
  • the electrodes stimulate the hearing nerve
  • the hearing nerve sends teh signal to the brain for processing
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18
Q

Hearing Aids Vs Cochlear Implants

A

Hearing Aids:

  • acoustically amplify signal
  • rely on the responsiveness of healthy, inner ear sensory cells

Cchlear implants

  • converts speech info into electrical signals
  • bypasses the inner ear sensory cells & stimulates the hearing nerve directly
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19
Q

Inpatients VS Outpatients

A

Inpatients: patients still in the hospital after a traumatic event

Outpatients: patients dismissed from hospital but who still require speech/language therapy

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20
Q

Work settings fpr Speech-Language Pathology (SLP)

A

Home health care (provide therapy in patient’s home)

Clinics

Schools (therapy for kids age 3-22)

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21
Q

What does an SLP do?

A

Evaluate

provide therapy

teach tools/strategies to help clients communicate AND help family members and caregivers communicate with clients

  • educate the client and family
  • continuing education
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22
Q

signs of dysarthria

A
  • Slurred, choppy, or mumbled speech that may be difficult to understand
  • slow rate of speech
  • rapid rate of speech with a mumbling quality
  • limited tongue, lip and jaw movement
  • abnormal pitch and rhythm when speaking
  • changes in voice quality, such as a hoarse or breathy voice or speech that sounds nasal or stuffy
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23
Q

Causes of Dysarthria

A

Damage to nervous system pathways results in the inability to send proper messages from brain to the muscles involved in speech

  • stroke, brain injury, tumors
  • parkinsons, lou gehrigs, huntingtons, MS
  • cerebral palsy (damage to motor control venters of the developing brain during pregnancy, birth, or shortly after
  • progressive neurological disease
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24
Q

Upper Motor Neurons *UMN”

A
  • originate in the motor cortex
  • axons synapse on cell bodies of lower motor neurons in brainstem and spinal cord
  • cell bodies and axons totally contained within central nervous system (CNS)
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25
Q

Lower Motor Neurons (LMN)

A
  • originate in brainstem and spinal cord
  • receive info from upper motor neurons
  • axons synapse on muscle fibers
  • cell bodies contained within CNS; axons leave CNS
  • form a final common pathway for information descending from cerebrum to periphery
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26
Q

two Motor Pathways

A
  • Pyramidal Tract –> direct pathway from cortex to periperal nerves in the body
  • Extrapyramidal Tract –> indirect to areas involved in coordination, involuntary movements
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27
Q

Ataxia

A

Incordinated movement

like intoxicated speech

lesion in cerebellum

loss of full control of body movements

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28
Q

Mixed Dysarthria

A
  • Affects more than 1 part of the motor system
  • characteristics will vary depending on whether the upper or lower motor nerons remain most intact
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29
Q

Acquired Dysarthria Classification

A
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30
Q

Dysarthria Assessment

A
  • Oral Motor examination: look for reduction in strength, speed, ROM, and coordination
  • Standardized Protocols
  • Speech and non-speech tasks
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31
Q

Dysarthria Treatment

A

Speech Therapy

Surgery

Medication

AAC

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32
Q

What is language

A

socially shared rules/mapping that create a medium for communication

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33
Q

Phonology

A

How sounds are put together to form words (tents vs ntet)

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34
Q

Lexical Knowledge/Semantics

A

Mappings from words to meanings

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35
Q

Morphology

A

How words are combined from smaller pieces (happy, happiness, happily)

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36
Q

Syntax

A

How words are put together to form phrases and sentences

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37
Q

Pragmatics

A

How language is used/language meaning in context (would you mind moving your foot? vs get off my foot!)

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38
Q

Lateralization of function

A

Major differences between the role of left and right cerebral hemispheres in language function

Left hemisphere: speech, finding words, grammar

Right hemisphere: discourse, metaphor, jokes

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39
Q

Lateralization of Language in left hemisphere

A

speech, finding words, grammar

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40
Q

Lateralization of Language in right hemisphere

A

discourse

metaphor

jokes

41
Q

Lateralization of language can be tested through

A

wada test

split brain research

42
Q

Wada Test

A
  • used to determine which hald of the brain is primarily responsible for language, primarily in patients with epilepsy prior to surgery
  • administration of sodium amobarbital to carotid artery. one hemisphere is temporarily put to sleep
  • patient typically counts backward upon injection, which disrupts counting, and the contralateral (opposite) side of the body lose control
  • if language is lateralized to the hemisphere that has been put to sleep, then counting stops, patient wont be able to speak, patient will not have verbal memory for items encountered while that hemisphere is anesthetized
43
Q

Wada Test: for most patients, language lateralizes to _________

A

Left hemisphere;

when LH asleep, they have no verbal memory of the object/cant verbally identify it

-can identify object by picking it up withthe left hand

When right hemisphere is asleep:

-can verbally identify object; can identify object by picking it up with right hand

44
Q

Which hemisphere is dominant for language?

A

left

  • 98% of right-handers are LH dominant for language
  • left-handers have more varied brain organization
  • 70% LH dominant, 15% RH dominant, 15% bilateral for language(not impaired during Wada test)
45
Q

commisurotomy

A

surgically cutting the nerve fiber tracts connecting the two hemispheres. Complete splits include the corpus callosum and other inter-hemispheric tracts, including the anterior and posterior commissures

Use to be a cure for epilepsy.

Outcomes: seizures often subsided with largely normal behavior

46
Q

Fiber tracts connecting the two hemispheres

A

corpus callosum: major fiber tract containing 200 million axons

Primarily homotopic (connects corresponding regions of the 2 hemispheres)

Also heterotopic (connects different regions across the hemispheres

Anterior fibers connect anterior areas of cortex (frontal lobes)

Posterior fibers connect occipital and parietal cortex

47
Q

Split Brain Patients

A

Left hemisphere shows normal language use (production and comprehension)

Right hemisphere shows only some rudimentary word recognition

48
Q

Limitations of split-brain patient studies

A
  • only a few cases have been intensively studied
  • these patients didnt have normal brains to begin with (all were being treated for epilepsy)
  • some connections remain intact after surgery in all/most patients
  • lateralization of language is prevalent, but may still be somewhat variable
49
Q

Communication problems in split-brain patients

A
  • moderate memory deficits
  • patients have pragmatic deficits in conversations
    • inappropriate/exaggerated politeness
    • slight tendency to confabulate
  • reading long texts is difficult
  • LH has difficulty connecting relevant information together into a larger structure on its own
50
Q

What is aphasia

A
  • impairment of the ability to use or understand language, usually acquired after a stroke or other brain injury
  • damaged brain areas are in the left hemisphere
  • most common cause of aphasia is stroke
    • can also be from head injury, brain tumor
  • most severe right after injury; many patients improve over time
  • can be accompanied by other symptoms: paralysis or weakness in right side of body
51
Q

Broca’s Aphasia

A
  • early distinctions: productive; motor
  • Lesion in the LH
  • damage to lower rear portion of frontal lobe adjacent to motor cortex
    • inferior frontal gyrus
    • brodmann’s area 44/45
  • halting and telegraphic speech, as if there is a need to conserve energy
  • speech is agrammatical
  • anomia: inability to produce the name for an object
  • in severe cases, speech may be repetitive (tan)
52
Q

Wernicke’s Aphasia

A
  • Early distinctions: receptive; sensory
  • Lesions in the posterior portion of the brain (left temporal lobe) cause impairment of auditory comprehension of language
  • exhibit logorrhea and will talk until you interrup them due to poor self-monitoring skills
  • articulation is preserved
  • word salad
  • frequent paraphasias (jumbled speech/errors in language)
53
Q

Paraphasias

A
  • two forms
    • literal: phonologucal errors (tootbrust for toothbrush)
    • verbal: semantic errors, often related to the intended term. (knife instead of fork)
54
Q

Wernicke-Geschwind Model

A
  • arcuate fasciculus runs between the mid temporal lobe and the frontal lobe via the parietal lobe
  • according to this model, the arcuate fasiculus is the primary route by which linguistic messages, formulated in Wernicke’s area are transmitted to Broca’s area
55
Q

Conduction Aphasia

A
  • comprehension and articulation are intact
  • difficulty repeating speech
  • Wernicke was wrong about the prediction that conduction aphasia results from damage to arcuate fasciculus
  • lesions in parts of parietal cortex that knock out underlying white matter can produce conduction aphasia
  • patients with damage only to the arcuate fasiculus are not aphasic
56
Q

Wernick’s 3 predictions

A
  • there are two language centers
    • broca’s (spech articulation)
    • Wernicke’s (language comprehension)
  • third syndrome: “disconnection” syndrome, or conduction aphasia, due to damage to the arcuate fasiculus [which turned out to be wrong]
57
Q

Surgery that affects only Broca’s area has ______________

on language abilities

A

no lasting effects

58
Q

Removal of ____________ has no lasting affects on __________

A

Removal of Wenicke’s area has no lasting effects on language abilities

59
Q

No one-to-one correspondence for lesion-site and function

A
  • traditionally defined language areas are either
    • not entirely responsible for the wernicke-geschwind model’s functions
    • easily assumed by nearby brain areas (plasticity)
  • neither alternative is compatible with the idea of innately specified language modules
60
Q

Problems with Wernicke-Geschwind Model

A
  • Wernicke’s model assumes that aphasia refelcts damage to a single module, but symptoms may reflect damage to separate anatomical neighbors
  • no obvious one-to-one correspondence with lesion site and deficits
  • data suggest aphasia symptoms dont reflect famage to a single brain area
  • broca and wernicke may have slightly mislocalized areas subserving motor representation of spech and auditory representation of speech
61
Q

4 Specific Behaviors used in distinguishing between different types of aphasia

A
  • spontaneous speech production (fluency)
  • comprehension
  • repetition
  • word finding/naming

aFasia (aphasia) CRW

62
Q

Broca’s Aphasia: writing and reading

A

Writing

  • patients write like they speak: slowly and laboriously
  • usually pring, not cursive

Reading

  • fewer problems compared to wernicke’s
63
Q

Wernicke’s Aphasia: Writing and Reading

A

Writing

  • resembles their speech: writing is better than with Broca’s in that letters are more well-formed, patients write with ease and it is legible
  • most will use cursive
  • logorrhea also happens in writing

Reading

  • impaired in both spoken and written comprehension
64
Q

Angular Gyrus (BA 39)

A
  • important for processes in reading and writing
  • damage can cause
    • alexia: reading impairment
    • agraphia: writing impairment
    • alexia with agraphia can cause both reading and writing impairments
    • alexia without agraphia
      • rare form of alexia
      • disconnection of angular gyrus from visual input
      • requires damage to inputs to angular gyrus from left occipital lobe, but NOT to the angular gyrus itself
65
Q

Patients with right hemisphere damage have largely preserved _______ skills. They have impairments with _____

A
  • preserved language skills (including grammar and word meaning
  • impairments with pragmatics

pragmatic interpretation: appropriate interpretation

semantic interpretation: literal interpretation

66
Q

Impaired production in RH damage

A
  • may not establish common ground with conversational partner
  • reduced sensitivity to the listener, including reduced eye contact and talking more
  • conversations may be egocentric
  • may change topic without warning or make remarks that are only tangentially related
  • could also have reduced speech, rather than increased. difficulty initiating conversation
    • speech may lack cohesion
    • speech may not be appropriate for the context, including use of inappropriate humor
    • intention of speech may not be clear
    • speech may be too vague or too detailed
67
Q

Impaired comprehension in RH damage

A
  • impairments are primarily with non-literal uses of language
    • irony/sarcasm/idioms
  • indirect requests: can someone get the lights
  • humor interpretation
  • problems making inferences
  • problems activating appropriate meanings (may interpret a word with two meanings in the wrong context)
68
Q

Dementia

A
  • Neurophysical disorders with memory impairment and deficits in at least one other cognitive function
  • acquired; may be progressive
  • produce occupational or social disability
  • symptoms present for 6 months or longer
69
Q

Types of dementia

A
  • alzheimers
  • dementia with lewy bodies
  • frontotemporal degeneration
  • vascular dementia
  • also associated with
    • parkinsons
    • huntingtons
    • ALS
    • MS
70
Q

Signs and symptoms of dementia

A
  • confusion
  • difficulty on job
  • getting lost in familiar areas
  • problems handling personal affairs
  • depression (hallucinations, apthy, agitation, REM sleep behavior disorder)
  • personality changes
  • significant memory loss
  • difficulty following simple directions
  • decreasing communication skills
  • difficulty swallowing
  • by the final stages: inability to feed themselves, walk independently, or speak intelligibly
71
Q

Neuropsychological assessment for demntia include these 5 examinations

A
  1. attention
  2. memory
  3. language
  4. visuospatial skills
  5. executive function

M.A. L.oV.E.

72
Q

Alzheimer’s Disease (AD)

A
  • most common form of dementia (60-70% of cases)
  • increasingly common worldwide
  • typically lasts a decade from onset to death
  • a diagnosis of definite AD requires clinical symptoms while living and evidence of AD at autopsy (or from cerebral biopsy)
  • 6th leading cause of death in US
  • 2/3 americans with AD are women
  • prevalence doubles approx. every 5 years after the age of 60
73
Q

Risk Factors for Dementia

A
  • Age (greatest risk–most over 65)
  • female gender
  • family history
  • genetics
  • history of head trauma
74
Q

Stages of AD

A
  • Mid-early stage
    • function independently
    • forgetting common words/misplacing things
    • family begins to notice
  • Moderate-middle stage
    • lasts many years
    • needs more help/care–difficulty w/ routine tasks
    • frustration–trouble expressing thoughts
  • Severe-late stage
    • unable to respond to environment
    • minimal conversational skills
    • difficulty controlling movement
    • needs help with daily activities
    • extreme shrinkage of cerebral cortex
    • severely enlarged ventricles
    • extreme shrinkage of hippocampus
  • Plaques and tangles
75
Q

Alzheimers and Language

A
  • syntax okay
  • poor working memory
  • poor comprehension of inferential material
76
Q

Treatment for AD

A
  • medication to temporily reduce rate of cognitive decline
  • psychotropic drugs to treat behavioral disturbances and neuropsyhiatric symptoms
  • working with caregivers to provide them with appropriate compensatory strategies
77
Q

Parkinson’s Disease

A
  • degenerative neurological disease
  • dopamine-generating cells in the substantia nigra die resulting in motor symptoms
  • shaking, tremor, slowness, difficulty with walking and hait
  • cognitive and behavioral problems
    • dementia, sleep problems, emotional problems
78
Q

Frontotemporal degeneration

A
  • caused by degeneration of the frontal (and often the temporal) lobe
  • 3 clinical syndromes
    • frontotemporal dementia
    • progressive nonfluent aphasia
    • semantic dementia
79
Q

Dementia with Lewy Bodies

A
  • anatomically characterized by presence of Lewy bodies (clumps of protein in neurons)
  • overlaps clinically with AD and Parkinson’s
    • fluctuating cognition
    • hallucinations
    • motor features of Parkinson’s
80
Q

Vascular Dementia

A
  • Dementia due to problems with blood supply to brain
  • 2nd most common form of dementia in older adults
  • Multi-infarct dementia (MID) is one type of vascular dementia following multiple strokes
  • early detection and accurate diagnosis important: MID is partially preventable
81
Q

Potential Theories to prevent Dementia

A
  • moderate alcohol
  • bilingualism
82
Q

Speech and language changes characteristics of dementia

A
83
Q

What is TBI

A
  • An insult to the brain
    • not degenerative or congenital
    • caused by external physical force
    • may oroduce a diminished or altered state of consciousness
  • results in an impairment of cognitive abilities, physical functioning, and disturbance of behavioral or emotional functioning
    *
84
Q

A significant TBI can be sustained ______ a person receiving a blow to the head

A

without

ex: whiplash from being rear-ended

85
Q

2 ways of classsfying TBI

A
  1. Penetrating (open)
    1. meninges are ruptured but to
      1. tearing by skull fragments
      2. brain is penetratedby a projectile
      3. lacerated by bone fragments
    2. associated with more focal brain damage
  2. Nonpenetrating (closed)
    1. meninges remain intact, skull my be fractured
      1. diffuse brain damage
      2. majority of TBIs in civillian are nonpenetrating
86
Q

Open Head Injury Damage

A
  • Primary damage
    • low velocity
      • force cases fracture of the skull with debris entering brain
      • destruction of tissue at the site of impact
    • high velocity
      • a projectile enters the brain
      • destruction of tissue around projectile path
        • ex: phinneas gage
  • Secondary Damage
    • extracerebral bleeding into the meninges
    • intracerebral bleeding into the brain (stroke)
87
Q

Brain damage in TBI

Primary effects vs Secondary effects

A
  • Primary effects
    • occur at the moment of impact
    • linear acceleration causes contusion at the point of impact and contusion opposite the point of impact
  • Secondary effects
    • accumulation of fluid over the first few hours causes swelling and intracranial pressure
    • lapsing into a coma
88
Q

TBI Risk Factors

A
  • males are at greater risk (ages 15-24)
  • childhood: abuse, accidents, falls
  • teenagers: sports, accidents
  • elderly: falls
89
Q
  • Describe the severity of mild, moderate, and severe TBIs
A
90
Q

MIld TBI

A
  • Injury to the head arising from blunt trauma or acceleration/deceleration forces
  • injury is not visible with medical imaging
  • individual may appear to be fine
  • any period of confusion
  • Mild TBI does not mean mild impairment!
91
Q

Moderate TBI

A
  • up to 24 hours loss of consciousness or coma
  • may have fractures, bruises, or bleeding in the brain
  • injury is visible with medical imaging
    *
92
Q

Severe TBI

A
  • Coma longer than 24 hours
  • long term support will be required at home, in school, and in the community
  • the severity of the injury does not equate to the functioning level of the patient
93
Q

Difference between concussion and mild TBI

A
  • concussion: injury to the brain resulting from impact to head
    • not life threatening injury
    • can cause both short and long-term problems
    • results from closed-head injury and doesnt include injuries in which there is bleeding under the skull or into the brain
    • mild concussion: no/brief loss of consciousness
    • severe concussion: loss of consciousness w/ delayed return to normal
    • function may be interrupted, but there is no structural damage
94
Q

Repercussions of TBI

A

impact on cognitive functions:

  • memory
  • attention
  • flexibility
  • organization
  • physical function
  • impulse control
  • decision making
  • speech/language
  • emotion
95
Q

Speech and Language after TBI

A
  • Motor speech disorders
    • apraxia and/or dysarthria
    • dysarthria is most persistent disorder
  • typically, people show minimal deficits on standardized language tests but have significant difficulty w/ communicative abilities of daily life
  • have cognitive-communication disorders
    • impairment in linguistic and metalinguistic skills as well as impairments in attention, memory, reasoning, and perception
96
Q

Language Impariments inTBI

A
  • comprehension
    • pragmatics and discourse
    • trouble understanding the meaning; trouble getting the gist of info; tend to be overly literal; poor comprehension of sarcasm
  • production
    • anomia; fewer cohesive ties when describing events in a sequence
  • word-finding problems, poor verbal fluency, difficulty understanding complex commands
  • ambiguities
  • inferences
  • drawing conclusions
  • impulsivity during language production
  • figurative language (metaphors)
  • humor
97
Q

Memory Impairment after TBI

A
  • short term memory impariment
  • long term memory impairment
    • retrograde: forget things before injury
    • anterograde: forget things after injury
98
Q

Anosognosia

A
  • seems unaware of or denies the existence of disability
  • linked to frontal lobe damage
99
Q

TBI can often look like ______

A

RHD (right hemi damage)

Cognitive Science (5 decks)

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