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CSD 277 > exam 2 > Flashcards

exam 2 Flashcards

1
Q

What is audiology

A

Branch of science that deals with hearing and balance

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2
Q

What is an audiologist?

A

Primary health-care professionals who evaluate, treat, and manage hearing loss and balance disorders in adults and children

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3
Q

Being an Audiologist requires what

A

Doctorate of Audiology (AuD), Doctorate of Philosophy (PhD), or occasionally a Masters of Science (MS), or Doctorate of Science (ScD)

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4
Q

What are audiologist not?

A
  • Not medical doctors (MDs), or (ENTs)
  • Not hearing instrument specialist
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5
Q

What does private practice primarily do? (Audiology)

A
  • Hearing aids
  • Some diagnostics and Cls
  • some increased flexibility
  • May have longer with each patient
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6
Q

Licensure vs. Certification

A

Licensure: credential required that legally defines the professional practice of audiology. A license is required to legally practice audiology. Issued by the state

Certification: Voluntary process through a private organization provided to individuals who have successfully met all requirements and demonstrated ability to perform their profession competency. Typically, not mandatory

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7
Q

Presbycusis

A

sensorineural hearing loss typically associated with aging

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8
Q

Air-conduction

A

sound sent to inner ear by way of outer and middle ear

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9
Q

Bone-conduction

A

sound sent to inner ear by way of skull vibrations

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10
Q

Pitch corresponds to ____ & is measured in _____

A

frequency, Hertz

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11
Q

Loudness/amplitude responds to ____ & is measured in _____

A

intensity, decibles

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12
Q

Humans can hear

A

20 Hz to 20,000 Hz

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13
Q

Peripheral Auditory System

A
  1. Outer ear
  2. Middle ear
  3. Inner ear
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14
Q

Central Auditory System

A
  1. Brainstem
  2. Primary Auditory Cortex
    - temporal lobe
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15
Q

What does the external or outer ear consist of?

A
  • pinna (auricle)
  • External Auditory canal (meatus)
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16
Q

What does the pinna do?

A
  • enhances the collection of sound
  • shape and location helps us to locate sound
  • enhances signals in 2k-7kHz
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17
Q

Middle ear anatomy includes

A
  • tympanic membrane (TM)
  • Ossicular chain
  • Stapedius and tensor tympani muscles
  • eustachian tube
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18
Q

Ossicular Chain

A

– Connects TM to the oval window of the cochlea
– Malleus attaches to the TM.
– Stapes footplate is sealed to the oval window of the cochlea.
– Vibration of OC creates the wavelike motion necessary to stimulate the cochlea.

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19
Q

Eustachian Tube

A

– Tube that connects ME to the nasopharynx
– Allows air to pass from nasopharynx to the ME
– Equalizes the pressure in the ME cavity
- Allows for the optimal TM movement

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20
Q

The hair cells are responsible for

A

converting the mechanical sound waves into electrical impulses that can be transmitted to the central nervous system.

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21
Q

3 main sections of Cochlea

A
  • Scala Vestibuli (perilymph)
  • Scala Media (endolymph)
  • Scala Tympani (perilymph)
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22
Q

Basilar Membrane

A

– Separates the Scala Media from Scala Tympani
– Organ of Corti sits on top of the BM

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23
Q

Maximum stimulation of the cochlea/BM depends on

A

the frequency of the sound.

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24
Q

The incoming sound wave (created by ossicular chain) displaces the

A

BM, organ of corti, and tectorial membrane.

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25
Q

High frequency sounds stimulate the

A

basal end of the cochlea

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26
Q

low frequency sounds stimulate the

A

apical end of the cochlea.

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27
Q

8th Cranial Nerve (i.e. the auditory nerve)

A

– Nerve fibers leave inner ear through the internal auditory canal of the temporal bone.
– Enters the brainstem at the cerebellopontine angle (CPA) and terminates at the cochlear nucleus complex.
– Preserves the tonotopic organization of the cochlea.

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28
Q

4 major sites of Brainstem

A

– Cochlear Nucleus Complex (CNC)
– Superior Olivary Complex (SOC)
■ 1st site of binaural communication
■ Sensitive to interaural timing and intensity cues.
– Lateral Lemniscus (LL)
– Inferior Colliculus

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29
Q

Medial Geniculate Body of Thalamus

A

Relay station to Primary Auditory Cortex

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30
Q

Primary Auditory Cortex

A

– Heschl’s Gyrus
– Broadmann’s Area 41

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31
Q

Sensorineural (sensory-neural):

A

Hearing loss that occurs along the bone-conduction pathway (cochlea). Typically thought of as permanent hearing loss.

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32
Q

Conductive:

A

Hearing loss caused by attenuation or decreased sound strength related to the outer or middle ear.

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33
Q

Signs and Symptoms hearing loss

A

■ poor academic performance,
■ delayed language and speech production development,
■ behavioral concerns
■ “muffled” hearing
■ asking for repetition
■ tinnitus
■ difficulty paying attention
■ speaking too loudly or too softly
■ difficulty understanding speech in noise
■ turning the volume up on the television/music
■ thinking others “mumble”
■ difficulty understanding speech on the telephone
■ difficulty understanding speech, particularly of women and children
■ not participating in activities/isolating one’s self

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34
Q

Hearing

A
  • Involuntary
  • little effort
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35
Q

Listening

A
  • requires intent
    -discrimination/comprehension
  • active attention/concentration
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36
Q

signs of a language disorder in children

A
  • does not smile or interact with others (birth and older)
  • does not babble (4-7 months)
  • Makes only a few sounds or gestures like pointing (7-12 months)
  • does not understand what others say (7 months-2 years)
    -says only a few words (12-18 months)
  • words are not easily understood (18 months-2 years)
  • Does not put words together to make sentences (1.5-3 years)
  • has trouble playing and talking with other children (2-3 years)
  • has trouble with early reading and writing skills (2.5-3 years)
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37
Q

What can parents do

A
  • listen and respond to your child
  • talk, read, and play with your child
  • talk with your child in the language you are most comfortable using
  • know it is good to teach your child to speak a second language
  • talk about what you are doing and what your child is doing
  • use a lot of different words with your child
  • have your child play with other children
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38
Q

Language disorders may involve

A
  • form
  • content
  • use
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39
Q

How to create a quality interactive environment

A
  1. being responsive
  2. extending interactions
  3. model developmentally appropriate & meaningful language
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40
Q

Dysphagia

A
  • Disordered swallowing
  • affects all age groups
  • multiple signs and symptoms
    -numerous complications
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41
Q

Dys meas

A

bad or disordered

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42
Q

Phag- means

A

eat

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43
Q

Complications of dysphagia

A

malnutrition (weight loss, weakness, death), dehydration (electrolyte and metabolic problems, death), and aspiration (pneumonia, respiratory distress, death)

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44
Q

Mastication

A

Chewing

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45
Q

Bolus

A

food that has been collected and missed with saliva and collected into a small ball

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46
Q

Aspiration

A

Food or drink entering the trachea below level of vocal folds

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47
Q

NPO

A

nil per os- “nothing through the mouth” (latin). “nothing by mouth” (medical term)

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48
Q

What can lead to dysphagia in adults

A

CVAs
TBIs
Dementia
Neuromuscular disease
cancer
trauma
edema

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49
Q

What can lead to dysphagia in children

A
  • Developmental disability
  • neurological disorders
  • structural abnormalities
  • genetic syndromes
  • sensory issues
  • complex medical conditions
  • Medication side effect
  • Behavioral factors
  • social, emotional, and environmental issues
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50
Q

Sometimes the cause of dysphagia cannot be ____

A

identified

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51
Q

SLP and swallowing

A
  • assess and treat
  • need strong anatomical/physiological background of head/neck
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52
Q

what percentage of SLPs are involved with the management of dysphagia

A

30%

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53
Q

Four phases of normal swallowing

A
  1. oral preparatory phase
  2. Oral transport/transit phase
  3. Pharyngeal transport phase
  4. Esophageal (transport) phase
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54
Q

Dysphagia can occur at ___ or ___ phases of swallowing

A

one, more than one

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55
Q

Oral preparatory phase

A
  • Chewing and manipulation of food into bolus
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56
Q

Oral transport phase

A
  • Bolus begins to move posteriorly (back) in the oral cavity, toward oropharynx
  • soft palate elevates
  • posterior pharyngeal walls move to accept bolus
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57
Q

Pharyngeal transport phase

A
  • directs the food from the pharynx to the esophagus
  • airway protection
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58
Q

Esophageal transport phase

A
  • food travels to the stomach
  • peristalsis: involuntary constriction and relaxation of the esophageal muscles
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59
Q

Dysphagia evaluation

A
  • bedside clinical evaluation
  • review patient’s history
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60
Q

Direct therapy (swallowing)

A

involves the presentation of food and/or liquid trials during therapeutic activities

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61
Q

Impact of hearing loss on adults

A
  • depression
  • social isolation
  • cognitive decline
  • impaired memory
  • safety concerns
  • lower quality of life
  • not hearing a cry for help
  • increased anxiety
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62
Q

impact of hearing loss on children

A
  • delayed language development
  • academic under achievement
  • social isolation
  • higher risk of injuries
  • increased poverty
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63
Q

Conductive hearing loss example causes

A
  • fluid
  • allergies
  • foreign objects
  • ruptured ear drum
  • impacted ear wax
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64
Q

Sensorineural hearing loss example causes

A
  • aging
  • ototoxicity
  • loud noise
  • blast/explosion
  • tumors
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65
Q

What 3 causes of hearing loss are shared between sensorineural and conductive?

A
  • genetic disease
  • virus, disease, or infection
  • head trauma
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66
Q

aural rehabilitation interventions

A
  1. devices (hearing aids, cochlear implants)
  2. counseling
  3. training
  4. strategies
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67
Q

one hearing aid is enough
T or F

A

False

68
Q

A hearing aid is not necessary until the hearing loss is severe
T or F

A

False

69
Q

Hearing aids cost too much to be affordable
T or F

A

False

70
Q

Hearing aids are covered by insurance
T or F

A

For children - True- in kentucky
For adults - false- some exceptions

71
Q

Outcomes with hearing aids

A
  • improved understanding in quiet and overall communication function
  • overall positive satisfaction with HAs, but some still end up in the drawer
  • reduces loneliness
72
Q

Most children get 2 cochlear implants
T or F

A

TRUE

73
Q

Cochlear implant is brain surgery
T or F

A

False

74
Q

Insurance will cover cochlear implants
T or F

A

True

75
Q

Speech processor defintion

A

selects and arranges sounds picked up by the microphone

76
Q

A transmitter and receiver/stimulator

A

receives signals from the speech processor and convert them into electric impulses

77
Q

Electrodes

A

collects the impulses from the stimulator and send them to the brain

78
Q

Counseling

A
  • informational counseling (degree, type, impact, untreated hearing loss)
  • psychosocial adjustment counseling (acceptance and coping)
  • group or individuals (families of children with HL, adults with HL, children with HL)
79
Q

Direct training, drill like activities with the purpose to hear differences among

A
  • environmental sounds
  • speech sounds
  • words
  • phrases
  • sentences
80
Q

strategies for person with HL and communication partner

A
  • make eye contact
  • have your mouth visible
  • get their attention before you start speaking
  • encourage hearing aid use
  • speak clearly, but don’t yell
  • be patient
81
Q

What is fluency

A

Effortless flow of speech

82
Q

Disfluency

A

anything that disrupts flow of speech; it is an interruption of speech

83
Q

Stuttering onset can be between

A

18 months of age and puberty

84
Q

Individualized treatment

A
  1. Child-centered therapy or person-centered therapy
    - educate client about stuttering
    - SLP must receive all the education they can about facts, approaches (one size does not fit all)
  2. Listening
    - learn the client’s story, journey, path
    - learn the client’s experiences of stuttering
  3. strategies used
    - preferences
  4. attitudes and feelings about stuttering
    - yesterday, today, tomorrow?
  5. solutions/ plans to consider
85
Q

Older teens and adults effects of stuttering

A

Advanced stuttering
- age is older than 13 years
- learned conditioned behaviors may be stronger
- negative self-concept may be stronger
- fear and avoidance of speaking situations may occur
- fear and avoidance of stuttering may occur

86
Q

School age children (stuttering)

A
  • age is 6-13 years
  • fear of stuttering may be present
  • reacts to fear by avoiding
  • may have more blocks, repetitions and prolongations of sound
87
Q

Preschool children (stuttering)

A

Preschool child may have normal disfluency
- 2-3.5 years of age
- typically the child rarely notices their disfluencies
- no particular feelings or attitudes towards disfluencies

If disfluencies continue, it may become beginning stuttering
- 3.5 to 6 years of age
- child is aware
- feels frustration
- may ask “why can’t I talk?”
- shows some fear

88
Q

Repetitions

A

sound (b-b-b-boy), syllable (ba-ba-baby) or single syllable words (my, my, my)

89
Q

Blocks

A

Air is stopped (in the word “baby” - the lips are pressed tightly together for /b/ placement but no airflow

90
Q

Prolongations

A

(m—y); sounds continues or air flow continues but articulator movement stops

91
Q

Secondary behaviors (stuttering)

A

Escape behaviors
~ a speaker is stuttering and tries to terminate the stuttering
~ eye blinks, head nods, interjection of sounds, or others

Avoidance behavior
~ A speaker anticipates that he or she may stutter and remembers that negative feelings associated with stuttering
~ eye blinks, head nods, or others

92
Q

Consider (in terms of stuttering)

A
  • feelings and attitudes
  • core behaviors
  • secondary behaviors
  • underlying processes
93
Q

Theories about stuttering

A
  • brain organization
  • speech timing
  • multifactorial/dynamic
  • communicative failure and anticipatory struggle
  • capacities and demands
94
Q

Research studies on stuttering

A
  • physical and motor skill development (ex. between 2-5 years of age, there is a rapid growth in the child’s speech muscles
  • speech and language development (ex. children rapidly develop speech and language between 2-5 years of age)
  • cognitive development (ex. children with developmental delays may develop speech and language at slower rates)
  • environmental studies (ex. parents may react differently to a child’s speech (fluent and disfluent)
95
Q

Clinician’s expertise on stuttering

A
  • do not jump to conclusions
  • ask questions to determine client’s needs
  • show acceptance
  • follow client’s privacy rights - HIPAA
  • establish trust and credibility
96
Q

Male to female ratio

A
  • for children and adults: 3 to 1
  • for very young children who start to stutter: 1:1
  • girls recover more often in young childhood
97
Q

Recovery of stuttering without treatment

A

75% of children

98
Q

Incidence of stuttering

A

5% - how many people have stuttered at some point

99
Q

Prevalence of stuttering

A

1% - how many people who stutter or how widespread is the disorder

100
Q

Has the cause or causes of stuttering been determined?

A

No but numerous theories exist

101
Q

Stuttering can consist of

A
  • part or whole word repetitions
  • prolongations
  • sound or syllable repetitions
  • interjections
  • broken words
  • blocking
  • circumlocution (word substitutions)
102
Q

Stuttering onset can be between

A

18 months of age and puberty

103
Q

stuttering onset is usually before

A

6 years of age

104
Q

What is voice

A

Sound made by vocal fold vibration

105
Q

Voice productions involves 3 subsystems

A
  1. respiratory system
  2. phonatory system
  3. resonator
106
Q

Vagus Nerve

A

main nerve for the muscles in the larynx

107
Q

Voice disorder

A

Is a type of communication disorders where problem with voice production is the primary cause for a difficulty with speech production

108
Q

A voice disorder exists when

A

a person’s quality, pitch, and loudness differ from those of similar age, gender, cultural background and geographic location

109
Q

Dysphonia

A

Abnormal voice, as judged by the listener, involving either pitch, loudness, quality, flexibility, or some components of all four

110
Q

Aphonia

A

The voice is either severely breathy or whispered.

111
Q

Prevalence of voice disorders for adults (general public)

A
  • 29.9% (nearly 1/3) affected at some point in their life
  • 6.6% at any given point in time
  • Risk factors: sex (women), age (40-59 years), voice use patters and demands, esophageal reflux, chemical exposures, and frequent cold/sinus infections
112
Q

Prevalence of voice disorders in adults (teachers)

A
  • 57.5% (more than 1/2) is affected at some point in their life
  • 11% at any given time
113
Q

Prevalence of voice disorders in children

A
  • 6% (clinician report) - 11% (parental report) at age 8
  • risk factors: having older siblings and genders (male)
  • 6-23% across childhood
  • more than 1 million children in the united states affected by chronic dysphonia
114
Q

Top occupations associated with laryngeal pathologies:

A
  • teachers, sales people, secretaries
  • singers/professional voice users
  • homemakers
  • factory workers
  • executives/managers
  • nurses
  • retired persons (age)
115
Q

What causes voices disorders

A
  • Lesion on the vocal fold
  • problem with VF mobility
  • excessive tension of the laryngeal muscles
116
Q

Lesion on the vocal fold

A

organic: malignant
-cancer of the larynx
organic - benign
-vocal abuse/misuse:
vocal fold nodules, polyps, cysts
-viral:
laryngeal papillomatosis, upper respiratory infections
- Inflammatory:
Gastroesophageal reflux (heartburn)

117
Q

Problem with VF mobility

A

neurological
- vocal fold paralysis
- parkinson’s disease
- spasmodic dysphonia

118
Q

Excessive tension of the laryngeal muscles

A

functional dysphonia

119
Q

Laryngeal Cancer

A
  • malignant
  • need immediate medical attention
    Treatment:
  • Surgery, chemotherapy, radiation, voice rehabilitation
  • Removal of the entire larynx (laryngectomy) may become necessary in some cases
  • Trachea is repositioned to form a stoma for breathing
120
Q

vocal fold nodules

A
  • benign: injury to the vocal fold mucosa (vocal overuse/misuse/abuse)
  • could have negative impact on social, occupational function (QOL), but not life-threatening
  • Treatment: (voice therapy, surgery is an option AFTER voice therapy)
121
Q

contact ulcer

A

Inflammatory
- tissue in a healing process

  • usually located on the posterior third of the vocal fold, which corresponds to the vocal process of the arytenoid cartilage
  • patient typically able to point to site of pain, especially with phonation
  • often associated with laryngopharyngeal reflux (acid reflux)
122
Q

Vocal fold paralysis

A
  • neurological: CNS or PNS (vagus nerve)
  • could result in aspiration pneumonia
  • voice quality could be breathy and weak
  • Treatments: voice, therapy, surgery
123
Q

Spasmodic Dysphonia

A
  • neurological - CNS
  • spasm of vocal folds upon speech
  • intelligibility is moderate to severely reduced
  • treatments: voice therapy, botox injection (paralytic agent)
124
Q

Functional voice disorders

A
  • conversion/somatoform disorder
  • severe tension of laryngeal muscles
  • otherwise the larynx functions normally
    -treatment (voice therapy)
125
Q

Voice team

A
  • patient
  • parent/spouse
  • slp
  • classroom teacher
  • radiologist
  • neurologist
  • allergist
  • endocrinologist
  • psychologist
  • speech/voice scientist
126
Q

Clinical flow

A
  1. identification of problem
  2. evaluation
  3. treatment
  4. re-evaluation
127
Q

Typical voice evaluation

A
  • history
  • perceptual voice analysis
  • instrumental voice analysis
  • quality of life measuring
  • laryngeal imaging
128
Q

Treatment modalities of voice disorders

A
  • surgical
  • pharmacological
  • behavioral
129
Q

Perceptual voice analysis

A
  • subjective assessment
  • describe severity and type of dysphonia by using commonly used attributes
  • not only auditory: also observes respiratory, behaviors, posture, visible effort, etc.
130
Q

What did Dr. Kanner believe was the cause of autism?

A

parents who were too rigid and unbended

131
Q

1 in __ children are affected by ASD

A

36

132
Q

The lifetime cost to care for an individual with ASD is

A

$3.6 million dollars

133
Q

What are the costs to the U.S. for autism per year?

A

$7 trillion

134
Q

Lifelong care costs can be reduced by __ with early diagnosis and intervention

A

2/3

135
Q

Criteria is established by

A

psychiatrists, psychologists, and physicians with extensive experience

136
Q

Criteria for ASD diagnosis

A
  1. persistent difficulties in social communication and social interactions across multiple contexts
  2. Restricted, repetitive interests or patterns of behavior (at least 2)
  3. Symptoms must be present in early childhood
  4. limit and impair everyday functioning
  5. Overall difficulties are not explained by
137
Q
  1. Persistent difficulties in social communication and social interactions across multiple contexts
A
  • deficits in social-emotional reciprocity
  • deficits in nonverbal communication behaviors
  • deficits in developing, maintaining, and understanding age- appropriate social realtionships
138
Q
  1. Restricted, repetitive interests or patterns of behavior
A
  • repetitive use of objects
  • mannerisms
  • insistence on sameness, upset with very small changes in routines
  • high restricted interests
  • hyper- (over) or hypo (under) reactive to sensory stimuli
139
Q
  1. Symptoms must be present in early childhood
A
  • often noticed before second birthday
  • in some cases may not be apparent until later in childhood or adolescence until social demands exceed abilities.
140
Q
  1. Limit and impair everyday functioning
A
  • social
  • occupational
  • communication
141
Q
  1. Overall difficulties are not better explained by
A
  • intellectual disability
  • global developmental delay
142
Q

IDEA defines autism as:

A
  1. significantly affecting verbal and nonverbal communication and social interaction
  2. adversely affects the student’s educational performance
  3. includes other characteristics such as repetitive behaviors and interests
  4. individual states have their criteria for eligibility for early intervention and special education under the disability category of ‘autism’.
143
Q

Benefits of ASD classification system

A
  • helpful for determining the outcomes of research
  • gives clinicians a “common language” for describing the disorder
144
Q

Prevalence

A

number of cases of a condition that exists at a particular time in a defined population

145
Q

Incidence

A

the rate of new cases of a disease occurring in a specific population over a particular period of time

146
Q

Regression usually occurs at

A

18 months of age

147
Q

Boys are more affected than girls TRUE OR FALSE

A

TRUE

148
Q

Average male to female ratio for ASD

A

4:1

149
Q

In the U.S., the average age of diagnosis of ASD is _ years

A

4

150
Q

What causes ASD

A
  • environment
  • epigenetic
  • genetic
151
Q

Studies involving dizygotic (fraternal) twins (ASD)

A
  • When one twin was diagnosed the concordance for ASD diagnosis was low - The risk of ASD for siblings of those identified on the spectrum is 15% to 20%, considerably higher than the population risk (.05%-.01%)
152
Q

Autism screening

A
  • All children should be screened for autism spectrum disorder as part of their well-child healthcare visits at 18 months and 24 months
  • SLPs play a central role in screening individuals
153
Q

ADOS-2

A
  • standardized means of observing behavior
  • Gold standard assessment
154
Q

__ of individuals with ASD do not acquire functional, verbal communication

A

30%

155
Q

Relatives of those with ASD have an increased frequency of lesser variants/symptoms of ASD, known as the broader autism phenotype (BAP)

A
  • Challenges with social skills and or language development
  • Presence of repetitive behaviors and interest
  • Known as “subclinical” features
156
Q

Differences in the structure and function of the brain ASD

A
  • Head circumference is normal at birth but enlarged by 6-14 months of age
  • Overgrowth of the brain continues through the first 2 years of life
  • Overgrowth is probably due to dysregulation of layer formation and layer-specific neuronal differentiation, which occurs during prenatal development
  • The most likely cause is excess neuron numbers due to dysregulation of neurogenesis, or lack of normal neuronal pruning and connecting of the neurons
  • There could be axonal overconnectivity in the frontal lobes and the amygdala
157
Q

Motor speech disorders

A

are a group of speech (not language) disorders resulting from damage to the CNS and/or PNS

158
Q

Dysarthria (informal)

A

Dysarthria is a neurological motor speech impairment characterized by slow, weak, uncoordinated movements of the speech musculature.

158
Q

Apraxia

A

Apraxia is a neurologic speech disorder that makes it hard to perform purposeful movements, even though the muscles work normally, and the person understands what they want to do.

159
Q

Dysarthria can be

A

congenital (e.g., cerebral palsy) or acquired (e.g., MS, Parkinson’s disease, brain injury, stroke).

160
Q

Flaccid dysarthria

A

→ damage in brainstem nuclei (in blue-colored area) and/or cranial nerves (yellow arrows pointing from brainstem toward head and neck muscles)
→ damage results in muscle weakness and paralysis, and wasting of muscles (lower motor neuron disease)
→ speech characteristics
breathy voice
hypernasality
imprecise consonants

161
Q

Spastic dysarthria

A

→ damage to descending fibers (called the corticobulbar tract) from cortical motor neurons to motor nuclei in the brainstem (yellow arrows pointing from cortex to pons and medulla in brainstem)

→ damage results in muscle weakness and hypertonic and hyper-reflexive muscles (upper motor neuron disease)

→ speech characteristics
slow speaking rate
strain-strangled voice
monopitch
reduced stress
imprecise consonants

162
Q

Ataxic dysarthria

A

→ damage to cerebellum, and/or to fibers tracts connecting it to all parts of CNS (see yellow arrows)

→ damage results in difficulty maintaining a consistent rhythm, and in controlling the force of muscle contractions; often the force of muscle contraction is inconsistent with the task (e.g., too much force), and movements are jerky, and uncoordinated

→ speech characteristics
excess and equal stress
irregular articulatory breakdown
“drunk-sounding” speech
imprecise consonants

163
Q

Hypokinetic dysarthria

A

→ loss of dopamine-producing cells in the substantia nigra (located in midbrain—see blue oval), reducing level of dopamine delivered to basal ganglia for control of movement (yellow arrows show dopamine pathway from substantia nigra to basal ganglia)

→ dopamine deficiency and other damage to the brain results in resting tremor, rigid (stiff) muscles, slow, small movements; patients may have episodes of inability to move

→ speech characteristics
monopitch
reduced stress
monoloudness
weak voice

164
Q

Hyperkinetic dysarthria

A

→ damage to one (or several) structures of the basal ganglia (subcortical nuclei and their connections, see blue oval in image); there are several basal ganglia diseases associated with movement disorders; information is provided in text on two of these diseases—Huntington’s disease, and dystonia

→ in Huntington’s disease the movement disorder is associated with jerks, tics, and sudden, uncontrolled movements; in dystonia there are sustained contractions that build up and are maintained for several seconds or longer, creating unwanted and uncomfortable postures

→speech characteristics (combined for both diseases)
prolonged intervals (e.g., sustained vowels)
reduced stress
variable speaking rate
harsh voice or voice (phonation) stoppages
imprecise consonants

165
Q

Mixed dysarthria

A

→ combination of two or more of the five types (flaccid, spastic, ataxic, hypokinetic, hyperkinetic) of dysarthria, presumably due to damage to two separate parts of the CNS or CNS + PNS

→ Examples
Multiple sclerosis (MS) often has lesions (damage) in both the corticobulbar tract (upper motor neuron disease) and cerebellum; the expected mixed dysarthria is called a spastic-ataxic dysarthria

Amyotrophic lateral sclerosis (ALS) may have damage in both the corticobulbar tract (upper motor neuron disease) and brainstem (lower motor neuron disease); the expected mixed dysarthria Is called a spastic-flaccid dysarthria

166
Q

Unilateral Upper Motor Neuron Dysarthria

A

→ a relatively milder form of dysarthria in which only one of the two (paired) corticobulbar tracts is damaged

→ spastic dysarthria is typically the result of damage to both corticobulbar tracts

→ speech characteristics (mild)
imprecise consonants
harsh voice
slow speaking rate

CSD 277 (6 decks)

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