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107 Cards in this Set

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Fluency - definition
Aspect of speech production referring to continuity, smoothness, rate, and/or effort with which phonologic, lexical, morphologic, and/or syntactic language units are spoken
Fluency disorder
A fluency disorder is a “speech disorder” characterized by deviations in continuity, smoothness, rhythm, and/or effort with which phonologic, lexical, morphologic, and/or syntactic language units are spoken.
Disfluency refers to breaks in the continuity of producing phonologic, lexical, morphologic, and/or syntactic language units in oral speech.
Normal developmental disfluencies
Higher than adult levels of normal disfluencies that occur in preschool children as they learn language normally. Approximately half of nonstuttering children go through an identifiable period of “increased normal developmental disfluency” during this time
Same as stuttering.

According to Wingate (1984), the “dys” and “dis” prefixes are quite different. The “dys” prefix implies abnormality, such that a word beginning with “dys” denotes an abnormal condition. . . . However, most recent texts still prefer the term stuttering.
Stuttering 1 of 4
Stuttering refers to speech events that contain monosyllabic whole-word repetitions, part-word repetitions, audible sound prolongations, or silent fixations or blockages. These may or may not be accompanied by accessory (secondary) behaviors (i.e., behaviors used to escape and/or avoid these speech events).
Stuttering refers to a moment in time - per Dr. Flint
Stuttering 2 of 4
Stuttering consists of speech events that are reliably perceived to be stuttering by observers.
Stuttering 3 of 4
Stuttering refers to the private, personal experience of an involuntary loss of control by the person who stutters. As such, it often affects the effectiveness of the speaker's communication.
Stuttering 4 of 4
Stuttering refers to disordered speech that occurs as the result of: (a) certain physiological, neurological, or psychological deviations; (b) certain linguistic, affective, behavioral, or cognitive processes; or (c) some combination thereof.
Secondary behaviors
Accessory (or secondary) behaviors include the entire range of reactions, strategies, “tricks,” and avoidance or escape behaviors that stutterers perform either when they stutter or in anticipation or fear of stuttering.
Effort with re to stuttering
Effort refers to the amount of perceived exertion a speaker experiences during speaking.
Suprasegmental features
Suprasegmental features are dimensions of speech that extend across phoneme or allophone (i.e., “segment”) boundaries, and include such things as rhythm, prosody, melody, and inflection. Like rhythm and prosody.
Rhythm refers to the pattern (timing and duration) of stressed and unstressed syllables in speech.
Prosody refers collectively to syllable stress, juncture, and intonation contours in speech.
Naturalness refers to the degree to which speech (and language) sounds like that of normal, native speakers.
Cluttering is a fluency disorder characterized by a rapid and/or irregular speech rate, excessive disfluencies, and often other symptoms such as language or phonological errors and attention deficits.
Neurogenic stuttering
Neurogenic stuttering refers to stuttering, often transient, that began with—or is maintained as a result of—a specific, identifiable neurological insult or lesion.
Psychogenic stuttering
Psychogenic stuttering is stuttering that is clearly related to psychopathology.
Dr. Flint's def of disorder of stuttering
Not defined simply by frequency of moments of stuttering; diagnosis requires that 2 people agree that stuttering is present (family + professional, e.g.).

Professionals and laypeople usually agree on what constitutes stuttering.
Can the word fluency be used to refer to stuttering?
No - fluency refers only to the flow of speech, rhythm, rate, prosody. Discontinuity is better word, per Dr. Flint.
Is "rate" considered to be associated with stuttering?
Yes and no -- rate is measured, but is not a problem of stuttering
PWS &/or CWS
Reflects current use of person first language
Can be considered symptoms of disorder of stuttering (confirm this with Dr. Flint)
Variability of stuttering
All comm disorders show variability - but not to the degree seen in stuttering
What varies in disorder of stuttering?
Frequency of stuttering events

Severity of stuttering events
Frequency refers to
Number of stuttering events
Severity refers to
Usually to length or other factors
3 ways stuttering can vary - overview
1) over time
2) within utterance
3) by condition or situation
Varies over time
Moment to moment, day to day
Thus, cannot measure one time (or situation, or place) to determine disorder of stuttering
Varies within utterance
Loci of stuttering
Single sample can result in variability (idiosyncrasies exist) so must take more than one speech sample
This factor is the only one of the 3 that is true of stuttering - and NOT true of normal disfluencies
Loci of stuttering (cont.)
Place where stuttering occurs is more likely to occur:
a) in the 1st 3 words in a sentance
b) On content words moreso than function words
c) within longer words
d) words that begin with consonants
e) within a word - on stressed syllables (usually), and at beginning part of word
Overall -- stuttering tends to occur in clusters
Universal ways that show a decrease in stuttering
Altering way speak (see next card for more on this), and
Environmental conditions
FIC that tend to show DECREASE in stuttering
ALTERED SPEECH: (all about altering phonation)
Using unfamiliar accent
Slow rate
Alter rhythm
Speak in monotone
Prolonging speech (drawing it out)
Environmental situations that tend to show DECREASE in stuttering
Chorus reading
Introduction of masking noise
Suggestion (proved to be untrue?)
Adaptation task
Methods of increasing fluency that are NOT due to environmental conditions
Now thought to be due to altered speech:
Presence of metronome (alters speech
DAF (increases prolongation of speech)
Speaking to animals and young children
Delayed Auditory Feedback (DAF)
Likely has nothing to do with stuttering -- reflects changes in speech by altering speech (prolonging)
Does decrease in communicative pressure decrease stuttering?
No - study proved this to be untrue
Hypnosis – worked temporarily, not therapeutic, likely to be purely environmental

Placebo – therapeutic suggestion is suggested to stutterers, usually where one starts therapy, but is only temporary
Adaptation effect
Same passage read over and over
Works for most everyone
About 5th time of reading, stuttering decreases by 50%
Where read 6th time, realize have plateaued at 5th reading
This phenomena must be explained by any theory that purports to explain etiology of stuttering
Factors that tend to INCREASE stuttering events
Speaking to:
Large audience
Authority figure
Emotional arousal (both +/- emotions)
Waiting to speak
Telephone – usually a problem for stutterers
Theories about etiology of stuttering
3 categories
WE DO NOT KNOW WHAT CAUSES STUTTERING, the theories fall into one of the below:
Environmental (Onslow only)
Physiological theories – overview
Cerebral Dominance theory
Auditory deficit HP (several)
Cerebral dominance theory
Initially thought that stuttering was related to handedness
Orton & Travis 1920s proposed:
A) either wrong (right when it should be the left) hemisphere is trying to dominate, or
B) there is no dominant hemisphere
Forced to change handedness
Was popular for awhile but has been debunked
Auditory deficit theories
Various theories about something being wrong with auditory feedback in stutterers
Masking noise was formally used to support these theories
Defective auditory feedback
Why no longer?
Masking effect not valid
Flawed logic – saying DAF causes stuttering is not valid
Location of stuttering – frequently, stuttering occurs at the initial word – thus PRIOR to auditory feedback
Psychological theories
Freudian and useless to SLP
Stuttering as a neurosis is not widely accepted and even the proponents say their treatment doesn’t work well
Environmental theories
Onslow said that Normal disfluencies and the child’s reaction to same cause stuttering
W. Johnson followed Onslow
Diagnosogenic (Dx) theory
Wendell Johnson
Parental misdiagnosis of normal disfluencies as stuttering causes stuttering
Parental reaction is abnormal, child becomes anxious, increase in disfluencies follows
NOW debunked
Problems with Dx theory
1) Can’t disprove it because it’s not testable (can’t be there in the room at the moment the parents react to instance of disfluencies)
2) Genetic factor not explained by Dx theory
3) Early evidence refuted
a. Name for stuttering was said not to exist in Native American community
4) Cognitive therapy would work better than it does (where you presuppose a link between anxiety and stuttering – if you treat the anxiety, the stuttering should, but doesn’t, disappear)
5) Claim that decrease in stuttering prevalence due to Dx theory is simply not true (ref’ed only to decrease in Tx referrals due to Dx therapy)
6) Calling attention to stuttering in young child can make it better – not worse
a. Puppet study for early 1970s
Spontaneous Recovery (S/R)
View of layperson “will grow out of it” but actually:
Data is flawed, which leaves the rates (as high as 80%) questionable
Dr. Flint believes the number of actual SR are ___
How define “recovered” with re to SR?
SR means the disorder IS COMPLETELY ABSENT
Recovery can be gradual but is not considered attributable to formal treatment
How verify recovered?
1) Had d/o to being with
2) Recovered w/o treatment
3) Did in fact recover (per above)
What is probably the largest factor in high number of SR cases?
High number of individuals with NORMAL disfluencies
Four groups of SR
1) never had the d/o
2) not completely recovered
3) true/actual cases of SR, and
4) Recovered via treatment
True cases of SR
Internal (maturation) effects
External factors – studies have revealed that parents were conducting treatment themselves, whereas adults were self-treating
Is there a causal factor in cases of actual SR?
Yes – didn’t simply occur naturally
Treatment considerations with re to SR
Why treat? Why wait?
Evidence suggests that if wait too long (and child turns out to have developmental stuttering – and does not SR) stuttering can get much worse
In fact, with re to children – the only time “cure” is used is with children because they tend to respond so well to treatment for stuttering
Assessment of Stuttering – overview
Always look at ALL areas of language when assessing

Think of assessment as: 1) collect data 2) analyze data
What do you measure when assessing stuttering?
1) Actual stuttering events, and
2) Everything else that should be measured
What do we measure with stuttering events?
Frequency, duration and type
Other things that are measured
Secondary behaviors
Speech rate
What are secondary behaviors?
Postponement devices or starters
Other physical movements that accompany stuttering
Avoidance behaviors
Attitudes about speaking, communication and personal feelings
Why measure speech rate?
Not just about slowing down, unless that’s what treatment is focused on
Must measure rate even if not involved in treatment to verify and est baseline
Why measure naturalness?
Some treatments involve creating very unnatural speech – when time comes to return to natural speaking patterns may want to know where you were to begin with
Natural refers to more than rate
It’s not formally measured
Researchers do so, and we may end up formally measuring it
How determine severity?
A compilation of many things – refer to SSI (which is open to debate)
What does SSI measure?
Frequency, duration and physical concomitants
Does the clinician decide something about severity?
Often yes – open to clinician interpretation
May take avoidance behaviors into account, because many times even where actual stuttering events are mild, the avoidance behavior is severe because it’s handicapping to the individual
What is frequency?
Considered Core behavior
Primary measurement of stuttering events
% syllables stuttered
Most often measured at SYLLABLE level because it’s more sensitive than at word level
Percent syllables stuttered (%SS)
Used to make comparisons – before and after treatment
How calculate the % SS?
# of stuttering events / total # syllables spoken x 100
How calculate speech rate?
Calculate the total # of syllables spoken, then divide by time – either minutes or seconds
Example: time sample, count number of syllables produced, divide the # of secs in a minute (60) by the # of secs in the sample, multiply by the # of syllables in the sample

Example: 20 second sample, 62 syllables produced, 60 / 20 = 3; 62 x 3 = 186 SPM
What are the 2 methods of finding %SS?
1) record and transcribe, marking all places where stutter occurred (very time consuming)
2) listen to recorded sample twice – once to count syllables, then to could stutters
What counts as a stutter?
Any attempt at a syllable
Single attempt = single stutter
How do we measure duration?
Quantitatively (using #s)
Qualitatively (describing events with words – like “most stuttering moments were fleeting” (will use most or few for duration – not true with measuring frequency)

With duration, will want to measure QUALITATIVELY not quantity: Why - CHANGE is shown better via qualitative measures

With severity - length of block (not type) - they're equal in severity - thus no reason to measure quantitative
How do treatment goals influence therapy?
Adults either want to be completely free of stuttering, or want to lessen severity
With treating stuttering the clinician usually sets the goals – but in treating adults, want to take their feelings/ thoughts into account in determining goals
Thus – where want to lessen severity, treatment may be aimed at duration
Also, where want to eliminate it, may not care about lessening duration – so won’t be part of assessment
Where want to eliminate stuttering (in adult clients) how approach measuring duration?
Use more non-precise measures of duration or don’t measure at all?
Where want to modify moments of stuttering (in adults) how approach measuring duration?
Need more precise measurements
Quantitative measurement of duration
1) transcribe, mark MOS, then measure duration of each one with stop watch – can average and arrive at proportion – problems: very unreliable, fleeting moments are <.5 secs – not humanly possible to measure
2) mark transcript as those that are longer than fleeting – will improve reliability, but takes much time
3) % of stutters that were fleeting – e.g., 50% fleeting, 50% longer – then measure average duration of longer stutters
4) mark as either fleeting or long and lump into categories
ALL OF THESE require transcripts which are very time consuming
May simply use SSI way of labeling and be more objective (quantifies duration – average 3 longest MOS in sample, plug into table)
Why calculate duration, per Dr. Flint?
Not really useful, not precise – how decide which 3 were the longest? Dr. Flint uses descriptive measures instead.
Why not worry about measuring quantitatively?
Change is shown better via quality not quanity
Is measuring TYPE of stutter important to treatment?
No; we need to show changes over time - thus, need to measure in qualitative way
Why measure type?
Only reason presently is need overall description of disorder - a profile of disorder
Other reasons for measuring type relate to research
RQ1) does the type of disfluency determine if child is normally disfluent or stuttering? (don't know)
RQ2) does type help to distinguish between those who will SR v. those who won't SR?
RQ3) Can one predict treatment success, and make better decisions in intervention? not conclusive
Taxonomy is needed - why?
Problems - there are several, not all terms are descriptive enough, have overlapping terms, & need to eliminate wastebasket terms (too broad)

A taxonomy is a system of classification
Examples of terms not descriptive enough
syllable repetition = dysrhythmic phonation
Example of overlapping terms
syllable repetition and word repetition (same with one-syllable words)
Example of wastebasket terms
dysrhythmic phonation can refer to blocks, repetitions within words,
Same behavior, same word
block, silent prolongation, tense pause (only at beginning of word)
Proposed taxonomy
1) Repeated movements (repetition)
A) incomplete syllable rep'n (not a full vowel)
B) syllable rep'n
C) multisyllable rep'n
2) Fixed postures (articulators are stuck - mouth is in position to make the sound)
D) Audible
E) Inaudible
3) Superfluous behaviors (extra things being added)
F) Verbal (um, like, ya'know)
G) Non-verbal (physical mvmts, like head jerk - but these are not truly disfluencies though)
What was wrong with Tudor study - re treatment?
Treatment was not explicitly stated - e.g., observations are assumed to have occurred, but were not documented - what actually occurred in treatment is unknown and we can only speculate
What was wrong with Tudor study - perceptual data?
At the beginning of the experiment, there was no appreciable difference in the mean scores of the groups
a) between children who stutter v. the non-stutterers
b) in pre and post trmt severity ratings
c) no differences at the end of the study
d) additionally -- the trends shown for each group are "insignificant" but are also headed in the wrong direction - e.g., IA (stutterers labelled as normal) had decreased fluency, IIA (normal fluent labelled as stutterers) had improved fluency
What was wrong with Tudor study - posttreatment?
None of the posttreament children were labelled as a stutterer
Why was Dyer (reporter) wrong in conclusion that stuttering was established?
Reporter looked at the perceptual data and concluded that stuttering was established as a result of the study -- he was wrong!
His conclusion is not supported by the data. In fact, one of the people interviewed by reporter showed the greatest improvement in fluency - and this guy was reported to have DEVELOPED stuttering as result of the study
Wrong in that: 1) NOT designed to induce stuttering, 2) NOT suppressed by Johnson, and 3) Participants were NOT driven to stutter
What does Tudor's data (summarized at p. 197) indicate about whether the children developed stuttering?
Tudor's notes do not confirm the development of stuttering and are consistent with the advent of low self-esteem re speaking abilities
What about participants - besides being orphans
Were not representative because they were raised w/o parents, and had low IQ (confounding factor)
Evidence against Dx theory
1) Nature of normal disfluencies: stutterers are said to have different speech from day one
2) Experimental punishing of stuttering - did not show a decrease - in fact, calling attention to it can help a child
3) Parents actually help stuttering child by correcting their speech - stop/slow down
4) Evidence now shows that stuttering may be genetic - at least non-environmental
Ethical issues re Tudor study
1) use of human subjects
a) setting - gave erroneous info to staff
2) Assigned responsibility
3) Behavior of others - Mercury news released personal information w/o consent
Anticipatory Struggle (AS) theory
Bloodstein 1961
Similar to Johnson
Causal theory
Tension and fragmentation (speech apprehension) occur because child's belief in difficulty in speech
People stutter because they BELIEVE speech is difficult
Per Bloodstein - stuttering occurs due to a feeling of impending difficulty in speech which disrupts speech motor planning and execution
Strengths of AS theory
Provides explanation of consistency effect (same words) - which is words are representative of past failure and apprehension - they function as stimuli for speech breakdowns
Cons of AS theory
*Cognition in stuttering (Bloodstein suggests PPL could recover if they forget they stutter); HOWEVER, cognitive therapy alone is of ltd use in eliminating stuttered speech
*Role of anxiety in stuttering - there is no link btwn anxiety and stuttering
*Genetic evidence remains unaccounted for
Trait = inherent level of anxiety
State = situation specific
Craig study of causal relationship btwn anxiety and stuttering
204 subjects, 102 stutter, 102 non-stutterers
Results = before trmt, stutterers were more highly anxious than fluent controls
Problems with Craig study
External validity weakened - phone call was to stranger, so results pertain only to that situation
No random selection
PPL must be highly motivated to take part in intensive trmt
Q: does this group resemble the anxiety of all stutterers? Perhaps they were atypical; possibly highly anxious to eliminate their stuttered speech
Miller & Watson study
Questionnaire measure of anxiety found NO DIFFERENCE in state or trait anxiety btwn stuttering and control group
Kraaimatt study
Reported that PWS were significantly less anxious than social phobics
Weber & Smith
Found higher autonomic levels correlated with disfluent speech; but all measures were within normal range
Research on link between stuttering and anxiety
Has not been demonstrated

To a clinician, this is a non-starter as the clinician will adapt trmt to situation accordingly
Lincoln & Onslow showed that not everyone who stutters is anxious
Clinical scenarios on anxiety and stuttering
1) anxiety is not a clinical issue
2) anxiety is presenting problem
3) stuttering eliminated but anxiety remains (may want to combine trmt with anxiety mngmt)
4) anxiety eliminated with stuttered speech (anxiety ceases with stuttering)
5) anxiety becomes apparent during trmt