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Stuttering > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Wingate’s definition (3 components, ‘64)

A
  1. kernel speech characteristics (part word repetitions and prolongations), 2. accessory features (secondary, abnormal speech-related or not movements such as pursed lips, tongue out, jerking head, stomping feet, starters like “you know”), 3. associated features (emotions, stress); Perkins added “involuntary” to this definition in ‘91
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2
Q

WHO definition

A

disorders of rhythm of speech in which the individual knows precisely what he wishes to say, but at times is unable to say it because of involuntary, repetitive prolongation or cessation of sound

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3
Q

WHO disability vs. handicap

A

limitations on ability to communicate (activity) vs. lack of fulfillment of social life, job, school, etc. (participation)

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4
Q

parts of other definitions

A

timing of syllables caused by discoordination of various systems; result of MULTIPLE (not singular) coexisting, physiological, psychological factors; stoppages include reps of sounds, syllables, or 1-syllable words, prolongations of sounds, blocks of airflow or voicing (important!)

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5
Q

secondary behaviors of escape or avoidance

A

escape from block with head turn, etc. or circumlocutions, situation avoidance

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6
Q

Conture’s definition

A

within word and between word disfluencies

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7
Q

stuttering stats

A

childhood disorder: 18 mos. to 5 yrs.; sex ratio 2-1 in children and 5-1 (3-1+?) in adults; probably congenital; originally thought there were primary and secondary stutterers (younger and older children), but later found more categories and stages

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8
Q

overall stuttering definition

A

domain of motor speech production and its disruption by speech disfluencies

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9
Q

Yairi’s stuttering-like disfluencies statistical model

A

typical: partial word repetitions, single-syllable word repetitions, disrhythmic phonation (prolongations and blocks)–especially children; also tense pauses and broken words –all

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10
Q

More phonatory or respiratory difficulties?

A

Probably phonatory

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11
Q

Where do things like head turns and stomps come from?

A

Sometimes learned compensatory techniques

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12
Q

Why do children often increase speech rate?

A

To get it out before stuttering monster hits

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13
Q

Yairi’s definition

A

Stuttering is an involuntary disruption of the smooth execution of a speaker’s intentional speech act

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14
Q

Where did SLP start?

A

School of Rhetoric and Theater at U of Iowa in ’20s

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15
Q

Why do people stutter on name?

A

One theory is communicative responsibility: relaying important info.

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16
Q

Is reading or spontaneous speech usually better?

A

Reading, because lower cognitive load; telephone worst of all

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17
Q

Who defines what cure is?

A

The patient

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18
Q

Is it important if someone stutters 18% vs. 22% of the time?

A

Not very

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19
Q

Blocks are of

A

airflow and voicing

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20
Q

Steps of speech

A
  1. exhale 2. make noise 3. turn noise into speech
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21
Q

Hutchinson definition

A

complex, unique, integrated, hierarchical

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22
Q

devp’t of stuttering

A

traditional view was unitary or progressive disorder that develops from normal disfluencies (simple easy repetitions without tension, awareness, emotions, etc.); so, there must be a critical period when disfluency changes to stuttering (need to divert stuttering back to normal fluency)

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23
Q

Bloodstein’s Model

A

based on cross-sectional study; uses 5 parameters: type of disfluency, loci, physical tension, cognitive awareness, emotional reactions

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24
Q

Bloodstein’s Developmental Phases

A

1: 2-6 yrs. onset; episodic, usually under stress, excitement, etc., mostly repetitions, mostly at beginning of utterances; content and non-content words; little concern on children’s part; 2: 4-5 yrs., chronic; children aware of stuttering; mostly content words; low concern about speech; influence of rapid speech or excitement; 3: 8-adult, specific situations, words, sounds; substitutions and circumlocutions; avoidance rare; 4: 10+ yrs.; fearful anticipation; know trigger words; frequent avoidance, circumlocutions; fear and embarrassment

25
Q

Van Riper Tracks (developmental heterogeneity)

A

based on: age of onset, type of onset, type of stuttering, concomitant problems; one of first researchers to recognize rapid onset of stuttering; subgroups of stutterers

26
Q

Van Riper Tracks

A

1: traditional (most @ 50%), 2.5-4 yrs., previously fluent, gradual onset, episodic, syllable repetition, no tension, frustration, awareness; 2: artic/lang. (25%), onset with first sentences, never fluent, gradual onset, poor artic., fast, irregular reps, no tension, frustration; 3: organic (15%), onset after trauma, sudden, previously fluent, slow, careful rate, significant tension, awareness, struggle; 4: strange child (10%), onset after 4, sudden, erratic, no remission/consistent pattern, awareness, but no frustration/fear

27
Q

Daly’s Supportive Study

A

mostly confirmed Van Riper’s tracks, although no children in track 4/strange child (overall, 83% placed in tracks); tx techniques were slow rate, easy voice onset, breathstream management; track 3 = best gains, then 1, then 2

28
Q

Conture’s 3 tracks

A

50% brief speech production issues leading to repetitions, no other problems, recovery likely; 50% brief problems, repetitions, develop into block and prolongations; 10% sudden onset and severe, need counseling

29
Q

New Castle study

A

longitudinal, ‘64, birth to high school, nurses visited homes; most stuttering before age 5, no new after 11; 3 types of stutterers: transient/developmental (normal non-fluency between 2-4, for six months); temporary (more than 6 months, but stopped); persistent (didn’t stop)

30
Q

incidence and prevalence based on New Castle

A

incidence (chance of occurring over period of time, have you ever?)=5%; prevalence (have disorder at given time)=1%; recovery rate = 80%

31
Q

spontaneous recovery

A

some get better on own (4% difference between incidence and prevalence)=80%

32
Q

risk for persistent and recovered stuttering

A

1%= prevalence/persistent; 4% = recovery; 5% = incidence/ all stuttering; but higher risk for boys

33
Q

Much higher risk if

A

relatives who stutter; highest risk is male relatives of female probands; females have higher thresholds requiring more genetic factors, so they have more to transmit to males

34
Q

penetrance

A

degree of expression given susceptibility gene: reduced for males and greatly reduced for females in stuttering

35
Q

observed vs. expected PERSISTENT stutterers

A

stuttering is familial and strong genetic factor; MUCH higher percentage of persistent stuttering when familial proband

36
Q

recovery chance of males and females

A

5.3% vs. 2.7% (due to larger numbers)

37
Q

% of recovered from probands of recovered stutterers is much greater than expected except for

A

female stutterers of male probands

38
Q

observed vs. expected RECOVERED stutterers

A

observed for recovered 2-3 times greater than gen. population, so recovered is less familial than persistent and MAY have great environmental component

39
Q

single most reliable predictor of persistent stuttering

A

family history

40
Q

how genes are expressed subject to

A

environmental influences and actions and interactions of many genes

41
Q

phenotype vs. genotype

A

observable traits or characteristics that are genetically controlled vs. sum total of genes, 1 copy for each parent

42
Q

genes (genotype) transmits?

A

susceptibility for features that may play a role in disorders

43
Q

environmental aspect types

A

external and internal, shared or unique

44
Q

are males or females more likely to have stuttering relatives?

A

females

45
Q

high rate of recovery from stuttering during X months?

A

12

46
Q

how many stutterers have positive family history?

A

71% (43% first degree)

47
Q

When should therapy start for CWS with persistent family history?

A

right away (ask parents if recovered or not; if persistent and onset more than 12 mos. ago, more probelmatic)

48
Q

do environmental factors play a role?

A

yes

49
Q

sex ratio

A

2:1 children; 3:1 or higher adults

50
Q

What is difficult about stuttering eval for children?

A

TX needed? Recovered or persistent?

51
Q

neurologic components of stuttering: soft signs

A

attending problems, auditory processing problems, sentence formulation problems, oral-motor problems (most; DDK, artic., etc.)

52
Q

structural brain differences between PWS and NFS

A

atypical R to L asymmetry (Wernicke’s correlate same or larger in RH for S., but larger in L for N); disturbed white matter tracts (including corpus callosum); abnormal fibers in pyramidal tracts, premotor cortex, supramarginal gyrus; larger corpus callosum so greater RH participation; reduction of gray matter volume in cerebellum and medulla

53
Q

brain functioning differences

A

communication between left sensorimotor cortex, Broca’s, temporal regions disturbed; sequencing of cortical activation during speech production different (normal is programming in inf. frontal cortex before motor prep. in motor cortex); B. & W. in LH reduced activity, but increased RH activity when stuttering (in corresponding section); maybe because RH becomes wired for speech but can’t handle complexity, or LH neural network failure, so RH for compensatory

54
Q

cerebral functioning differences

A

stutterers can’t use LH as well as nonstutterers, so use RH which is not as quick, instead (more activation in RH and less in LH); also note that RH for emotions (already busy with emotions, so inefficiently dealing with emotional overload)

55
Q

auditory processing differences

A

reduced activity in LH auditory association an Wernicke’s (maybe using less aud. feedback); can’t fix what you can’t recognize; but how to explain difficulty getting started?

56
Q

reaction time in PWS

A

slower: articulation, respiration, laryngeal; 3 aspects include analysis of signal, planning response, executing response

57
Q

hypothesis re: reaction time

A

practicing slow regular speech may help synchronize disturbed speech signal between systems (slower systems in general: longer vowel duration, slower transitions, delayed VOT for voiceless)

58
Q

post rx or fluent (spontaneous recovery)

A

RH over-activation decreases, LH increases; auditory cortex more normal in singing or choral speaking; tx may be reestablishing functions where they belong

59
Q

incidence of coexisting issues (artic., lang., etc.)

A

higher than in general population, especially artic; BUT can’t use SSD as predictor, although CWS did stutter more on word-inital CCs when misarticulated, and there MAY be a delay early on; persistent stuttering may be predict artic. issues, though; with language, no significant differences either

Stuttering (3 decks)

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