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Stuttering > Test 2 > Flashcards

Test 2 Flashcards

1
Q

What does a general theory do?

A

Describes behaviors, contributing factors, course (figment of author’s imagination)

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2
Q

3 types of stuttering theories

A

biological, psychological, integrated

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3
Q

challenges for stuttering theories

A

stuttering at onset, change over time, inconsistent (episodic), ethical limitations

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4
Q

Charles Van Riper’s story

A

learn how to stutter

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5
Q

psychoemotional basis of stuttering in 20s-50s

A

trauma, emotional disturbance, personality

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6
Q

what is a manifestation?

A

block, repetition, prolongation

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7
Q

psychoemotional and anxiety

A

Greiner: higher anxiety for PWS; Craig: higher state[response to st]/trait anxiety; Craig: greater anxiety for PWS; Guitar: reactive temperament may predispose child to stutter; Hauner: sensitivity for all w/ comm. disorders

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8
Q

anxiety and st.: Ezrati-Vincour and Levin (2004)

A

trait anxiety higher for PWS; state anxiety increases with stuttering severity; authors say to assess state anxiety to see which situations trigger; however, all PWS in study were seeking tx (more likely to stutter)

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9
Q

psychobehavioral

A

theories

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10
Q

classical conditioning: Pavlov

A

stimulus (paired with something) and reaction; for people who stutter, a situation or person can be what’s paired with stuttering to produce the anxiety reaction

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11
Q

operant conditioning: Skinner

A

positive reinforcement, negative reinforcement, punishment/extinction (eventually stop working without reinforcement)

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12
Q

diagnosogenic theory (still psychobehavioral)

A

anticipatory apprehensive hypertonic avoidance reaction; parents disapproval and labeling of stuttering (after normal disfluency) causes the child anxiety, which leads to tension, and then stuttering, which becomes more severe with more disapproval; parents blamed; harmful b/c then wouldn’t seek therapy

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13
Q

more psychobehavioral theories

A

conflict (approach-avoidance): Sheehan–tx leads to master y over FEAR so approach can increase–competing desires to speak and hold back lead to maladaptive behaviors

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14
Q

more

A

two-factor: Brutten & Shoemaker: classical and operant conditioning; tx to reduce ANXIETY and desensitize; stuttering as involuntary byproduct of anxiety

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15
Q

more

A

demands and capacities: Starkweather: tx to reduce demand because the system breaks down when the task demand is too high, as is the case for speech sometimes; capacity may be good with normal demands (so situational)

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16
Q

psycholinguistic theory

A

retrieval and assembly of ling. components overwhelm the system (relative/related example); tx to slow down; Covert Hypothesis example of this

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17
Q

Covert Repair Hypothesis: Postma and Kolk

A

based on perceptual loop theory (Levelt), where you have phonological issues which you process when you are saying something, and then try to repair the future damage during or before it comes out; external loops–internal for speaker (processing), external for listener

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18
Q

more CRH

A

disfluencies are byproducts of covert repairs of internal speech errors as soon as error is detected, speech halted to repair error–comes out as stuttering as opposed to repair; fillers may be used to help listener understand the repair and hold your turn; prolongations as repair before continuant; blocks as problem on initial sound; CWS have lesser capacity during artic./lang. growth

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19
Q

psychological theories

A

psychoemotional: anxiety; psychobehavioral: classical, operant conditioning, diagnosogenic; psycholinguistic: perceptual loop, covert repair

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20
Q

biological theories

A

genetic, neurophysiological, physiological

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21
Q

Drayna et al. genetic study of families in Cameroon found

A

40/100 family members are PWS; chromosome 3 and 12 mutations

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22
Q

genetics

A

not sure what is transmitted, but could be structural anomalies, biochemical pathways, brain processing, motor skills, temperament, etc.

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23
Q

neurophysiological

A
  1. cerebral dominance theory, which was debunked (handedness related to leader hemisphere–lefties stuttered bc RH more activated); 2. auditory processing, relevant, since deaf population has lower stuttering, and researchers showed decreased stutter in noise condition (Shane), defect in feedback loop, and lagging feedback
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24
Q

Lombard effect

A

you become louder in background noise

25
Q

brain dysfunction in PWS

A

overactivation of RH

26
Q

CWS

A

deficiency in L hemisphere showed increased risk for CWS (Chang)

27
Q

articulatory differences include

A

poor speech programming and abnormal lip movement (stability and sequencing)

28
Q

phonatory/respiratory differences

A

Conture: simultaneous contraction of VF adductors/abductors (working against each other); Denny: insufficient laryngeal muscle activity; Johnston: insufficient lung volume

29
Q

whisper study by Perkins et al., 1976

A

reading passage with 3 conditions: voiced, whispered, lip movement; stuttering @ 24.6% ss–syllables stuttered, 10.3% ss, .8% ss; implication is that phonation (whisper) and respiration (lip movement) are involved, at least for some

30
Q

when is the mean onset of stuttering across genders (total)?

A

33 mos., with a SD of 8 (by age 3, by age 4 with SD); 60% start by 3; 85% by 3;6; 90% by 4; usually not before 2; 50% demonstrated secondaries; stuttering does NOT arise from normal disfluencies

31
Q

onset of stuttering type

A

sudden 40%, gradual 27%, intermediate in the middle with 32% (if combined, gradual 60/sudden 40)

32
Q

onset characteristics of severity

A

70% mild, 30% mod/severe

33
Q

onset characteristics of stress and profile

A

43% had stress; 26% had no stress + fam. history, while 20% of gradual had no stress and no fam. history

34
Q

instruments to predict stuttering (persistent)

A

Cooper Chronicity Prediction Checklist; Pindzola’s protocol; Stuttering Prediction Instrument; Yairi’s formula; SSI-3 Severity Scale (chronicity = persistence)

35
Q

Cooper Chronicity Prediction Checklist

A

HISTORICAL indicators (history of chronic; 2+ year history of stuttering); ATTITUDINAL indicators (perceive self as stutterer); BEHAVIORAL indicators (PW rep characteristics and prolongation characteristics); disclaimer saying it’s not based on longitudinal studies (based on literature) and shouldn’t be only thing used to make judgment; questions are NOT weighted; 93% of Ss 14 y.o. or older!

36
Q

Protocol for Differentiating the Incipient Stutterer (Pindzola)

A

AUDITORY BEHAVIORS (type, size, frequency, duration, audible effort, work/phrase substitutions, circumlocutions, avoidance/starter) + VISUAL EVIDENCE (facial grimaces/artic. positioning), head movements, body involvement)

37
Q

More Pindzola

A

awareness + concern; length problem existed; consistent/episodic; reaction to stress; phoneme/word/situation fears; family history; weighted, range of 14-42; if borderline, use family history to decide (KEY CONTRIBUTION from Pindzola, along with weighting)

38
Q

stuttering prediction instrument (SPI): Riley

A

history (no score); reactions (12); part word repetitions (4); prolongations (12); frequency (9); speech sample; weighted score; some overlap with persistent vs. non, but use family hx and length of st. as tie breaker; a little sketchy based on age of participants

39
Q

Illinois Prediction Criteria

A

primary, secondary, tertiary factors; fam. hx, gender, SLDs, duration of stuttering, age at onset, disfluency length, sound prolongations/blocks; 2: severity, head/neck movement, phonological skills; 3: concomitant disorders

40
Q

secondary and tertiary factors

A

severity: NOT factor in first 8-12 mos.; age at onset: greater risk for later onset (4-5 y.o.); phonology (st. may predict phono.); lang.: not clear; secondaries=greater risk; concomitant disorders/awareness/emotional reactions=not risk predictors, but may complicate stuttering

41
Q

familial hx of persistency gives a child a ? chance of following the trend, and ? of recovery?

A

65% that will follow, 35% that will recover (and vice versa)

42
Q

speaking rate Kloth et al. study

A

high risk preschoolers; no difference in language; CWS had faster articulation rate; speech motor control may be factor in developing stuttering; later followed up and found that of recovered, had slower speaking rate, and mother’s interaction style was nondirective and language was less complex

43
Q

family history and subgrouping stutterers (Poulos & Webster)

A

66% fam. hx only 2.4% reported birth/childhood factors associated with stuttering; with NO fam. history, 37% percent reported a factor or event; may be subgroups of genetically vs. early brain damage

44
Q

early life incidents that may relate to stuttering (nothing in particular jumps out in terms of likelihood)

A

anoxia, premature, anesthesia, head injury or accident, mild cerebral palsy, intense fears

45
Q

Conture’s within-word disfluencies (=kernel characteristics of stuttering or SLDs)

A

sound syllable repetitions, sound prolongations, monosyllabic whole-word repetitions, within-word pauses; 3 or more per 100 words has some fluency concerns

46
Q

Ambrose & Yairi 1999 SLDs vs. ODs (stuttering-like disfluencies vs. other disfluencies)

A

part word repetitions, single syllable word repetitions, disrhythmic phonation (=prolongations and blocks) vs. interjections, revisions, abandoned utterances, phrase repetitions; repetition units/iterations not included, not SLDs (RU are the # of extra productions divided by incidents)

47
Q

Ambrose & Yairi 1999 CWS vs. CWNS

A

ratios for SLDs= PWR 10:1; SSR 5:1; DP 30:1 whereas almost the same for ODs

48
Q

Yairi’s weighted formula

A

[(pw + ss) x ru] + 2 dp (dp heavily weighted); frequency, type, extent; 4 is the cutoff (no overlap) for mild (-9.99); 10-29.99 mod; 30+ severe; make sure you can apply this formula!!! (see PPT); results should 38, 47, 15 % for mild, mod, severe

49
Q

Pellowski & Conture (2002)

A

stuttering behaviors in 3 and 4 y.o. children: study similar to Yairi’s, showing that total disfluencies and SLDs can be used to differentiate CWS from CWNS (Yairi total disfluencies for CWS 15%, 72% of total disfluencies are SLDs; for CWNS: 6-8 and 34); WEIGHTED SLDs well over 10x greater difference, so good predictor; over 4 on weighted SLDs differentiates 97% of CWS

50
Q

criteria for Yairi’s study

A

below age 6, hx not longer than 8 mos., at least 3 SLDs per 100 syllables, no neurologic disorder, parents believe child stutters and 2 researchers agree

51
Q

Throneburg & Yairi (2001)

A

almost no difference between persistent (P) and recovered (R) close to onset; overall level of SLDs not a sign of P; R more severe at onset; for both, PW reps majority; iterations, DPs no diference

52
Q

genetic basis of R and P

A

females recover more: R/P transmitted; common genetic etiology; P particially due to additional genetic factors such as delayed phonological development

53
Q

Curlee & Yairi comparing R & P close to onset

A

children who stop are younger, began before 3 y.o., are female, have fam. hx of recovery; recovery takes places by 12-14 mos. post onset; fewer SLDs after 12 mos.–if increased or same, more likely to persist

54
Q

More Curlee & Yairi

A

more head and neck movements for persistent, persistent have multiple iterations as compared to just 1-2 (pretty much never more) for nonstutterers

55
Q

prolongations and secondaries

A

over one second = stutter; 75% of CWS have some degree of physical movement during stutter

56
Q

diagnostic info. (Runyan’s protocol)

A

time since onset, family hx, gender, age at onset

57
Q

danger signs for persistent

A

fam. hx of persistence, more than 2/100 SLDs (no. not going down), over 4 on weighted Yairi scale, 2 or more iterations, rapid talker, male, more than 12 mos. post onset, began stuttering after 3, secondary behaviors of tension and movement

58
Q

Yairi & Ambrose predictive factors

A

primary, in order of importance: family hx, gender, SLD trends (down= good, even if high freq.), duration of stuttering (more than 1 year), age at onset (before 4), disfluency length (reduced iterations = good), sound prolongations/blocks (fewer = good)

Stuttering (3 decks)

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