Introduction
The following exercise is a case study of a boy (‘DL’) who was studied by Matthews et al. (Reference Matthews, Williams and Pring1997). DL has a moderate to severe stutter. He attended a local clinic for 17 weeks along with his parents. The case study is presented in five sections: primer on developmental stuttering; client history; speech and language evaluation; parent–child interaction therapy; and speech outcome.
Primer on developmental stuttering
Developmental stuttering is by far the most extensively studied disorder of fluency. Notwithstanding this fact, it continues to pose a considerable assessment and treatment challenge for fluency professionals. Wingate (Reference Wingate2002: 9) defines stuttering as a ‘unique anomaly in the flow of speech characterised by iterative and/or perseverative speech elements involving word/syllable-initial position’. Although the general population prevalence of developmental stuttering is typically taken to be 1%, Yairi and Ambrose (Reference Yairi and Ambrose2013) have recently argued in a review of the epidemiology of the disorder that a lifespan prevalence of 0.72% appears to be a reasonable estimate. There is evidence that the prevalence of stuttering is higher in certain special populations such as individuals with intellectual disability or genetic and chromosomal syndromes. Bloodstein and Bernstein Ratner (Reference Bloodstein and Bernstein Ratner2008) reported that estimates of the prevalence of stuttering among individuals with Down's syndrome range from 21% to 48%. The lifespan incidence of stuttering has standardly been reported at approximately 5%. (Yairi and Ambrose (Reference Yairi and Ambrose2013) have described this as a conservative figure, which should be revised upwards to approximately 8%.) There is a significant gender bias in adults who stutter, with a male:female ratio of 4:1 or larger standardly reported. However, Yairi and Ambrose (Reference Yairi and Ambrose2013) reported that considerably smaller ratios are found in very young children who are near stuttering onset.
Although there is general agreement that stuttering has its onset in early childhood, there has been considerable variation between studies on the mean or median age at onset. Yairi and Ambrose (Reference Yairi and Ambrose2013) state that 95% of the risk for stuttering onset is over by age 4. There is a high level of natural recovery from stuttering, that is, recovery in the absence of intervention. Using data from the Twins Early Development Study, Dworzynski et al. (Reference Dworzynski, Remington, Rijsdijk, Howell and Plomin2007) examined parental reports regarding stuttering at 2, 3, 4 and 7 years. Based on the number of children who were still reported to be stuttering at 7 years, these investigators calculated a 69% recovery rate for children with stuttering onset at 2 years, a 79% recovery rate for children with stuttering onset at 3 years, and a 53% recovery rate for children with stuttering onset at 4 years. Children who stutter can present with a range of other disorders including speech and language problems. In a survey-based study of 1,184 speech-language pathologists serving 2,628 children who stutter, Blood et al. (Reference Blood, Ridenour, Qualls and Hammer2003) reported the presence of articulation disorders in 33.5%, phonology disorders in 12.7%, learning disabilities in 15.2%, literacy disorders in 8.2% and attention deficit disorders in 5.9%.
Stuttering has adverse psychosocial implications for the person who stutters and his or her family. McAllister et al. (Reference McAllister, Collier and Shepstone2013) examined the impact of parent-reported adolescent stuttering on the psychological distress of people who stutter at age 42 years. Members of a British birth cohort who were reported to stutter (217 subjects) had higher psychological distress scores than controls in the study. However, they were not found to be at an increased risk of serious mental health difficulties. Erickson and Block (Reference Erickson and Block2013) reported that adolescents who stutter have below average self-perceived communication competence, heightened communication apprehension and are teased and bullied more often than their fluent peers. The families of these adolescents experienced high levels of emotional strain and family conflict. There is also evidence that certain occupational roles are deemed to be unsuitable for people who stutter. Gabel et al. (Reference Gabel, Blood, Tellis and Althouse2004) asked 385 university students to report their perceptions of appropriate career choices for people who stutter. These respondents considered 20 careers, including speech-language pathologist, audiologist and occupational therapist, to be unsuitable for people who stutter. The extent to which this vocational stereotyping actually influences the careers pursued by people who stutter remains unclear.
Unit 34.1 Primer on developmental stuttering
(1) Which of the following are true statements about the speech features of developmental stuttering?
Iterations and perseverations in stuttering are distinct from normal non-fluencies.
Iterations are most commonly found in word-final position.
Iterations typically involve full syllables.
Perseverations are the prolongation of phonemes beyond their normal duration.
Iterations and perseverations decrease in frequency when the person who stutters is made aware of speech errors.
(2) The significant gender bias in adults who stutter is less evident in very young children who are near stuttering onset. What does this tell us about the process of natural recovery?
(3) In their study of the persistence of and early recovery from stuttering, Dworzynski et al. (Reference Dworzynski, Remington, Rijsdijk, Howell and Plomin2007) found that concordance rates were consistently higher for monozygotic than for dizygotic twin pairs. What does this finding tell us about the aetiology of stuttering?
(4) Why do speech-language pathologists have to be attentive to comorbid conditions in stuttering?
(5) Clinicians must increasingly consider the psychosocial implications of communication disorders in their clients. Which of the following statements characterise those implications in regard to stuttering?
Psychosocial implications extend well into adulthood.
Psychosocial implications must be addressed in the management of the person who stutters.
Psychosocial implications are usually time-limited in nature.
Psychosocial implications are limited to the person who stutters.
Psychosocial implications can have an adverse impact on the occupational domain.
Client history
DL was aged 4;2 years at the outset of the study. He was from a two-parent family and had one younger sister who was aged 1;7 years. An interview with DL's parents revealed a significant family history of stuttering. DL's father, paternal grandfather and uncle had all stuttered. DL's mother was also dysfluent as a child. The parental interview revealed a number of other noteworthy points. The information from this interview suggested that DL had immature attention and delayed speech motor processes. The interview also identified DL's birth history as a possible significant physiological factor. The family had recently undertaken a stressful move. The interview revealed that there were difficulties in managing DL's behaviour. The parents reported considerable anxiety about DL's dysfluency. DL was also described as having a sensitive and anxious nature.
Unit 34.2 Client history
(1) The onset of DL's stuttering was prior to 4 years of age. Given the information about onset in pp. 241–2, is DL's onset typical of stuttering?
(2) Which feature of DL's history indicates that he has an increased genetic risk of stuttering?
(3) The history suggests that DL is also at risk of comorbid disorders. Name two such disorders.
(4) Are there any environmental factors that may be contributing to DL's stutter?
(5) DL was reported to have a sensitive, anxious nature. The relationship between anxiety and stuttering is complex. Which of the following are true statements about anxiety in stuttering?
There is a high rate of social anxiety disorder among people who stutter.
Social anxiety is a psychological concomitant of stuttering.
Social anxiety is typically only found in adolescents who stutter.
Social anxiety causes stuttering.
Collaboration between speech-language pathologists and psychologists is required in order to assess and treat social anxiety in people who stutter.
Speech and language evaluation
DL's speech and language skills were assessed. In terms of DL's dysfluencies, these were characterised by whole- and part-word repetitions, prolongations and blocking of sounds on 8.4% of words. A number of non-verbal behaviours, including hand-flapping, facial grimacing and avoidance of eye contact, were concomitant with these dysfluencies. Both content words and function words were affected. Single words could display several dysfluencies. An example of DL's spoken output is ‘Its its ha-ha-haaa:vn't got got a window’. When questioned about his speech, DL did not display any concern. However, DL's parents reported that he was frustrated about his speech at home. Combined with his concomitant behaviours, this suggested that DL was aware of his dysfluency. DL's rate of speech was 3.8 syllables per second. The Clinical Evaluation of Language Fundamentals: Pre-school (CELF-P; Wiig et al., Reference Wiig and Secord1992) was used to assess DL's receptive and expressive language skills. The CELF-P revealed a considerable language delay, with DL's overall age equivalent 12 months below his chronological age.
An analysis was also undertaken of parent–child interaction. Video-recordings were made of DL in play with each of his parents separately. This analysis revealed a number of behaviours which were subsequently addressed in therapy. DL's mother displayed a fast speech rate and rapid turn-taking. She often interrupted DL's attempts to communicate and failed to wait for his responses. She made excessive use of questions to initiate conversation. Eye contact with DL was rarely achieved. DL's father also used a rapid rate of speech. However, this was reduced somewhat by his dysfluency. He was highly directive in his play sessions with DL. He tended to dominate verbally the interaction through his use of many questions, imperatives and by taking lengthy turns. He used extended explanations which were too complex in terms of their syntax and semantics for DL's delayed language skills.
Unit 34.3 Speech and language evaluation
(1) Conture (Reference Conture, Curlee and Siegal1997) argues that if a child exhibits three or more within-word (stuttered) speech dysfluencies per 100 words of conversational speech, then he or she is at risk of continuing to stutter. Based on this figure, is DL at risk of continuing to stutter? Provide evidence to support your answer. The percentage of stuttered words is only one measure of stuttering frequency. What other measure do clinicians use to assess stuttering severity?
(2) How would you characterise the dysfluencies in the utterance ‘Its its ha-ha-haaa:vn't got got a window’?
(3) Respond with true or false to each of the following statements:
(4) Describe three verbal behaviours which suggest that DL's parents are not particularly attuned to his language difficulties.
Parent–child interaction therapy
The parent–child interaction therapy proposed by Rustin et al. (Reference Rustin, Botterill and Kelman1996) was undertaken. For 17 weeks, DL attended a local clinic along with his parents. For the first six weeks, DL's parents were video-recorded as they took it in turns to play with him for 20 minutes. During recordings, the other parent and clinician remained in the room. The observed parent was told to use whatever toys in the room that he or she wanted to use. However, no advice was given on the way in which the toys should be used or on any other aspect of the session. Transcriptions of DL's utterances from the recordings were used to calculate the number of dysfluencies produced per 100 words. This figure was calculated both for the mother-led and father-led play sessions, resulting in two measures of dysfluency every week. To ensure that this measure was reliable, a speech and language therapist specialised in dysfluency viewed recordings from three of the weekly sessions. There was 95% agreement between the judges.
Therapy was delivered during the next six weeks. First, video-recordings were made of the parents playing with DL. These were then viewed by the parents and clinician. DL's parents were encouraged to identify one positive aspect of their interaction with him, and one negative aspect which they would like to change. If these identifications were difficult for the parents, the clinician guided them to parts of the recordings which they were encouraged to describe in detail. The parents were asked to consider how changes to their behaviour might be helpful to DL. They also had the opportunity to put their ideas into practice during the session. The target behaviours that were identified in the session became the focus of a home activity. This activity was a five-minute playtime which each parent agreed to undertake five days a week. DL had the choice of play during this activity. The parents recorded his choice as well as their success in implementing their target behaviours. In subsequent sessions with the clinician the parents had the opportunity to reflect on their progress during these playtimes with DL.
DL's parents were offered specific advice during this six-week period. Both parents were advised to reduce their use of questions and to replace them with comments. Additionally, DL's mother was encouraged to have eye contact with him during communication. In order to gain DL's attention, techniques such as using animation, touch and calling his name were encouraged. DL's father was advised to be less directive when playing with him, and to allow DL to lead activities, to make his own decisions and to solve his own problems. The father's use of imperatives was discouraged, and he was advised to comment on DL's play. He was also encouraged to reduce his speech rate and to use vocabulary that was appropriate for DL's language skills. In the final five-week period, measures of DL's dysfluency continued to be made. The parents also worked on their special playtimes with DL at home, and reflected on their progress each week. However, there was no new information or advice given to the parents at this stage.
Unit 34.4 Parent–child interaction therapy
(1) During the first six weeks of contact with DL and his parents, the clinician did not undertake direct therapy. What purpose within the overall intervention do you think this period served?
(2) Why do you think video-recordings were used when audio-recordings could have provided the authors of the study with the transcribed utterances that were used to measure dysfluencies?
(3) Which of the following statements best characterises parent–child interaction (PCI) therapy?
PCI therapy aims to desensitise the child to stuttered speech.
PCI therapy aims to teach the child fluency-modification techniques such as smooth speech.
PCI therapy aims to increase the child's fluency by modifying how parents communicate with their child.
PCI therapy aims to change parental attitudes towards stuttering.
PCI therapy aims to teach the child techniques for how to stutter more easily.
(4) The parents in this case received specific advice on how to modify their communication with DL. Explain how and why DL's parents were encouraged to modify their use of speech acts during communication with him.
(5) During the last five weeks of contact with DL and his parents, the clinician offered no new information or advice. What purpose within the overall intervention do you think this period served?
Speech outcome
The percentage of dysfluencies per 100 words was collected every week for both parents. These measurements are collated and tabulated below. The collated measurements also display the mean rate of dysfluency for each week of the investigation. The tabulated results are reproduced from Matthews et al. (Reference Matthews, Williams and Pring1997: 352).
| Week | Rate of dysfluency with father | Rate of dysfluency with mother | Mean rate of dysfluency | |
|---|---|---|---|---|
| Phase A | ||||
| 1 2 3 4 5 6 |
8.7 5.9 7.74 8.82 13.3 11.69 |
10.6 7.28 9.86 9.78 7.01 7.34 |
9.65 6.59 8.8 9.03 10.16 9.52 |
|
| Phase B | ||||
| 7 8 9 10 11 12 |
9.95 2.5 1.94 5.47 3.6 5.84 |
8.39 10.49 3.12 4.36 5.7 3.3 |
9.17 6.5 2.53 4.92 4.65 4.57 |
|
| Phase C | ||||
| 13 14 15 16 17 |
2.07 1.21 7.18 8.01 4.04 |
3.43 3.55 7.58 5.5 9.35 |
2.75 2.38 7.28 6.76 6.7 |
Statistical analysis of the baseline period (Phase A) revealed a non-significant result, suggesting that there was no observable trend during this time. However, analysis of Phases A and B produced a significant result. This supported the claim that there was a significant decrease in the number of dysfluencies during the treatment phase. During Phase C, there was an increase in the number of dysfluencies produced by DL. However, statistical analysis revealed that this was not a significant increase. There was no significant difference in the number of dysfluencies used by DL during mother-led and father-led sessions. Although there was no formal recording of DL's language skills during the three phases of the study, he was noted by the end of the study to be using more utterances and longer utterances.
Unit 34.5 Speech outcome
(1) Is there any evidence from this study that DL's dysfluency was improving spontaneously, i.e. without direct intervention? Provide support for your answer.
(2) There is considerable fluctuation in DL's dysfluency during Phase A of the study. How might this inconsistency pose a problem for an intervention that uses as its baseline a single measure of dysfluency that is based on a discrete point in time?
(3) Although parent–child interaction therapy is not a language intervention per se, is there any evidence that DL's language skills improved following this therapy?
(4) For young, dysfluent children, clinicians have found it helpful to conceive of intervention in terms of balancing the demands on and the capacities of the child. Explain how this way of conceiving of intervention can be applied to the case of DL.
(5) The authors of the study attributed the (non-significant) increase in dysfluency in Phase C to a number of ‘distracting and uncontrollable variables’ which may have created emotional anxieties for DL. These variables included a family holiday and the parents’ marriage. What linguistic variable may have contributed to the increase in DL's dysfluency towards the end of the study?
Introduction
The following exercise is a case study of a 29-year-old man (‘Mr A’) who was studied by Leder (Reference Leder1996). Mr A was initially diagnosed with acquired stuttering related to a conversion reaction. However, this diagnosis was subsequently revised to acquired neurogenic stuttering in the presence of a Parkinsonian-like syndrome. The case study is presented in five sections: primer on acquired stuttering; client history and presentation; speech pathology evaluation; psychiatric and neurological evaluation; and fluency therapy.
Primer on acquired stuttering
The onset of dysfluency in adulthood is known as acquired stuttering. There are two forms of acquired stuttering in adults. In acquired psychogenic stuttering, the onset of dysfluency is associated with a traumatic event, psychological distress, or the presence of a psychiatric disorder. Raphael and Schoenfeld (Reference Raphael and Schoenfeld2006) described the case of a 44-year-old woman with bipolar affective disorder and a history of childhood sexual abuse who presented with severe stuttering. A neurological evaluation of this woman was negative. In acquired neurogenic stuttering, the onset of dysfluency is caused by neurological injuries and disorders. Strokes or cerebrovascular accidents are the single biggest cause of neurogenic stuttering. Theys et al. (Reference Theys, van Wieringen, Sunaert, Thijs and De Nil2011) reported neurogenic stuttering in 17 (5.3%) of 319 subjects who sustained a stroke. Stuttering persisted for more than six months in at least 2.5% of these subjects. Individuals with comorbid aphasia displayed a significantly higher frequency of stuttering compared to those without aphasia. Traumatic brain injury, progressive supranuclear palsy (a form of parkinsonism) and multiple sclerosis are less common causes of neurogenic stuttering (Kluin et al., Reference Kluin, Foster, Berent and Gilman1993; Mower and Younts, Reference Mower and Younts2001). Some cases of acquired stuttering have both neurological and psychological factors in their aetiology. Mattingly (Reference Mattingly2015) described the case of a service member returning from war with the comorbid diagnoses of post-traumatic stress disorder and a mild traumatic brain injury who experienced the onset of stuttering.
The speech features of acquired stuttering differ in significant ways from those of developmental stuttering. Helm-Estabrooks (Reference Helm-Estabrooks and Curlee1999: 260) states six features which, she claims, help to distinguish neurogenic stuttering from developmental stuttering in adults: (1) dysfluencies occur on grammatical words nearly as frequently as on substantive words; (2) the speaker may be annoyed but does not appear anxious; (3) repetitions, prolongations and blocks do not occur only on initial syllables of words and utterances; (4) secondary symptoms such as facial grimacing, eye blinking, or fist clenching are not associated with moments of dysfluency; (5) there is no adaptation effect whereby there are fewer and fewer dysfluencies on repeated readings of a passage; (6) stuttering occurs relatively consistently across various types of speech tasks. However, the results of some studies indicate that it may not always be possible to perceptually distinguish neurogenic from developmental stuttering, as these criteria would appear to suggest. Van Borsel and Taillieu (Reference Van Borsel and Taillieu2001) presented a panel of professionals with random speech samples from four developmental and four neurogenic stutterers. The results indicated that based on verbal output alone, it is often difficult to distinguish neurogenic from developmental stuttering.
Unit 35.1 Primer on acquired stuttering
(1) The epidemiology of acquired stuttering is not as well investigated as the epidemiology of developmental stuttering. Name one feature of the epidemiology of developmental stuttering which does not appear to hold true of acquired stuttering.
(2) Which of the following is not a cause of acquired neurogenic stuttering?
(3) Which of the following scenarios describes acquired stuttering of mixed aetiology?
A 40-year-old man exhibits stuttering following a head injury sustained in a road traffic accident.
A 30-year-old woman, who first received fluency therapy in childhood, participates in an intervention for adults who stutter.
A 55-year-old woman, who had a recent family crisis, experiences sudden onset of dysfluency.
A 40-year-old man, who has been under medical supervision for psychological distress following a head trauma sustained in a violent assault, is referred to speech-language pathology for fluency evaluation.
A 77-year-old man exhibits stuttering following an intracerebral haemorrhage.
(4) The following speech is produced by a 36-year-old man with multiple sclerosis who was studied by Mower and Younts (Reference Mower and Younts2001). What two speech features characterise this extract?
‘Well, we-we-we-we-we in-in-in port mo-most of time and-and when-when-when I got-got married, got-got-got-got-got-got an apar-par-partment.’
Client history and presentation
Mr A is a 29-year-old white male who is a graphic designer at a university. He was referred by his primary care physician to speech pathology following the sudden onset of dysfluent speech on 21 November 1993. Mr A has no prior history of dysfluency. His only medical complaint is headaches for which he takes aspirin. He reports that for some months he has been under considerable stress at work as he prepares a museum catalogue. On the day when Mr A first experienced dysfluency, he could not say the word ‘paper’. The following day Mr A's dysfluency increased during the morning and by early afternoon he was severely dysfluent. Although his vocal pitch was normal at the time, it did increase over the next three to four days. Mr A's pitch returned to normal over the next month but his severe dysfluency persisted. Writing was also disrupted. Although lower case printing and cursive writing were unimpaired, Mr A was unable to write in capital letters. Capital letters were used extensively in Mr A's work as a graphic designer. His problem with writing persisted for seven days, and then resolved spontaneously. Also in November 1993, Mr A underwent a neurological evaluation. EEG, MRI without gadolinium, CT scans and lumbar puncture were all normal. With one exception, there was no history of neurological disease in Mr A's family. Mr A's father, who was 58 years old, had suffered complex partial seizures since his early twenties.
Unit 35.2 Client history and presentation
(1) On the basis of this history and presentation, what type of acquired stuttering do you think Mr A has? Provide evidence to support your answer.
(2) On the basis of this history and presentation, which of the following might be considered a cause of Mr A's dysfluency?
(3) Alongside the onset of dysfluency, Mr A displayed two communicative features which are seldom reported in acquired stuttering. What are these features?
(4) Mr A was able to form lower case letters but was unable to write upper case or capital letters. Is this impairment suggestive of writing difficulties in a neurodegenerative disorder?
(5) Which of Mr A's neurological examinations excluded epileptic seizures as a cause of dysfluency?
Speech pathology evaluation
Mr A underwent a speech pathology evaluation on 9 December 1993. This was 19 days after the onset of stuttering. He displayed frequent syllable and word repetitions while blocks on syllables and words were infrequent. Multiple repetitions and/or blocks were present on every syllable and word. For example, during conversational speech and oral reading 20 or more repetitions per syllable were routinely noted. Mr A's stuttering pattern was unaltered during choral reading. Stuttering was also present when words were mouthed without voicing during conversational speech and reading. Mr A's vocal pitch had increased following what appeared to be tension in the shoulder and neck areas. He did not make use of starters or secondary characteristics. He exhibited no avoidances or word or situational fears (e.g. telephone use). In this early, post-onset period there were no tremors or lingual fasciculations. Tremors and fasciculations appeared in March 1994, and necessitated a referral for a further neurological evaluation. Mr A's cognitive functions and expressive and receptive language were intact. Mr A was both distressed about his stuttering and motivated to correct it.
Unit 35.3 Speech pathology evaluation
(1) Describe two ways in which the repetitions exhibited by Mr A differ from the iterations of developmental stuttering.
(2) Name one speech feature which is present in developmental stuttering but which is absent in Mr A's case.
(3) Mr A's stuttering behaviour differs in other significant respects from developmental stuttering. State three such respects.
(4) In the early, post-onset period, Mr A did not display lingual fasciculations, although he later went on to develop them. What are lingual fasciculations? What type of neurological damage causes fasciculations?
Psychiatric and neurological evaluation
Based on an initial diagnosis of a conversion reaction, Mr A started receiving psychiatric treatment in December 1993. He was prescribed 200 mg doxepin hydrochloride at night for depression and sleep. A biweekly telephone call between the psychiatrist and speech-language pathologist was used to discuss the behavioural and psychiatric strategies that were used to address Mr A's dysfluency. However, by March 1994 there had been no improvement in dysfluency and the psychiatrist concluded that Mr A's stuttering had an organic origin.
On 23 August 1994, a second neurological evaluation of Mr A was performed. Normal proportions of dopamine were revealed by SPECT scanning. With the exception of markedly slow tongue movements Mr A's cranial nerve examination was also normal. A sensory examination was normal. During a cerebellar examination, Mr A was able to perform normal finger to nose movements in procession. However, movements were slow. A tremor, which did not increase in amplitude, persisted during these movements. There was a tremor at rest in both arms (right more than left), and a slight tremor at rest in the right leg. Mr A could stand but was unable to walk on either his heels or toes. Pushing on his chest and back produced mild instability with no reflexive compensatory movements of his arms. Mr A's face was without expression. Movements were slow to begin and to complete. He was unable to perform rapid alternating movements. Mr A was prescribed carbidopa-levodopa. An initial dose of four times a day (August 1994) was gradually reduced to once a day (May 1995) as improvements occurred in speech and motor skills. Stuttering increased in severity as the dose of drug was decreased.
Unit 35.4 Psychiatric and neurological evaluation
(1) After a period of psychiatric intervention it became clear that Mr A's dysfluency was not related to a conversion reaction. What were the two main features of this intervention? Did either of these features result in an improvement in speech?
(2) There are four cardinal signs of Parkinson's disease. What are these signs? Does Mr A exhibit each sign?
(3) In relation to the results of SPECT scanning, the author of the study concludes that there is either no biochemical basis for Mr A's symptoms or that his symptoms are the result of receptor dysfunction. Explain this conclusion.
(4) Mr A exhibited the mask-like facial expression that is characteristic of clients with Parkinson's disease. Give a description of this expression.
(5) Mr A's speech and motor symptoms displayed a good response to carbidopa-levodopa. Along with neurological findings, what does this suggest about the aetiology of Mr A's stuttering?
A psychogenic aetiology is still plausible as a cause of Mr A's stuttering.
A relapse in developmental stuttering appears to be the most likely cause of Mr A's stuttering.
The aetiology of Mr A's stuttering is likely to be neurogenic in nature.
Mr A's stuttering has no known cause and is idiopathic in nature.
Mr A's stuttering is one symptom of a wider parkinsonian syndrome.
Fluency therapy
Fluency therapy took place three times a week for a three-month period. Among the therapy techniques used were the use of soft contacts in stop and fricative phonemes and relaxation of the shoulders and neck area. Also, Mr A was encouraged to adopt a continuous breath flow as a means of promoting an open glottis. This was followed by producing a whisper and then progressing to voicing by humming vowels and nasal continuants /m, n/. Mr A was successful in using these techniques in the initial session in order to control his stuttering and increase his fluency. There followed a discussion with Mr A which focused on responsibility for and control of his stuttering. Through his use of breath flow, soft contacts and negative practice, Mr A was able to exhibit control of fluent and stuttered speech production. The following fluency-shaping goals were pursued: (1) breath flow, soft contacts and relaxation were attempted first on rote speech tasks (e.g. counting) then short, overlearned phrases (e.g. How are you?), and finally on conversational speech, while maintaining fluency; (2) the rate of speech was increased while maintaining fluency; (3) the loudness of speech was increased while maintaining fluency; and (4) appropriate vocal pitch was pursued by decreasing tension in the neck and shoulders. Daily telephone contact was used to support maintenance, carry-over and generalisation to conversational speech. With the exception of pitch, which returned to normal, Mr A did not continue to show improvement.
Unit 35.5 Fluency therapy
(1) Which of the following techniques and approaches were used in fluency therapy with Mr A?
(2) Which of the techniques shown in question (1) was used to address Mr A's vocal pitch anomalies? These anomalies improved while other aspects of Mr A's stuttered speech did not. Why do you think this was the case?
(3) One of the fluency-shaping techniques employed with Mr A was the use of soft contacts. Describe what is involved in this technique.
Introduction
The following exercise is a case study of a boy (‘Michael’) who was studied by Daly and Burnett (Reference Daly and Burnett1996). Michael was first evaluated at 9;7 years of age. He subsequently received a course of therapy and was re-evaluated when he was 11;8 years of age. The case study is presented in five sections: primer on cluttering; client history; pre-intervention speech-language evaluation; cluttering therapy; and post-intervention speech-language evaluation.
Primer on cluttering
Although there is no consensus on a definition of cluttering, a widely used definition, and one that is accepted by the International Cluttering Association, states that:
cluttering is a fluency disorder characterized by a rate that is perceived to be abnormally rapid, irregular, or both for the speaker (although measured syllable rates may not exceed normal limits). These rate abnormalities further are manifest in one or more of the following symptoms: (a) an excessive number of disfluencies, the majority of which are not typical of people who stutter; (b) the frequent placement of pauses and use of prosodic patterns that do not conform to syntactic and semantic constraints; and (c) inappropriate (usually excessive) degrees of coarticulation among sounds, especially in multisyllabic words.
The key elements of this definition are consistent with the features of cluttering that are reported in clinical studies. In a survey of 29 clutterers in 12 articles, St Louis (Reference St. Louis1996) identified 53 symptoms that were used by the authors of these articles to characterise cluttering. The three most commonly reported symptoms were excessive dysfluencies, rate of speech too fast and rate of speech too irregular.
The epidemiology of cluttering is still a vastly under-investigated aspect of this fluency disorder. This is confirmed by the fact that there has been no study of the prevalence and incidence of cluttering in the general population since Becker and Grundmann (Reference Becker and Grundmann1970) reported the incidence of cluttering to be 1.5% in 7- and 8-year-olds in a German school. Cluttering is more common in certain special populations than in the general population. Coppens-Hofman et al. (Reference Coppens-Hofman, Terband, Maassen, van Schrojenstein Lantman-De Valk, van Zaalen-op't Hof and Snik2013) examined dysfluencies in the spontaneous speech of 28 adults with mild and moderate intellectual disabilities. Of the 22 (75%) of subjects who showed clinically significant dysfluencies, 21% were classified as cluttering, 29% as cluttering-stuttering and 25% as clear cluttering at normal articulatory rate. St. Louis et al. (Reference St. Louis, Filatova, Coşkun, Topbaş, Ozdemir, Georgieva, McCaffrey and George2010) reported a male:female sex ratio for cluttering of 4.5:1. Genetic and neurological factors appear to be integral to the aetiology of cluttering. The presence of cluttering in children with genetic and chromosomal syndromes, including Down's syndrome and fragile X syndrome, suggests that genetic factors may play a role in developmental cluttering (Hanson et al., Reference Hanson, Jackson and Hagerman1986; Van Borsel and Vandermeulen, Reference Van Borsel and Vandermeulen2008). Acquired cluttering has been reported in adults with neurodegenerative disorders including dementia and idiopathic parkinsonism, and in individuals who sustain cerebrovascular accidents (Hashimoto et al., Reference Hashimoto, Taguchi, Kano, Hanyu, Tanaka, Nishizawa and Nakano1999; Lebrun, Reference Lebrun1996; Thacker and De Nil, Reference Thacker and De Nil1996).
Unit 36.1 Primer on cluttering
(1) Which of the following are true statements about cluttering?
(2) The neural correlates of cluttering were investigated by Ward et al. (Reference Ward, Connally, Pliatsikas, Bretherton-Furness and Watkins2015). These investigators found that the caudate nucleus and putamen were overactive in adults who clutter. Which of the following neuroanatomical structures does this study suggest is compromised in cluttering?
(3) The epidemiology of cluttering has only rarely been investigated. Why do you think this is the case?
(4) A person who clutters says [wʌfɪl] for ‘wonderful’. What term is used to describe this speech behaviour?
(5) True or false: Cluttering is often associated with poor reading skills.
Client history
Michael was first seen for evaluation in May 1993 when he was 9 years 7 months old. He was a third grade student. At school, he received the support of a learning disability teacher for a reading disorder. He also received treatment from the school speech-language pathologist. The focus of earlier SLP intervention was speech rate, ‘clearness’ and intelligibility of articulation. Michael was seen by the speech-language pathologist during the 1993/94 and 1994/95 school years. Additionally, he also received SLP intervention in a hospital speech programme in the spring and summer of 1994. This intervention consisted of 16 treatment sessions.
Parental report indicated that Michael was just within normal limits for motor developmental milestones. However, speech and language development was significantly delayed. The mother of Michael stated that baby talk had persisted, and that family members had increasingly experienced difficulty in understanding him. According to Michael's mother, his speech intelligibility problems were related to misarticulations, an unusually fast speech rate and the presence of repetitions, which started between 2.5 and 3 years of age. A family history of fast talking and stuttering was reported by the mother. Although Michael had received intervention for speech articulation at school for several years, his mother reported that there had only been minimal improvement.
Unit 36.2 Client history
(1) Michael was just within normal limits for motor developmental milestones. State when normally developing children should attain three motor milestones.
(2) Does Michael have other communication problems in addition to cluttering? If so, are these problems typical of people who clutter?
(3) What aspect of Michael's history indicates that he may have been at an elevated genetic risk of having a communication disorder?
(4) What key speech feature of cluttering is evident from parental report?
Pre-intervention speech-language evaluation
The initial evaluation of Michael's speech and language skills was performed at 9 years 7 months. The report of the school psychologist indicated that Michael's IQ was within the high-to-average range. Scores on arithmetic were above average, and Michael was placed in a gifted programme for mathematics and science. Although Michael's verbal skills fell in the high-to-average range, his reading ability was below average. Also, the school psychologist remarked of Michael's conversational speech that it displayed ‘excessive speed, slurred or omitted syllables and sounds, and had a low volume, especially at the ends of sentences’.
The initial evaluation revealed some noteworthy speech and language problems. The organisation and formulation of language, topic maintenance, the rate and tempo of speech, prosody and intelligibility were all judged to be problematic. Additionally, Michael appeared to be largely unaware of his difficulties and his listener's difficulty in understanding him. However, there was an improvement in his speech when a recorder was introduced. Auditory memory abilities and oral motor coordination skills were below those of Michael's peers. This profile of impairments was suggestive of cluttering and so a checklist of cluttering behaviours was performed. The overall score on the checklist confirmed the clinical impression of cluttering. The nine areas which were most characteristic of Michael's speech were rapid rate, slurred articulation, speech better under pressure, reading disorder, ability to think is faster than the ability to talk or write, above average mathematical and abstract reasoning abilities, poor rhythm, timing or musical ability, other family members with the problem and lack of self-awareness.
Unit 36.3 Pre-intervention speech-language evaluation
(1) The school psychologist reported that Michael's conversational speech exhibited slurred or omitted syllables and sounds. What speech feature of cluttering does this description capture?
(2) Michael undertook diadochokinetic speech tasks as part of his evaluation. What skills are assessed by means of these tasks?
(3) The checklist revealed that Michael's speech was better under pressure, for example, during short periods of heightened attention. What observation during the initial evaluation confirms this finding?
(4) Many individuals who clutter only seek professional help for their speech problems when they are encouraged to do so by colleagues, friends and family members. Which checklist finding might explain this?
(5) People who clutter have impaired pragmatic language skills (Teigland, Reference Teigland1996). Which feature of the initial evaluation suggests that Michael has some impairment in the area of pragmatics?
Cluttering therapy
The findings from the checklist were used to plan Michael's therapy. It was decided that the focus of therapy should be on oral motor coordination, speech rate, language abilities, awareness of deficits and reading difficulties. Language abilities included the formulation of stories, topic maintenance and sequencing of events. These areas were treated by school and hospital speech-language pathologists (SLP). The school SLP saw Michael twice a week. To address Michael's oral motor coordination difficulties, the Oral Motor Assessment and Treatment programme (Riley and Riley, Reference Riley and Riley1985) was used. The school SLP reported that although Michael had initially found the production of three-syllable sets very difficult, all sets were produced with accuracy and an even flow by the end of the semester. Rate tapes were produced in order to facilitate reduction of speech rate and improve awareness and intelligibility. The school SLP noted significant improvements during the 1994/95 school year in rate and self-monitoring during conversational speech. The hospital SLP, who had diagnosed cluttering with central auditory processing disorder, focused on the following areas during treatment: improving concentration and memory; increasing specificity of language; language skills (thought organisation, narrative production and topic maintenance), and improving self-monitoring. Substantial improvements in all areas were reported.
Unit 36.4 Cluttering therapy
(1) Cluttering has both motoric and linguistic components. Explain how these components are reflected in the intervention that Michael received.
(2) Aside from motoric and linguistic components, it is clear that cluttering also has significant cognitive components. Describe three ways in which these cognitive components are reflected in therapy.
(3) Michael was treated by a school and a hospital speech-language pathologist. However, the emphases of these interventions were quite different. How would you characterise the differing emphases of these interventions?
Post-intervention speech-language evaluation
More than two years after the initial evaluation, Michael was assessed for a second time. He was 11 years 8 months old at this time. The cluttering checklist was re-administered. Michael's overall score had significantly improved. Areas of improvement were rate, articu-lation, rhythm and awareness. These areas were all directly targeted in therapy. Michael's mean speaking rate had decreased from 126 words per minute to 116 words per minute. Where Michael had previously achieved 70% accuracy on the articulation of multisyllabic words, he now had 85% accuracy on these words. He undertook self-correction of his errors and had a positive response to minimal cuing. Michael displayed auditory memory for 23 syllables (the 12-year-old mean for auditory memory is 26 syllables). His oral motor skills for single syllables, double syllables and tri-syllables were largely consistent with 12-year norms. The one exception was single syllables, with Michael achieving times between 3.3 to 3.9 seconds (4.0 to 4.5 seconds is the 12-year norm).
Michael's language skills also showed improvement. At the initial evaluation, Michael had deviated from the topic three times in a 60-second sample. However, no topic deviations in a 60-second sample were noted at his re-evaluation. His language was no longer disorganised with multiple revisions and he was able to sequence events. It was observed during the evaluation session that Michael displayed more reserved behaviour and used a generally low volume. Michael's low volume did reduce his intelligibility to a degree. However, volume did not diminish at the end of sentences, as had been noted by the school psychologist. Michael was also observed to keep his hands in front of his mouth. He used very brief responses and only improved his eye contact upon cuing. In association with linguistic revisions and other speech production difficulties, Michael also displayed instances of blinking his eyes in a rapid, repetitive fashion. The authors of the study recommended that these behaviours should continue to be monitored.
Unit 36.5 Post-intervention speech-language evaluation
(1) At Michael's re-evaluation, there was a mixed set of prosodic findings. Identify one prosodic aspect which had clearly improved following therapy, and one prosodic aspect where improvement was not so evident.
(2) Was there any improvement in Michael's pragmatic language skills as a result of intervention? Provide support for your answer.
(3) Identify two cognitive skills which improved or were at least age-appropriate following therapy.
(4) Is there any aspect of Michael's presentation at his re-evaluation which is suggestive of stuttering? Provide support for your answer.
(5) Michael displayed non-verbal behaviours at re-evaluation which were not present at his initial assessment. What are these behaviours? How might the emergence of these behaviours be explained?