McGill University Health Centre, 1650 CedarAvenue, Montreal, Quebec H3G 1A4
Two cases of adult onset stuttering are_ presented, one of neurological origin, one functional. Neither had any history of stuttering behaviour nor any other speech or language abnormality prior to onset of dysﬂuency at ages 28 and 42 respectively. LF presented with an atypical pattern of multiple syllable and word repetitions following a stroke. TN presented with a severe stutter which had gradually developed over a period of weeks. Neurological findings, stuttering behaviours, and response to treatment will be compared and contrasted. Implications for" the nature and development of stuttering will be discussed.
Those who present with a clear adult onset of stuttering do so most often from some discrete neurological event, such as cerebrovascular accident, head injury, degenerative neurological disease, or drug toxicity. Although relatively rare, neurogenic stuttering has been reported in the literature for many years. Two important studies, Canter (1971) and Helm—Estabrooks (1993), deﬁned criteria for the differential diagnosis of neurogenic versus developmental stuttering. Ringo and Deitrich (1995), in a review of published studies on the disorder, determined the ﬁve most frequently reported characteristics for the diagnosis of neurogenic stuttering as follows:
- The tendency for stuttering to occur on grammatical as well as substantive words (90% of reported cases)
- A relative lack of anxiety about the stuttering (80% of reported cases).
- The tendency for dysfluencies not to be restricted to initial syllables (75% of reported cases)
- Absence of secondary symptomatology (approximately 70% of reported cases).
- Failure to exhibit an adaptation effect (60% of cases where this was studied)
According to Helm—Estabrooks (1995) it might be argued that the dysﬂuency arising from a neurological event in adulthood is not “stuttering” at all, but a side effect of aphasia, dysarthria, or apraxia of speech. She concludes, however, that neurogenic stuttering is a distinct speech manifestation which may not necessarily be correlated with or accompanied by other more typical speech and language disorders. This view is also held by Curlee (1995). He argued that until the similarities between neurogenic and developmental stuttering are shown to have etiologic, diagnostic, and treatment signiﬁcance, the terms stuttering associated with acquired neurological damage (SAAND) and stutter-like dysﬂuencies (SLD) should be used to describe this disorder and its speech disruptions.
The term “psychogenic stuttering” has in the past been deﬁned as a conversion reaction. Using the criteria of Deal (1982) and Roth et al. (1989), Mahr and Leith (1992) in reviewing the literature and four cases of their own proposed that a diagnosis of stuttering as a conversion reaction be made if all of the following deﬁning criteria are present as well as at least one of the associated symptoms:
- A change in speech pattern suggesting stuttering
- A relationship to psychological factors, as evidenced by the onset of symptoms associated with emotional conﬂict, the apparent symbolic signiﬁcance of the symptoms, and/or the presence of primary or secondary gain
- An absence of organic etiology
- Past history of mental health problems
- Atypical features, such as
- Stereotyped repetition of initial or stressed syllables of words
- Speech pattern not affected by choral readings, white noise, or trial of delayed auditory feedback.
- No islands of ﬂuency
- No secondary symptoms, no avoidance, and no attempts to inhibit stuttering
- La belle indifference
The following are two very different cases of adult onset stuttering. They are presented as further examples of differences in etiology, symptoms, and response to treatment. The second case more closely parallels developmental stuttering than what has been described as psychogenic stuttering.
- Case #1 — LF
2.1 Neurological ﬁndings
Serial CT Scans following the initial stroke revealed a left parietal infarct and a right peri- caudate lacunar infarct. MRI showed small hypodense areas around the right caudate head, anterior- most aspect of the putamen, and anterior—most aspect of the internal capsule, as well as a left posterior parietal infarct. Etiology of the stroke was never clearly determined, but was thought to be related to a hypercoagulable state. Past medical history had included migraine headaches, Raynaud’s syndrome, hypothyroidism, and asthma. She was smoking and on the birth control pill at the time of the stroke.
2.2 Other investigations
Because of a conﬂictual relationship with her mother and the sudden death of her father two years prior to the stroke, possibly by suicide, LF’s psychological status was initially questioned and a psychogenic etiology to her stuttering considered. However, a neuropsychiatric evaluation during her early hospital stay showed no psychiatric illness. A complete neuropsychological battery was also conducted while at the MNH.
2.3 Speech and language skills
Language skills were initially tested using the Boston Diagnostic Aphasia Examination (Goodglass & Kaplan, 1972), later with the Psycholinguistic Assessment of Language (Caplan & Bub, 1990), and the Minnesota Test for Differential Diagnosis of Aphasia (Schuell, 1965). When ﬁrst seen by the author at ten months post—onset, LF’s oral expression, though replete with easy syllable and word repetitions, did not show any syntax nor any signiﬁcant word ﬁnding problems. LF spoke in grammatical sentences without any particular searching for words. Auditory comprehension was functional although memory deﬁcits were evident both on testing and in everyday life. Writing was grammatical yet ﬁlled with spelling errors, most words written phonetically. Reading comprehension was nonfunctional. Certain words were visually familiar, but most required sounding out, a laborious and unsuccessful approach. The following is a writing sample at 20 months post—onset:
2.4 Stuttering behaviour
LF’s stuttering was characterized by simple rhythmic syllable and word repetitions without visible struggle (see below). Repetition behaviour was evident on almost every word and on the majority of syllables (7l%SS). Repetitions could occur on any part of speech and sometimes crossed word boundaries, e.g., "Than—than—than-than—kyou—kyou-kyou" for “thank you”. Number of repetitions was typically 2 or 3, but ranged up to 10. The pattern was evident on automatized sequences, singing, and mouthing sentences. She denied difﬁculty with any particular sound. She denied substituting easier words. Although sometimes frustrated by it, she was not particularly anxious about her speech. A transcript of a speech sample (32 seconds) is shown below:
2.5 Treatment history
Traditional ﬂuency enhancing techniques associated with slowing down rate of speech and relaxing muscles were impossible for LF to learn. Attempts at simple exercises to inhale, exhale, and prolong a vowel, for example, were unsuccessful due to an obvious apraxia. Also unsuccessful was the use of a pacing board as a compensatory strategy. LF never exhibited any sense of control over her stuttering, either in a structured therapy exercise or the easiest of real life situations. Ultimately, LF was referred to a psychiatrist, a recommendation that had been made throughout the course of her rehabilitation and that LF was now ready to accept. The goal was to help her adjust to her stroke sequelae and to explore the issues in her past that had been thought by some to be the root of her dysﬂuency. 502 Theory, research and therapy in ﬂuency disorders
2.6 Ten year follow-up
Contact was made with LF ten years after her stroke, about eight years after the completion of all forms of rehab therapies. LF was married and was busy raising her 23 month old son. She had continued her counselling until giving birth. She was closely followed by haematology for the blood disorder that had been thought to be the cause of her stroke. She remained on high doses of Coumadin, Aspirin, and an analgesic for constant pain in her right arm. The reading, writing, and memory behaviours persisted, more or less to the same degree. The stuttering persisted, but was somewhat less frequent. The pattern remained. She now admitted to having difficulty with certain sounds (plosives) and would substitute words if she anticipated difficulty. LF reported that she continues to be made fun of or questioned about her speech about twice weekly.
- Case #2 — TN
3.1 Stuttering behaviour
Stuttering was characterized by frequent part-word and whole—word repetitions and silent laryngeal blocks accompanied by secondary features involving head turning to the left, eye closing, and hand movements. Moments of stuttering lasted several seconds. He complained of neck pain and occipital headaches. Avoidance behaviour was noted in the form of word substitutions, spelling, or writing with his ﬁnger. He reportedly avoided some speaking situations. He noted his speech to be worse in the morning and easier in the evening when he was more tired and tended to stutter less. Although annoyed by it, he did not seem particularly concerned about the stuttering and continued to run his business, speaking with his clients as usual.
3.2 Treatment history
TN was seen for individual sessions to teach ﬂuency enhancing skills and for counselling regarding slowing the pace of his lifestyle. He was seen initially once a week, later decreasing in frequency, over the course of a few months. He was motivated and worked hard on practice exercises and on making lifestyle changes. There was noticeable improvement in TN’s speech at each successive session. Despite the severity, with secondary characteristics and some avoidance behaviour, it was readily apparent that his problem was reversible.
3.3 One year follow-up
TN was seen 18 months after the onset of his stuttering and almost a year after his last regular therapy session. Speech was ﬂuent, save for one self—corrected moment of stuttering, and natural sounding throughout the session. He reported normally ﬂuent, spontaneous speech most of the time, but with some mild stuttering during his busiest periods at work. Although he maintained an incredibly hectic pace, he continued to practice ﬂuency techniques and coping with stress strategies as needed. Besides the improvement in his ﬂuency, his other physical complaints had all subsided except for his irritable bowel syndrome. He attributed his reversal of stuttering to a combination of ﬂuency techniques (slowing down and not forcing out the words) and coping with stress strategies.
Table 1. Comparison of two cases of adult onset stuttering
LF was clearly a case of neurogenic stuttering, meeting all ﬁve of Ringo and Dietrich’s (1995) criteria. The question of whether this is truly stuttering is valid in this case. Certainly an oral apraxia was evident in addition to the easy repetitions. Perhaps stuttering-like dysﬂuencies and stuttering associated with acquired neurological damage is more appropriate terminology. The neurological ﬁndings support Helm—Estabrooks’ (1993) statement that bilateral lesions are necessary for the dysﬂuencies to persist.
TN on the other hand did not ﬁt the criteria for psychogenic stuttering as deﬁned by Mahr and Leith (1992). Although there was no evidence of organic etiology, there was also no true psychopathology. In fact, TN presented more like a developmental stutterer with onset in adulthood, where “demands” far outweighed “capacities” in many aspects of this man’s life. Interestingly, not only did he deny any stuttering—like behaviour or fast speech as a child, he came upon an audio sample that showed his speech to be much slower prior to the onset of his stuttering. Like everything in his life, the pace of his speech seemed to be spiraling out of control. What was evidenced over a three ‘month period was a steady progression from simple repetitions, to blocks, secondary behaviours, and beginning avoidance of talking. The relative brevity of the symptoms allowed for the quick reversal of the pattern, not unlike early childhood stuttering.
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