2003 IFA Congress: Montreal, Canada

Two Very Different Cases of Adult Onset Stuttering

Jill Harrison
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.

  1. Introduction
Clinicians who specialize in the treatment of adult fluency disorders typically see people who have stuttered since childhood. Less often are they called upon to evaluate and treat adult onset stuttering. These two cases shed light on our understanding of different types of fluency disorders beginning in adulthood.

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:
  1. The tendency for stuttering to occur on grammatical as well as substantive words (90% of reported cases)
  2. A relative lack of anxiety about the stuttering (80% of reported cases).
  3. The tendency for dysfluencies not to be restricted to initial syllables (75% of reported cases)
  4. Absence of secondary symptomatology (approximately 70% of reported cases).
  5. Failure to exhibit an adaptation effect (60% of cases where this was studied)
Except for the occipital lobe, most other cortical and subcortical areas of the brain have been implicated in neurogenic stuttering (Rosenbek et al., 1978). Helm—Estabrooks (1993) reported that the disorder seldom persists longer than a few weeks unless bilateral lesions are present.

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:

Defining Criteria
  1. A change in speech pattern suggesting stuttering
  2. 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
  3. An absence of organic etiology
Associated Symptoms

  1. Past history of mental health problems
  2. Atypical features, such as
    1. Stereotyped repetition of initial or stressed syllables of words
    2. Speech pattern not affected by choral readings, white noise, or trial of delayed auditory feedback.
    3. No islands of fluency
    4. No secondary symptoms, no avoidance, and no attempts to inhibit stuttering
    5. La belle indifference
Today the term psychogenic stuttering is less often used and is cautioned against in Asha’s Terminology Pertaining to Fluency and Fluency Disorders: Guidelines (1999), unless there is a diagnosed psychopathology. Indeed the validity of the term as a diagnostic entity is questioned.

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.

  1. Case #1 — LF
LF was 28 years old and studying for her Master’s degree in Social Work when she experienced a stroke. Initial symptoms included ataxia, dysphasia, right homonymous hemianopsia, and “unusually dysfluent speech”. After being seen by various medical and rehab specialists in a small hospital in the community where she was studying, she was transferred to the Montreal Neurological Hospital for a second opinion, particularly regarding her medical condition. She was re—evaluated and followed extensively in physiotherapy, occupational therapy, and speech therapy at the MNH, then at convalescence and an out—patient rehabilitation centre before being referred to the author at ten months post—onset for her persistent stuttering behaviour. Prior to referral for exclusive treatment of the dysfluency, she was treated in speech therapy predominantly for her dyslexia and agraphia after unsuccessful attempts had been made to address the stuttering.

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:
Greatings frum Amsterdam. It’s a bewtaful city, lawts of twolips — very cheerful! Enjoying the time weth my frnd doing fun things. Grate food, spicee, you wood enjoy it. The shoping is expensive — lawts of nice potery and grate wood peases. See you in April.

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:
In—In the su—su-um—um-mer I li-li-like to go-go-go to ba—ba-base—ball-ball ga—ga—games. Um to-to—night-night we’re go-go—go—go—going t0—to see—see the—the—the-the—the Ex—Ex—Expo—po— pos play-play a ba—ba—ba-baseball-ball—ball ga—ga—ga—game again—gain—gainst...I for—for—get- get—get the te—te-te—team, San—San-San Fran-Fran—Fran—cis-is—is—co-co.

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.

  1. Case #2 — TN
TN, a 42 year old owner of a catering business, was referred by the neurologist because of a recent onset of stuttering. Neurological exam and CT scan were normal. TN reported having begun to stutter significantly over the course of a week. He denied any history of stuttering prior to this and there was no stuttering in the family. He felt that his stuttering and other physical complaints of skin rashes, heart burn, patches of his beard falling out, and irritable bowel were the result of stress and the hectic pace of his catering business. The various doctors he had seen had come to the same conclusion. At the time of the evaluation he was averaging about 3-4 hours sleep a night and working 7 days a week. He had been prescribed antidepressant and anti—reflux medications.

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. 

  1. Discussion
A comparison of the two cases can be summarized in Table 1.


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.

  1. Conclusion
Cases of adult onset stuttering are rare and those resulting from neurological damage are not always seen by specialists in fluency disorders. The first case demonstrates that we may not always be able to alleviate the dysfluencies using our traditional methods. The second case reinforces the importance of speech pathology intervention as early as possible in the development of a stuttering pattern without neurological cause. Documenting cases such as these will lead to a better understanding of the etiology, development, and treatment of different types of fluency disorders.


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Canter, G. (1971). Observations on neurogenic stuttering: A contribution to differential diagnosis. British Journal of Disorders of Communication, 6, 139-143.

Caplan, D., & Bub, D. (1990). Psycholinguistic assessment of aphasia. Miniseminar presented at the annual convention of the American Speech-Language-Hearing Association, Seattle, WA. Curlee, R. F. (1995). Comments on “Neurogenic stuttering: An analysis and critique”. Journal of

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Deal, J. L., (1982). Sudden onset of stuttering: A case report. Journal of Speech and Hearing Disorders, 47, 301-304.

Goodglass, H., & Kaplan, E. (1972). The Assessment of Aphasia and Related Disorders, Lea & Febiger Publishers. .

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Curlee (Ed.), Stuttering and Related Disorders of Fluency (pp.205-219). New York: Thieme Medical Publishers.

Helm-Estabrooks, N. (1995). Comments on “Neurogenic stuttering: An analysis and critique”. Journal of Medical Speech-Language Pathology, Vol 3, No. 2, 123-124.

Mahr, G., & Leith, W. (1992). Psychogenic stuttering of adult onset. Journal of Speech and Hearing Research, 35, 283-286.

Ringo, C. C., & Deitrich, S. (1995). Neurogenic stuttering: An analysis and critique. Journal of Medical Speech-Language Pathology, Vol 3, No. 2, 111-122.

Rosenbek, J., Messert, B., Michael, C., & Wertz, R. (1978). Stuttering following brain damage. Brain and Language, 6, 82-96.

Roth, C. R., Aronson, A. E., & Davis, L. J. Jr. (1989). Clinical studies in psychogenic stuttering of adult onset. Journal of Speech and Hearing Disorders, 54, 634-646.

Schuell, H. (1965). The Minnesota Test for Dyferential Diagnosis of Aphasia. Mineapolis, MN: University of Minnesota Press.
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