About the authors:

Tessa Byrd is currently a second year graduate student striving to attain her Master’s Degree in Communication Sciences and Disorders at Western Carolina University (Cullowhee, North Carolina, USA). For her Bachelor of Science Degree, she studied Communication Sciences and Disorders at the same university. She fell in love with the program and decided the charming school tucked into the mountains was her heaven. Tessa is blessed with two loving, supportive parents who recently moved to North Carolina. She is eager to work with all people who have communication disorders and is particularly interested in serving people who stutter.

Beth Baxley, MS, CCC/Speech-Language Pathology, is a clinical Speech-Language Pathologist who has been in practice for 31 years. She has worked primarily in hospitals, home health agencies, and skilled nursing facilities, specializing in adult neurogenic speech, language, and swallowing disorders. She is a former adjunct faculty member of Western Carolina University (Cullowhee, North Carolina, USA).  She is also a beekeeper and is currently assisting her husband, Steve, and daughter, Lauren, in pursuing their lifelong dream of opening a chocolate shop in Sylva, North Carolina (USA).

David A. Shapiro, Ph.D., CCC/Speech-Language Pathology, is a Fellow of the American Speech-Language-Hearing Association, a Board Certified Specialist in Fluency and Fluency Disorders, and the Robert Lee Madison Distinguished Professor at Western Carolina University (Cullowhee, North Carolina, USA). For 38 years, Dr. Shapiro has taught workshops, provided clinical service, and conducted research on six continents. His book, Stuttering Intervention: A Collaborative Journey to Fluency Freedom (2011, PRO-ED, www.proedinc.com) is in its 2nd edition and continues to find a wide international audience. Dr. Shapiro is actively involved in the International Fluency Association (IFA) and International Stuttering Association (ISA), received IFA’s Award of Distinction for Outstanding Clinician, and served as IFA’s President from 2012-2014. Dr. Shapiro is a person who stutters, has two adult children with his wife, Kay, and lives near the Great Smoky Mountains National Park.

There are relatively few cases of psychogenic acquired stuttering reported in the literature. This paper addresses one such case, which revealed “a solution in search of an explanation” (Dworkin, Culatta, Abkarian, & Meleca, 2002, p. 222).

What is Psychogenic Acquired Stuttering?

Psychogenic acquired stuttering typically begins in adulthood in association with a psychological disturbance or emotionally traumatic event, with no association of a history of developmental stuttering or neuropathology. With some variation, the speech disfluency resembling stuttering begins abruptly, is characterized by repetition of initial or stressed syllables, is without secondary symptoms (i.e., learned reactions to the stuttering) or episodes of spontaneous  fluency, and does not reduce with fluency facilitating contexts (e.g., choral reading, white noise, delayed auditory feedback, singing, and different communication contexts). The person with psychogenic acquired stuttering may demonstrate atypical interpersonal interaction, consistent eye contact, absence of a stuttering pattern related to content or function words, absence of an adaptation effect (i.e., there is no reduction in stuttering with continued conversation or repeated readings), a history of previous mental health issues, and indifference personally to the disruption caused by stuttering (i.e., la belle indifférence). One of the hallmarks of psychogenic acquired stuttering is symptom reversibility, complete or near complete resolution of symptoms, as a consequence of a short term of management (Shapiro, 2011).

Case Summary

Harry (fictitious name), a man in his 20s, expressed concern about stuttering, which reportedly began suddenly within hours of a neurology appointment scheduled less than one month prior to a speech evaluation. Harry interpreted being told by the neurologist that his seizure disorder would cause progressive brain damage. Harry’s aunt, who accompanied him, corroborated this event as the precipitator of Harry’s stuttering. Harry wears a helmet to protect himself from potential harm during the seizures, which he indicated occur, with some variation, every day and evening. He stated that the seizures trigger headaches, loss of breathing, and unconsciousness, all of which he documents in a journal.

Significantly, the neurologist reported that Harry demonstrated “no difficulty speaking” and that his speech was “clear and appropriate.” He also reported that a previous emergency room evaluation for seizure activity was negative and that the seizures “represent psychogenic events.” There was no evidence of neuropathology, however, there was a positive history of mental illness (i.e., anxiety, conversion disorder, depression, and insomnia).

Harry reported no situations in which fluency improved (i.e., although fluency worsens when he is emotional, in pain, or trying to reduce disfluency), discussed various traumatic life events, and expressed a desire to make a presentation at an upcoming conference to discuss his struggle with stuttering. In an attempt to encourage others, Harry reported frequenting an electronic chat room designed for people with disabilities and interacting with people who stutter. Harry expressed an awareness of the literature on stuttering and a high level of personal anxiety and frustration related to his stuttering.

A conversational speech sample collected at the initial meeting revealed disfluency on 100% of the words spoken without secondary or learned reactions. Eye contact was consistent. All disfluencies were part-word repetitions, specifically replication of word-initial phonemes, ranging from two to seven units of repetition. Harry’s disfluency demonstrated no change in response to choral reading, singing, gentle onset, rhythmic speech, and tapping with reduced rate. There was no difference in degree or type of disfluency on content or function words and no observed adaptation effect.

Following the evaluation, Harry was seen for two treatment sessions. Both fluency shaping (behavioral procedures to eliminate stuttering) and stuttering modification (practice to alter the type and degree of stuttering, combined with discussion of related thoughts, feelings, and attitudes) were used, resulting in minimal change in disfluency. Intervention focused on transferring the observed fluency in the medial and final positions of words to the initial position. Speaking to the beat of a metronome, whether slow or fast, resulted in no change in disfluency. However, during slow, rhythmic speech, Harry reported a painful headache that only occurred when he tried to suppress disfluencies, so the activity was concluded. There seemed to be no identified phonemic pattern of disfluency; consistent disfluency continued on all word-initial sounds, whether vowel or consonant.

At the second treatment session, the clinician shared that the neurologist reported Harry’s speech to be without disfluency and seizures to be of non-neurogenic origin. Harry expressed being unable to explain the neurologist’s observations. When probed, Harry altered what he previously reported, now indicating that stuttering began more gradually the day before the neurology appointment. The session was concluded with a subsequent session scheduled.

A few days later, before the third scheduled treatment session, Harry left a voicemail message for the clinician, saying that his disfluency resolved completely in all speaking situations after the second treatment session. He stated that the onset of stuttering was related to lack of consistency in taking his medications and that the elimination of stuttering was due to greater medication compliance. Because Harry terminated treatment, the clinician followed up with two phone calls to Harry. Both revealed Harry’s speech to be without stuttering.

Discussion 

Consistent with the profile mentioned above, particularly symptom reversibility, Harry’s stuttering appeared to be of psychogenic origin. One exception was that Harry reported and demonstrated anxiety related to stuttering. Indeed, determining the type of disfluency can be challenging. Harry did not present a history of developmental stuttering, so this diagnosis was eliminated. Distinguishing between neurogenic and psychogenic acquired stuttering can be particularly challenging. Baumgartner (1999) concurred, stating “The presence of neuropathology does not mean the patient’s stuttering is neurogenic, and the presence of psychopathology may not mean it is psychogenic. Neurogenic and psychogenic disorders often coexist and the presence of one does not render a patient immune to the other” (p. 276).

We looked more closely at the possibility of neuropathology. As noted, the neurologist reported no evidence of neuropathology and that the seizures were likely psychogenic in origin. Nevertheless, it is possible that neuropathology went undetected. If that were the case, Spain, Mandel, and Sataloff (2006) have reported that epileptic seizures can induce stuttering. Furthermore, Rosenbek (1984) indicated, “About the only sites within the nervous system which have not been associated with stuttering are the occipital lobes of the brain, which are devoted primarily to vision and the cranial nerves once they leave the brainstem” (p. 43).

As stated, Harry demonstrated no neurologic evidence of seizures. Vossler et al. (2004) examined 230 patients experiencing seizures. Using a video-EEG, they found that 113 experienced true epileptic seizures and 117 experienced psychogenic non-epileptic seizures. All of the patients who exhibited disfluencies experienced psychogenic non-epileptic seizures. Often psychogenic stuttering and non-epileptic seizures co-occur. Reports of epileptic seizures inducing psychogenic disfluencies are few; more frequently non-epileptic seizures accompany psychogenic acquired disfluencies (Spain et al., 2006).

Another possible undetected neurogenic factor is antiepileptic medications, which also have been associated with stuttering. Gabapentin, a seizure medication, was reported to induce stuttering in one patient; that patient’s disfluency disappeared when he ceased use of the medication (Nissani & Sanchez, 1997). Harry had been on a long-term gabapentin prescription, which was not altered before or during the course of speech therapy. His other medications were researched and none were found to contribute to stuttering. It is unlikely, therefore, that Harry’s medications contributed to disfluency.

Malingering (i.e., pretending or faking stuttering) was another consideration due to the personal gain associated with receiving ongoing financial support for a disability from the government and anticipation of receiving praise for dealing with stuttering at the upcoming conference. Although malingering and neurogenic acquired stuttering were not completely excluded as possible contributing factors, psychogenic acquired stuttering better represented the client’s symptom and recovery patterns.

Harry is no longer receiving fluency treatment but continues to see a general practitioner, neurologist, psychologist, and counselor for his seizure disorder. Regardless of the precise diagnosis, Harry now is experiencing remarkable fluency success. Indeed we have found “a solution in search of an explanation.”

Additional Questions to Consider

Flower (1985) confessed, “Our unending questions and our ceaseless doubts in no way discredit our profession or our discipline. They may well be among our greatest assets” (pp. 24-25). In this positive and constructive spirit, many questions remain for consideration and further discussion.

• Why is it important to differentiate between stuttering and other fluency disorders?
• How can one distinguish between developmental stuttering, neurogenic acquired stuttering, psychogenic acquired stuttering, and malingering? What are the similarities and differences between the disorders in terms of behavioral, cognitive, and affective considerations? How might treatment considerations differ with each disorder?
• Baumgartner (1999) indicated that neurogenic and psychogenic acquired stuttering can coexist and the presence of one does not eliminate the possibility of the other. How can the two disorders be distinguished? What might be the characteristics and treatment methods if a person has evidence of both?
• Why is it still important to determine the type and cause of a fluency disorder after a solution was found and Harry is no longer stuttering?
• Why is it beneficial to share clinical cases such as Harry’s? How does such sharing contribute to our understanding of fluency and fluency disorders?
• Flower (1985) concluded that the most appropriate, honest, and positive salute to our profession and our discipline is “To bewilderment!” How might this toast relate to the questions raised by this paper and the challenges presented by Harry?

References

Baumgartner, J.M. (1999). Acquired psychogenic stuttering. In R. F. Curlee (Ed.), Stuttering and related disorders of fluency (2^nd ed., pp. 269-288). New York: Thieme.

Dworkin, J. P., Culatta, R, A., Abkarian, G. G., & Meleca, R. J. (2002). Laryngeal anesthetization for the treatment of acquired disfluency: A case study. Journal of Fluency Disorders, 27, 215-226.

Flower, R. M. (1985). Asking questions. Asha, 27 (12), 21-25.

Nissani, M., & Sanchez, E. A. (1997). Stuttering caused by gabapentin. Annals of Internal Medicine, 126 (5), 410.

Rosenbek, J. C. (1984). Stuttering secondary to nervous system damage. In. R. F. Curlee & W. H. Perkins (Eds.), Nature and treatment of stuttering: New directions (pp. 31-48). San Diego, CA: College-Hill.

Shapiro, D. A. (2011). Stuttering intervention: A collaborative journey to fluency freedom (2^nd ed.). Austin, TX: PRO-ED.

Spain, R., Mandel, S., & Sataloff, R. T. (2006). The neurology of stuttering. Journal of Singing, 62 (4), 423-433.

Vossler, D. G., Haltiner, A. M., Schepp, S. K., Friel, P. A., Caylor, L. M., Morgan, J. D., & Doherty, M. J. (2004). Ictal Stuttering: A sign suggestive of psychogenic nonepileptic seizures. Neurology, 63 (3), 516-519.