Neurological issues may drive common voice disorders : Hyperfunctional voice disorders (HVDs) are hard to describe but easy to hear. People with the condition produce a grab-bag of forms of unusual voice behaviors that make them more difficult to follow. Nodules on the vocal cords may trigger the condition, but it may linger after the nodules are removed by surgery. Voice exercises or other treatments sometimes work and sometimes do not.
And although HVDs are the most common class of voice disorders, afflicting about 3% of the U.S. population, their causes are not well understood. Doctors typically attribute the condition to emotional stress that affects the performance of muscles involved in speech.
A study by researchers at Boston University College of Health & Rehabilitation Sciences: Sargent College, however, suggests that a neurological problem affecting those muscles also can be to blame.
“We show the first evidence that some HVDs may be due to a motor control disorder, in which patients improperly process what they hear,” says Cara Stepp, an assistant professor of speech, language and hearing sciences at Sargent College. “This is a very small study, but it’s important because no one previously showed a neurological cause for this condition.”
“Calling this condition ‘hyperfunctional’ suggests that it is something that you should just be able to stop doing, but that’s clearly not true,” says Stepp, the lead author on a paper about the research in the Journal of Speech, Language, and Hearing Research.
In some cases, she notes, people can regain their normal voices after rigorous massages or other treatments, but these successes are often followed by a relapse of the condition.
Stepp and her colleagues hypothesized that some HVD patients might have neurological difficulties in integrating audio cues into their voice control, a breakdown that occurs in many other types of communication disorders.
The team tested their theory with experiments on two groups of nine people—one group with HVD and one group without. Participants were outfitted with headsets and microphones, and told to repeat a series of “ahs”, maintaining their pitch and volume as well as possible, while listening to their own voices in the headsets. The researchers very slowly raised the pitch of the participant’s voice until it was higher by one semitone (the interval between two adjoining piano keys), and then returned it to the original pitch.
As they heard their voices rise in pitch, people with normal vocal control lowered the pitch of their speech to try to compensate. “When we move the pitch up, your brain realizes that it’s higher than your target, so next time you produce your pitch a tiny bit lower,” says Stepp who runs the Sensorimotor Rehabilitation Engineering Lab.
Five of the people with HVD, however, instead raised the pitch of their speech, “which was extremely strange,” she says. And when they heard their voices on the headsets return to the original pitch, these five participants did not go back to the baseline.
“This finding suggests that they have a problem with properly utilizing auditory feedback to control their voice,” Stepp says.
The results correspond closely with some clinical observations, she adds. “It’s quite common for someone with HVD to say that the condition started when they had a cold, and then it just never went away. That’s an interesting match with our findings—when the perturbation we create is done, they ramp up their pitch even further and create a voice that’s even worse.”
Through recent funding from the National Institutes of Health, her lab is collaborating with the Massachusetts General Hospital Center for Laryngeal Surgery and Voice Rehabilitation to recruit participants for a larger five-year HVD project. The researchers will examine a larger group of participants in greater detail, adding other forms of audio-feedback tests.
“We then can make individual computational models of the vocal motor control system for each participant, which will get us much closer to understanding the mechanisms,” she says.
This work will exploit a model of speech motor control called DIVA (Directions Into Velocities of Articulators) developed by Frank Guenther, a BU professor of speech, language and hearing sciences.
DIVA can help to highlight activity in specific areas of the brain, potentially allowing researchers to design brain imaging experiments that highlight the precise neurological pathways that go astray with HVDs, Stepp says.
Her group also will compare motor-control behaviors of HVD patients both before and after successful voice therapy. These analyses may demonstrate either that people who are successful at voice therapy learn to compensate for their abnormal motor-control responses, or that the rehabilitation actually fixes the neurological glitches, she says.
“By cataloguing exactly what happens during voice therapy, we hope to tease out the relationship between who resolves these responses and what kinds of therapies did they get, which is how this research could directly lead to better rehabilitation,” Stepp says. “We have a lot of work ahead of us, but we’ll know a lot more in five years.”
Other co-authors on the paper, all from Boston University, included Rosemary Lester-Smith, Defne Abur, Ayoub Daliri, J. Pieter Noordzij and Ashling Lupiani.
Method One female speaker with ADSD was recorded reading an interview script at two time points: (a) pre-BOTOX injection (severe), and (b) post-BOTOX injection (mild). Thirty-two HRPs evaluated the recording in one of the two conditions via a qualitative structured interview. HRPs gave their recommendations regarding when and how to disclose ADSD.
Results In the mild condition, no HRP perceived that the applicant had a voice disorder. Disclosure was not recommended as often, as an impairment was not initially noticed. However, 15/16 HRPs commented on the applicant’s voice in the severe condition, with most suspecting she was a smoker or had lung/throat cancer. Disclosure in the severe condition was recommended more often, as it clarified symptoms that were noted at the outset.
Conclusions Symptom severity in ADSD influences employer perceptions during the phone interview process. Incorrect assumptions may be made about applicants with severe symptoms, and apparentness of symptoms influences whether or not disclosure is recommended. Results have implications for counseling individuals with ADSD who are navigating the job interview process.
Derek D. IsettiDepartment of Speech Language Pathology and Audiology, University of the Pacific, Stockton, CA
Carolyn R. BaylorDepartment of Rehabilitation Medicine, University of Washington, Seattle
Michael I. BurnsSpeech and Hearing Sciences, University of Washington, Seattle
Tanya L. EadieSpeech and Hearing Sciences, University of Washington, Seattle
Disclosure: The authors have declared that no competing interests existed at the time of publication.
Correspondence to Derek D. Isetti: email@example.com
Editor: Krista Wilkinson
Associate Editor: Preeti Sivasankar
Copyright © 2017 American Speech-Language-Hearing Association
SD is formally classified as a movement disorder, one of the focal dystonias, and is also known as laryngeal dystonia. Supporting evidence that SD is a neurological disorder includes:
- SD may co-occur with other neurological movement disorders such as blepharospasm (excessive eye blinking and involuntary forced eye closure), tardive dyskinesia (involuntary and repetitious movement of muscles of the face, tongue, body, arms and legs), oromandibular dystonia (involuntary movements of the jaw muscles, lips and tongue), torticollis (involuntary movements of the neck muscles), or tremor (rhythmic, quivering muscle movements).
- Spasmodic dysphonia runs in some families and is thought to be inherited. Research has identified a possible gene on chromosome 9 that may contribute to the spasmodic dysphonia that is common to certain families.
Histological examination of the nerve to the vocal cords in patients with SD demonstrates that the percentage of abnormally thin nerve fibers was higher than in normal controls
Functional MRI signal is reduced in sensorimotor cortices associated with movement of the affected body part in laryngeal dystonia, supporting a dystonic basis for this voice disorder