The Valsalva Stuttering Network

J. FLUENCY DISORD. 10 (1985), 317-324




Member of the Philadelphia, Pennsylvania Bar and the National Stuttering Project

Reprinted from the December 1985 issue of the Journal of Fluency Disorders.

Copyright © 1985 by Elsevier Science Publishing Co., Inc., 52 Vanderbilt Ave., New York, NY 10017.

This note presents the hypothesis that the excessively forceful closure of the mouth or larynx associated with certain types of stuttering may involve a neurological confusion between speech and the human body's Valsalva mechanism, which is designed to increase pulmonary pressure by forceful closure of the upper airway to assist in many types of physical effort. It is suggested that such behavior may result from excessive neuromotor tuning of the Valsalva mechanism prior to speech, especially in situations where the stutterer anticipates the need to "try hard" to speak properly. Such tuning may both interfere with phonation and render the Valsalva mechanism overexcitable to triggering stimuli, such as the increase in subglottal pressure that accompanies the start of articulation.


I am an attorney who has spent most of his life attempting to resolve a severe stuttering problem. Over the years I have tried a wide range of treatments, including elocution lessons, attitude therapy, psychotherapy, psychoanalysis, metronome training, biofeedback, and airflow therapy - none of which provided satisfactory long-term relief. Since my termination of therapy several years ago, I continued to explore the problem on my own, through extensive review of the existing literature, personal experimentation, and, more recently, consultations with professional researchers in the fields of laryngology and speech pathology.

My stuttering was primarily characterized by some form of excessively forceful, prolonged, or repeated closure of the upper airway, at the level of either the mouth or the larynx. The stuttering of initial vowel sounds involved tight closure of the larynx, including both the vestibular and the vocal folds, such as occurs during effort closure. These laryngeal closures were subsequently observed through a nasally inserted, fiberoptic nasopharyngoscope by Dr. Joseph P. Atkins, Jr., Chief of Otolaryngology at the Pennsylvania Hospital in Philadelphia, and video recorded.

During severe blocks, my mouth or larynx would clamp shut, while my abdominal and thoracic muscles would contract, as if straining to force air through the closure, which, in turn, seemed to tighten more than ever. As I studied my behavior more carefully, I noticed that my stuttering (even when less severe) was preceded and accompanied by tension in certain muscles in and around the larynx, in the abdomen, and in the rectum, as well as difficulties or delays in initiating phonation. When I consciously relaxed my abdominal and rectal muscles, phonation became easier and stuttering was substantially reduced.

As a result of my personal research, I have formulated a hypothesis as to my own problem, based on a possible relationship between stuttering and the Valsalva mechanism - a powerful alliance of laryngeal, respiratory, abdominal, and rectal muscles that are often activated to create pulmonary pressure to assist in many types of physical effort, as well as defecation. As shall be discussed below, the involvement of this mechanism in certain types of stuttering behavior might help to explain a stutterer's involuntary use of excessive force in speaking, and why stuttering is more severe in situations where the person feels the need to "try hard" to "force out" the words.

Although I have found this hypothesis to be my own key to fluency, I recognize that its general validity has yet to be established. Indeed, the possible involvement of the Valsalva mechanism seems to have been totally ignored by the existing literature. Because I do not have the necessary laboratory facilities at my disposal, I am therefore writing this note for the limited purpose of stimulating empirical research into this question.


The term Valsalva mechanism (after the Italian anatomist Antonio Maria Valsalva, 1666-1723) refers to those muscles that are neurologically coordinated for simultaneous contraction in the performance of a Valsalva maneuver, which may occur during many kinds of physical exertion (Carlson, Johnson and Cavert, 1961; Ardran and Kemp, 1967; Fink, 1973, 1975; Fink and Demarest, 1978). Usually such a maneuver involves tight closure of the vocal and vestibular folds of the larynx (called effort closure) for the purpose of sealing off the respiratory tract, accompanied by contraction of the parietal muscles of the abdomen and thorax (Fink, 1975; Fink and Demarest, 1978).

The resulting increase in pulmonary pressure can serve two important functions: (1) bracing and stiffening the trunk of the body, forming a base for the limbs to perform strenuous tasks and (2) permitting abdominal pressure to be used more efficiently to expel visceral contents, as in defecation, urination, and childbirth (Ardran and Kemp, 1967; Fink, 1975; Fink and Demarest, 1978; Dickson and Maue-Dickson, 1982). When the straining effort is not for the purpose of defecation, the anal sphincter is closed, and closure is reinforced by contraction of the puborectalis muscle, to help prevent evacuation (Fink, 1975).

The various elements of the Valsalva mechanism appear to be linked neurologically so that they tend to contract simultaneously. For example, electromyographic studies have indicated that the thyrohyoid muscle is automatically excited or activated in proportion to the contraction of the abdominal wall muscles and the resulting increase in sublaryngeal pressure (Fink, 1975; Fink and Demarest, 1978). Abdominal straining is always associated with complete closure of the larynx in young, normal people (Ardran and Kemp, 1967). Likewise, contraction of the rectal muscles will also stimulate a reflexive closure of the larynx-a fact that could be visually observed during the fiber optic study performed on me by Dr. Atkins. This is not meant to imply that straining and defecation cannot occur without effort closure, or that persons cannot voluntarily refrain from closing the larynx in such instances (Ardran and Kemp, 1967).


The hypothesis suggested by this note may be briefly summarized as follows:

1. Certain types of stuttering behavior may be preceded by excessive "tuning" of the neural pathways to the muscles of the Valsalva mechanism.

Research into muscular activity has indicated that the onset of movement is preceded by preliminary tuning of the excitability of all participating sensory and motor elements in accordance with the motor program for the intended act (Zimmerman, Smith, and Hanley, 1981). Such tuning either promotes or inhibits the excitability of the various motoneuron pools, and thereby enables groups of muscles to act as functional units, called coordinative structures, which are activated by the appropriate triggering signals. In the case of a stutterer, the degree of such tuning might be influenced by psychological and emotional factors, and would more likely occur in those instances when the stutterer feels a particular need to "try hard" to speak.

2. The tuning of the Valsalva mechanism would increase the excitability of those muscles to stimuli that would trigger a Valsalva maneuver.

Such stimuli might (but not necessarily) include the abrupt increase in subglottal pressure that usually occurs at the beginning of articulation (Ladefoged, 1968). The pressure increase would be sensed by mechanoreceptors found in the subglottic portion of the laryngeal mucous membrane (Wyke, 1971) and transmitted to the central nervous system. These stimuli might then be misinterpreted as indicating the beginning of a Valsalva maneuver, resulting in a responsive triggering of the Valsalva mechanism. The reported reduction of stuttering by methods that emphasize a "gentle onset" of voice and articulation (e.g., Perkins, 1973; Webster, 1974) might therefore be attributed to the avoidance of abrupt increases in subglottal pressure.

3. The triggering impulses might be sent to the muscle groups comprising the Valsalva mechanism (as well as to the oral structures that caused the closure of the upper airway) to stimulate their simultaneous contraction, so as to continue the increase of subglottal pressure.

These contractions might include effort-type closures of the larynx during the stuttering of initial vowel sounds, as were observed in the fiber optic study performed on me by Dr. Atkins. Van Riper (1973) has also described such closures as consisting of occlusion at the level of the larynx with both the vocal folds and ventricular folds closed tightly. However, effort closure of the larynx would not necessarily occur when closure of the upper airway is already being accomplished by the various oral structures, such as by the lips and the tongue in the articulation of certain consonants.

Such lack of effort closure would be consistent with the behavior of the larynx observed in the fiber optic study when I used my lips for upper airway closure during a Valsalva maneuver. (Of course, mere visual observation might not reveal the full extent of laryngeal muscular activity during such a maneuver.) Therefore, the validity of the Valsalva hypothesis would not require visible effort closure of the larynx during stuttering that involves oral closures.

My hypothesis proposes, instead, that the oral structures (primarily those whose closure had initiated the rise in air pressure), might be neurologically recruited to assist the Valsalva mechanism. During both stuttering and straining, I have found the overall sensation to be the same, regardless of whether closure is at the oral or laryngeal level. Wyke (1971) has stated that an increase in subglottal air pressure may reflexively induce spasm of the laryngeal and oral musculature.

4. As subglottal pressure rises, the oral or laryngeal structures blocking the upper airway would be stimulated to close with proportionately greater force, so as to resist the increased pressure.

In this way, the increased subglottal pressure would serve as a continuing stimulus for the contraction of the Valsalva muscle groups, creating a vicious cycle that would render fluent speech impossible for as long as the maneuver continues. The stutterer may also adopt various secondary behaviors in an attempt to terminate or avoid such blocks, including inspiratory gasps and attempts to begin speech with little or no available air in the lungs (Van Riper, 1971, 1973; Adams, 1974). Such behaviors may themselves interfere with phonation in other ways, such as by failing to provide sufficient airflow to sustain vibration of the vocal folds.


The possible relationship between difficulty in phonation and stuttering has been suggested by several researchers (e.g., Wingate, 1969, 1976; Wyke, 1971; Adams, 1974; Perkins, et al., 1976). This difficulty might be explained, at least in part, by the possibility that the neuromotor tuning of the Valsalva mechanism may interfere with the larynx's readiness to produce phonation, by preparing it instead to take part in a Valsalva maneuver.

EMG studies have observed neuromotor tuning occurring in the intrinsic laryngeal muscles some 0.05 to 0.55 sec prior to audible phonation (Wyke, 1971). However, tuning of the Valsalva mechanism might supersede the normal prephonatory tuning, because the laryngeal muscles would become set for their role in effort closure rather than phonation. That is, the laryngeal muscles might not be prepared to place the vocal ligaments in the proper position, to give them the necessary tension, or to permit them to vibrate in the manner required for phonation (Fink and Demarest, 1978). This might help to explain, at least in part, the delay in vocal reaction time and voice onset that has been observed in stutterers (Adams and Reis, 1971; Adams, 1974; Starkweather, Hirschman, and Tannenbaum, 1976; Starkweather, Franklin, and Smigo, 1984).

Because a Valsalva maneuver does not normally occur during inspiration, a stutterers' vocal reaction time might be expected to improve when inspiratory phonation is used. In a study by Reich, Till, and Goldsmith (1981), the stutterers' average reaction time was 208.2 msec for inspiratory phonation and 236.8 for expiratory phonation of a vowel sound. The corresponding reaction times for nonstutterers were 182.1 and 177.0 msec, respectively. Although the stutterers' reaction times were somewhat slower than those of nonstutterers as to every task, whether manual or laryngeal, the stutterer-nonstutterer difference was more than twice as great for expiratory phonation than for inspiratory phonation.

If tuning of the Valsalva mechanism does, in fact, interfere with the phonatory function of the larynx, then, conversely, it would seem to follow that tuning of the larynx for phonation might tend to reduce the excitability of the Valsalva mechanism in general. This effect may help to explain the reported reduction of stuttering when vocalization is emphasized (Wingate, 1969, 1970, 1976; Weiner, 1978).


As Henry Freund (1966) has written, one of the primary experiences of stuttering is that of "an obstacle which needs force to overcome it"; however, such effort by the stutterer "only increases the force of the closure." In my own case, I have found the Valsalva hypothesis to be an effective solution to this paradox. I believe it highly plausible that, as a 4-yr-old child experiencing anxiety, emotional conflict, and perhaps some simple disfluency in expressing himself, I may have unconsciously sought help from the Valsalva mechanism, which had previously served me well in defecation and other types of effort, and thereby established my stuttering behavior.

This behavior may have been reinforced by my perception that the increased physical effort was ultimately successful in forcing the words out (Freund, 1966). Activation of the Valsalva mechanism may have achieved certain psychological gains as well. For example, I may have felt that this display of effort would demonstrate to adults "how hard I was trying" to please them, thereby reducing the danger of punishment. The Valsalva hypothesis would seem to provide a common nexus between the psychological and the physiological components of stuttering. It would seem to explain why stuttering is more frequent at the beginnings of words and on stressed syllables (Froeschels, 1961; Soderberg, 1966), instances in which abrupt increases in subglottal air pressure are probably most likely. More important, it would help to explain some of the psychosocial and linguistic variables in stuttering. As summarized by Starkweather (1982), stuttering is more frequent in content words and meaningful speech than in function words and non-meaningful speech, and is more likely to occur at points of high uncertainty or high information load, precisely those instances when a speaker might tend to use increased effort while speaking.


A determination of the validity of the Valsalva hypothesis in explaining certain types of stuttering behavior will require broad-based empirical research. Therefore, I would urge researchers to consider the question of Valsalva mechanism involvement when designing future experiments.

For example, it may be helpful if future EMG studies of muscular activity during stuttering would include some of the significant laryngeal, abdominal, and rectal muscles associated with the Valsalva maneuver. Biofeedback experiments might also test whether stuttering is affected by relaxation of muscles in various parts of the Valsalva mechanism.

I wish to express my most sincere thanks to Dr. Joseph P. Atkins, Jr., of the Pennsylvania Hospital Department of Otolaryngology, for his advice and assistance in this matter, and to the Journal of Fluency Disorders for allowing me the opportunity to share these ideas.


Adams, M.R. A physiologic and aerodynamic interpretation of fluent and stuttered speech. Journal of Fluency Disorders, 1974, 1, 35-47.

Adams, M.R. and Reis, R. The influence of the onset of phonation on the frequency of stuttering. Journal of Speech and Hearing Research, 1971, 14, 639-644.

Ardran, G.M. and Kemp, F.H. The mechanism of the larynx: 11. The epiglottis and closure of the larynx. British Journal of Radiology, 1967, 40, 372-389.

Carlson, A.J., Johnson, V., and Cavert, H.M. The Machinery of the Body. Chicago: University of Chicago Press, 1961.

Dickson, D.R. and Maue-Dickson, W. Anatomical and Physiological Bases of Speech. Boston: Little, Brown, 1982.

Fink, B.R. The curse of Adam: Effort closure of the larynx. Anesthesiology, 1973, 39,325-327.

Fink, B.R. The Human Larynx: A Functional Study. New York: Raven Press, 1975.

Fink, B.R. and Demarest, R. Laryngeal Biomechanics. Cambridge, MA: Harvard University Press, 1978.

Freund, H. Psychopathology and the Problems of Stuttering. Springfield, IL: Charles C. Thomas, 1966.

Froeschels, E. New viewpoints on stuttering. Folia Phoniatrica, 1961, 13, 187-201.

Ladefoged, P. Linguistic aspects of respiratory phenomena. Annals of New York Academy of Sciences, 1968, 155, 141-151.

Perkins, W.H. Replacement of stuttering with normal speech: 11: Clinical procedures. Journal of Speech and Hearing Disorders, 1973, 38, 295-303.

Perkins, W., Rudas, J., Johnson, L., and Bell, J. Stuttering: Discoordination of phonation with articulation and respiration. Journal of Speech and Hearing Research, 1976, 19, 509-522.

Reich, A., Till, J., and Goldsmith, H. Laryngeal and manual reaction times of stuttering and nonstuttering adults. Journal of Speech and Hearing Research, 1981, 24, 192-196.

Soderberg, G. The relations of stuttering to word length and word frequency. Journal of Speech and Hearing Research, 1966, 9, 584-589.

Starkweather, C.W. Stuttering and laryngeal behavior: A review. ASHA Monographs, 1982, 21, 1-45.

Starkweather, C.W., Franklin, S., and Smigo, T.M. Vocal and finger reaction times in stutterers and nonstutterers: Differences and correlations. Journal of Speech and Hearing Research, 1984, 27, 193-196.

Starkweather, C.W., Hirschman, P., and Tannenbaum, R.S. Latency of vocalization: Stutterers vs. nonstutterers. Journal of Speech and Hearing Research, 1976, 19, 481-492.

Van Riper, C. The nature of stuttering. Englewood Cliffs, NJ: Prentice-Hall, 1971.



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