Professor P.T. Macklem researched the Del Ferro method


We investigated the role of respiratory muscle incoordination during stuttering by measuring esophageal, gastric, and transdiaphragmatic pressures to obtain subglottic pressure (Psg) and indices of diaphragmatic, rib cage, and abdominal muscle contraction during speech in normal volunteers and in severe stutterers. We found in contrast to the relatively constant subglottic pressure during normal conversational speech that speech in stutterers was characterized by failure to control Pag because of contraction of the diaphragm, rib cage, and abdominal muscles singly or in various combinations. As a result, Pag varied substantially and sometimes chaotically from 100 high to 100 low, rendering normal speech impossible. During periods of fluency, Pag was much better controlled. We conclude that incoordination of the respiratory muscles is a major problem in stuttering, resulting in failure to control the pressure difference across the vocal cords. It is unclear if this is a primary abnormality or is a secondary response to a primary abnormality elsewhere.


A remarkable feature of normal speech is the mechanism by which the respiratory muscles control the pressure across the vocal cords, namely, the difference between subglottic and atmospheric pressure (Psg). During conversational speech, Psg remains nearly constant if the loudness of the voice is constant (1-5). There are pressure fluctuations for particular sounds (1, 2, 6) and these are reflected in fluctuations of EMG amplitude of respiratory muscles (I, 2). A complex and precise interaction among respiratory muscle groups is necessary to achieve this degree of control, and failure to properly coordinate these muscles would be expected to severely disrupt the normal speech pattern.

Therefore, we have assessed the coordination of the respiratory muscles during stuttering speech to test the hypothesis that inability to control Psg plays a role in stuttering. We present evidence in support of the hypothesis.


Data were obtained from 10 stutterers and live subjects with normal speech who served as controls. The control subjects were all male Italian laboratory volunteers 24 to 47 yr of age. The stutterers were made up of five male Italians 15 to 44 yr of age, three male Dutchmen in their 20s, and two Canadians. None of the subjects had known abnormalities of the respiratory system or history of respiratory diseases. Subjects were tested in the seated position. Esophageal and gastric pressures were measured during quiet breathing by conventional balloon-catheter systems (7, 8), coupled with Honeywell (Denver, CO) or Validyne (Northridge, CA) DP I5 differential pressure transducers. The balloons were 5 cm long and were positioned in midesophagus and stomach, respectively. Esophageal pressure was used to estimate Psg during speech (l, 2, 5, 9). Each balloon-catheter was also connected to one side of a third differential pressure transducer to obtain the difference between gastric and esophageal pressure or transdiaphragmatic pressure, which is a measure of diaphragmatic contraction. Rib cage (RC) and abdominal (AB) motion was obtained by means of Respitrace (Ambulatory Monitoring, Ardsley, NY) bands centered at the level of the nipples and umbilicus, respectively. These signals were used as qualitative measures of lung volume. The Respitrace gains were adjusted so that RC and AB deflections were equal during quiet breathing. All variables were simultaneously recorded during quiet breathing and phonation on a multichannel chart recorder (Battaglia—Rangoni, Bologna, Italy or Graphtec WR 3101, Tokyo, Japan). Data from five subjects were also stored on FM tape (RACAL Store TDS): in these cases, the subject’s voice was recorded, via a microphone placed 30 cm from the subject’s mouth, and served tor synchronization of acoustic and pressure events, during data replay. In the two Canadian stutterers, integrated phonograms and tape recordings of speech were made to assess fluency qualitatively, along with measurement of esophageal pressure. In these subjects, gastric and transdiaphragmatic pressures are not reported.

The subjects were given two tasks: spontaneous conversation and reading aloud at conversational intensity. We report the pressures in stutterers without specifying the degree of fluency with which they were speaking at that particular moment except in the two in whom we recorded vocal phonograms. The other eight were severe stutterers who had great difficulty in speaking at all times and were dysfluent during the speech records we report.

No objective measure of loudness was made; however, the intensity of conversational voice at data replay was satisfactorily constant.

To a close approximation, Psg is alveolar pressure relative to atmospheric pressure. There is a pressure drop between the alveoli and the vocal cords caused by the frictional resistance of the airways, but during speech it is small because the expiratory flow rates are small. We assumed it to be negligible. Alveolar pressure is more positive than pleural and esophageal pressures by an amount equal to the elastic recoil pressure of the lung. At the end of a normal quiet breath, pleural and esophageal pressures are approximately — 4 cm H20, where as alveolar pressure is atmospheric because there is no flow between the alveoli and the atmosphere. When speech starts (figure 1), esophageal pressure rises above the end expiratory value, and this rise, to a close approximation, is Psg. Thus. we took esophageal pressure during speech relative to esophageal pressure at the end of a normal expiration as Psg.

We analyzed qualitatively the activity of the inspiratory muscles of the rib cage (parasternals, scalene, inspiratory intercostals), the diaphragm, and the expiratory muscles (abdominals, triangularis sterni, expiratory intercostals). Transdiaphragmatic pressure gave us a direct measurement of diaphragmatic contraction, Inspiratory RC muscle contraction was inferred when Psg was too low and the diaphragm remained relaxed with a trans-diaphragmatic pressure of zero, or its contraction was too weak to account for the abnormally low Psg. Expiratory muscle activity was inferred when Psg was too high. Various combinations of respiratory muscle activity ar described further in the results. we report only limited data on RC and AB displacements because the major abnormalities we describe were found in the pressure tracings, and abnormalities of RC and AB displacements were secondary to these.

Figure 1

From top to bottom. Changes in esophageal (Pas). gastric (Pga), and transdiaphragmatic (Pdi) pressures, and in rib cage {RC) and abdominal (AB) motion during quiet breathing and phonation in one subject with normal speech. Vertical lines indicate onset and end cl phonation. Horizontal lines in the pressure tracings are end-expiratory levels. Upward detections are positive pressure changes and increases in thoracoabdominal dimensions.


A typical example of esophageal, gastric, and transdiaphragmatic pressures and RC and AB motion during normal speech is shown in figure 1. Speech starts at the point in the tracing marked by the first vertical line and ends at the second. The onset of speech occurs at the end of a normal inspiration, but gastric pressure remains elevated after the diaphragm has relaxed instead of falling as it does during quiet expiration. Because the pressure across the diaphragm is zero, the elevated AB pressure is transmitted to the pleural space, and esophageal pressure rises by about 7 cm H2O over its normal end-expiratory value (indicated in the figure by the horizontal line). Virtually all of this increase in pleural pressure is transmitted to the vocal cords, and Psg is about +7 cm H2O. Thus, in this and in all subsequent figures, the horizontal line on the esophageal pressure tracing represents zero Psg with respect to atmosphere. The horizontal line on the gastric pressure tracing represents AB pressure in the absence of either expiratory muscle or diaphragmatic activity. Where gastric pressure is above this line, it is either because the diaphragm has contracted or the expiratory muscles have contracted or both. The horizontal line on the transdiaphragmatic pressure tracing is a transdiaphragmatic pressure of zero. When this tracing is on this line, the diaphragm is relaxed. When the diaphragm contracts, transdiaphragmatic pressure becomes positive and the tracing is above the horizontal line. During speech, esophageal pressure changes little although tending to increase slightly as lung volume decreases. This increase is necessary to maintain Psg constant: as lung volume decreases, the elastic recoil pressure of the lung decreases as well. Because, to a close approximation, Psg is the sum of esophageal pressure and elastic recoil pressure, as the latter decreases with lung volume, esophageal pressure must increase to maintain Psg constant.

Inspirations during speech are accompanied by sharp falls in esophageal pressure, increases in transdiaphragmatic pressure, and outward movement of RC and AB. They are considerably more rapid than inspirations taken during quiet breathing. When speech ends (right-hand vertical line in figure 1), there is a positive value for transdiaphragmatic pressure of about 3 cm H2O. This does not indicate an active contraction of the diaphragm, but rather a passive stretching of the diaphragm’s fibers by the larger expiratory displacements of RC and AB that occurred just before speech stopped. In fact, in normal conversational speech, the diaphragm always remains relaxed (3-5). All pressures after stopping speech immediately reverted to the quiet breathing pattern.

Tracings of esophageal pressure during dysfluent speech in the eight Italian and Dutch stutterers are shown in figure 2. As before, the horizontal line in each tracing represents a Psg of zero. In contrast to normal conversational speech when Psg is relatively constant at about +7 cm H20, there is marked variability of Psg in stutterers. This reveals that a feature of stuttering speech is a failure to control Psg Subsequent figures analyze various abnormalities of muscular control of Psg in greater detail.

In figure 3, several abnormalities in Subject 3 are illustrated. With the onset of speech (A), the rise in gastric pressure is considerably less than in the normal subject so that Psg only increases by about 3 cm H2O. Thereafter, gastric pressure increases progressively and is accompanied by prominent inward AB displacement, indicating AB muscle recruitment. Although transdiaphragmatic pressure rises during this episode of speech. This is probably due to passive stretching of the diaphragm because of AB muscle contraction. After the subsequent inspiration and with resumption of speech (B), gastric and esophageal pressures and Psg were again abnormally low, increasing by only about 2 cm H20, and Psg was sometimes negative between B and D. In this instance, the low values of Psg were due to contraction of the diaphragm as there was no evidence of passive stretching caused by inward AB motion and an excessive gastric pressure. Diaphragmatic contraction during conversational speech is abnormal and results in a Psg too low for effective speech. Between B and D there were little RC or AB displacements, indicating little or no expiratory flow and thus no speech. During this time, there were two rapid contractions of the AB muscles, the first taking place at C, which increase gastric pressure.


Figure 2

Tracings of esophageal pressure during speech in eight stutterers. Horizontal lines are end-expiratory levels for each subject and represent zero subglottic pressure (see text). Upward deflections are increases in pressure. Bar illustrates pressure scale, common to all tracings. On the right the subject number is given. Compare with figure 1 (top tracing): unlike in normal speakers, subglottic pressure in stutterers was never kept at a constant positive value during phonation. Note marked intrastutterer and interstutterer variability in pressure pattern and wide fluctuations during single attempts at speech. Individual patterns are analyzed in detail ln following figures.

These increases were transmitted, as shown on the esophageal pressure tracing, to the vocal cords. At D there was a twitch like contraction of the diaphragm so that Psg became negative with almost no change in RC and AB dimensions. The failure to inspire indicates that the glottis was closed or almost so. The rest of the tracing shows a rather chaotic pattern of esophageal pressure and Psg with marked fluctuations caused by diaphragmatic contraction (E) and sudden relaxation of expiratory muscles (F).

In figure 4, obtained in Subject 2, an initially normal pattern is shown, with increases in gastric and esophageal pressure and therefore Psg at the onset of speech (A) and a transdiaphragmatic pressure that remained zero. Before long, however, speech was interrupted by repeated twitch like diaphragmatic contractions such as that illustrated at B, which were more rapid (< 0.2 s in duration) than normal inspirations and which lowered Psg to sub atmospheric values, rendering normal speech impossible. At C, quiet breathing resumed.


Figure 3

From top to bottom. Changes in esophageal (Pee), gastric {Pgs). and transdiaphragmatic (Pdi) pressures, and in rib sage {RC) and abdominal (AB) dimensions during speech in Stutterer 3. Horizontal lines indicate end-expiratory pressure levels. Speech starts at A and continues throughout figure, with intercurrent brief inspirations. Several abnormalities are shown, marked by vertical lines: abnormally low Pos (B to D) twitchlike contraction of AB muscles (C) and of diaphragm (E]; sudden AEI muscle relaxation (F). See text for details.

It can be seen in figure 5 that Subject I failed to increase esophageal pressure and Psg at the onset of speech. During most oft he tracing, Psg remained sub atmospheric (below the horizontal line) so that speech was impossible Indeed, starting at B is a prolonged period where, as shown on the esophageal pressure trace, Psg remained negative and there was no evidence of expiratory flow as revealed by the constancy of RC and AB dimensions even though the subject was trying to speak. Throughout this period, the diaphragm was relaxed so that the sub atmospheric values of Psg must have resulted from sustained inspiratory RC muscle contraction. At C, normal breathing resumed.


Figure 4

Tracings of esophageal [Pes). gastric (Pga), and transdiaphragmatic (Pdi} pressures in Stutterer 2 during speech [A to C) am during quiet breathing (right of C). Horizontal lines indicate end-exploratory pressure levels. Twitchlike diaphragmatic contractions (such see one at B) repeatedly lower Pee and subglottic pressure during phonation. See text for details.

In figure 6 from Subject 5, a failure of the diaphragm to relax at the onset of speech is revealed, resulting in a failure of Psg to rise. Between A and C a tonic but fluctuating diaphragmatic contraction caused Psg to be sub atmospheric except for a brief rise at point B caused by a twitch like contraction of the expiratory muscles and a brief relaxation of the diaphragm. Subsequently, the diaphragm relaxed, but Psg retrained sub atmospheric because of a contraction of the RC inspiratory muscles between C and D.


Figure 5

Changes in esophageal (Pes). gastric (Pga), and transdiaphragmatic (Pcli) pressures. and in rib cage (FIC) and abdominal (AB) dimensions recorded in Stutterer 1 during quiet breathing and during speech (A~C). Horizontal lines indicate end-expiratory pressure levels. Vertical line labeled B marks beginning ot sustained RC muscle contraction lowering Pes and subglottic pressure during phonation. Diaphragm remains relaxed. as indicated by zero Pdi. See text for details.


Figure 6

Records of esophageal (Pes), gastric (Pga). And transdiaphragmatic (Pdi) pressures. and of rib cage (RC) and abdominal [AB) displacement during speech in Stutterer 5. Horizontal lines indicate end-expiratory pressure level. Lew Pes was due to tonic diaphragmatic contraction (positive Pdi] between A and C: to RC muscle contraction (zero Pdi) between C and D. B marks twitch like abdominal muscle contraction. See text for details.

In figure 7 from Subject 4, chaotic fluctuations in esophageal pressure and Psg are revealed with similar chaotic fluctuations in transdiaphragmatic pressure during attempts to speak (B) compared with a normal breathing pattern (A). These tracings show not only a failure to relax the diaphragm during speech, but that contractions were excessive, with the strength of contraction varying in a seemingly random way while the subject tried to speak.


Figure 7

Changes in esophageal (Pee), gastric (Pga), and transdiaphragmatic (Pcii) pressures in Stutterer 4 during quiet breathing (A] and during phonation (S). Horizontal lines indicate and-aspiratory pressure levels. Failure to relax diaphragm during speech and superimposed chaotic contractions render Pes abnormally low and widely fluctuating. See text for details.

All stutterers showed abnormal patterns of respiratory muscle activation during phonation, as inferred from respiratory pressure recordings. All had unstable Psg during stuttering, in contrast with the essentially constant values observed in all normal subjects during speech. Six of the eight Italian and Dutch stutterers had abnormally low (or sub atmospheric) Psg and positive transdiaphragmatic pressures during stuttering speech, indicating diaphragmatic contraction. In three, sub atmospheric Psg and zero transdiaphragmatic pressure indicated inspiratory RC muscle contraction during attempts at speech. Rapid, twitch like diaphragmatic contractions occurred in six of them. Evidence of expiratory muscle in coordination (i.e., failure of gastric pressure to rise and/or excessively high gastric pressure) resulting in an inappropriate Psg occurred in all stutterers. In both Canadian stutterers, in which gastric and transdiaphragmatic pressures were not measured, attempts at Speech with too low or too high Psg were observed. These abnormal patterns of respiratory muscle activation during speech were alternating with normal ones in all but one subject (Subject 4).

In the two Canadian stutterers, Psg and integrated phonograms were simultaneously recorded, allowing us to match patterns of Psg generation with fluency. As shown for one subject in figure 8, during relative fluency (figure SA), Psg was well controlled at approximately +9 cm H20, but when the subject was dysfluent, as indicated by a first prolonged attempt followed by silence on the bottom traction in figure 8B, there was a failure to control Psg. In this case, Psg was subatmospheric to relax, as indicated by the diaphragmatic electromyogram.


Figure 8

Changes in esophageal pressure (Pee), integrated voice phonogram, and diaphragmatic EMG (Edt) recorded during speech in one additional stutterer A. Period of relative fluency, as indicated by regularly occurring spikes in phonogram; note good control of Pes. The vertical arrow labeled A in the command by the operator to start speaking. Speech started at the vertical arrow labeled B. EL Period of stuttering, as indicated by small and irregular spikes in phonogram; note lack of control of Pes. and particularly its low value associated with diaphragmatic contraction (Edl) during first attempt at phonation.


This investigation reveals one salient feature common to all stutterers studied: a failure to control Psg. In contrast to normal subjects during conversational speech, in whom Psg is almost constant and the diaphragm is relaxed (1-5), in stutterers Psg may be too low or too high and may fluctuate between these extremes. As tight control over Psg is essential for normal speech, this represents an important abnormality in speech mechanics, resulting from incoordination of the respiratory muscles.

All the respiratory muscles may be involved. The diaphragm may remain contracted to nicely or speech may be interrupted by twitch like diaphragmatic contractions that render Psg too low for effective speech. Expiratory muscle contraction, which is essential for normal speech (1-5), may be absent, also resulting in low Psg, or excessive, making Psg too high. Psg may be too low even though the diaphragm is relaxed, indicating abnormal contraction of inspiratory RC muscles. These abnormalities may all be present in the same person, but all stutterers do not show abnormalities of all three muscle groups.

Although our data clearly show respiratory muscle incoordination during stuttering speech and resulting failure to control Psg, the study does not reveal whether or DOI this is the primary abnormality.

It is possible that the respiratory muscle contraction is a secondary struggle behavior characteristic of severe stuttering. Alternatively, abnormality of Psg control may be an integral part of the underlying abnormality. As we studied respiratory muscle dysfunction in detail in only eight stutterers, we were unable to determine if there were some distinct patterns of dysfunction separating different groups of stutterers, Perhaps some patterns would have emerged if we had studied more and, if so, this might be helpful in localizing central nervous system abnormalities.

Motor control disturbances associated with stuttering have been reported, involving abnormalities in synchronization of motor activities (10-12) and in reaction time latencies to visual and acoustic stimuli (13-16). Perkins and coworkers (17, IS) postulated that stuttering is a temporal discoordination of the phonatory and respiratory systems. Discoordination ofthe phonatory system in stuttering is indisputable, but we have been unable to find much published evidence of concomitant discoordination of the respiratory system.

Apart from sparse and no conclusive reports on “respiratory blocking” during phonation (19) and “excessive neuromotor tuning in muscles responsible for the Valsalva mechanism” (20), most of the previous work focuses on events between a stimulus to speak and the onset of speech (13-16, 21, 22). In this time period. Peters and Boves (23) measured Psg directly and described three abnormal types of Psg build-up: (I) no monotonous increase in Psg, including decreases to sub atmospheric levels; (2) excessive increases in Psg; (3) exceedingly slow increases in Psg with phonation starting at very low pressure levels. A fourth type of abnormality was described in which Psg build-up was normal but phonation was abnormally delayed after Psg reached normal phonatory levels. We have found similar abnormalities in Psg after the onset of phonation.

Our results then are quite consistent with the hypothesis that stuttering is a temporal discoordination of the phonatory and respiratory systems, and to the best of our knowledge is the first conclusive demonstration of respiratory muscle discoordination during speech in stutterers. The most striking abnormality found in stuttering speech is diaphragmatic contraction. Diaphragmatic activity during phonation has been detected only during singing at high lung volumes and IBD-id phonatory changes (9), and it is known to be absent during normal conversational speech (1-5). Transdiaphragmatic pressure may rise at the end of sustained utterances because of passive stretching of the diaphragm by the increase in abdominal pressure (3-5).

Failure to relax the diaphragm at onset of speech is presumably responsible for the first and third type of abnormal Psg build-up reported by Peters and Boves (23). However, three of the stutterers we studied (Subjects 6 to B} failed to show abnormal diaphragmatic contractions during speech even though their stuttering was severe. All three had been attending a clinic where control over diaphragmatic activity during speech was taught, and this may have altered their pattern of respiratory muscle activation. ln these stutterers, abnormally low Psg resulted from inspiratory RC muscle recruitment. Inspiratory RC muscles are normally activated during phonation to reduce Psg in a number of situations: (I) at high lung volume, to counteract excessive Psg caused by the elastic recoil of the respiratory system (1-5); (2) during strong AB muscle contraction (as in singing), to counteract excessive Psg caused by high AB pressure (1-5); (3) throughout normal phonation in brief bursts of activity, to secure rapid and delicate modulation of Psg, taking part in an economical and precise interplay between agonist and antagonist muscle groups (3-5). The intercostals muscles are particularly adept to perform this precision task because of their highly developed proprioceptive feedback control system (5, 9). In the three stutterers who showed sustained inspiratory RC muscle activation during attempts at phonation, lung volume was in the normal quiet-breathing range and the AB muscles were not contracting (see figures 5 and 6). This abnormality was such as to render normal speech impossible.

Various therapeutic approaches and strategies to reduce stuttering have been proposed and sometimes successfully employed. Some of these (though indirectly) involve techniques favoring respiratory muscle coordination such as pacesetting by metronome or arm-swinging, singing, chorus reading (10, 13, 22, 24-26). These strategies can be view cd as making vocalization possible by imposing an organized motor “skeleton,” through repetition of routine standardized patterns of muscle activation in contrast to the variable ones used during free speech {24). Biofeedback programs based on other muscle activity (laryngeal, lips, masseter) have been employed in treatment of stuttering, with inconsistent results (27-30). The results of the current study suggest that programs to teach coordination of respiratory muscle activity during speech might also be beneficial.

If restoration of coordination restored fluency, this would be strong evidence that respiratory muscle discoordination was primary in stuttering. One possible approach would be to teach coordination with singing. A curious feature of stutterers is that they can sing perfectly normally (5) though singing is a form of phonation that requires just as much (if not more) respiratory muscle coordination as speech. lt might therefore be beneficial if stutterers could be taught to carry over their normal respiratory muscle coordination during singing to speech. Alternatively, or in combination, biofeedback therapy using Psg as the biofeedback signal might restore fluency. As current forms of treatment in stuttering are not entirely satisfactory, it might be most useful to try a different approach and teach stutterers to control Psg.


The writers thank Dr. Claudio Fracchia of the Centro Medico di Montesano for referring four of the stutterers and for participating in some of the studies.


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