STUTTERING:

A DISORDER

OF MOVEMENT

GERALD ZIMMERMANN
University of Iowa, Iowa City

Based on the data and discussion in the two preceding papers a preliminary model for
disfluency is proposed. Stuttering is identified as movement patterns associated with
perceptually judged disfluencies. It is suggested that the speech structures operate
within certain ranges of variability in terms of their movement parameters and interarticulator temporal and spatial relations. This variability may be influenced by emotional,
perceptual and/or physiological events. When the "normal" ranges are exceeded, the
afferent nerve impulses generated alter the gains of associated brainstem reflexes. Altering of the reflex gains throws the articulatory system out of balance and a breakdown in
behavior occurs, often manifested as oscillations or static positioning. The influence of
physiological and environmental variables on neuromotor processes leading to these patterns is emphasized. The model suggested has been developed from inferences from
movement patterns of the upper articulators. Thus, the patterns discussed involve these
structures. It is suggested, however, that an understanding of the many behaviors associated with stuttering will be understood only by analyzing the behavioral and
neurophysiologicaI interactions among the respiratory, laryngeal, and supraglottal structures.
Ideally, any theory of stuttering must be consistent with many p h e n o m ena that have b e e n d e s c r i b e d in the literature (Bloodstein, 1975; Van
R i p e r , 1971). W h e t h e r a l e a r n i n g t h e o r y , a p h y s i o l o g i c a l t h e o r y , a
p s y c h o d y n a m i c theory, or some hybrid, it must account for both perceptually fluent and disfluent portions of the speech of stutterers. It must include the precipitation of disfluencies as well as the escapes or releases
from the "blocks." It must account for the well-known effects of environmental variables such as emotional stimuli, as well as for the known effects o f whispering, choral reading, adaptation, etc. In accounting for all
these p h e n o m e n a any theory must relate the variables which it incorporates (such as contingencies, anal fixation, or muscle output) to a breakdown in motor p e r f o r m a n c e d u r i n g s p e e c h p r o d u c t i o n . In effect, any
c o m p l e t e theory must be able to explain how the learning~ analytic, or
organismic variables interact with the motor control system for speech.
It is well d o c u m e n t e d that normal speakers manifest disfluencies similar to those seen in stutterers (Davis, 1939; Williams et al., 1969). For the
sake o f parsimony a n d for the sake o f limiting assumptions about the differences b e t w e e n the stuttering and normal populations a t h e o r y should
account not only for the disfluency in behavior of stutterers, but also o f
n o r m a l s p e a k e r s . T h e d e v e l o p m e n t o f s u c h a t h e o r y d e p e n d s on:
(1) k n o w l e d g e of the control mechanisms involved in normal s p e e c h production, (2) k n o w l e d g e o f d i f f e r e n c e s in the o p e r a t i o n of the s p e e c h
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production systems of stutterers and nonstutterers, and (3) knowledge of

how environmental and learning variables interact with the neuromotor
processes underlying speech production.
Clearly, such a complete theory of stuttering must await scientific advances to fill the major gaps in our knowledge of speech production.
However, preliminary models may be useful in guiding investigations and
giving specific direction to general areas of inquiry. The purpose of this
communication is to put fo~h a preliminary model of disfluency which
has evolved from an analysis of structural movements and articulatory positions of stutterers reported previously (Zimmemaann, 1980 a, b). These
analyses and recent advances in the understanding of reflex interactions
among brainstem and higher level structures, have led to a model which I
believe is consistent with much of the data and many of the theories of
stuttering. It directs attention to the effects of both environmental and
organismic variables on speech production processes.
The central tenet of this preliminary model is that disfluent behavior is
caused by changes in reflexological interactions among the respiratory,
laryngeal, and supralaryngeal structures. The discussion will center on the
upper articulators because these are the structures that have been studied.
A speaker produces f u e n t speech by moving his articulators within certain ranges of velocity and displacement and within certain ranges of interarticulator positioning and timing. Once these ranges are exceeded interarticulator reflex pathways become abnormally facilitated or inhibited
and repetitive or tonic behaviors develop. Evidence that (1) reflexological
interactions can disrupt ongoing behavior of orofacial structures coupled
with the findings that the (2) movement patterns of a group of stutterers
differ from those of normal speakers (Zimmermann, 1980a) and that (3)
aberrant relationships between articulators are associated with repetitive
and tonic behaviors (Zimmermann, 1980b) have led to the speculative
model discussed below. Three lines of evidence have led to this speculative model.

Interactions Among Brainstem Structures

Investigations into the neuromotor processes underlying complex orofacial behaviors suggest a perspective with which to interpret the movement and muscular p h e n o m e n a associated with stuttering behavior. Recently investigations into mastication and swallowing have l e d t o an
improved understanding of the extensive influences which brainstem nuclei exert on each other. For example, the effects of electrical and mechanical stimulation of certain structures directly controlled by brainstem nuclei have been documented. The effects of afferent feedback to brainstem
structures have been shown to have a modulating effect on behaviors elicited by stimulating descending pathways (Murakami, Lund and Rossignol,
1977). It has been shown that brainstem structures are capable of producing behaviors such as mastication and swallowing without the aid of
ZIMMERMAN:Stuttering

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123

specific cortical inputs (Lund and Dellow, 1971). Table 1 shows a sample
of effects of interactions among brainstem structures that have been demonstrated. The investigations shown in Table 1 make it clear that electrical and mechanical stimulation of perioral and intraoral structures, cranial
nerve, auditory pathways and other structures have many effects on orofacial behavior. An extensive review of these studies can be found in
Bratzlavsky (1976).
TABLE 1. Summary table of studies showing interaction among structures innervated by
brainstem pathways.

Structures Stimulated

Type of
Stimulation Species

Effects of Stimulation

Effects of Perioral Stimulation

Orbicularis oris (Larson and
Sutton, 1978)

mechanical
(stretch)

monkey

Inhibition of orbicularis oris

superior (6-8 msec latency)
Less consistent inhibition in
MPT (6 msec)

Perioral area (comer of the

mouth) (Larson et al., submitted)

mechanical
(stretch)

man

Reflex amplitude elicited in labial muscles was linearly related to the logarithm of the
stimulus velocity.

Perioral area (comer of the

mouth) (McClean, 1978)

mechanical
(stretch)

man

Increase in excitability of labial

muscles prior to onset of voluntary activity.

Perioral (labial) area (Bratzlavsky, 1973; Yu et al., 1973)

exteroceptive
electrical

mail

Pause in digastric activity (at

high levels of stimulation and
only during active chewing)
Bilateral early and late pauses
in masseter activity (10-15 and
30-60 msee latencies)

Peridontal and gingival

structures (Goldberg, 1971)

electrical

man

Excitatory response in masseter

muscles

Upper lip, intraoral stimulation, hard palate, alveolar

mucosa, incisive papilla (Yu,
Schmitt, and Sessle, 1973)

mechanical
and electrical

man

With stimulation of upper lip

they found a complete or partial
inhibition of EMG activity of
masseter muscle. The intensity
of the stimulus' and the level of
muscle activity maintained by
Ss were found to influence the
incidence and duration of the
inhibitory period

Labial and lingual surface of

maxillary incisor (Lund,
McLachlan and Dellow,
1971)

mechanical
(pressure)

rabbits

Activation of contralateral
zygomatico-mandibular and anterior temporalis muscles
Activation of digastric
External p t e r y g o i d fired on
both sides
Other muscle ipsilateral to
stimulus were inhibited

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TABLE 1. (continued)

Structures Stimulated

Type of
Stimulation Species

Effects of Stimulation

Effects of TMJ Stimulation

T e m p e r o m a n d i b u l a r joint
(Greenfield and Wyke, 1966;
Kawamura et al., 1967)

mechanical

cats

Both inhibitory and excitatory

reflexes in jaw muscles

Nerves subserving TMJ

(Klineberg et al., 1970;
Schwaluk, 1971)

electrical

cats

Reflex inhibition of jaw closers

and reflex jaw opening

TMJ anesthetization (Thilander, 1961)

local
anesthesia

man

Impairment of jaw position

Jaw displacement (Hannam,

1972)

mechanical

man

Masseter reflex facilitated with

increased levels of voluntary activity

Mandibular position (Lowe

and Sessle, 1973)

mechanical
position
changes

cat

Rhythmic change s in genioglossus activity and in hyperglossal

nerve

Effects of Stimulation of Lingual Nerve and Other Intraoral Sites

Lingual nerve, teeth, hard
palate, givgivae, tongue, lip
(Miller and Sherrington,
1915; Sherrington, 1917)

electrical
and mechanical

cat

Jaw opening reflex and tongue

movement

Lingual nerve and gingivae

(Goldberg, 1972)

electrical

cats and
monkeys

Jaw opening (linguomandibular

reflex recorded)
Increase in digastric and m.n.
activity
Decrease in masseter m.n. activity
Short latency excitatory reflex
in jaw closers

Lingual nerve (Blom and

Skoglund, 1959; Blom, 1960)

electrical

cats

Hypoglossal excitation

Lingual nerve (Morimoto et

al., 1968)

electrical

cats

Differential effects on tongue

protruders and retractor m.m.s

Tongue surf~tce (Bratzlavsky

and Vander Eecken, 1974)

electrical

man

Pause in activity of tongue protruders

Lingual nerve, inferior alveolar nerve (Goldberg and

Nakamura, 1968)

electrical

cats

Hyperpolarization of masseter
motoneurons

man

Excitatory response in masseter

muscles

Peridontal and gingival

structures (Goldberg, 1971)
Proprioceptive afferent of
jaw closing muscles (Kidikoro et al., 1968)

electrical

cat

No influence on digastric m.n.s.

Teeth (Sessle and Schmitt,

1972)

mechanical

man

Inhibition of jaw closers

ZIMMERMAN: Stuttering

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125

TABLE 1. (continued)

Structures Stimulated

Type of
Stimulation

Species

Effects of Stimulation

Effects of Stimulation of Other Cranial Nerves

Inferior dental nerve
(Yemm, 1972)

electrical

man

Did not elicit digastric reflex

Anterior digastric (Sauerland

and Thiele, 1970)

electrical

cats

Depolarization of primary afferents of lingual and glossopharyngeal nerve terminals

Laryngeal stimulation
(Schmidt et al., 1973)

electrical

cats

Tongue protrusion reflex

Peripheral Sites (Lowe,

Gurza, and Sessle, 1976): infraorbital, lingual glossopharyngeal, superior laryngeal,
maxillary and mandibular
branch of V

electrical

cats and
monkeys

Effects on genioglossus:
Stimulation of IX elicited excitation of genioglossus (6-12
msec latency)
Stimulation of lingual nerve,
palatal stimulation and tooth tap
led to excitation of genioglossus
Both excitatory and inhibitory
effects were produced by stimulation of branches of V and sites
supplied by it

electrical

cats

Facilitation followed by inhibition of alpha m.n.s.

Excitation of gamma followed
by an inhibition of gamma
m .n .s.
No effect on digastric m.n.s.

Peripheral Sites (Sessle,

1977):
masseter and temporalis
nerves

digastrie nerve

No effect on alpha m.n.s, in

masseter or temporalis muscles
No effect in gamma m.n.s, in
masseter and temporalis
No effect on digastric alpha
m.n.s.

glossopharyngeal nerve

No effect on alpha m.n.s, of

masseter and temporalis muscles
No effect on gamma m.n.s, of
masseter and temporalis muscles
Excitatory effect on digastrie
m.u.s.

I n s t u d i e s b y L u n d a n d D e l l o w (1971), M u r a k a m i , L u n d , a n d R o s s i g n o l
(1977) a n d S u m i (1969), p e r i p h e r a l s t i m u l a t i o n h a s b e e n s h o w n to i n f l u ence systematically and interfere with movements involved in complex
o r o f a c i a l b e h a v i o r s . S u m i (1969) s h o w e d t h a t c o r t i c a l l y i n d u c e d c h e w i n g
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March 1980

can be interrupted by peripheral stimulation that elicits swallowing. Lund

and Dellow (1971) studied the influence of electrical stimulation to various peripheral sites on masticatory movements in rabbits. They found that
certain peripheral stimulations inhibited cortically induced mandibular
movements while stimulation of other intraoral sites were facilitory to a
subthreshold central stimulus. The findings on Lund and Dellow suggest
that peripheral stimulation of the intraoral region can modulate input arising at the cortex to alter mandibular movements. Murakami et al. (1977)
demonstrated that stimulation of the upper lip during subthreshold cortical stimulation in the rabbit evokes rhythmical movements resembling
normal mastication. They showed that such stimulation evokes a long duration burst of activity in the digastric muscle, after which a period of
rhythmical mastication may follow. They reported also that when such
stimulation of the lip is given during masticatory movements the effect
depends upon the phase of movement in which it occurs. When given
during jaw closing and the early part of jaw opening, the chewing cycle
time is increased by 20%. But when the stimulus occurs during the final
phase of jaw opening the cycle is shortened by up to 10%. It is unchanged
if stimulation occurs in the intervening period.
Using stimulation of the cortex to elicit rhythmical jaw movements,
Murakami et al. (1977) found that the cycle length was dependent upon
the phase relation between the stimulus and the movement. When a cortical stimulus is given at maximal jaw opening the cycle length is reduced
to 75% of the mean. The gradual displacement of the stimulus away from
this point led to an increase of the cycle length up to a maximum 25%
longer than the mean. This occurs when the cortical stimulus is presented
just before maximal jaw opening. Thus, there is an interaction between
peripheral (upper lip) and central (cortical) stimulation in controlling the
mastication cycle. The peripheral stimulation is most effective when presented during jaw closing and the early part of jaw opening and at the
final phase of jaw opening. The largest effects of cortical stimulation of
cycle time occurs when stimulation is presented at maximal jaw opening
and just before maximal openings.
The results of the investigations summarized in Table 1, the review by
Bratzlavsky (1976) and anatomical studies (Dubner and Kawamura, 1971)
showing the proximity and overlapping of many of the brainstem nuclei,
suggest the existence of functional interactions between structures involved in oral behaviors. Any patterned oral behavior then, such as mastication, swallowing, or speech, is likely to result in the stimulation of many
sensory systems and it is probable that under normal conditions a large
amount of afferent activity is generated. Each of the excited receptor sites
is capable of acting in a reflexogenic manner, given adequate stimulation,
to alter the input to the motoneuron pools controlling many brainstem
structures (Sessle, 1977). The degree to which peripheral reflexes are effective during normal speech is unknown. However, each of these reflex
pathways is available and could influence speech production, particularly
ZIMMERMAN:Stuttering 127

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if the normal patterning is somehow interrupted, as has been shown for

other behaviors (Grillner, 1975).
That some of these pathways are available and can effect speech gestures has been demonstrated. Folkins and Abbs (1975) investigated the
on-line compensatory movements of the lips and jaw. They abruptly arrested the movement of the mandible during speech and observed an online compensatory labial activity. These results suggest that reflex pathways were operative, at least when the mandible was perturbed.
McClean (1978) studied the activity of the orbicularis superior muscle
in response to a mechanically induced stretch to the corner of the mouth
prior to muscle contraction for speech. McClean reported systematic increases in perioral reflex amplitude as a function of the interval between
mechanical stimulation and onset of voluntary muscle contraction.
If speech processes are similar to those of other motor systems, then the
ability to modulate the activity of the reflex pathways is important to the
production of speech, as well as any motor task. The inability to modulate
reflex activity which may result in an imbalance of gains in longer loop
pathways and in the traditional reflex are, has been observed to interfere
with ongoing motor activity. Stein and Oguztoreli (1976) have posited that
reflex modulation must be employed to avoid instability and oscillation.
They showed that imbalances in gains or changes in phases among pathways lead to oscillatory behavior. Others also have indicated that the inability to modulate reflex activity during movements results in rigidity observed in Parkinson's patients (Houk, 1972; Lee and Tatton, 1975; Neilson
and Lance, 1976). An inability to modulate reflex activity has also been
shown to result in clonus (Gottlieb and Agarwal, 1973).
Thus, with the stimulation of receptor sites in the oral, laryngeal and
respiratory systems during speech, the brainstem motor nuclei are bombarded by an enormous number of ascending and descending impulses.
. Imbalances in these afferent-efferent signals may lead to disruptions of
motor performance. As suggested earlier, peripheral stimulation can elicft
brainstem reflexes that disrupt ongoing orofacial behavior.
The model suggested below is based on the premise that certain behaviors often associated with stuttering are produced by aberrations in
activity among reflex pathways involved in speech production. Furtherrnore, this activity is hypothesized to be associated with an increased
variability in both movement patterns.

A Preliminary Model of Disfluency

Figure 1 describes in schematic form the events involved in fluent and
disfluent speech production. The central commands for speech might
exist as spatially coded targets (Lashley, 1951; MacNeilage, 1970), auditory targets (Ladefoged, DeClerk, Lindau, and Papcum, 1972), or some
hybrid. Whatever the representation of the code, the commands must be
executed to achieve the critical spatial-temporal relationships necessary
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ZIMMERMAN:

Stuttering

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129

for intelligible speech. How the input is c o d e d is a moot issue at this point
and is not relevant to the present discussion. What is important is that
certain temporal and spatial relationships of the articulators must be
achieved throughout a speech gesture and that fluent m o v e m e n t patterns
are d e p e n d e n t on such relationships (Zimmermann, 1980b). These must
be accomplished by the proper neuromotor input via the cranial nerve
nuclei and motoneuron pools to proper muscles or muscle systems at the
proper time. The portion in Figure 1 labeled spatial coordinate system
represents these goals. This is not to suggest that the code is in terms of a
spatial target, but rather that in the execution of the higher level commands, certain articulatory relationships are achieved.
Invariance of articulatory relationships is not implied. The movements
involved in achieving these goals, the contacts made, and the positions
achieved result in the stimulation of many intraoral and perioral receptor
sites. It is posited that w h e n a person speaks he usually operates the respiratory, laryngeal, and supralaryngeal systems within certain ranges of
variability. That is, he usually stays within certain limits in velocities, displacements, accelerations and interarticulatory spatial and temporal relationships. For instance, though the lower lip and jaw move more-or-less
simultaneously toward given targets some normal variation occurs in lipjaw synchrony.*
When these normal ranges are e x c e e d e d the afferent nerve impulses
generated are p r e s u m e d to increase the gains of associated brainstem reflex pathways. If excitation reaches a "threshold" level, oscillation and/or
tonic behaviors occur. Such reflex connections have b e e n shown to disrupt ongoing patterned behaviors (Sumi, 1969; L u n d and Dellow, 1971;
Murakami et al., 1977) b y altering afferent input and changing muscle
length and tension which affect the gains and phases of these pathways
(Stein and Oguztoreli, 1976).
Stein and Oguztoreli (1976), in modeling tremor behavior, suggested that
small amounts of sensory feedback are necessary to reduce deviations from
steady state length of muscle, but that larger amounts of feedback can
produce oscillations. If the strength of sensory feedback is sufficient, either
the mechanical oscillations (due to the interaction of the muscle with its
load) or reflex oscillations, or both, can grow with time. Thus, the same reflex
pathways used to stabilize the biomechanical systems may, under conditions
of increased afferent feedback and/or changes in the interactions of reflex
pathways, lead to the destabilization of a muscle system.
*It must be emphasized that not only have interactions been found among the orofacial
muscles, but that stimulation of receptors and afferent fibers in the laryngeal muscles also
can have a direct or conditioning effect on the structures of the upper artieulatory system
(Sessle, 1977; Wyke and Kirchner, 1976). Furthermore, receptors in the trachea which are
sensitive to ehanges in lung volume or airflow may also effect both laryngeal behavior and
orofacial behavior, Such interactions are also necessary to take account of in understanding
the processes involved in speech production, and the behaviors associated with stuttering,
many of which involve complex interactions and interruptions in respiratory, laryngeal, and
supralaryngeal activity (Adams, 1974).
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In line with this reasoning, the schematic in Figure 1 suggests that increased variability in the movement parameters may lead to aberrant spatial relationships. Either the increased variability of movement parameters
or the aberrant spatial relationships alone may result in afferent information which leads to an instability in the afferent-efferent system. This instability, resulting from the inability to modulate these incoming signals
to the motor nuclei results in oscillatory or tonic behavior. As shown in
the upper line of blocks, however, if the velocity and displacement and
the spatial relationships remain below "threshold levels" of variability so
as not to increase reflex effects, fluent production occurs--the stability
and integrity of the system is maintained, the usual feedback mechanisms
are employed and the speech process continues. It is suggested that by
keeping velocity of movement down and by using more time to complete
a gesture (Adams, Runyan, and Mallard, 1975; Zimmermann, 1978a) the
stutterer remains below his threshold leve'l. Any increase in these parameters might lead to an increase in variability and increase the probability of
disruption.
When the system is thrown into oscillation or tonic behavior due to the
bombardment of reflex pathways by afferent input, the system is able to
accommodate its movements to regain stability. For instance, when the
simple repetitive movements or brief Ionic behaviors (normal disfluencies) occur, the system makes the necessary adjustments immediately.
Such an accommodation may be analogous to that proposed by Shik and
Orlovski (1965, 1976) who put forth a mathematic model of interlimb
coordination involving cat stepping which incorporates the ability of the
system to accommodate its stepping cycle to environmental perturbations.
Shik and Orlovskii's model accounted for data which showed that if one
limb is prevented, temporarily, from initiating its transfer stage so that its
stepping cycle is out of its usual phase relation to the other limb, it is
gradually brought back into phase over several stepping cycles. This is
effected by the muscles in a way that alters the stepping cycles of the
unperturbed limbs, particularly the other limbs of the same girdle as the
perturbed limb. They concluded that the ~indings confirm that intralimb
coordinative structures are organized into larger systems that regulate
interlimb coordination. Similarly, Zimmermann (1980b) suggests that interactions exist among the articulators and that these interactions account
for the precipitation and release of oscillatory and static behaviors. For
instance, a more inferior jaw position was found to correlate with the termination of oscillatory behavior involved in the production of the bilabial
/p/(Zimmermann, 1980b, Figure 1). Also, repositioning of the tongue dorsum to a position that approximated the tongue dorsum in its resting position was correlated with the termination of static (prolonged) tongue
tip-dental or tongue tip-palatal behaviors. In both cases it is likely that
activation of inappropriate muscles, i.e., the jaw closers, or the muscles
influencing the tongue dorsum position, had a disruptive effect, via reflex
pathways, on the muscles necessary for fluent production.
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It is only when the inputs to these "inappropriate" muscles are inhibited, as manifested (possibly) by jaw opening and a normal shape of the
tongue dorsum, that the adverse reflex effects on the labial and tongue tip
musculature are eliminated, and fluent production can be accomplished.
These inputs along with the data showing interactions among articulators
(Kent and Moll, 1972; Kent, Carney, and Severeid, 1974; Folkins and
Abbs, 1975; Hughes and Abbs, 1976; Lindblom, Lubker, and Gay, submitted) suggest that the structures of speech are organized into larger systems
that regulate interartieulator coordination. Such a position has recently
been put forth by Fowler (1977).
The emphasis thus far has been on accounting for behaviors associated
with perceptually j u d g e d disfluencies rather than on the diagnostic
categories, stutterers and nonstutterers. The goal has been to put forth a
preliminary model from which hypotheses can be developed and tested
concerning the neuromotor processes related to disfluent events.
An answer is needed to the obvious and important question, of why
these types of disfluent events occur more in stutterers than in normal
speakers? Assuming the validity of the threshold construct, a number of
explanations might account for the differences found:
(1) Stutterersmaybe those on the low end of the thresholdcontinuumfor excitingreflex
pathways. That is, the speech neuromotorsystems for stutterers might be more susceptible to destabilization than those of normal speakers. Hence,a given amountof
neuromotormovementvariabilitymay excitereflexpathwaysin stutterers but not in
normal speakers.
(2) Stutterers may have thresholds similar to those of normal speakers but have more
variable motorics.
The validity of these explanations is empirically testable and relevant investigations are underway.
For both explanations, the ideas put forth raise certain questions and
suggest specific predictions. For instance the model suggests that situations which have been shown to induce fluency (whispering, choral reading, adaptation, etc.) should be characterized by reduced variability in
movement patterns. Though demonstrating that a reduction in movement
variability is correlated with increased fluency will not dispel an "anxiety
reduction" explanation, it will emphasize the need to relate ideas concerning emotional states to their effects on motor control. Such results
might suggest alternative explanations. In other words, a reduction in
movement variability may be attributable to repeated performance in the
case of adaptation; simplified neuromotor demands as in whispering; or
an imposed rhythm as in singing.

Behaviors Other Than Simple Repetitions and Tonic Positioning:

Behaviors Associated with Stutterers
It has been explicit in the foregoing discussion that oscillatory and tonic
behaviors result from an instability in the motor system. Certainly many
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other behaviors must be accounted for by any model of stuttering. The

coping behaviors (escape, avoidance, etc.) take on many forms and have
been distinguished from part-word repetitions and prolongations on the
basis of their differences in susceptibility to modification by response contingencies (Brutten and Shoemaker, 1967), their differences in morphology, and by the observation that normal speakers manifest repetitions and
prolongation but are, for the most part, devoid of coping behaviors. Thus,
coping behaviors have been included in the schematic shown in Figure 1.
The diagram shows that the response produced stimulation associated
with aberrant positions can serve as conditional stimuli which can occasion what have been traditionally called escape or avoidance responses.
Whether they are escape or avoidance is largely determined by when disfluency in the aberrant chain of events stuttering occurs. The stimuli can
also occasion more adaptive responses such as relaxation or repositioning
which bring the articulators into balance in terms of afferent-efferent patterns.
If the system isn't stabilized immediately following the onset of oscillation and/or tonic activity, the stimulation derived from these behaviors
and their afferent input (pressure receptors, tactile, auditory, etc.) may
produce movement patterns associated with what have been called coping
behaviors. In the sophisticated stutterer these stimuli might occasion relaxation and/or repositioning while in the unsophisticated stutterer they
might cause more maladaptive, hypertonie escape behaviors.
The loop is completed in the model by showing that afferent feedback
derived from the coping behaviors influences both the ascending and descending inputs to the motoneuron pool.

Emotional States and Stuttering

The role of arousal and/or emotional states also must be considered in
any model of stuttering. Within the present framework the critical questions concern the effects of emotional states on the neuromotor processes
involved in speech production. It might be constructive to ask questions
concerning the effect of emotional arousal on movement, muscular, and
other variables related to interarticulatory coordination that may be predictive of stuttering. Investigations such as those into the effect of sympathetic innervations to muscle spindles (Granit, 1970) will lead to a
better u n d e r s t a n d i n g of the physiological processes involved in the
breakdown of motor behavior under emotional stress. Chase and his colleagues (1970a,b) reported two studies related to the effects of stimulation
of ~agal afferents on somatic reflex activity. They found that stimulation of
vagal fibers similar to those whose excitation induces E E G patterns correlated with emotional arousal, leads to systematic facilitation and inhibition
of monosynaptic (masseteric) and polysynaptic (digastric) brainstem reflexes in the cat. Such autonomic effects may account for changes in reflex
activity of the respiratory, laryngeal and supralaryngeal structures that
ZIMMERh~N: Stuttering

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133

m a y b e a causal factor for oscillatory m o v e m e n t s and static p o s i t i o n i n g o f

the articulators.
It s h o u l d b e e m p h a s i z e d that the p h y s i o l o g i c a l f r a m e w o r k p u t forth in
no w a y i m p l i e s a m i n o r role for l e a r n i n g a n d e m o t i o n a l p r o c e s s e s associated w i t h stuttering. It does, h o w e v e r , lead to q u e s t i o n s a b o u t effects
of l e a r n i n g and e m o t i o n a l states on the n e u r o m o t o r p r o c e s s e s u n d e r l y i n g
specific p a r a m e t e r s o f t h e b e h a v i o r s . F o r i n s t a n c e , l o w e r i n g stress in
s p e a k i n g situations m a y serve to r e d u c e d i s f l u e n c y b y l o w e r i n g gains of
reflex p a t h w a y s a n d / o r r e d u c i n g m o v e m e n t variability.
T h e q u e s t i o n arises of h o w this f r a m e w o r k will lead to a b e t t e r und e r s t a n d i n g o f stuttering. Past t h e o r i e s o f stuttering h a v e e m p h a s i z e d the
d e f i n i t i o n o f s t u t t e r i n g , t h e role o f l e a r n i n g a n d e m o t i o n , a n d / o r diff e r e n c e s in the n e u r o l o g i c a l organization o f stutterers a n d n o n s t u t t e r e r s .
T h e p r e s e n t f r a m e w o r k may g u i d e investigations w h i c h will lead to: (1) an
u n d e r s t a n d i n g of the n e u r o m o t o r p r o c e s s e s u n d e r l y i n g specific b e h a v i o r s
associated with stuttering, a n d (2) an u n d e r s t a n d i n g o f the role that emotional, p h y s i o l o g i c a l , p e r c e p t u a l , etc., factors p l a y in d i s r u p t i n g t h e s e
p r o c e s s e s . F r o m this p e r s p e c t i v e r e s e a r c h into stuttering finds a c o m m o n
focus. T h e p h e n o m e n a that h a v e b e e n d e s c r i b e d in the literature m a y b e
i n t e r p r e t e d in terms o f the effects that the e n v i r o n m e n t a l , e m o t i o n a l and
p h y s i o l o g i c a l variables h a v e on m o v e m e n t p r o c e s s e s i n v o l v e d in s p e e c h
production.
Some r e s e a r c h q u e s t i o n s are s u g g e s t e d to test this p r e l i m i n a r y m o d e l :
(1) Are stutterers more variable than normals in the execution of speech gestures?
(2) Does an increase in variability of kinematic parameters lead to an increase in the
probability of deviant positional relationships among articulators ?
(3) Are changes in the variability of interarticulatory positions and/or movement predictive of disfluency in stutterers? In normal speakers?
(4) Are stutterers and normal speakers equal in their ability to modulate reflex activity?
(5) Do conditions that induce fluency, i.e., whispering, choral reading, rhythm, etc.,
alter the kinematics or organization of speech gestures in stutterers? In normal
speakers?
ACKNOWLEDGMENT
This research was supported by PHS Grant #NS07555, National Institute of Neurological
and Communicative Disorders and Stroke, and DE-00853, National Institute of Dentral Research. Thanks to Pamela Mueller for her help in preparation of the manuscript. Requests for
reprints should be sent to Gerald Zimmermann, Ph.D., Department of Speech Pathology and
Audiology, University of Iowa, Iowa City, Iowa 52242.
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March 1980