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Stuttering: A view from psychiatry


What is stuttering?
Who stutters?
What causes stuttering?
What are the treatments for stuttering?

What is stuttering?

Stuttering is defined as an observed disruption in the normal fluency and time pattern of speech.  This disruption in speech has been recognized since antiquity – stuttering is depicted in Egyptian hieroglyphics.1  Also the famous physicians, Hippocrates (460-377 B.C.) and Galen (131-200 A. D.) wrote of stuttering. Like the descriptions of the ancients, the current definition of stuttering is based on observed speech patterns.

There are characteristic dysfluencies observed in stuttering.2 Simply, the nature of dysfluencies can be classified as occurring within words or between words or phrases.

Dysfluencies that occur within words:

1)      sound and syllable repetitions

“Wh-Wh-What time is it?”

2)      sound prolongations

“Wh------------at time is it?”

3)      broken words

“Wh (pause) at time is it?”

Dysfluencies that disrupt the flow of speech between words:

1)      interjections

“What ummmm time is it?”

2)      audible and silent blocking (The person attempts to speak, while no or little sound is emitted.) 

“What (pause) time is it?”

3)      circumlocutions (Word substitutions to avoid problematic words or paraphrasing the intended sentence using different words.)

“Wh---- Do you have the time?”

4)      monosyllabic whole-word repetitions

“I-I-I have the time.”

The dysfluency in stuttering can vary widely among different individuals, and most individuals who stutter tend to have a waxing and waning course of dysfluency; that is, those who stutter tend to have times when they stutter more and times when they do not.  Also, stuttering usually occurs at specific points in conversation - at the beginning of sentences or phrases.  

In addition to the dysfluency, people who stutter may display secondary motor behaviors.  Facial and neck tics, eye blinking, lip and tongue tremors, and other body movements may accompany stuttering.

Interestingly, there are maneuvers that can induce fluency in persons who stutter.  Singing, impersonating another’s voice, speaking alone, speaking in unison with other individuals (choral speech), speaking with a metronome, auditory masking (using white noise or other masking noise to prevent stutterers from hearing themselves speak), and delayed auditory feedback (a maneuver where an individual hears what he or she is speaking approximately two to three hundred milliseconds after he or she has spoken) all can evoke fluency.3

In addition to observed speech, stuttering can be further defined as developmental or acquired.  Developmental stuttering is by far the most common form and begins in childhood – usually with a gradual onset.  Acquired stuttering can begin at any age and is almost associated with some type of brain insult, such as, stroke, brain trauma, or even neurosurgical procedures.4,5 Also, some medications can induce acquired stuttering.6 

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Who stutters?

Stuttering is recognized worldwide, and all cultures recognize and have words that describe stuttering.  Stuttering is a common affliction.  The incidence of developmental stuttering, the number of individuals who start stuttering, is approximately five percent, while the prevalence, the number of people who currently stutter, is approximately one percent.  This means that about eighty percent of the population who has ever stuttered, recovered and conversely, about twenty percent of those who stutter as children stutter as adults.  The reason for this recovery is unknown, but this recovery percentage has been documented for decades and is a reflection of the course of developmental stuttering.

Developmental stuttering typically emerges between ages two and six and, for the fortunate majority, resolves by adulthood.  Interestingly, the incidence and recovery from stuttering is related to gender.   At age of onset, more boys stutter than girls – about a two to one sex ratio.  This ratio is not constant over time, and by adulthood the male-to-female ratio is approximately four to one.  The reason for the change in sex ratio over time is unknown.  Females may have a higher recovery rate or may have better compensation techniques.7 The end result is that most adults who stutter are male.

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What causes stuttering?

The etiology of stuttering is unknown, though throughout history, medicine has proposed many theories on the cause of stuttering.  Roman physicians attributed stuttering to an imbalance of the four “humors,” yellow bile, blood, black bile, and phlegm.  Treatment was directed as correcting an imbalance.  Humoral manipulation continued to be the mainstay of treatment up until the eighteenth century.  By the 1700s, anatomy and its pathology became the template for disease, and these concepts were applied to stuttering.  Giovanni Morgani (1682-1771), the Italian pathologist, attributed stuttering to deviations in the hyoid bone.   He came to this conclusion via autopsy – making a causal relationship between variations in the hyoid bone and stuttering.  Anatomy continued to be the focus of study for the next century.  Surgical intervention, via resection of a triangular wedge from the posterior tongue to prevent spasms of the tongue, was tried.  Also, tubes were placed behind the tongue to ensure proper airflow – as abnormal airflow was thought to contribute to stuttering.8  By the early twentieth century, psychological and neurological conflict became implicated in stuttering.  For example, Joseph Sheehan, the American speech pathologist, proposed that a component of stuttering was a conflict between a desire to speak and a fear from speaking.9 Also, Lee Edward Travis, the American speech pathologist, presented a theory of cerebral dominance that was based on conflict between the two brain hemispheres.  This conflict created mistiming of nerve impulses to the bilateral speech musculature.10

There have been other theories of stuttering – ranging from psychodynamic formulations to disturbances of the voice apparatus.  None have been ideal, and treatments based on these concepts have not ameliorated stuttering.  However, recent progress in medical research has shed some more light on the nature of the stuttering and offers the chance for new, efficacious treatments.

Because of the observation that individuals who stutter can speak fluently under certain conditions; for example, while singing, investigation has switched from anatomical abnormalities in speech mechanism to evaluation of the system of speech production.  Since the brain orchestrates the motor production of speech, it has become the forefront of stuttering research.  Some of the strongest tools used in psychiatric research have been applied to stuttering, revealing some interesting observations.  Below is a summary of some findings of recent inquiry. 


As some people who stutter already know, stuttering tends to run in families.  This observation has been also been documented in scientific study.  Familial studies reveal that about two-thirds of those who stutter have a family member who also stutters.11,12 Also studies of identical twins, who have the same genetic constitution, and fraternal twins, who share about fifty percent of their genes, reveals differences in the incidence of stuttering among the different pairs.  The incidence of identical twins who both stutter is higher than the incidence of fraternal twins who both stutter.  In about three quarters of the population of identical twins, where one twin stutters, the other twin also stutters.  The percentage of fraternal twins who both stutter is lower, ranging from nine to nineteen percent.13,14 Because the incidence of dual stuttering in identical twins is not one hundred percent, nongenetic factors must contribute to the expression of stuttering and thus stuttering cannot be completely ascribed to genetics. Though, these familial and twin studies support a genetic connection to stuttering. 

Brain imaging

Structural brain imaging, where the gross anatomy of the brain can be visualized and analyzed has not shown an anatomical difference between the brains of those who stutter and those who do not.15 However, functional neuroimaging, where processes in the brain can be observed, has shown some differences in the state of stuttering.  There is no consensus on which areas of the brain are active or inactive during the state of stuttering, but several positron emission tomography (PET) studies of this state have found distinct changes brain activity.   Differences in brain activity have been observed in areas that are associated with speech motor function, e.g., the area of the primary motor cortex that controls mouth movements and areas associated with perceiving and decoding sounds.  Also, the areas involved with the formulation and expression of language, which in the vast majority of individuals are located in the dominant left cerebral hemisphere, appear to be expressed in the right hemisphere or bilaterally in those who stutter.16-18

PET has also been used to measure the activity of neurotransmitters (the molecules in the brain that allow brain cells to communicate with each other) in stuttering.  Increased dopamine, a neurotransmitter, activity has been found in the medial prefrontal cortex – an area that modulates the motor production of speech, areas of the limbic system, and in part of the auditory cortex.19 Recently reported, is a PET study of four individuals who stutter that reports the same pattern of brain activity in stutterers when they stutter and when they imagine they are stuttering.20


Psychopharmacology refers to the effects of medication on brain function.  The induction of stuttering in individuals by medicines known to affect brain function, and the subsequent return of fluency when these medications are discontinued is evidence that the brain is involved in stuttering.  A wide variety of medications have been reported to induce stuttering.6 

There are also observations of medications inducing fluency.  These medications target specific chemicals and circuits in the brain and are discussed in the below treatment section. 

Observations of Acquired stuttering

Further implication of brain involvement in stuttering are reports in the medical literature of brain damage with the onset of stuttering.  Brain cell injury affects brain function and head trauma and stroke have been associated with acquired stuttering.4 Observations of where the damage in the brain has occurred have not revealed a specific brain area where damage induces stuttering.  For example, there are multiple reports of patients with strokes who develop stuttering, who have lesions affecting different areas of the brain.21-23   However, there are reports of patients who have undergone neurosurgical procedures, and as a complication, there are those who have developed stuttering and who have also had their stuttering alleviated.5,24 In these patients, the area where the neurosurgical intervention occurred was the thalamus.  Simply, the thalamus is an area of the brain that processes sensory information.  Surgical destruction or stimulation of the thalamus does not always induce or ameliorate stuttering, but these cases implicate that the thalamus is involved in speech production and may have a role in stuttering.

So, in light of the above observations, the question arises again: What causes stuttering?  The answer is still unknown, but there is strong evidence that genetics and the brain contribute to the phenomenon. 

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What are the treatments for stuttering?

The first step in treatment is to decide who would benefit.  This is easy for adults.  In children, referral is not as simple.  Dysfluency is a normal aspect of early childhood and is expected as a child learns to speak.  There is no consensus among physicians when a child should be referred for treatment.  However, a reasonable proposal in medical literature suggests treatment if the child is over the age of four, has been stuttering for more than three months, shows consistent stuttering, demonstrates tension or struggle behavior when stuttering, or if the parents show great concern.25

Once treatment has been suggested, treatment aims need to be delineated.  The treatment goals of developmental stuttering are two fold.   The first, the obvious goal, is to decrease the amount of stuttering.  The second goal is to decrease the amount to anxiety associated with the fear of stuttering, which is termed anticipatory anxiety.  Research, surprisingly, has demonstrated that these aspects of stuttering are not directly related to each other; that is, some of the individuals who have the most severe forms of stuttering do not have as much anxiety as some with mild forms.26 Anxiety seems to be related to the self- perception of communication.   Nonetheless, anticipatory anxiety has been shown to exacerbate stuttering and probably contributes to the social avoidance for those who stutter. 

Currently, the mainstay of treatment is behavioral and cognitive therapy under the guidance of a speech pathologist.27  There are many different nuances employed by speech pathologists.  Simply, the individual is taught to reduce the rate of speech and different means of producing sounds.  Also, confidence is instilled in the individual through repetition and positive feedback to alleviate the anxiety associated with stuttering.  Approximately seventy percent of individuals with developmental stuttering benefit from this treatment.28  Also, study shows that therapy is of most benefit in younger patients, that is, younger patients tend to respond best to therapy.  Thus the same type of therapy given to pre-school population that stutters, may be more successful – possibly over a shorter period of time – than the same therapy given to an older population that stutters.29

To add to this success rate, research has been directed at evaluating pharmacological compounds that act in the brain and target brain function.  This research is based on the above-mentioned discoveries of the role of the brain in stuttering.  Many medications have been used, with limited success, to decrease stuttering.  However, only two have proven to be effective under the gold standard of medication evaluation: A double-blind, placebo-controlled trial.  A double-blind medication trial is one where the investigators and the patients are “blinded,” that is, both parties do not know if the patient is taking placebo or the medicine and the two medications that have passed this evaluation are haloperidol and risperidone.30,31

Unfortunately, haloperidol is associated with side effects that limit its compliance and is rarely used.  Risperidone is a medication that is related to haloperidol, but is not associated with as many side effects.  The largest study, and only double-blind, placebo-controlled study, of risperidone for stuttering was completed here at UCI.  The medication induced fluency and was well tolerated by the participants.  Also the worrisome side effects observed with haloperidol, such as, extrapyramidal symptoms and akathisia were not found with the use of risperidone.  However, sedation was common and some of the participants developed transient sexual and menstrual-cycle side effects that resolved with discontinuing the medication or with a reduction in the dose of the medication.  These side effects are thought to be due the elevation of the hormone “prolactin.”  Risperidone and haloperidol have both been observed to raise prolactin levels in some patients, and these patients may display sexual or menstrual-cycle side effects.32

Olanzapine is another medication similar to risperidone and haloperidol, however it does has a different side effect profile and does not appear to raise prolactin levels to any significant level.  Most recently, olanzapine has been used to successfully treat developmental and acquired stuttering in children, adolescents, and adults.33,34 Some of the patients in the preliminary studies developed side effects of sedation, increased appetite, and moderate weight gain ~ two to ten pounds.  These side effects were controlled by reducing the medication or by implementing a diet and exercise program.  Due to the promising results observed in the preliminary studies, olanzapine is currently being evaluated in a double-blind, placebo-controlled manner in a larger population that stutters.  The results will be available by the summer of 2001, and at that time we should know how well olanzapine induces fluency and its exact side effect profile in those who stutter. 

While the treatments for stuttering have vastly improved over a short time, there is still no medication that can “cure” stuttering.  The best ones only decrease the symptoms of stuttering.  However, reflecting on two thousand years of futile treatments, this is quite an accomplishment.  Furthermore, as medicine advances and the circuits that mediate stuttering become clearer, the prognosis for those who stutter can only improve.  The future is bright, hopeful, and exciting for both physicians and those who stutter.

Nathan E. Lavid, M.D., with a grateful thank you to the many at UCI and elsewhere who reviewed and critiqued this work.
March, 2001

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