Are people who stutter really tongue-tied?

June 21st, 2022

Written by: Sophie Liebergall

For the majority of people, speaking is such a natural process that they can barely perceive any distance between their thoughts and the words that come out of their mouth. But for people who stutter, translating thoughts into speech is hardly automatic. All speakers occasionally have interruptions to the flow of their speech known as disfluencies, such as repeating a word or using “like” or “um.” A person who stutters, however, will have disfluencies that occur as a result of being physically unable to say an intended word. These can manifest as repetitions of a single syllable, prolongations of a single syllable, or the inability to start speaking at all, and are accompanied by an uncomfortable or tense feeling. For people who don’t stutter, it is easy to forget that nearly all of our daily tasks, from ordering at a coffee shop, to attending a work meeting, to going to the doctor, require speech. In an often impatient and unsympathetic world, these simple tasks can become excruciating for a person who stutters.

Stuttering is a relatively common speech condition that generally has its onset in childhood. Most cases begin when a child is 2 to 4 years old, and can start either gradually or suddenly. However, up to 90% of childhood stutters will resolve before adulthood.¹ Some adults can also begin to stutter suddenly after a major head injury or other neurological insult, but this makes up a small percentage of the overall cases of stuttering.² Though no two individuals’ stutters are exactly alike, many people who stutter report remarkably similar experiences. People who stutter often describe that they can feel a stutter word coming before they say it. This means that many individuals are able to swap out an anticipated stutter word for a safer word to avoid disfluencies. Furthermore, a person who stutters tends to have certain “problem syllables.” For example, a person may tend to block on words that specifically start with “n.” Someone’s set of “problem syllables” can evolve over time – they may tend to block on words starting with “n” for a few years, but then start blocking on words starting with vowels or “y.” In fact, the overall severity of an individual’s stutter can evolve over time as well, day to day and even year to year.

Though these interesting patterns can give us clues about the underlying mechanism of stuttering, the exact cause of this relatively common condition remains unclear. Nevertheless, throughout the scientific history of stuttering many researchers have proposed both psychologic and neurologic theories of its mechanism. Initially, most of the major theories of the causes of stuttering were psychologic. For example, some psychologists postulated that a stutter is the result of having a certain “temperament” in which someone is more anxious and shy.³ However, stuttering seems to occur at similar rates across different cultures and in different languages. And for people who have experienced a stutter block, it hardly feels volitional or the product of psychological factors. As our technology for assessing brain function has advanced, scientists have gathered evidence that stuttering is a neurologic condition that is caused by a structural or functional differences with the brain itself, rather than only a social or psychological phenomenon.

There are three major neurologic theories of stuttering. The first is that stuttering is caused by changes in cerebral laterization. Cerebral lateralization means that some of our cognitive functions are mostly handled by one side of the brain. For example, areas in the brain involved in speech production and speech comprehension are almost exclusively handled on the left. As such, in studies in when scientists image the brain activity of non-stuttering individuals while talking, in the moments leading up to speech there are patterns of activity that occur predominantly on the left side of the brain. But some studies have shown that in people who stutter, the left-dominance of this pre-speech activity is decreased, and they actually have more changes in activity on the right side of the brain relative to fluent speakers.⁴ This could mean that during a stutter the brain is confused about which side to use, almost like fumbling while trying to write with your non-dominant hand.

Other studies that have imaged the brain activity of people who stutter show changes in white matter compared to fluent speakers. White matter brain is composed of the cables that connect neurons. This means that white matter is important for neurons to be able to send messages to each other, especially when these messages need to be sent quickly over long distances. There is evidence that the cables that connect the areas of the brain that prepare speech and the areas of the brain that execute speech may be missing or misshapen in people who stutter.⁴ There may also be changes in the cables that connect the areas of the brain that execute speech and the areas of the brain that monitor the speech that is already coming out of your mouth. For both the cerebral lateralization and white matter theories, however, it is difficult to tell whether these changes seen in imaging studies are the cause of stuttering. They could instead be compensatory changes that occur over time as a result of stuttering.

In the last major theory of stuttering, some scientists have argued that stuttering is the result of damage to the basal ganglia. The basal ganglia are a group of structures located deep in the brain that control movement, particularly starting and stopping a movement. There are a number of lines of evidence that suggest that the basal ganglia may be a major player in stuttering. Firstly, in the rare cases of stuttering that occur in adulthood after damage to the brain from a stroke or injury, the patients often have damage in the basal ganglia or in structures that connect the basal ganglia to other brain regions.⁵ Secondly, the only class of drugs that seem to have an effect on the frequency of stuttering are drugs that manipulate the dopamine system in the brain.⁶ Drugs that block dopamine can reduce the frequency of disfluencies in some people who stutter; whereas, drugs that cause increased levels of dopamine can cause a medication-induced stutter in people who didn’t stutter before.⁶ Dopamine’s primary role is to modulate the activity of the basal ganglia, suggesting that the effects of these drugs on stutter are due to manipulating basal ganglia function. Lastly, there is a theory that at least some cases of stuttering are an immune reaction to an infection with Group A Streptococcus pyogenes bacteria (commonly known as “strep throat”) that targets the basal ganglia.⁷ Historically, the number of cases of stuttering have declined as the number of strep infections have declined, and a number of cases studies show stuttering that occurs after strep throat infection. It is known that after some strep infections, the body makes antibodies to try to target the bacteria. These antibodies mistakenly also target and damage the basal ganglia. Given the circumstantial evidence connecting stuttering and strep infection, it is possible that this classical strep-induced basal ganglia damage may cause some cases of stuttering as well.

Even if we do figure out the cause of stuttering, is it a neurological condition that we should necessarily try to treat medically? In many ways, stuttering can be seen as a speech difference, rather than a defect. A great deal of the suffering that many people who stutter experience is not a result of the dysfluencies themselves, but rather is a product of the ignorance to and intolerance of stuttering and other speech differences by our society at large. That being said, for some people who stutter there can be an intrinsic frustration with not being able to easily express oneself in spoken word. While there are many alternative ways to communicate, speaking remains perhaps the most efficient and widespread way for an individual to connect with those around them. Whether or not a medical treatment for stuttering is on the horizon, further research into the cause of stuttering can not only provide answers for the millions of individuals worldwide who experience this neurologic condition, but also may provide clues to the complex and poorly understood mechanism by which the human brain translates thoughts to speech.

References

1.         Yairi, E. & Ambrose, N. Epidemiology of stuttering: 21st century advances. J. Fluency Disord. 38, 66–87 (2013).

2.         Mawson, A. R., Radford, N. T. & Jacob, B. Toward a theory of stuttering. Eur. Neurol. 76, 244–251 (2016).

3.         Alm, P. A. Stuttering in relation to anxiety, temperament, and personality: Review and analysis with focus on causality. J. Fluency Disord. 40, 5–21 (2014).

4.         Chang, S. E., Garnett, E. O., Etchell, A. & Chow, H. M. Functional and Neuroanatomical Bases of Developmental Stuttering: Current Insights. Neuroscientist 25, 566–582 (2019).

5.         Alm, P. A. Stuttering and the basal ganglia circuits: A critical review of possible relations. J. Commun. Disord. 37, 325–369 (2004).

6.         Maguire, G. A., Nguyen, D. L., Simonson, K. C. & Kurz, T. L. The Pharmacologic Treatment of Stuttering and Its Neuropharmacologic Basis. Front. Neurosci. 14, 1–8 (2020).

7.         Alm, P. A. Streptococcal Infection as a Major Historical Cause of Stuttering: Data, Mechanisms, and Current Importance. Front. Hum. Neurosci. 14, 1–20 (2020).

Cover photo by Volodymyr Hryshchenko on Unsplash.