Causes of Stuttering

Stuttering is most likely to develop between the ages of 2.5 and 4.5 years. This period is critical both for speech development and for the onset of stuttering. Stuttering less commonly begins during school age; cases of onset in adolescents and adults are rare. What accounts for this timing? Why does one child begin to stutter while another does not?

The great majority of people who stutter can be divided into two subgroups. The first, smaller subgroup (approximately 25%) consists mainly of healthy children who were born without birth trauma and have no history of serious illness, but who have had prolonged contact with people who stutter. These children have no period of fluent speech — they have stuttered from the time they began to speak.

Stuttering by imitation. Many researchers have noted that stuttering occurs more frequently in families where relatives stutter than in the general population. This has been used as a basis for genetic theories of stuttering. We believe, however, that the higher frequency of stuttering in such families may simply mean that these families contain factors that provoke the onset of stuttering through imitation. Our research shows that prolonged contact between a child and a person who stutters during the period of speech development can cause the child to begin stuttering. In most cases, it is relatives who are present with the child during this period. The degree of the family relationship is not relevant — what matters is the duration of the child's contact with the person who stutters. The more time a stuttering relative spends with the child, the greater the likelihood that the child will develop stuttering by imitation.

In our practice we have encountered cases that do not support the genetic theory of stuttering. We had a patient who began stuttering in infancy by imitating his stepfather. There was a four-year-old boy who started stuttering by imitating a stuttering friend. Living in a family with stuttering relatives does not always lead to stuttering in a child. Some women with severe stuttering deliberately limited their contact with their own children during the period of speech development. For example, two of our patients placed their children in the care of grandmothers until the children reached the age of three. Despite the mothers' severe stuttering, their children — two in one case and three in the other — have normal speech.

Thus, it is not the fact of direct family relation but contact with a person who stutters during the period of speech development (ages 0–3) that is one of the primary risk factors for the onset of stuttering.

Sudden fright. The second subgroup accounts for approximately 75% of all people who stutter, according to our data. These are children who experienced birth trauma, received antibiotics in early childhood, or both. Due to the sensitivity and fearfulness of such children, certain events in their lives can cause severe stress and trigger the onset of stuttering.

Many clinicians are familiar with incidents that people who stutter and their parents associate with the beginning of the condition. Most often, stuttering begins when a child is startled unexpectedly. Analysis of the triggering incidents shows that most of them occur in the life of every child: all children have been frightened by dogs, have been briefly left alone without their parents, have experienced their first days at kindergarten, have had dental treatment, have fallen, and so on — yet only a very few children began to stutter as a result. Therefore, an unexpected fright, which in most cases precedes the onset of stuttering, cannot be considered its sole cause. There are a number of factors that determine why one child starts stuttering after being frightened while another does not.

It turned out that most of our children whose stuttering began after a sudden fright had a history of birth trauma — neonatal asphyxia.

Birth trauma. The physical and neurological status and behavior of children who stutter and children who have experienced asphyxia are very similar.

In the behavior of children who have experienced asphyxia, functional psychoneurological disturbances are observed that indicate increased nervous excitability. After birth trauma, digestive disturbances, abnormal muscle tone, elevated intracranial pressure in early childhood, and signs of seizure activity on EEG are frequently noted. Such children adapt poorly to new conditions and are prone to crying. Parents report sleep disturbances — difficulty falling asleep, light and shallow sleep, night terrors, and unprovoked fearfulness.

This fearfulness and sensitivity in children who have experienced asphyxia, together with heightened excitability and restlessness, may turn certain environmental stimuli into supra-threshold triggers. As a result, a dog rushing at the child, an unexpected loud noise, or a visit to the doctor can cause severe stress with activation of seizure-like processes in the nervous system. Any environmental agent can provoke stress and stuttering in a fearful and excitable child, while the same event produces no stress response in an ordinary child. The incidents that parents associated with the onset of their child's stuttering were often quite minor and would not normally be expected to cause severe stress. For example, one three-year-old boy saw a worm on the wall; another was frightened during sleep; a third was unexpectedly called out to and tapped on the shoulder. It is clear that an ordinary child would not have begun stuttering after such incidents.

Subsequently, stuttering may intensify even when the patient is not experiencing severe stress, which is apparently related to the nature of seizure-like processes in the nervous system.

The incidents after which children without a history of asphyxia begin to stutter are significantly more serious. For example, a thirteen-year-old girl spent a night alone with her mother who had died in her presence; a six-year-old girl was caught in a bombing; a four-year-old boy underwent painful daily procedures following surgery and was forcibly restrained by nurses despite his screams and attempts to break free. These children began to stutter even though none of them had a history of birth trauma.

Not every child who has experienced asphyxia begins to stutter, but the combination of neurological and behavioral characteristics makes the onset of stuttering after severe stress highly probable in such children. We therefore identify neonatal asphyxia as one of the most important risk factors for the development of stuttering in children.

Antibiotics in early childhood. We found no data in the literature on the effects of systemic antibiotic administration on seizure activity in the nervous system, but it turned out that approximately 30% of the stuttering subjects in our study had received large doses of antibiotics in early childhood. Ten of them began to stutter within a month of completing the course of treatment, with no apparent cause.

Despite the absence of direct evidence, we hypothesize that systemic use of antibiotics in early childhood, before speech development is established, may be a provoking factor for the onset of stuttering.

Thus, antibiotic use in early childhood, alongside neonatal asphyxia and stuttering in the family, is a risk factor for the onset of stuttering in early childhood.

In summary, we identify three main risk factors that provoke stuttering: contact with a person who stutters, neonatal asphyxia, and antibiotic use in early childhood. Each of these risk factors may act independently or in combination with the others, increasing the likelihood of stuttering developing in a child.

Pathological muscle activity. Stuttering is associated with abnormal activity of the muscles involved in speech. The first study of laryngeal muscles in people who stutter using a flexible fiberoptic nasolaryngoscope was conducted in 1977 by Conture and colleagues. The data revealed the presence of pathological motor activity in the laryngeal muscles during speech. Subsequent research found that during speech, people who stutter exhibit spasmodic movements including trembling and twitching of the tongue, strong lateral constriction of the pharynx, rapid up-and-down movements of the larynx, and paradoxical attempts to open the vocal folds at the moment of intending to speak (Freeman & Ushijima, 1978; Monfrais-Pfauwadel et al., 2005).

In addition, in people with severe stuttering, the jaw, lips, and laryngeal muscles display rhythmic tremor-like oscillations of myographic activity (Kelly et al., 1995; Smith, 1989; Smith et al., 1993). Stuttering is also accompanied by disruption of the normal interaction between the laryngeal, articulatory, and respiratory systems (Conture et al., 1985; McClean & Runyan, 2000; Zimmermann, 1980).

It is clear that pathological muscle activity represents the peripheral component of the pathogenesis of stuttering. The central mechanisms of stuttering have not been fully studied. The literature contains EEG data indicating the presence of signs of pathological paroxysmal activity in the central nervous system of people who stutter. In many of them, a focus of polymorphic activity is evident, characterized by a predominance of sharp waves, slow oscillations, and sharp-wave–slow-wave complexes.