Regular studies of theoretical and clinical aspects of stuttering identify it as a disease having different aspects of pathogenesis - physiological, psychological, and genetic. Ambrose et al. (1993) reported of high risk for stuttering in children growing up in families with stuttering relatives. By different authors, the probability of stuttering in such children varies from 12 to 69 percent. It is generally accepted that stuttering is a disturbance of motor control (Smith, 1990). Studies of motor control (including articulation) and activity of laryngeal muscles (Conture et al., 1977; McClean et al., 1984) give evidence that stuttering is accompanied by pathological muscle activity. Numerous review articles point to laryngeal muscle activity as being one of the reasons of stuttering state (Freeman et al., 1978; Fudjita, 1966). It has been found out that stutterers have increased muscle tone (Kalotkin et al., 1979; Murray et al., 1984) and specific pattern of muscle pair “co-contraction” (Freeman & Ushijima, 1978; Guintal et al., 1988).

Electroencephalographic (EEG) studies testify to the presence of pathological convulsive activity in most of the stuttering patients. Ivanova et al. (1990) observed paroxysmal activity in EEG of 39% of the examined patients. Hyperventilation for 2 - 2.5 minutes induced an increase in the background paroxysmal activity in 75% of the cases. Lokhov (1994) revealed paroxysmal activity in EEG of 43% of the examined children, which enhanced after hyperventilation in 75% of cases. A distinct focus of polymorphous high-voltage activity (up to 100 μV) in the parietal-occipital area of the right hemisphere was found by this author in 77% of the patients.

Similar patterns were observed in EEG of adult stutterers. Fesenko (1994) recorded paroxysmal activity in 68% of stuttering children and clear-cut epileptiform activity in 58% of these cases. The above mentioned phenomena hardly ever occur in healthy adults and children.

Thus, from a certain moment of stuttering development, the nervous and muscular systems begin to function in the specific manner with convulsive components.

Stuttering most probably begins in children aged 2.5-4.5 years. This age is critical both for speech development and the onset of stuttering. Seldom stuttering appears later, at the school age. In adolescents and adults stuttering begins in exceptional cases.

What factors determine stuttering origin? Why does one child begin to stutter and another does not? Many clinical physicians well know about the incidents, which stutterers and their relatives associate with stuttering appearance. It usually occurs when a child gets a sudden fright. Every child undergoes stress in his life, but not every child, after being frightened by a terrible dream, angry dog or unexpectedly loud sound begins to stutter. Therefore, unexpected fright that provokes this disorder in most cases cannot be considered as a reason for stuttering. There exist some risk factors, which make a child to begin stuttering after a definite provoking incident.

The present study was carried out in an attempt to reveal the prerequisites to the disease. With this purpose 60 stuttering persons of both sexes and at different age were examined and questioned. Data about conditions immediately preceding and accompanying stuttering onset were obtained from the patients and their mothers and from individual medical case histories.

Methods

Subjects

The study incorporates data obtained from 60 persons (38 males and 22 females) aged from 2.4 to 24 years. They were referred by a wide network of sources such as special nursery school, speech pathologist and by parents responding to newspaper advertisements. Exclusion criteria included the pretreatment level of stuttering frequency and the absence of any treatment in the past 3 months. Among the selected persons, approximately two thirds of the subjects received previous medicamental treatment (sedative and tranquilizing drugs), psychotherapy, reflexotherapy, and speech training. Despite this, for the moment of examination patients demonstrated a remarkable level of stuttering assessed by speech therappist as grave (23 persons) and medium (37 persons). Hearing acuity was not assessed, since no subject reported of any hearing problems. All information about the disorder onset and its course was obtained from:

(1) Objective speech estimation;

(2) interviews with subjects and their parents;

(3) examination of personal case histories (medical card).

Objective investigation

Subjects’ speech was assessed (a) during talking with the speech therapist; (b) from the reports of family members talking with the outpatients in home environment. Speech pathologist (the author of the paper) assessed oral reading and conversational speech of an outpatient in order to diagnose stuttering. Each of the 60 participants was classified as a stutterer on the basis of the following criteria: production of at least 3 within-word speech disfluencies (i.e., sound/syllable repetitions, sound prolongations, within-word pauses) per 100 words of speech (Conture, 1990). Unnatural hesitations, interjections, restarted or incomplete phrases and unfinished or broken words were also considered as indications of stuttering.

Interviews with patients’ mothers

In the talks with mothers most attention was concentrated on the course of pregnancy and delivery, the general state and behavior of a child during the first months of infancy, medical history preceding the onset of stuttering, medications, circumstances associated with the onset of stuttering, and the time since the onset.

The period which preceded the onset stuttering was scrutinized: the stressful events thought by the parents to be responsible for the disorder were taken into account as well as the detailed personal history of stuttering. Moreover, we elucidated whether stuttering was observed in the family and how close child’s intercourse with stuttering relatives was; contacts with other stuttering persons were also taken into consideration.

All the data about delivery, diseases, medical diagnoses, recommended treatment procedures and medicines reflected in the personal medical case history were used as additional objective information.

Results

Objective study

All the subjects stuttered while reading and talking at home and in the laboratory. Extent of stuttering varied in relation to the extent of speech independence, complicity of a linguistic task, and the level of CNS excitation. Stuttering was least pronounced during reading and maximally expressed in conversation with the therapists. These distinctions were sharper in the elder subjects. Approximately from the age of 7 all participants used some special subterfuges, which facilitated speech (such as within-word and within-sentence pauses, attendant movements, unnatural hesitations, and interjections).

Parents picked different strategies regarding their child’s stuttering. In 55 families they didn’t pay attention to the disorder, and parents of 5 children episodically made some remarks such as “don’t hurry”, “try again”, “speak slowly”. These children were classified as patients with less severe stuttering. It is likely that it was the result of their parents’ behavior. Those 55 subjects, whose parents followed the opposite line, demonstrated moderate and strong stuttering.

Subjects having stuttering relatives

Within the period of speech formation, 14 subjects had continuous close contacts with stuttering fathers (n = 5), mothers (n = 4), grandmothers (n = 2), a grandfather (n = 1), elder sisters (n = 2), and an uncle (n = 1).

As revealed from the talk with the mother and case history examination, there was one case of pathological delivery, which resulted in asphyxia neonatorum, and one case of complicated pregnancy. The remaining children had no birth-trauma. In 11 subjects there were no behavioral deviations, beginning from the early childhood. One had a surgical operation at the age of 2 and took antibiotics within 2 weeks. No one of the parents could give the exact date of stuttering onset and correlate its origin with a definite incident in the child’s life. In their opinion, a child began stuttering “approximately between two and two and a half” (n = 4), “about two years old” (n = 4), “began to stutter just when began talking” (n = 6). Stuttering relatives of 13 children constantly lived together with a subject. Only in one case the stuttering elder sister departed when her younger sister was 3 years old and was already stuttering.

Parents noted that their children began from a slight and insignificant stuttering. Later on stuttering increased, and to the moment of examination every participant demonstrated more pronounced stuttering in comparison with his/her stuttering relatives.

Stress and illness enhanced stuttering. With age this disorder became more pronounced. At the moment of examination, there was no significant difference in severity of stuttering between the children with and without stuttering relatives.

Subjects without stuttering relatives

From the case histories and conversation with patients’ mothers it was found out that the overwhelming majority of participants began their lives from birth-trauma (n = 46). There were the following factors: pathological pregnancy (n = 15), artificial delivery because of poor birth activity (n = 30 ), delivery lasted for 6-38 hours (n = 38), pharmacologically stimulated delivery (n = 18). There were no cases of abdominal delivery. The asphyxia neonatorum of different gravity (n = 40) and fetus hypoxia (n = 3) were the consequences of pregnancy and delivery complications.

Medical histories point to increased intracranial pressure (n = 32) and increased muscular tone (n = 38) in the early childhood (up to 6 months). Parents reported about the anxious behavior of their children within the first 3 months after birth (n = 38), frequent unreasonable crying (n = 41), falling asleep with difficulties (n = 39), sleep problems (n = 38), appetite and digestion (n = 39) disturbances, allergic reactions (n = 28), disposition to respiratory diseases (n = 41). Parents noticed that their children differed from the others by poor attention and concentration (n = 29), easy fatigability (n = 37), restlessness (n = 41), long-lasting falling asleep (for 0.5-1 hour, n = 39). High sensitivity, irritability, anxiety, and “jitteriness” were also marked too. Some children (n = 29) prior to stuttering onset took antibiotics by medical indications; 10 of these children began to stutter within 1 month after termination of the treatment course following a provoking stressful incident or without it. All the parents considered the speech of their children before stuttering to be normal and for the most part associated beginning of stuttering with a definite incident (n = 39). The following episodes were mentioned by the parents as a reason for stuttering onset:

- fright of a dog, which had suddenly appeared or unexpectedly rushed at a child (n = 8);

- fright of a terrible dream at night (n = 4);

- other kinds of frights, for instance, thunderstorm, insects, etc., n = 11);

- stress on the first day of staying in preschool institutions, when a child cried for a long time without mother (n = 5);

- the first visit to a dentist, especially if during the treatment procedure a child had been hold by force (n = 4);

- forced immobilization during the first drug injection (n = 4);

- falling accompanied by head contusion (n = 2);

- current stroke (n = 1).

Parents of the remaining 7 subjects could not recall any occurrence associated with the onset of stuttering or immediately preceding it.

The above listed incidents occurred at the age of 2.5-3.5 years (n = 30), about 4 years (n = 6), at the age of 5 (n = 2), and only in one of the children it happened at the age of 6 (n = 1). Stuttering began within the day after an incident (n = 12), 3-10 days later (n = 16), about 12-20 days later (n =11). Different estimations of time period between the event and onset of stuttering can depend on whether or not the onset of stuttering was immediately noticed by parents. It seems very likely if to take into consideration the common pattern of stuttering development. By our observations, stuttering usually begins from word (sometimes word/syllable) repetition. Some parents cannot identify such mode of speech as stuttering or think it to be the usual speech errors of a 2-3-year-old child. Further speech deterioration is associated with syllable (sometimes syllable/ consonant) repetitions. Then aggravation of stuttering occurs at the expense of consonant pronunciation difficulties and later, if stuttering intensifies, a pathological speech pattern develops which includes some difficulties with pronunciation of vowels.

Quiet atmosphere slows down stuttering development, but every subsequent stress aggravates the speech. In one patient stuttering has been substantially intensified after stresses during service in the forces at the age of about 19.

Discussion

Subjects having stuttering relatives

Our study demonstrates that continuous contacts with stutterers in the course of speech formation period can become a reason for stuttering. Child’s surroundings in this period are usually confined to his family. It seems that the degree of relationship does not matter, but the duration and intimacy of contacts are important. The longer is the time period spent by a stutterer with a child, the higher is the probability of stuttering origin.

In our 20-year practice we observed some facts (none included in the present study) that don’t corroborate the genetic theory of stuttering (Ambrose et al., 1993, Yairi et al., 1996). We had a patient, who lived with his stuttering stepfather from the early childhood; another 4-year-old boy had an intimate friend who stuttered and began to stutter himself while imitating his friend. Stay in the family with stuttering relatives not always results in stuttering. Some intensively stuttering mothers especially restricted their contact with their children till the period of speech formation. For instance, two women (the first of them having 2 children and the second 3 one) asked grandmothers to bring up their children till the age of 3. Despite the strong stuttering of mothers, their children have normal speech. Some parents try to speak better and less with their children, and due to this strategy, they do not stutter. The greater incidence of child stuttering in families with stuttering members in comparison with the general population suggests the existence in these families of the factors, which provoke stuttering by imitation. Thus, the intercourse with a stuttering person in the period of speech formation (1-3 years old) rather than direct relationship is one of the main risk factors for development of the disorder.

Yairi et al. (1996) established that more than 70% of children have grown up in the families with history of stuttering. In our study we have obtained a different incidence - 23%. Our 20-year practice confirms this finding: approximately a quarter of all examined by us stuttering persons were brought up in families with stuttering history. Different ratio between two stuttering groups given by different authors can probably be explained by country-specific conditions of pregnancy and delivery.

Subjects without stuttering relatives

Asphyxia neonatorum. Our studies demonstrate that actually not every child begins to stutter after stressful incidents. Analysis of the events which can give impetus to stuttering shows that a lot of children have experienced such type of events: they have been frightened of a dog, for a short time stayed alone without mother, endured the first days in a kindergarten, have been ill, visited physician, fell down. However, only few of the children became stutterers.

The overwhelming majority of our participants had birth-trauma, i.e., the asphyxia neonatorum in anamnesis. In order to clear up the asphyxia consequences for the CNS, turn to the data of literature. The main brain injury resulting asphyxia includes furnace necrosis of neurons and lesions in parasaggital cortical area, basal ganglia, and thalamus. In consequence an arterial pressure fluctuations and a vascular tone central regulation disorders brain blood circulation has disturb. Asphyxia has result a sharp blood-filling and perivascular oedema in a newborn brain. Brain oedema can raise the intracranial pressure in such degree that it may considerable increase brain vessels pressure. As result perfusion pressure is falling and insult begins developing (Minkovski, 1952; Victor, 1986).

Behind the primary changes in the capillary ending the dystrophic phenomena develop in neurons and neuroglia (Essbach, 1961). Abnormal brain development was mentioned in 20-25% of children born in severe asphyxia. Pathomorphological studies showed that punctuate hemorrhages related with asphyxia was diffuse and evenly distributed not only in different brain regions, but other organs and tissues as well (Elizarova, 1977). Pyramidal cells in the neocortical motor area are most sensitive to asphyxia, which is the reason of motor disorders (Solov’eva, 1971). Brain circulation disturbances include hemorrhages, ischemia and hemorrhagic infarcts which are localized, as a rule, in brain white substance (Mochalova et al., 1984). In children perished from asphyxia at the age of about 1 month there was a diffuse swelling of myelinated fibers, some of them had destroyed segments. The number of Schwann cells diminished. Phenomena of myelin disintegration were revealed in the child who had been lost at the age of 3 week. In some cases myelin degeneration was noticed with demolition of axis cylinders (Petrukhin, 1974).

Thus, under the influence of asphyxia myelination of the nervous fibers disturbs. A lot of specific and nonspecific metabolic and circulatory strokes can suppress or retard myelination (Petrukhin, 1974; Duncan, 1990). Children which have had asphyxia have reduced conduction velocity in the motor fibers of peripheral nerves, and this characteristic is known to reflect the general state of myelination process in the central nervous system (Duncan, 1990; Petrukhin, 1974). The functional impportance of myelin in the nervous system and the requirement for its normal formation are highlighted in myelin mutant mice, where disturbances of the normal myelinating process lead to severe neurological dysfunction with tremor, ataxia and seizures (Duncan, 1990). Mutant dystrophic mice with spontaneous demyelization develop a progressive seizure syndrome because their nervous system has swollen axons and restricted extracellular space (Rosenbluth, 1990), which provide the substrate for the ephaptic transmission (Rasminsky, 1980; 1982).

There is no direct evidence for participation of asphyxia and myelin pathology in the central mechanisms of stuttering. However, such participation seems likely because descriptions of stuttering children, including the EEG data, are comparable with characteristics of children after asphyxia. The pathological EEG activity was recorded in 90% of one-year-old children after medium and severe asphyxia: sharpened waves obliterate spike-wave complexes, differently pronounced paroxysms (Solov’eva, 1971). In the EEG of such children Elizarova (1977) observed hypersynchronyzed slow waves, focal spike-wave complexes, and equivalents of epileptiform seizures. Different intracranial hemorrhages are thought to be one of the reasons of seizures (Basca, 1981b). Convulsive activity in the CNS the first days of life is manifested in tremor, seizures, and tone disorders. Muscular spasticity and hyperkineses were observed in cases of severe (6-10 min.) asphyxia (Petrukhin, 1974; Solov’eva, 1971; Zemlyanskaya, 1972). In some children the neurological deviations were discovered later, at the end of the first year of life. They consisted in disturbances and asymmetry of the muscle tone and brief tonic convulsions (Solov’eva,1971; Zemlyanskaya, 1972). Hypo-, hyper-, or distonic disturbances in the newborn period usually appear in infants with brain injuries due to asphyxia or hypoxia (Basca, 1981b; Zemlyanskaya, 1972).

The functional psychoneurological disorders were observed in children with asphyxia. They testify to increased nervous excitability (Elizarova, 1977). Derangements in the limbico-reticular system were manifested in poor adaptation to new conditions, tearfulness, causeless fearfulness, and sleep disorders (Basca, 1981b; Solov’eva, 1971): falling asleep problems, light, short, and superficial sleep, quivering in sleep (Solov’eva, 1971; Elizarova, 1977). Sometimes anxiety was manifested by a loud cry with simultaneous attack of face flushing (Solov’eva, 1971).

Together with the above mentioned delay in physical development, which persists up to 3 - 5 years old (Solov’eva, 1971; Elizarova, 1977), a number of authors note indigestion in these children. It has been shown in guinea-pigs that moderate asphyxia causes a reduction of the blood inflow to the stomach and the upper and lower gastrointestinal tracts without diminution of cardiac output (Milborat, 1981; Elizarova, 1977). Decrease in oxygenation in muscles and digestive system results from blood circulation redistribution with predominant supply of vital organs, i.e., brain and heart (Schabalov et al., 1989).

The above mentioned may be summed up as follows: physical and neurological state and behavior of stutterers and patients, who have had asphyxia, are similar. The features such as disturbances of tone, indigestion, increase in intracranial pressure, and convulsive manifestations in EEG activity appear long before the onset of stuttering and reflect an alteration of the physical and neurological state after birth-trauma.

Higher timidity and sensitivity of children, which have had asphyxia, together with the increased excitability and anxiety probably, change some environmental stimuli into super threshold irritants. In this way, a rushing dog, a sudden loud sound, or the first visit to a physician induce a no adequate powerful stress with actualization of convulsive processes in the CNS. The same environmental agents can be stressful for sensitive children, who have endured asphyxia, and be indifferent for healthy children. Later on this disorder necessarily augments even if the subject no more experiences strong stresses. This may be associated with the nature of convulsive processes.

In a healthy child the same event did not induce stress reactions. The incidents which do induce stuttering in children, who had not endured asphyxia or hypoxia, must be substantially more serious. For example, 13-year-old girl spent the whole night together with her dead mother; 6-year-old girl got into bombing; 4-year-old boy endured painful procedures every day after surgery. Despite his loud crying and attempts to free himself, he was forcibly immobilized by hospital nurses. All these children became stutterers, although no one of them had any birth-trauma in the personal history.

Not every child who has suffered from the asphyxia neonatorum begins to stutter, but the complex of neurological and behavioral reactions of this child after his birth- trauma makes stuttering very probable after a strong stress. Thus, we think that the asphyxia neonatorum is one of the most important, but not exclusive, risk factors for stuttering.

Antibiotics. It is well known that application of penicillin induces convulsive activity in the neocortex of animals (Ochs, 1965; Pockberger et al., 1984a, b). In Ochs’ opinion, antibiotics increase the sensibility of certain neuronal groups; their activity synchronizes and evokes discharges in the neighboring cells. The mechanisms of excitation spreading from groups of cells with seizure activity to other regions, evidently, are very complicated. The local drug application evokes not only local spikes but discharges in the cortical areas which receive projections from the irritated region (Ochs, 1965). It has been shown by means of local cortical destruction between the primary and secondary foci that excitation spreads by the cortico-cortical axons (Lashley, 1929).

In the literature we have not found evidence for facilitative action of systemically administered antibiotics on seizure activity, however, about 50% of our subjects took antibiotics in early childhood (before the period of speech formation). It is worth noting that 10 children from the group of our subjects began stuttering within a month after the termination of treatment without a clear-cut reason. Incidents given by the parents as a reason for stuttering onset were insignificant and must not have induced strong stress. For instance, a 3-year-old boy saw a worm on the wall, another boy was frightened by a bad dream, a third one was unexpectedly hailed and tapped on the shoulder. It is evident that a healthy child would not have stutter after such events. On the other hand, children with physical and physiological disorders are more susceptible to different infections due to the birth-trauma, which call for treatment with antibiotics.

There is no direct evidence to this supposition, but probably, systemic intake of antibiotics before speech formation period is a risk factor for stuttering. Our observations and experience suggest that in a child that took a considerable amount of antibiotics within the first year of life the probability of stuttering is very high even without provoking stress.

Thus, taking antibiotics in the early childhood along with neonatal asphyxia and family stuttering is a risk factor for stuttering onset.

Conclusions

Relying on our observations, we conclude that for the most part, stutterers may be divided in 2 subgroups. The first, less numerous (25%) consists essentially of practically healthy children without birth injury and severe physical disease but brought up with stuttering relatives. They begin to stutter gradually, as they imitated the speech manner of a stuttering relative.

The second subgroup includes (on evidence derived from our studies) 75% of all stutterers. These are children which were born with asphyxia neonatorum and/or took antibiotics. Due to sensitivity and “jitteriness” of these children some stressful events can provoke initiation of stuttering.

Finally, we distinguish three main risk factors for stuttering origin: stuttering in family, asphyxia neonatorum, and antibiotics. The three factors singly or in combination can serve a reason for stuttering initiation.

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