Neurological Incidents May Cause stuttering

By Per Alm, Ph.D.
Lund University, Sweden,
and The Stuttering Information Center of Denmark

alt textFrom the Stuttering Foundation's winter 2008 newsletter

Several studies of heredity and genetics have shown that genes play an important role in the causal background of stuttering. In addition, these studies have shown that non-genetic factors also play a significant role. The nature of these non-genetic factors has been obscure. However, there is mounting evidence indicating that some early neurological incidents may contribute to the risk for development of stuttering.

Higher frequency of early incidents in cases without stuttering relatives
One way to find indications about non-genetic factors is to compare groups of stuttering persons with and without stuttering relatives. An early study of this type was performed by Robert West and coworkers (1939), comparing two groups of about 100 stuttering persons each, with and without stuttering relatives. The result indicated that several background factors were more common in the group without stuttering relatives, for example infectious disease, diseases of the nervous system, injuries, and surgery.

The same tendency was found in a more recent study, by Poulos and Webster (1991). Early incidents were reported in 21 of 57 cases without family history of stuttering, to be compared with only 3 out of 112 cases with stuttering relatives. Most of these factors were physical, such as head injury or birth complications, but also three cases of intense fear were included.

Prevalence of stuttering in groups with early neurological incidents?
Another way to investigate this question is to study groups with suspected neurological incidents. B-hme (1968) investigated a group of 802 children and adults with supposed cerebral lesions, related to early adverse events. According to this report the prevalence of stuttering was surprisingly high. In the group with normal intelligence 24% were diagnosed as stuttering. Interestingly, the prevalence of stuttering was lower in groups with impaired intelligence, with only 2.4% in the group regarded to have the lowest intelligence. Some specific risk factors mentioned were concussion, with stuttering in 6 out of 11 cases, and premature birth with forceps delivery, with stuttering in 5 out of 5 cases.

A possible relation between concussion and stuttering was also reported by Segalowitz and Brown (1991). In a survey of high-school students 16% of 607 nonstuttering adolescents reported head injury with unconsciousness, to be compared with 6 of the 9 stuttering students in this survey (i.e., 67%). The frequency of all reported head injuries, also without unconsciousness, was 30% in the nonstuttering group, in contrast to 8 out of 9 stuttering students.

New study in Sweden
New data regarding the role of early neurological incidents comes from a study of stuttering adults, at Lund University, Sweden, recently published in Alm and Risberg (2007). In this study background factors and heredity were analyzed in relation to childhood traits of attention deficits, using a questionnaire for retrospective diagnosis of childhood ADHD or ADD (Attention Deficit Hyperactivity Disorder or Attention Deficit Disorder, without hyperactivity). The questionnaire was a subset of the Wender Utah Rating Scale (WURS).

Of the 32 stuttering adults 41% showed childhood ADHD/ADD scores above the maximum score for the control group. The high scores were related to the following aspects, in descending order: (a) being inattentive, daydreaming; (b) being tense, restless; (c) concentration problems, easily distracted; (d) tendency to be or act irrationally; (e) anxious, worrying; (f) hot- or short-tempered, low boiling point; (g) acting without thinking, impulsive. However, most of the stuttering cases had scores below the level for diagnosis of ADHD, meaning that they showed some traits of ADHD or ADD but should not be regarded as having this diagnosis.

When splitting the stuttering group into two halves, with low versus high scores for childhood attention deficits, it was clear that early neurological incidents were more common in the high-ADHD-group. The following list is a comparison of various background factors in the group with high versus low ADHD/ADD scores (n = 16 in both groups)- 

a) Premature birth, average two months: 3 versus 0 persons.

b) Other birth complications: 4 versus 1 person.

c) Head injury, resulting in unconsciousness or medical care: 6 versus 1 person.

The high and low ADHD groups also differed with regard to heredity: 13 cases showed "only heredity", i.e., they had at least one stuttering relative but no report of early incidents. Eleven of these 13 cases were found in the low-ADHD/ADD-group. In contrast, 7 cases showed "only neurological incidents", i.e., no report of stuttering relatives but reports of early physical incidents. Six out of these 7 cases were found in the high-ADHD/ADD-group.

The link between traits of ADHD and the background factors indicates that these traits were not secondary effects of the stuttering, but rather direct neurological effects of the background factors. However, it should be noted that traits of ADHD often are genetically transmitted, and results from Oyler (1994) indicate that such traits in stuttering children may well be familiar. In other words, traits of attention deficits in stuttering children should not be regarded as indications of neurological incidents.

What does "neurological incidents" imply?
If early neurological incidents are a factor behind some cases of stuttering, what does this imply with regard to possible cerebral lesions? It is known that early neurological incidents may result in attention deficit problems, related to the basal ganglia system and the frontal lobe. Some of the incidents discussed above were premature birth, birth complications, and concussion. Both premature birth and birth complications are often related to hypoxia. The effects of hypoxia depend on several factors, such as the degree, duration, if it is intermittent or not, etc. The effects may be subtle, for example affecting the dopamine system and resulting in loss of neurons within the basal ganglia. In fact, the high content of dopamine seems to make basal ganglia neurons especially sensitive to hypoxia. There are indications that males may be more sensitive to early hypoxia than females. Also concussion resulting in unconsciousness might have subtle effects in this region of the brain, because of forces in the upper part of the brain stem. In general, it seems as if lesions related to stuttering typically do not affect intelligence.

In summary, this study supports previous studies reporting higher frequency of early neurological incidents in a stuttering group without stuttering relatives.

Furthermore, the results indicate that these early incidents often result in mild traits of attention deficits. This association further strengthens the likelihood that early neurological incidents actually have a causal role in a substantial subgroup of developmental stuttering. The data from the recent study also suggest that genetic factors and early neurological incidents may have an additive effect. If this is the case, one would expect to find a continuum between two hypothetical extreme groups with "pure" genetic stuttering versus "pure" neurological incidents.

The factors discussed above relate to the biological basis for stuttering. The possible influence of the psychosocial environment during upbringing remains to be established.

There is a need for continued studies in this area, especially looking at stuttering children and the risk for persistence of stuttering.

Alm, P.A. & Risberg, J. (2007). Stuttering in adults: The acoustic startle response, temperamental traits, and biological factors. Journal of Communication Disorders, 40, 1-41.
B??hme, G. (1968). Stammering and cerebral lesions in early childhood. Examinations of 802 children and adults with cerebral lesions. Folia Phoniatrica, 20, 239-249.
 Oyler, M. E. (1994). Vulnerability in stuttering children. Doctoral dissertation, University of Colorado. UMI Microform, No. AAT9602431.
Poulos, M. G. & Webster, W. G. (1991). Family history as a basis for subgrouping people who stutter. Journal of Speech and Hearing Research, 34, 5-10.
Segalowitz, S. J. & Brown, D. (1991). Mild head injury as a source of developmental disabilities. Journal of Learning Disabilities, 24, 551-559.
West, R., Nelson, S., & Berry, M. (1939). The heredity of stuttering. Quarterly Journal of Speech, 25: 23-30.

Editor's Note: Given Dr. Alm's data and speculation, would we expect to see more stuttering in football players, boxers and soccer players (the latter hitting the ball with their head), especially if these sports were begun early in life.  And what about all those knocks on the head most of us experienced as children, why aren't more of us stuttering? These and related issues seem like intriguing possibilities requiring further study.