Genetics or Neurological Compromise in People Who Stutter
Edited from Per Alm, 2007
By Glyndon Riley
Leading researchers in stuttering over the last 70 years have suggested two types of vulnerability to develop stuttering, (1) a history of stuttering in close relatives and (2) a history of neurological compromise due to low birth weight, concussions, etc. West, Nelson, and Berry (1939), Bohme (1968), and Poulos and Webster (1991) are examples of studies that investigated the two types of vulnerability.
Alm (2007) divided 32 adults who stutter into a two groups, “High” and “Low” attending disorders (ADHD) based on there clinical symptoms. He determined the hereditary and neurological history of each person. He found that “it was clear that early neurologal incidents were more common in the high-ADHD group.” Premature birth, other birth complications, and head injury were higher (please see Table 1).
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Table 1. History of Neurological Incidents in Adults Who Stutter with High vs Low ADHD scores.
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Group Premature birth Other birth Head “injury”
complications complications
___________ _______________ ____________ ___________
High-ADHA 3 4 6
N = 16
Low-ADHD 0 1 1
N = 16
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High vs. low-ADD are strongly related to “only heredity” and “only neurological incidents.”
Most of the heredity subjects were in the low-ADD group while most of the neurological incident subjects were in the high-ADD group (please se Table 2).
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Table 2. Distribution of “Heredity only” and “Neurological incidents only” Subjects in the High-ADD and Low ADD groups. Total sample = 32.
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Group Heredity only Neurological incidents only
N = 13 N = 7
_________ ___________ ______________________
High-ADD 1 6
Low-ADD 11 1
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The medical literature describes neurological incidents related to ADHD that involve problems in the basal ganglia and frontal lobe. Anoxia (reduced oxygen to the brain) is
common during birth complications and may affect the dopamine system and reduce the efficiency of the speech motor functions that are controlled partially by the basal ganglia.
Wu, Maguire, Riley, et al (1997) reported that a group of adults who stutter had 50% to 300% more dopamine in the basal ganglia than a group of controls. This excess dopamine could be related to childhood neurological incidents or to heredity. Alm concludes, “The data from the recent study suggest that genetic factors and early neurological incidents may have an additive effect … one would expect to find a continuum between two hypothetically extreme groups with ‘pure’ genetic stuttering and ‘pure’ neurological incidents.”
Certainly, more of this type of research is needed.
References
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.
Bohme, G. (1968). Stammering and cerebral lesions in early childhood. Examinations of 802 children and adults with cerebral lesions. Folia Phoniatrica, 20, 239-249.
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.
West, R., Nelson, S., & Berry, M. (1939). The heredity of stuttering. Quarterly Journal of Speech, 25, 23-30.
Wu, J.C., Maguire, G.A., Riley, G.D., Lee, A., Keator, D., Tang, C., Fallon, J. & Najafi, A. (1997). Increased dopamine activity associated with stuttering. Neuroreport, 8, 767-770.
Recent developments in stuttering
There is a growing trend to view stuttering from a medical perspective.
* Evidence that stuttering has a strong genetic component is persuasive to most researchers and to people who stutter PWS). The pair-wise concordance rate for stuttering at 60% is above the 50% rate for schizophrenia.
* The idea that hemispheric differences exist between PWS and those who don’t has been studied for many years using a variety of methods. Recent studies using brain imaging techniques such as PET scans have added specific evidence for these differences. Taken together these recent studies produce similar but not identical evidence that PWS have activation in the left primary speech motor areas or increased activation in similar areas in the right hemisphere.
* The basal ganglia seems to play an important role in many but probably not all PWS. Reduced efficiency in areas of the basal ganglia such as the caudate, putamin, and thalamus appear to interfere with important speech timing functions related to fluent speech. Excessive dopamine may contribute to this reduced function so some researchers have tried dopamine blocking medications to reduce stuttering. Such medications seem effective in more than half of the PWS who have participated in clinical trials.
Suggested Readings:
Alm, P.A. (2004). Stuttering and the basal ganglia circuits: A critical review of possible relations. Journal of Communication Disorders, 37, 325-369.
Curlee, R.F. & Siegel, G.M. (1997). Nature and treatment of stuttering (2nd ed.). Boston: Allyn and Bacon.
Riley, G., Maguire, G., Franklin, D., & Ortiz, T. (2001). Medical perspectives in the treatment of stuttering. Contemporary Issues in Communication Science and Disorders, 28, 104-110.
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