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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).

Table 1. History of Neurological Incidents in Adults Who Stutter
with High vs Low ADHD scores.

Group     Premature birth complications Other Birth Complications Head "injury"


3 4 6
0 1 1

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 see Table 2).

Table 2.  Distribution of “Heredity only” and “Neurological incidents only”
Subjects in the High-ADD and Low ADD groups.  Total sample = 32.

Group     Heredity only
Neurological incidents only


1 6
Low-ADD 11 1

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.


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.


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