UNDERSTANDING STUTTERING What causes stuttering?


Presumably, anyone who stutters has reflected on the reasons why he or she is a person who stutters. A common experience is that the ability to speak fluently varies a lot between situations, or between days. I have often met with the reasoning that because the speech is fluent at times, there cannot be anything physically wrong, it must be psychological. It is easy to see that the assumptions we make about the causes of stuttering will have a fundamental influence on how we approach therapy, but also for the identity and self-understanding of the persons who stutter. Likewise, it will affect how stuttering is viewed and portrayed by society in general.


One perspective that has come and gone, and come back again, is that stuttering should be viewed as variation within the normal range of diversity. This was a widespread view in the early 1980s in Scandinavia, based on influences from North America. More recently similar views have been put forward, linked to the neurodiversity movement. In this movement a ‘medical model’ is contrasted with a ‘social and relational model’ (Constantino, 2018). My personal view is that these two perspectives should not be incompatible. On the one hand, if progress in research makes it possible to improve actual speech fluency, it would be unethical to withhold such options, in particular from children. Stuttering can definitely imply a real difficulty with communication. On the other hand, a society accepting of diversity can be a good place to live for everyone.


As a person who stutters, my wondering about the nature of stuttering gradually turned into my work. It started with the assumption that any explanation of stuttering must include the functions of the brain, leading to the combination of psychology, medicine, and speech science. It is clear that the complexity of stuttering is such that no single method in itself will be able to capture its nature. For that reason, I have devoted a large part of my time to the detailed


14 by Per A. Alm, Ph.D.


study of the results from other researchers, in order to analyze and integrate their results into a, hopefully, coherent picture. Also, to integrate the results with the current general understanding of the brain and of physiology. The starting point for this type of work was in 2004, with an analysis of the possible role of the basal ganglia in stuttering (Alm, 2004). The pandemic resulted in more time for writing and publishing, generating three theory papers (freely available). I will briefly summarize them here.


In the first paper (Alm, 2020), it is argued that infections caused by Group A Streptococci (GAS) were a major, possibly the dominating, cause of stuttering, until the 1950s. This conclusion was based on (a) a large study of the medical history of stuttering children in the 1930s, showing a very high frequency of GAS infections before the onset of stuttering, compared with a control group; (b) a known mechanism, by which GAS can trigger an autoimmune reaction against the basal ganglia; and (c) a remarkable reduction in the number of stuttering children in US schools, in parallel with the reduction of rheumatic fever, an autoimmune reaction caused by GAS (correlation r = 0.95). The decline was particularly marked during the decade after the introduction of penicillin in 1943. There are a few current case reports (e.g., Maguire et al., 2010), suggesting that the development of stuttering may be interrupted if the infection is detected and treated early. The current incidence of stuttering related to GAS is unknown; it is likely to be low, but existing. There are indications that some of these children show signs of ‘PANDAS,’ i.e., Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. This is a condition caused by GAS, likely affecting the basal ganglia, see the link to information from NIH


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