The Paris Conference on the Neural Bases of Stuttering took place on 16th May 2008. Prof. Henny-Annie Bijleveld, who was one of the presenters, reports on the event.
The conference was dedicated to brain research and physiological aspects of stammering. A large panel of leading researchers in this field came to Paris to discuss the latest findings. The conference was organised by Anne-Lise Giraud and Christian Kell (Inserm-Paris), and was supported by the French stuttering association APB (Association parole-bégaiement).
All the papers pointed to the same key theme: typical differences in brain functioning of people who stammer, as based on neuroimaging studies. Ludo Max, for example, showed that people who stammer were slower in learning sensorimotor processing and execution of voluntary movements.
Sou-Eun Chang pointed to differences in white matter in the brain as a 'trait-related deficit' that may be related to the basis of developmental stammering. 'Trait-related' means something is inherent to the person, as opposed to 'state-related' where it is provoked by external factors such as stress, anxiety, or time pressure. Anne Foundas, on the other hand, suggested a 'state-related' approach - atypical brain activation may represent a 'predisposition' with which speech-language, and environmental variables interact to give rise to stammering. Different subgroups of people who stammer could respond to different therapies.
Brain research reveals the complexity of brain activity and the difficulty of interpreting results. This was made clear by Christy Ludlow who pointed to the fact that stammering often occurs together with other disorders. A genetic predisposition affecting brain development and cell migration would be one element in the complex of stammering.
Typical brain differences were also revealed by the research of R. Salmelin, who showed that people who stammer had different brain activation, even when speaking fluently. The problem with this sort of research is that it is based on the production of single words, not on conversational speech - and we know that stammering mainly occurs in conversational speech, during communication.
K. Watkins' study on abnormal activities during speech production in motor, premotor and prefrontal cortices and in the cerebellum of people who stammer, points to excessive dopamine production through abnormal functioning of the 'cortico-striatal-thalamocortical loops' in the brain of those who stammer. This was previously demonstrated by Alm (2004).
Christian Kell returned to an old and important element in therapy: the impact of rhythm and intonation in behavioural therapies. He showed that part of the brain called the Brodmann area 47/12 (left posterior orbitofrontal cortex) is involved in executive control of rhythm and has a connection to the basal ganglia. There is strong evidence of the role of the basal ganglia and dopamine in the process of stammering. Research is now being undertaken to examine its role in detail (Per Alm, Katrin Neumann and myself)
All these studies revealed brain abnormalities - in white matter, in grey matter, in activation, in feedback, in sensorimotor system and in rhythmic control - in people who stammer. Nevertheless some qualifications should be mentioned:
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