Abstract
Stuttering is a disorder characterized by intermittent loss of volitional control of speech movements. This hypothesis and theory article focuses on the proposal that stuttering may be related to an impairment of the energy supply to neurons. Findings from electroencephalography (EEG), brain imaging, genetics, and biochemistry are reviewed: (1) Analyses of the EEG spectra at rest have repeatedly reported reduced power in the beta band, which is compatible with indications of reduced metabolism. (2) Studies of the absolute level of regional cerebral blood flow (rCBF) show conflicting findings, with two studies reporting reduced rCBF in the frontal lobe, and two studies, based on a different method, reporting no group differences. This contradiction has not yet been resolved. (3) The pattern of reduction in the studies reporting reduced rCBF corresponds to the regional pattern of the glycolytic index (GI; Vaishnavi et al., 2010). High regional GI indicates high reliance on non-oxidative metabolism, i.e., glycolysis. (4) Variants of the gene ARNT2 have been associated with stuttering. This gene is primarily expressed in the brain, with a pattern roughly corresponding to the pattern of regional GI. A central function of the ARNT2 protein is to act as one part of a sensor system indicating low levels of oxygen in brain tissue and to activate appropriate responses, including activation of glycolysis. (5) It has been established that genes related to the functions of the lysosomes are implicated in some cases of stuttering. It is possible that these gene variants result in a reduced peak rate of energy supply to neurons. (6) Lastly, there are indications of interactions between the metabolic system and the dopamine system: for example, it is known that acute hypoxia results in an elevated tonic level of dopamine in the synapses. Will mild chronic limitations of energy supply also result in elevated levels of dopamine? The indications of such interaction effects suggest that the metabolic theory of stuttering should be explored in parallel with the exploration of the dopaminergic theory.
Highlights
IntroductionResearch on the neurological underpinnings of stuttering has made remarkable progress over the last two decades; yet, our understanding of the nature and mechanisms of the disorder can still be described as fragmentary, with a range of proposed theories
The main converging result was that all studies showed lower beta power compared with controls, and the overall tendency appeared to be a reduction of EEG power from the alpha band and higher, and some increase of power in the delta band
There was no statistically significant difference between the groups, and all the stuttering children were within the same range as the control children. These results indicate that the level of peripheral dopamine is normal in most cases of stuttering
Summary
Research on the neurological underpinnings of stuttering has made remarkable progress over the last two decades; yet, our understanding of the nature and mechanisms of the disorder can still be described as fragmentary, with a range of proposed theories. The present hypotheses and theory article was written as part of a series of articles aiming to analyze and integrate research findings on stuttering to date. The second article was a more general review of the anatomy and functions of the dopamine system, and the mechanisms for the automatization of movement sequences, in particular in relation to speech and stuttering (Alm, unpublished manuscript). The aim of the present article is to review and discuss indications that stuttering is related to the supply of energy to neurons. The article begins with a brief review of the energy metabolism in the brain, followed by a discussion of the findings and observations related to stuttering and cerebral metabolism, primarily considering the electroencephalography (EEG) power spectrum at rest, brain imaging of the cerebral blood flow at rest, genetics, and biochemical measures
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