In the last episode, I discussed how the authors of a paper on the neurology of stuttering were trying to use a model of normal speech control created by Jurgens to describe and explain stuttered speech. This led to the authors concluding that stuttering was primarily caused by brain “structural and functional abnormalities,” (disordered cerebral dominance seemed to be favored) while granting that there may be “psychological” and “emotional” factors that may be treated. According to the authors, the “most exciting explanation” was a theory of “delayed cerebral maturation” proposed by Ozge (2004), (a not-very-promising cul de sac.)
So, why is the Jurgens model important? Simply that it’s being used to guide a lot of stuttering research efforts, in particular, brain scanning studies.
Meanwhile, on the edges of Jurgens’ box are some very important systems and structures that the authors virtually ignore in their conclusions, including 1) auditory input, 2) proprioceptive input, 3) the anterior cingulate cortex, and 4) the periaqueductal gray (PAG). These are all elements of speech generation that are capable of transmitting disruptive or inhibitive inputs from the brains emotional/attention system to the speech system that comprises the Jurgens model. In fact, Jurgens himself discussed these elements in a presentation to the NIH which raised the (apparently, long forgotten) possibility that the amygdala, hippocampus, PAG, and anterior cingulate cortex are importantly involved in stuttered speech.
(This is not to say that the speech system of people who stutter (the “box”) is free from defects. It’s just that the violent nature of a lot of stuttering behavior is difficult to square with the relatively minor differences in the neurological performance of PWS when they are not stuttering, or those who are in recovery — without brain surgery, gene therapy, drugs, or stuttering inhibition aides. Or the lack of significant differences in many other activities.)
The stuttering research community steadfastly refuses to acknowledge that emotion is not a peripheral concern when it comes to stuttering, but is an integral part of the disorder. Indeed, since emotion is — in the broadest sense — a system for warning life forms the something is wrong and needs to be attended to, it can be argued that the reaction to speech disruption (i.e., stuttering) IS ITSELF an emotion.
This refusal has resulted in the inability of stuttering researchers to actually address the disorder. Instead, we have scores of papers characterising stuttering behavior by comparing it to fluent speech; earnest research efforts to analyze the types of words, phrases, and sentences that people might stutter on; quasi-phrenological studies of the shapes of brains of people who stutter; and tautological brain scan research that concludes: “that brain is sure not working properly when he stutters!”
Fortunately, there is reason for hope. At the conclusion of Dr. Dennis Drayna’s recently published talk on his team’s recent discovery of three gene mutations associated with stuttering, he notes that an analysis of gene expression for the resulting lysosomal mutations fingered the hippocampus.
The hippocampus, a brain structure that is not usually thought of as part of the “speech system,” but is part of a circuit associated with conditioning, emotional memories (particularly of places and situations), proprioceptive awareness, and epileptic seizures and motoric freezing, among a host of other behaviors.