Imaging studies continue to show differences in the brains of people who stutter. This suggests that stuttering may be the result of a neurologic dysfunction in the areas of the brain that process and output speech.

A 1995 PET scan study by Fox and Ingham found that when nonstutterers spoke, brain activation was higher in the left hemisphere than in the right in areas that control the muscle movements necessary for speech -- and also in the auditory areas that process incoming language formation. In stutterers, however, this dominance occurred in the right hemisphere. This difference persisted even during chorus reading (which induces fluency in most stutterers). This suggests an inherent difference in the way nonstutterers and stutterers process and output language. (updated note, November 26, 2012: the study actually "showed induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system." Ref:

Ludlow and Braun of the National Institute of Deafness and Other Communication Disorders (NIDCD) have published similar findings. They also found that when stutterers speak, the left hemisphere language areas seem to be less active compared to nonstutterers even when stuttering is suppressed (e.g., by chorus reading). Ludlow said this means that we can't look on stuttering as simply a motor-control disorder, but as a more fundamental disorder of the brain's interface between language and speech. She said that recent findings lean her toward the idea that stuttering may be caused by the failure of the brain to develop normal left-hemispheric dominance for language.

(This is certainly not a new idea, and I've been espousing this idea as a likely candidate for the cause of stuttering for over twenty years. That is, that stutterers might have bilateral language areas [one in each brain hemisphere], in competition with each other, which could cause a "bottleneck" in speech production. Signals to initiate speech are sent from two separate brain areas to speech articulator muscles at the same time. The speech articulator muscles need one dominant or consolidated set of signals, but are bombarded with two in stutterers. The greater the bottleneck, the more severe the speech block and stutter. As I'm fond of saying, words must get out of the brain before they can get out of the mouth.)

What this also suggests is that the even when a PWS is fluent, as many are when choral reading, speaking alone or to a pet, the neurologic flaw is still there. Many PWS and speech-language pathologists (SLPs) hold the misguided notion that this situational fluency experienced by PWS indicates that stuttering must be due to psychologic or emotional causes. Such situational fluency indicates only that developmental stuttering is probably not caused by a lesion or overt damage as is acquired stuttering, which tends not to show such variability. I believe that this situational fluency (the Primary Paradox) experienced by PWS can be explained by my excitation feedback component of stuttering, which may be due to a flaw in the brain's limbic areas in PWS

Ludlow goes on to say that these newer studies lend support to the view that speech therapy should start as soon as a child shows signs of stuttering. Treating the problem early, when language function may be more malleable, holds the best chance of actually influencing language development.

Before the newer brain imaging studies came on the scene, two studies by Webster (1986, 1988) showed differences in bimanual handedness for stutterers compared to nonstutterers. This may reflect a conflict in interhemispheric communication expressed through tasks requiring the use of both hands. In 1986, Webster reported that distinct differences for stutterers while tapping with one hand and while at the same time doing another motor task with the other hand. In 1988, Webster used a task that required subjects to write letters bimanually. Stutterers wrote significantly more slowly than nonstutterers, made more mirror reversals of letters (particularly with the nonpreferred hand), and showed poor quality of letter formation. In a 1989 study, Webster and Vaughn had similar findings, including the finding that nonstutterers were slightly more lateralized in handedness.

In 1995, PET scan studies by Gerald Maguire (a psychiatrist at the University of California at Irvine and a PWS himself) and colleagues show that stuttering appears to be associated with decreased activity in several brain areas, including the left language circuit (Broca's and Wernicke's areas), higher order association areas (superior frontal cortex), right cerebellum, and the posterior cingulate (limbic system).

Many of these areas become more activated (closer to normal function) when PWS are induced to be fluent (e.g., by chorus reading).

But a persistent defect is found in the left caudate nucleus during both fluent and stuttered speech in PWS. The caudate nucleus is part of the basal ganglia, which controls complex voluntary movements such as those required for speech. The left caudate nucleus does not function at full capacity even when a PWS is fluent, but at only about 40-50% of normal.

Maguire thinks that when a PWS speaks fluently, he may be using alternate speech production pathways (rather than the pathway for the usual stuttered speech). He says, "For instance, with chorus reading, delayed auditory feedback, the Edinburg Masker, or singing, I believe we're bypassing that loop. Or somehow activating it just slightly."

The limbic system (posterior cingulate) is our emotional modulator. This is the brain area that controls what Maguire calls our "internal anxiety" level. He points out that this "internal" anxiety is not the same as the anxiety caused by external stresses such as asking for a raise or making an important speech. Our internal anxiety levels are not under voluntary control and we may not even be aware of them.

There's an inverse relationship. The less active the limbic system, the higher the internal anxiety level. The more active the limbic system, the lower the internal anxiety level. During stuttered speech, the limbic system of PWS is less active, which indicates higher internal anxiety. During fluent speech (e.g., during chorus reading), the limbic system of PWS is more active, which indicates a lower internal anxiety.

Maguire's "internal anxiety" is another term for my excitation feedback component of stuttering.

Another thing Maguire found is that the substantia nigra area in the brain is slightly overactive when PWS speak fluently when compared to nonstutterers. He postulates that this area might be overcompensating and bypassing the caudate nucleus defect somehow.

In fact, one of Dr. Maguire's latest research projects is to examine the dopaminergic role of the substantia nigra. It's thought that dopamine levels in certain brain areas are too high in PWS. He plans to use a newer drug called risperidone -- similar to haloperidol -- but with less potential to cause serious side effects. Like haloperidol, risperidone antagonizes the effect of dopamine.

Maguire also studied the effects of nimodipine on stuttering. Nimodipine is a calcium-blocker similar to verapamil, but with more specific effects in the brain. A third of PWS taking nimodipine showed improvement and none of the PWS on placebo (inactive agent) did. The findings suggest that nim= odipine may be effective for some PWS, but further study is needed.

Maguire commented on the speculation by some researchers that calcium-blockers like verapamil and nimodipine work by stopping or easing tremors or spasms in the vocal cords: "I know that stuttering is much more than just a spasm in the larynx. It's not just one muscle group. It's a coordination of all of it. It's got to be in the brain."

I think it's time that we clarify our nomenclature. Instead of using terms such as "mental illness" or "mental disorder" (and "psychologic" or "emotional" disorder), let's use a term more descriptive of a condition's biologic origin -- for example, "neurobiologic disorder." That term more readily indicates that the origin of the disorder is in the brain. This removes much of the stigma associated with conditions such as Tourette's, attention deficit hyperactive disorder (ADHD), obsessive-compulsive disorder (OCD), clinical depression -- and stuttering. These disorders could then be recognized as the "medical" conditions they are. Which would also translate into more research funding and medical insurance coverage. The specific name of the disorder could be attached, for example: neurobiologic disorder/depression, neurobiologic disorder/OCD, neurobiologic disorder/ADHD, neurobiologic disorder/stuttering, and so forth.

For more information on the brain basis of stuttering, click on neuropatterning for stutterers.