Neuroimaging of Developmental Stuttering in Adults
Several neuroimaging studies have emerged in order to identify areas associated with stuttering. Brain imaging studies have primarily been focused on adults. In general, during stuttering, cerebral activities change dramatically in comparison to silent rest or fluent speech between people who stutter and people who do not stutter.
Studies utilizing positron-emission tomography (PET) have found during tasks that invoke disfluent speech, people who stutter show hypoactivity in cortical areas associated with language processing, such as Broca’s area, but hyperactivity in areas associated with motor function. One such study that evaluated the stutter period found that there was over activation in the cerebrum and cerebellum, and relative deactivation of the left hemisphere auditory areas and frontal temporal regions.
In non-stuttering, normal speech, PET scans show that both hemispheres are active but that the left hemisphere may be more active. By contrast, people who stutter yield more activity on the right hemisphere, suggesting that it might be interfering with left-hemisphere speech production. Another comparison of scans anterior forebrain regions are disproportionately active in stuttering subjects, while post-rolandic regions are relatively inactive.
Functional magnetic resonance imaging (fMRI) has found abnormal activation in the right frontal operculum (RFO), which is an area associated with time-estimation tasks, occasionally incorporated in complex speech.
Researchers have explored temporal cortical activations by utilizing magnetoencephalography (MEG). In single-word-recognition tasks, people who do not stutter showed cortical activation first in occipital areas, then in left inferior-frontal regions such as Broca’s area, and finally, in motor and premotor cortices. The people who stutter also first had cortical activation in the occipital areas, but, interestingly, the left inferior-frontal regions were activated only after the motor and premotor cortices were activated.
It is important to note that the neurological abnormalities found in adults does not conclude if childhood stuttering caused these abnormalities or if the abnormalities cause stuttering. Future research should address a longitudinal case study to track the development of brain structure in relation to stuttering.
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