Physiology Though neuroimaging studies have not yet found specific neural correlates, there is much evidence that the brains of adults who stutter differ from the brains of adults who do not stutter. Several neuroimaging studies have emerged to identify areas associated with<unk> . In general, during<unk> , cerebral activities change dramatically in comparison to silent rest or fluent speech between people who stutter and people who do not. There is evidence that people who stutter activate motor programs before the articulatory or linguistic processing is initiated. Brain imaging studies have primarily been focused on adults. However, the neurological abnormalities found in adults does not determine whether childhood<unk>  caused these abnormalities or whether the abnormalities cause<unk> . 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 overactivation in the cerebrum and cerebellum, and relative deactivation of the left hemisphere auditory areas and frontal temporal regions. 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 did 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 stutterers also first had cortical activation in the occipital areas but the left inferior-frontal regions were activated only after the motor and premotor cortices were activated. During speech production, people who stutter show overactivity in the anterior insula, cerebellum and bilateral midbrain. They show underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl's gyrus in the left hemisphere. Additionally, speech production yields underactivity in cortical motor and premotor areas. Abnormal lateralization Much evidence from neuroimaging techniques has supported the theory that the right hemisphere of people who stutter interferes with left-hemisphere speech production. Adults who stutter have anatomical differences in gyri within the perisylvian frontotemporal areas. A large amount of white matter is found in the right hemisphere of the brain, including the region of the superior temporal gyrus. This was discovered using voxel-based morphometry (VBM). On the other hand, lesser amounts of white matter are found in the left inferior arcuate fasciculus connecting the temporal and frontal areas in<unk>  adults. Results have shown that there is less coordination between the speech motor and planning regions in the brain's left hemisphere of men and women who stutter, when compared to a non-stuttering control group. Anatomical connectivity of the speech motor and planning regions is less vigorous in adults who stutter, especially women. Men who stutter seem to have more right-sided motor connectivity. On the other hand,<unk>  women have less connectivity with the right motor 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<unk>  subjects, while post-rolandic regions are relatively inactive. Bilateral increases and unusual right-left asymmetry has been found in the planum temporale when comparing people who stutter and people who do not. These studies have also found that there are anatomical differences in the Rolandic operculum and arcuate fasciculus. Denis Drayna suggests that brain imaging studies of people who stutter do not tell if the differences in the brain anatomy caused<unk>  or if they are the effect of<unk> ;In the mouse model for<unk>  created by Drayna and team, they noticed significant similarities between the vocalizations in mice (carrying GNPTAB mutation) and human<unk> . Researchers investigated the brain tissue from the mice mutants and reported a significant decrease in the number and density of astrocytes in their corpus callosum. Astrocyte is a star-shaped cell in the brain that supports the nerve cells by supplying oxygen and nutrients, and taking away the waste. The corpus callosum enables the communication between the left and right hemispheres of the brain. Follow-up experiments with the GNPTAB mutation introduced to brain cell types showed that the vocalization defects in mice were specific to the loss of astrocytes. Mice did not show<unk> -like vocalization defects when the mutation is engineered to other brain cell types. Other anatomical differences The corpus callosum transfers information between the left and right cerebral hemispheres. The corpus callosum, rostrum, and the anterior mid-body sections are larger in adults who stutter as compared to normally fluent adults. This difference may be due to unusual functions of brain organization in<unk>  adults and may be a result of how the<unk>  adults performed language-relevant tasks. Furthermore, previous research has found that adults who stutter show cerebral hemispheres that contain uncommon brain proportions and allocations of gray and white matter tissue. Dopamine Recent studies have found that adults who stutter have elevated levels of the neurotransmitter dopamine, and have thus found dopamine antagonists that reduce<unk>  (see anti-stuttering medication below). Overactivity of the midbrain has been found at the level of the substantia nigra extended to the red nucleus and subthalamic nucleus, which all contribute to the production of dopamine. However, increased dopamine does not imply increased excitatory function since dopamine's effect can be both excitatory or inhibitory depending upon which dopamine receptors (labelled D1 – D5) have been stimulated.
Stuttering
Hoarse voice
Drooling
Spasmodic dysphonia
Stilted speech
Facial toning
Kussmaul breathing
Sleepwalking