It was revealed that three genes controlling the level of dopamine in the brain are associated with the development of stuttering (D. Comings et al., 1996). They are also associated with hyperactivity syndromes,
attention deficit and Gilles de la Tourrette. However, the presence of these genes
alone is not enough for the development of stuttering. A starting factor is needed, often emotional stress. As a result, the interaction between the structures of the cortex and the subcortical structures is disturbed.
The occurrence of stuttering is also possible against the background of organic brain damage. Cases of stuttering due to hematoma in the right temporal lobe have been described (U. Hadar et al., 1991). When the damage is localized in the left hemisphere, apart from stuttering, patients may experience aphasia.
In patients with stuttering, even in the absence of an organic lesion of the central nervous system, changes in the regional blood supply to the brain are revealed, which, as a rule, are characterized by waviness and reversibility. Changes in the cerebral circulation take place not only during stuttering, but also with other neuroses, which disrupt the activity of nerve formations and play an important role in the pathogenesis of the disorders. During stuttering, a decrease in LMK was found in the structures responsible for fluency of speech — the left upper and middle temporal areas (BC Watson et al., 1992). However, other authors did not reveal LMK changes in patients with stuttering in the absence of speech stress (R. Ingham et al., 1996).