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In "Plastichnost e Strukturno-funccionalnaya Vzaimosvyaz Cory e Podkorkovikh Obrazovaniy Mozga" (Materials of the Brain Institute conference), 2003, p.65.
Electrophysiological indices of pathologic activity in stutterer's EEG.
Nabieva T.N.
Brain Institute of Russian Academy of Medical Sciences, 105064, per. Obukha 5, Moscow, Russia.
Objective study of stuttering pathogenesis is limited by electromyography, positron emission tomography, fMRI and electrophysiological investigations. Some data confirms the presence of pathologic paroxysmal activity in stutterers' central nervous system. Among the first was Schmoigl & Ladisich (1967) whom discovered slow paroxysmal activity (in 56% of all cases) and peak-wave complexes (6%) in stutterers' EEG. According to experimental data of Ivanov (1990), 39% of patient's demonstrated paroxysmal activity in background, 70% of stuttering participants had focus of polymorphous activity with prevalence of sharp waves, low oscillations, and "sharp wave-low wave" complexes in the area between parietal, temporal, and occipital regions of the right hemisphere. According to Lokhov's (1994) data, 33% of stuttering children demonstrated polymorphous picture of bioelectric activity with theta-wave predominance and a great deal of sharp waves in all leads. In an effort to investigate stuttering central mechanisms, we recorded electroencephalogram of 9 right-handed children with average stuttering of both sexes between the ages of 5 to 8. We revealed sharpened and disorganized alpha-rhythm; biphasic and threephasic sharp alpha-band waves and theta-band sharp wave groups were recorded in occipital and posterior temporal areas. In 6 cases we detected signs of pathological paroxysmal activity in the form of a great amount of sharp waves, "peak-waves" and "sharp wave-slow wave" complexes in all leads. Hyperventilation during 2 minutes resulted in strengthening of the local changes and disorganization of electric activity in all cases, as well as appearance in EEG of 5 participant's epileptiform activity in anterior and posterior leads. Mentioned phenomenon was not observed in healthy participants' EEG. Our investigation allows us to assert that the stutterers' EEG noticeably differs from the EEG of healthy persons by the presence of paroxysmal activity signs, both in background activity and after the hyperventilation.
Key words: stuttering, EEG, hyperventilation, stuttering pathogenesis mechanisms.
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