-Juvenile myoclonus epilepsy (JME) is a common epileptic syndrome, the etiology of which is genetically determined. Its onset occurs from 6 through 22 years of age, and affected patients present with myoclonic jerks, often associated with generalized tonic-clonic seizures -the most common association -and absence seizures. JME is non-progressive, and there are no abnormalities on clinical examination or intellectual deficits. Psychiatric disorders may coexist. Generalized polyspike-and-waves are the most characteristic electroencephalographic pattern. Usual neuroimaging studies show no abnormalities. Atypical presentations should be entertained, as they are likely to induce misdiagnosis. Prevention of precipitating factors and therapy with valproic acid (VPA) are able to control seizures in the great majority of patients. Whenever VPA is judged to be inappropriate, other antiepileptic drugs such as lamotrigine may be considered. Treatment should not be withdrawn, otherwise recurrences are frequent.KEY WORDS: juvenile myoclonic epilepsy, diagnosis, etiology, treatment. Epilepsia mioclônica juvenilRESUMO -A epilepsia mioclônica juvenil é uma síndrome epiléptica comum, cuja etiologia é fundamentada na genética. Inicia-se entre 6 e 22 anos e os indivíduos apresentam mioclonias, que podem ser acompanhadas por crises tônico-clônicas generalizadas -associação mais comum -e crises de ausência. A doença não é progressiva, e não há alterações detectáveis no exame físico ou déficits intelectuais. Distúrbios psiquiátri-cos podem coexistir. Polipontas-ondas lentas generalizadas constituem o padrão eletrencefalográfico ictal típico. Não há anormalidades em exames de imagem convencionais. Apresentações atípicas devem ser consideradas, pois predispõem a erros de diagnóstico. A prevenção de fatores desencadeantes e o uso de áci-do valpróico (VPA) controlam as crises epilépticas na grande maioria dos casos. Quando o VPA é inapropriado, outras drogas como a lamotrigina podem ser utilizadas. O tratamento não deve ser interrompido, visto que as recidivas são freqüentes.

We studied the influence of attention on the timecourse of Stroop-like conflict. Thirty-two volunteers performed a Stroop matching task in which they had to compare either the color (n = 16) or meaning (n = 16) of two stimuli. The first stimulus was always a color-name printed in yellow, red, or blue (i.e., Stroop stimulus), and the second stimulus was either a color-bar (Experiment 1) or color-word in white ink (Experiment 2). Stimulus onset asynchrony (SOA) was varied parametrically. Interference by incongruent Stroop stimuli was clearly modulated by SOA manipulation in both cases. The results are discussed in terms of interactions between translational and attentional models in which the degree of Stroop-like interference is attributed to time implementation of attentional mechanisms during color-to-color and color-to-word matching contexts.

Using a Stroop matching task, we evaluated how alcohol affects the time needed to overcome Stroop conflict and whether practice might reverse the effect of alcohol. Participants (n = 16) performed two sessions in which they had to compare the color of a color-word with the meaning of a color-word in neutral color. The two task stimuli were presented simultaneously or with a Stimulus Onset Asynchrony (SOA) of 200, 500, or 800 ms. For half of the subjects, alcohol was administered in the first session, and for the other half, alcohol was administered in the second session. The results showed that the Stroop effect was significant at the 0 and 200 ms intervals in the sober subjects. Moreover, in untrained intoxicated individuals, interference endured until the 500 ms interval, a result that was abolished in trained intoxicated subjects. In conclusion, alcohol increased the time needed for Stroop matching task conflict resolution. However, this deleterious effect was minimized by a previous practice session.