Thesis (M.S.)--Florida State University, 2005. / Advisor: Dr. Joseph K. Torgesen, Florida State University, College of Arts and Sciences, Dept. of Psychology. Title and description from dissertation home page (viewed June 16, 2005). Document formatted into pages; contains vi, 37 pages. Includes bibliographical references.

Thesis (M.A.) - Carleton University, 2007. / Includes bibliographical references (p. 163-170). Also available in electronic format on the Internet.

Thesis (M.A.) - Carleton University, 2007. / Includes bibliographical references (p. 124-126). Also available in electronic format on the Internet.

Title from first page of PDF document. Includes bibliographical references (p. 21-22).

Thesis (Specialist in Ed.)--Miami University, Dept. of Educational Psychology, 2005. / Title from first page of PDF document. Document formatted into pages; contains [1], v, 62 p. : ill. Includes bibliographical references (p. 43-45).

Thesis (Ph.D.)--Ohio University, June, 2006. / Includes bibliographical references (leaves 98-117)

Thesis (Ed. S.)--Miami University, Dept. of Educational Psychology, 2006. / Title from first page of PDF document. Includes bibliographical references (p. 35-39).

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 197-205).

Submitted by GABRIELA MELLONI ZUCULO null (gabriela.zuculo@gmail.com) on 2016-05-11T20:23:14Z No. of bitstreams: 1 DISSERTAÇÃO DEFESA GABRIELA ZUCULO PRONTO.pdf: 2423369 bytes, checksum: 1518ae3189c9a9ce35d3608fa0a5a980 (MD5) / Approved for entry into archive by Felipe Augusto Arakaki (arakaki@reitoria.unesp.br) on 2016-05-13T16:28:45Z (GMT) No. of bitstreams: 1 zuculo_gm_me_mar.pdf: 2423369 bytes, checksum: 1518ae3189c9a9ce35d3608fa0a5a980 (MD5) / Made available in DSpace on 2016-05-13T16:28:45Z (GMT). No. of bitstreams: 1 zuculo_gm_me_mar.pdf: 2423369 bytes, checksum: 1518ae3189c9a9ce35d3608fa0a5a980 (MD5) Previous issue date: 2016-04-19 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / As características comuns ao quadro do Transtorno do Espectro do Autismo (TEA) destacadas pelo DSM-5 são: déficit de comunicação, dificuldade em fazer amizades ou se relacionar, dependência de rotina, resistência a mudanças e obsessão por itens inapropriados. Tais comportamentos podem ser observados desde a infância, porém com variações em cada indivíduo, o que levou o TEA a ser considerado um “continuum” que varia de menos comprometido (leve) a muito comprometido (grave). Dentre a complexa sintomatologia do TEA nos diferentes graus destaca-se a alta prevalência de distúrbios de sono, com influência negativa nas alterações comportamentais, instabilidade de humor, déficits nas funções neurocognitivas, incluindo memória, atenção, criatividade verbal, flexibilidade cognitiva e raciocínio abstrato. Como possível causa dos distúrbios de sono nessa população, está o déficit na produção de melatonina, hormônio que tem dentre suas funções a modulação da qualidade do sono. Com o intuito de fornecer dados para futuros tratamentos visando à melhora da qualidade de vida de indivíduos com TEA, esse estudo teve como objetivo investigar parâmetros de ritmo sono-vigília, aspectos comportamentais e de fluência verbal, antes e após o uso de melatonina exógena em indivíduos com TEA leve. Indivíduos com TEA leve de ambos os gêneros, de 7 a 18 anos, foram avaliados por meio da Escala de sono para crianças (EDSC), actigrafia, Child Behavior Checklist (CBCL) e Teste de fluência verbal fonêmica antes e após o uso oral de melatonina (3mg). A análise estatística descritiva foi feita a partir da média e erro padrão da média ou do percentual nos diferentes parâmetros e a análise estatística inferencial foi feita a partir do teste Anova com o teste de Tukey (pós-teste) e o teste de correlação de Spearman. Os resultados mostraram que 55,5% dos participantes com TEA leve apresentam indicativo de ao menos um distúrbio de sono, sendo os maiores percentuais encontrados em distúrbios de hiperidrose de sono, distúrbios respiratórios de sono e distúrbios de início e manutenção de sono. O grupo que recebeu melatonina apresentou os menores percentuais de distúrbios de sono com exceção do distúrbio de hiperidrose do sono. A análise da actigrafia mostrou que: o grupo TEA leve melatonina apresentou maior tempo total de sono em comparação aos outros grupos. Houve divergência sobre o ritmo atividade-repouso entre os parâmetros de fragmentação e amplitude do ritmo, sendo encontrado que o grupo TEA leve melatonina apresentou: ritmo menos fragmentado segundo o Aczcm e o IVm; e maior amplitude de ritmo segundo RAd e menor amplitude de ritmo segundo Sumpim. Os resultados do inventário de comportamento indicaram que as crianças com TEA leve apresentam os maiores escores classificados como clínico em problemas de pensamento, ansiedade, retraimento, comportamentos internalizantes e comportamentos externalizantes. O grupo que recebeu melatonina apresentou menores percentuais de escores classificados como clínico pelo inventário CBCL. A média de acertos no teste de fluência verbal fonêmica no grupo TEA leve foi de 13,9 ± 1,6. Quando separado por letras, o resultado foi P= 5,4 ± 0,7, T= 4,3 ± 0,5, L= 4,6 ± 0,6. Houve correlação entre os distúrbios totais de sono e os problemas somáticos de comportamento apresentados pelo grupo TEA leve. Estes dados mostram que crianças com TEA leve apresentam alta incidência de distúrbios de sono assim como no TEA sem especificação de grau, porém em menor escala. Estes distúrbios afetam aspectos comportamentais destas crianças e o tratamento com melatonina pode levar a melhora deste quadro. A fluência verbal de crianças com TEA grau leve é similar a de crianças com desenvolvimento típico. / The features common to the ASD highlighted by the DSM-5 are: communication deficit, difficulty making friends or relating, routine dependence, resistance to change, inappropriate items obsession. Such behavior can be verified since childhood, but with individual variations, which led the ASD to be considered as a "continuum" ranging from less committed (mild) to very committed (serious). Among the complex symptoms of ASD there is the high prevalence of sleep disorders, with a negative influence on behavioral changes, mood instability, deficits in neurocognitive functions including memory, attention, verbal creativity, cognitive flexibility and abstract reasoning. As a possible cause of sleep disorders in this population is the deficit of the melatonin production, hormone that modulates the sleep quality. In order to collaborate with future treatments that improving the life quality of ASD individuals, this study aimed to investigate parameters of sleep wake rhythm, behavior and verbal fluency before and after exogenous melatonin use in mild ASD individuals. For this, mild ASD individuals of both genders, 7-18 years were assessed by Sleep Disturbance Scale for Children (SDSC), actigraphy, Child Behavior Checklist (CBCL) and phonemic verbal fluency test before and after oral melatonin (3 mg). Descriptive statistical analysis was analyzed by mean and standard error or by percentage of the different parameters and inferential statistical analysis was performed by ANOVA with Tukey test (post-test) and Spearman correlation test. The results showed that 55,5% of mild ASD participants showed at least one sleep disorder, with the highest percentages found in sleep hyperhidrosis, sleep-breathing disorders and disorders of initiating and maintaining sleep. The group receiving melatonin had the lowest percentage of sleep disorders with the exception of sleep hyperhidrosis disorder. The actigraphy showed that: the mild ASD melatonin group showed higher total time of sleep than other groups. There was disagreement about between fragmentation parameters and amplitude of the activity-rest rhythm, since was found that the group of mild ASD melatonin showed: less fragmented rhythm according to Aczcm and IVm; and greater amplitude following Rad and lower amplitude rhythm following Sumpim. The results of behavior indicated that children with mild ASD have the high scores classified as clinical problems in thinking, anxiety, withdrawal, internalizing behaviors and externalizing behaviors. The group receiving melatonin had lower percentages of scores classified as clinical CBCL inventory. The mean score on the verbal fluency test in the group of mild ASD was 13,9 ± 1,6. When separated by letter, the result was P= 5,4 ± 0,7, T= 4,3 ± 0,5, L= 4,6 ± 0,6. There was a correlation between total sleep disorders and somatic behavior problems presented by mild ASD group. These data show that children with mild ASD have a high incidence of sleep disorders as well as in the ASD level without specification, but to a lesser extent. These disorders affect behavioral aspects of these children and the treatment with melatonin can improve of the clinical condition. Verbal fluency of children with ASD mild is similar to typically developing children.

The aim of this thesis was to investigate the neural underpinnings of persistent developmental stuttering. We explored neural systems important for speech-motor integration and focused on subcortical control systems: the basal ganglia and cerebellum. A secondary aim of this work was to distinguish effects related to general traits of the disorder from those reflecting specific states of stuttered speech. To address these aims we used a variety of neuroimaging methodologies as well as an extensive neuropsychological and empirical test battery. Our examination of neural pathway microstructure using diffusion-tensor imaging replicated previous findings of widespread disorganisation of white matter in people who stutter. This disruption included all major white matter pathways leading in and out of the cerebellum. In our second, third, and fourth studies we examined functional activity at rest and during different types of speech. The brain networks used by people who stutter and controls largely overlapped. The brain regions that distinguished general traits and specific states of stuttering were somewhat task-specific. Subcortical activation in the basal ganglia and cerebellum was related to the frequency of dysfluent speech in the scanner. In our final study we examined performance on a variety of classical tasks of motor learning. We observed evidence of delayed learning in response to changes in environmental feedback in the stuttering group relative to controls. Within people who stutter, subgroups who differ according to heritability of the disorder may also differ in the balance of dopamine in the basal ganglia. Overall, we concluded that cerebellar alterations contribute to the general trait of stuttering, while basal ganglia disruption may reflect specific effects within stuttering. Our work supports a broader role of the subcortical system in speech production, generally.