MILBERTO SCAFF

(Fonte: Lattes)
Índice h a partir de 2011
8
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Neurologia, Faculdade de Medicina - Docente

Resultados de Busca

Agora exibindo 1 - 4 de 4
  • article 88 Citação(ões) na Scopus
    Stroke lesion in cortical neural circuits and post-stroke incidence of major depressive episode: A 4-month prospective study
    (2011) TERRONI, Luisa; AMARO JR., Edson; IOSIFESCU, Dan V.; TINONE, Gisela; SATO, Joao Ricardo; LEITE, Claudia Costa; SOBREIRO, Matildes F. M.; LUCIA, Mara Cristina Souza; SCAFF, Milberto; FRAGUAS, Renerio
    Objective. Little is known about the relevance of lesion in neural circuits reported to be associated with major depressive disorder. We investigated the association between lesion stroke size in the limbic-cortical-striatal-pallidal-thalamic (LCSPT) circuit and incidence of major depressive episode (MDE). Methods. We enrolled 68 patients with first-ever ischemic stroke and no history of major depressive disorder. Neurological and psychiatric examinations were performed at three time-points. We diagnosed major depressive episode, following DSM-IV criteria. Lesion location and volume were determined with magnetic resonance imaging, using a semi-automated method based on the Brodmann Cytoarchitectonic Atlas. Results. Twenty-one patients (31%) experienced major depressive episode. Larger lesions in the left cortical regions of the LCSPT circuit (3,760 vs. 660 mm(3); P = 0.004) were associated with higher incidence of MDE. Secondary analyses revealed that major depressive episode was associated with larger lesions in areas of the medial prefrontal cortex including the ventral (BA24) and dorsal anterior cingulate cortex (BA32) and subgenual cortex (BA25); and also the subiculum (BA28/36) and amygdala (BA34). Conclusions Our findings indicate that depression due to stroke is aetiologically related to the disruption of the left LCSPT circuit and support the relevance of the medial prefrontal cortex dysfunction in the pathophysiology of depression.
  • article 17 Citação(ões) na Scopus
    The association of post-stroke anhedonia with salivary cortisol levels and stroke lesion in hippocampal/parahippocampal region
    (2015) TERRONI, Luisa; AMARO JR., Edson; IOSIFESCU, Dan V.; MATTOS, Patricia; YAMAMOTO, Fabio I.; TINONE, Gisela; CONFORTO, Adriana B.; SOBREIRO, Matildes F. M.; GUAJARDO, Valeri D.; LUCIA, Mara Cristina S. De; MOREIRA, Ayrton C.; SCAFF, Milberto; LEITE, Claudia C.; FRAGUAS, Renerio
    Background: Anhedonia constitutes a coherent construct, with neural correlates and negative clinical impact, independent of depression. However, little is known about the neural correlates of anhedonia in stroke patients. In this study, we investigated the association of post-stroke anhedonia with salivary cortisol levels and stroke location and volume. Patients and methods: A psychiatrist administered the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition to identify anhedonia in 36 inpatients, without previous depression, consecutively admitted in a neurology clinic in the first month after a first-ever ischemic stroke. Salivary cortisol levels were assessed in the morning, evening, and after a dexamethasone suppression test. We used magnetic resonance imaging and a semi-automated brain morphometry method to assess stroke location, and the MRIcro program according to the Brodmann Map to calculate the lesion volume. Results: Patients with anhedonia had significantly larger diurnal variation (P-value =0.017) and higher morning levels of salivary cortisol (1,671.9 +/- 604.0 ng/dL versus 1,103.9 +/- 821.9 ng/dL; P-value =0.022), and greater stroke lesions in the parahippocampal gyrus (Brodmann area 36) compared to those without anhedonia (10.14 voxels; standard deviation +/- 17.72 versus 0.86 voxels; standard deviation +/- 4.64; P-value =0.027). The volume of lesion in the parahippocampal gyrus (Brodmann area 36) was associated with diurnal variation of salivary cortisol levels (rho=0.845; P-value =0.034) only in anhedonic patients. Conclusion: Our findings suggest that anhedonia in stroke patients is associated with the volume of stroke lesion in the parahippocampal gyrus and with dysfunction of the hypothalamic-pituitary-adrenal axis.
  • article 5 Citação(ões) na Scopus
    Executive function and depressive symptoms of retardation in nonelderly stroke patients
    (2014) SOBREIRO, Matildes F. M.; MIOTTO, Eliane Correa; TERRONI, Luisa; TINONE, Gisela; IOSIFESCU, Dan V.; LUCIA, Mara C. S. de; SCAFF, Milberto; LEITE, Claudia da Costa; AMARO JR., Edson; FRAGUAS, Renerio
    The depression-executive dysfunction syndrome, a late-onset depression of vascular origin with executive dysfunction and psychomotor retardation, has also been described after stroke. We verified whether this syndrome also occurs in nonelderly stroke patients by investigating the association between domains of depressive symptoms with executive functions in 87 first-ever ischemic stroke patients. The retardation domain of the 31-item Hamilton Rating Scale for Depression was associated with decreased performance on verbal fluency (assessed with FAS). The association was maintained for younger patients (aged <60 years) after adjusting for confounders. This result supports the clinical presentation of depression-executive dysfunction syndrome in younger stroke patients. Confirmation of this finding, its neural correlates, and clinical implication deserve further investigation.
  • article 35 Citação(ões) na Scopus
    The Influence of Depressive Symptoms on Quality of Life after Stroke: A Prospective Study
    (2015) GUAJARDO, Valeri Delgado; TERRONI, Luisa; SOBREIRO, Matildes de Freitas Menezes; ZERBINI, Maria Irene dos Santos; TINONE, Gisela; SCAFF, Milberto; IOSIFESCU, Dan V.; LUCIA, Mara Cristina Souza de; FRAGUAS, Renerio
    Background: Poststroke depressive symptoms have prospectively predicted impairment of health-related quality of life (HRQOL). However, it is not known whether such predictive effect is independent of HRQOL at 1 month after stroke. This study aimed to investigate the impact of depressive symptoms at 1 and 3 months after stroke on the 3-month poststroke HRQOL and to investigate the influence of the HRQOL measured at 1 month after stroke on these relationships. Methods: We prospectively evaluated 67 patients at 1 and 3 months after a first-ever ischemic stroke from 106 eligible patients who have been consecutively admitted to the neurology ward of a teaching hospital. A psychiatrist assessed the presence of depressive symptoms using the 31-item version of the Hamilton Rating Scale for Depression and the HRQOL was assessed with the 36-item Short-Form Health Survey from the Medical Outcomes Study. We used linear regression to measure the impact of depressive symptoms, HRQOL at 1 month, and potential confounders on HRQOL at 3 months. Results: We found an association between depressive symptoms at 1 month and HRQOL at 3 months after the stroke; however, this association was not significant when adjusting for the 1 month poststroke HRQOL. Depressive symptoms at 3 months were associated with HRQOL at 3 months after stroke, independently of the poststroke HRQOL at 1 month and potential confounders. Conclusions: Current depressive symptoms at 3 months are important for HRQOL at 3 months after stroke; however, regarding the prospective prediction, HRQOL at 1 month is the most relevant factor.