Perilesional and contralesional brain activations related to associative encoding of unfamiliar face-names pairs in adults with left chronic stroke with or without ischemic infarct on left inferior frontal gyrus.

The study of an Ischemic stroke infarction allows verifying how the lesion produces alterations in the neuronal networks resulting in cognitive deficits. It also allows the verification of adaptive and maladaptive cerebral reorganization related to the injury. In our previous fMRI study, we found that patients without ischemic vascular lesions in left inferior frontal gyrus showed an efficient compensation mechanism during the associative encoding of face name pairs, by the increased activation of ventrolateral and dorsolateral areas of contralesional hemisphere associated with better memory performance. While patients with ischemic vascular lesions on left inferior frontal gyrus (IFG) demonstrated worse memory performance and no signs of compensation mechanism. The present study explores more of these findings by analyzing perilesional and contralesional activations related to unfamiliar face name associative encoding in adults with chronic ischemic stroke, with or without left IFG lesion, compared to healthy controls. The main results showed that stroke survivors without lesions in IFG demonstrated increased activation in perilesional and contralesional prefrontal regions associated with better associative memory recognition, which are indicative of adaptive compensatory mechanisms. However, they also showed a negative correlation between the activation of right anterior prefrontal and inferior parietal regions and the associative memory performance, which may indicate the presence of maladaptive interhemispheric disinhibition. On the other hand, stroke survivors with IFG lesions demonstrated negative correlations in activations of the ipsilesional inferior parietal cortex and positive correlations in activations of the left middle frontal gyrus and left precentral cortex, which demonstrate the simultaneous occurrence of adaptive and maladaptive brain reorganization mechanisms in this group. However, the increase in perilesional prefrontal regions, associated with bilateral activation of the hippocampus and amygdala, was not enough to compensate for the inefficiency of associative memory performance. Finally, the differences in activation observed in stroke survivors reflect their clinical heterogeneity and demonstrate that adaptive or maladaptive compensatory mechanisms can coexist in the same group of patients. Furthermore, they reinforce the importance of the left IFG in the associative encoding of unfamiliar face name pairs and may suggest a deficit in associative memory related to injury in this region.

Anticoagulation and Stroke.

In 2019, the American Heart Association did not recommend the emergent use of anticoagulation to prevent recurrence or progression of acute ischemic stroke. However, its indication in patients with extracranial artery intraluminal thrombus with artery-to-artery cerebral embolization must be analyzed. In this article, we will also discuss other indications of anticoagulation. This treatment could be indicated in patients with ischemic stroke caused by embolization from cervical artery dissection, catastrophic antiphospholipid antibodies syndrome (APS) and some cases of Covid 19. For secondary prevention, anticoagulation is recommended for Cardioembolic stroke such as nonvalvular atrial fibrillation and other cardiopathies, some patients with cervical artery dissection, stroke associated with cancer, and thrombophilia such as APS. The timing to restart anticoagulation after a large ischemic stroke or after a cerebral hemorrhagic transformation always represent a challenge. Even in patients with high risk of thromboembolism it should be delayed at least two weeks, ideal after four weeks.

Anticoagulation and Stroke / Anticoagulação e AVC

Abstract In 2019, the American Heart Association did not recommend the emergent use of anticoagulation to prevent recurrence or progression of acute ischemic stroke. However, its indication in patients with extracranial artery intraluminal thrombus with artery-to-artery cerebral embolization must be analyzed. In this article, we will also discuss other indications of anticoagulation. This treatment could be indicated in patients with ischemic stroke caused by embolization from cervical artery dissection, catastrophic antiphospholipid antibodies syndrome (APS) and some cases of Covid 19. For secondary prevention, anticoagulation is recommended for Cardioembolic stroke such as nonvalvular atrial fibrillation and other cardiopathies, some patients with cervical artery dissection, stroke associated with cancer, and thrombophilia such as APS. The timing to restart anticoagulation after a large ischemic stroke or after a cerebral hemorrhagic transformation always represent a challenge. Even in patients with high risk of thromboembolism it should be delayed at least two weeks, ideal after four weeks.

Resumo Anticoagulação na fase aguda do acidente vascular isquêmico (AVCI) ainda é um tema bastante controverso. Em 2019, a American Heart Association (AHA) não recomendou o uso precoce da anticoagulação para evitar a progressão ou recorrência de AVCIs de grandes artérias. Mas sugere que a anticoagulação em pacientes com AVCI por embolização a partir de trombos intraluminais aderidos a parede de vasos extracranianos fosse analisada. Tanto a antiagregação como anticoagulação são opções terapêuticas nos casos de AVCI por dissecção arterial cervical. Mas em pacientes com AVCI por mecanismo de embolização, a anticoagulação poderia ser indicada. Pacientes com AVCI e sindrome catastrófica por anticorpos antifosfolípides devem ser anticoagulados além de receber tratamento específico. Outra indicação seriam casos de trombofilia como Covid 19. Nesse artigo de revisão será discutida a prevenção secundária de AVCI em situações específicas (AVCI cardioembólico em pacientes com fibrilação atrial não valvular ou outras cardiopatias, AVCI em casos oncológicos, além de outras trombofilias), além do período ideal para se introduzir ou reiniciar a anticoagulação após transformação hemorrágica.

Resting state functional connectivity and neural correlates of face-name encoding in patients with ischemic vascular lesions with and without the involvement of the left inferior frontal gyrus.

Face-name association is a relevant ability for social interactions and involves the ventral and dorsolateral prefrontal cortices, particularly in the left hemisphere, bilateral hippocampal, fusiform gyrus and occipital regions. Previous studies demonstrated the primary role of the hippocampus for this ability in healthy subjects. However, no study has examined the participation of the left inferior frontal area, specially the left inferior frontal gyrus (LIFG) in patients with ischemic vascular lesions. In the present study we addressed this issue and investigated the neural correlates and resting state functional connectivity of face-name memory encoding in ischemic patients with LIFG or without lesions in the left IFG (nLIFG) and healthy controls (HC) using fMRI. The main results showed that the nLIFG group demonstrated efficient compensation related to encoding and performance on face-name learning and recognition memory task, in addition to similar brain areas activated during task performance compared to healthy controls. Some of these areas were more activated in nLIFG group, indicating a compensation mechanism. In contrast, the LIFG group showed worse behavior performance, and no signs of an efficient compensation mechanism. Functional connectivity analysis suggested that the left IFG region seems to be important for maintaining the connectivity of the right fusiform gyrus or, perhaps, lesion in this area is associated to maladaptive reorganization. Our findings highlight the relevant role of the left IFG in face-name learning and encoding, possibly as a primary region in addition to the bilateral hippocampal formation and fusiform gyrus.

Screening for MELAS mutations in young patients with stroke of undetermined origin.

PURPOSE: It has been suggested that mitochondrial disease may be responsible for a substantial proportion of strokes of indetermined origin. We have preliminarily screened for MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) mutations in young patients with cryptogenic strokes. METHOD: The mitochondrial mutations A3243G and T3271C were investigated in 38 subjects aged less than 46 years. Group 1: 15 patients with cryptogenic strokes; Group 2: 3 patients with diagnosis of MELAS syndrome, including stroke-like episodes; Group 3: 20 healthy subjects. RESULTS: The A3243G mutation was absent in all subjects in Groups 1 and 3 but was present in all subjects in Group 2. CONCLUSION: Our results do not support screening for these mutations to diagnose oligosymptomatic forms of MELAS in cryptogenic strokes in the absence of other features of the syndrome. We suggest that clinical findings should guide mitochondrial genetic testing.

Screening for MELAS mutations in young patients with stroke of undetermined origin

PURPOSE: It has been suggested that mitochondrial disease may be responsible for a substantial proportion of strokes of indetermined origin. We have preliminarily screened for MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) mutations in young patients with cryptogenic strokes. METHOD: The mitochondrial mutations A3243G and T3271C were investigated in 38 subjects aged less than 46 years. Group 1: 15 patients with cryptogenic strokes; Group 2: 3 patients with diagnosis of MELAS syndrome, including stroke-like episodes; Group 3: 20 healthy subjects. RESULTS: The A3243G mutation was absent in all subjects in Groups 1 and 3 but was present in all subjects in Group 2. CONCLUSION: Our results do not support screening for these mutations to diagnose oligosymptomatic forms of MELAS in cryptogenic strokes in the absence of other features of the syndrome. We suggest that clinical findings should guide mitochondrial genetic testing.

PROPÓSITO: Foi sugerido que mitocondriopatias possam ser responsáveis por uma proporção substancial de acidentes vasculares cerebrais de etiologia indeterminada. Realizamos um estudo preliminar de pesquisa de mutações relacionadas à síndrome de MELAS (encefalomiopatia mitocondrial, acidose lática e episódios "stroke-like") em pacientes jovens com acidentes vasculares cerebrais criptogênicos. MÉTODO: As mutações mitocondriais A3243G e T3271C em 38 indivíduos com menos de 46 anos. Grupo 1: 15 pacientes com acidentes vasculares cerebrais criptogênicos; Grupo 2: 3 pacientes com diagnóstico de síndrome de MELAS, incluindo episódios "stroke-like"; Grupo 3: 20 voluntários saudáveis. RESULTADOS: A mutação A3243G esteve ausente em todos os indivíduos dos Grupos 1 e 3 mas esteve presente em todos os indivíduos do Grupo 2. CONCLUSÃO: Nossos resultados sugerem que não há utilidade em pesquisar estas mutações para diagnosticar formas oligossintomáticas de MELAS em acidentes vasculares cerebrais criptogênicos na ausência de características da síndrome. Sugerimos que o quadro clínico deva guiar a solicitação de pesquisas de mutações relacionadas a mitocondriopatias nestes pacientes.

Hepatic enzymes' level during chronic use of anticonvulsant drugs

Oitocentos e noventa e quatro epiléticos adultos tratados no período de 1983 a 1992 foram estudados retrospectivamente. Valores anormais de enzimas foram detectados em 49 por cento (n=438) dos casos. Em 200 pacientes (22.3 por cento), ao menos duas dosagens obtidas em momentos diferentes estavam alteradas. Estes últimos foram divididos em 3 grupos: GI, com alteraçoes de transaminases (3 por cento, n=6); GII com alteraçoes de gama-glutamil-tranferase (GGT) e fosfatase alcalina (AP) (72 por cento, n=144) e GIII com alteraçoes nos dois grupos de enzimas (25 por cento, n=50). Nenhum paciente desenvolveu sinais ou sintomas de doença hepática. O aumento de GGT e AP em pacientes em uso de drogras atiepiléticas é frequente e pode nao ter significado patológico. Pequenos aumentos de transaminases também podem ocorrer sem correçao clínica.

Imunizaçäo de crianças na idade escolar em Säo Paulo: Centro de Saúde Escola "Prof. Samuel B. Pessoa" -FMUSP / Vaccination status of school age children enroles at the \"Prof. Samuel B. Pessoa\" public health centre in São Paulo, Brazil

Analisa a situaçäo atual no Estado de Säo Paulo relativa às doenças infecto-contagiosas passíveis de prevençäo. Estuda a situaçäo vacinal de 389 crianças na idade escolar que frequentaram o Centro de Saúde Escola "Prof. Samuel B. Pessoa". Verifica que a mesma näo é satisfatória já que 31,11 por cento dos escolares encontram-se com imunizaçäo inadequada e incompleta. Sugere medidas para melhorar a situaçäo de imunizaçäo dos escolares