Abstract Objectives: to determine the effects of vitamin B12 supplementation on neuropsychological function and disease progression in middle aged and elderly patients with cognitive impairment. Methods: this was a prospective case-control study. From May 2020 to May 2021, 307 participants clinically diagnosed with cognitive impairment in the Department of Neurology of the First Affiliated Hospital of Chongqing Medical University were enrolled. A total of 115 patients were included in this study. Meanwhile, 115 participants with cognitive impairment were randomly assigned in equal proportions to two groups: vitamin B12 treatment group (n = 58, vitamin B12 500 mg/d intramuscularly for seven days, followed by cobamamide 0.25 mg/d and methylcobalamin 0.50 mg/d) and the control group (n = 57). Demographic characteristics and blood biochemical variables were obtained from all participants. Cognitive performance was measured using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Cognitive performance was measured at baseline and after six months. Results: the vitamin B12 supplementation treatment patients who presented with cognitive impairment showed significant improvement, especially in attention, calculation (p < 0.01) and visual-constructional ability (p < 0.05), in their neuropsychological function compared to their matched group. Conclusion: vitamin B12 supplementation may improve frontal function in patients with cognitive decline. Vitamin B12 levels should be investigated in all patients with cognitive impairment.

Resumen Objetivos: determinar los efectos de la suplementación con vitamina B12 en la función neuropsicológica y la progresión de la enfermedad en pacientes de mediana edad y adultos mayores con deterioro cognitivo. Métodos: se realizó un estudio prospectivo de casos y controles; se estudiaron 307 participantes, desde mayo de 2020 a mayo de 2021, diagnosticados clínicamente con deterioro cognitivo en el Departamento de Neurología, el Primer Hospital Anexado a la Universidad Médica de Chongqing. En el estudio se incluyeron un total de 115 pacientes con deterioro cognitivo que fueron asignados aleatoriamente en proporciones iguales a dos grupos: un grupo de tratamiento con vitamina B12 (n = 58, vitamina B12 500 mg/d intramuscular durante 7 días, seguido de cobamamida 0,25 mg/d y metilcobalamina 0,50 mg/d) y un grupo de control (n = 57). Se obtuvieron las características demográficas y las variables bioquímicas sanguíneas de todos los participantes. El rendimiento cognitivo se midió mediante el miniexamen del estado mental (MMSE) y la evaluación cognitiva de Montreal (Moca) al inicio del estudio y a los 6 meses. Resultados: los pacientes con deterioro cognitivo que recibieron tratamiento de suplementación con vitamina B12 mostraron una mejora significativa, especialmente en la atención, el cálculo (p < 0,01) y la capacidad visuoespacial (p < 0,05), en su función neuropsicológica en comparación con el grupo control. Conclusión: la suplementación con vitamina B12 puede mejorar la función frontal en pacientes con deterioro cognitivo. Los pacientes con deterioro cognitivo deben conocer sus propios niveles de vitamina B12.

This study aimed to estimate the incidence of central nervous system (CNS) metastases in patients with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) treated with trastuzumab. Studies were identified through a literature search of electronic databases. Random-effects meta-analyses were performed to estimate the incidence rate of CNS metastases, trastuzumab therapy duration, and time from trastuzumab therapy to CNS metastasis diagnosis. A meta-analysis of odds ratios was performed to evaluate the significance of a difference in CNS metastasis incidence between patients with and without trastuzumab treatment. Thirty studies (8121 trastuzumab-treated and 3972 control patients) were included. The follow-up duration was 18.9 months (95% confidence interval [CI]: 13.8, 24.1). The trastuzumab treatment duration was 9.0 months (95% CI: 7.0, 11.0). The median interval between the start of trastuzumab therapy and CNS metastasis diagnosis was 12.2 months (95% CI: 9.5, 14.7). The incidence of CNS metastasis after the start of trastuzumab therapy was 22% (95% CI: 16, 27). The incidence of CNS metastases was significantly higher in trastuzumab-treated than in non-trastuzumab-treated patients (odds ratio: 1.39 [95% CI: 1.06, 1.82], p=0.02). The survival time from the start of the study was 23.4 months (95% CI: 19.7, 27.1) in trastuzumab-treated patients and 18.4 months (95% CI: 12.7, 24.1) in patients treated with control regimens. The survival time after the development of CNS metastases in trastuzumab-treated patients was 19.2 months (95% CI: 15.6, 25.9). Approximately 22% of patients with HER2-positive MBC who were treated with trastuzumab developed CNS metastases. However, trastuzumab-treated patients had a longer survival than patients who were not treated with trastuzumab.

OBJECTIVE: Silent brain infarctions are the silent cerebrovascular events that are distinguished from symptomatic lacunar infarctions by their 'silence'; the origin of these infarctions is still unclear. This study analyzed the characteristics of silent and symptomatic lacunar infarctions and sought to explore the mechanism of this 'silence'. METHODS: In total, 156 patients with only silent brain infarctions, 90 with only symptomatic lacunar infarctions, 160 with both silent and symptomatic lacunar infarctions, and 115 without any infarctions were recruited. Vascular risk factors, leukoaraiosis, and vascular assessment results were compared. The National Institutes of Health Stroke Scale scores were compared between patients with only symptomatic lacunar infarctions and patients with two types of infarctions. The locations of all of the infarctions were evaluated. The evolution of the two types of infarctions was retrospectively studied by comparing the infarcts on the magnetic resonance images of 63 patients obtained at different times. RESULTS: The main risk factors for silent brain infarctions were hypertension, age, and advanced leukoaraiosis; the main factors for symptomatic lacunar infarctions were hypertension, atrial fibrillation, and atherosclerosis of relevant arteries. The neurological deficits of patients with only symptomatic lacunar infarctions were more severe than those of patients with both types of infarctions. More silent brain infarctions were located in the corona radiata and basal ganglia; these locations were different from those of the symptomatic lacunar infarctions. The initial sizes of the symptomatic lacunar infarctions were larger than the silent brain infarctions, whereas the final sizes were almost equal between the two groups. CONCLUSIONS: Chronic ischemic preconditioning and nonstrategic locations may be the main reasons for the 'silence' of silent brain infarctions.