Repositorio Institucional Fleni
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Barriers to access and utilization of multiple sclerosis care services in a large cohort of Latin American patients
No full textBackground: Multiple sclerosis (MS), is an emergent disease in Latin America (LATAM), which raises substantial socioeconomic challenges to a region where most countries remain as economies in development.
Objective: To assess barriers to access and utilization of MS care services in a regional cohort survey.
Methods: We conducted a cross-sectional study based on a self-reported survey. Patients with MS (PwMS) completed this regional survey in 12 Latin American (LATAM) countries. PwMS were also divided into those with healthcare insurance (including certain local national social security programs) and those without healthcare insurance (treated at public institutions).
Results: We surveyed 1469 PwMS and identified significant regional differences in relation to access to complementary tests, rehabilitation services, and prescription of disease-modifying therapies (DMTs). Between 44.4% and 73.5% of PwMS were unemployed and nearly 50% had completed higher education. PwMS receiving care from the private sector reported greater access to imaging, DMTs, and fewer problems obtaining DMTs compared to those treated at public institutions. Multivariate analysis showed that lack of private insurance (OR = 2.21, p < 0.001), longer MS duration (OR = 1.02, p = 0.001), lower level of education (OR = 0.66, p = 0.009), and unemployment (OR = 0.73, p = 0.03) were independently associated with inappropriate delivery of DMTs.
Conclusion: These findings suggest barriers to access and utilization of MS care services across LATAM are prevalent. We identified several factors predicting unmet healthcare needs in PwMS.Fil: Correale, Jorge. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.Fil: Contentti, Edgar Carnero. Hospital Alemán de Buenos Aires. Department of Neuroscience. Neuroimmunology Unit; Argentina.Fil: Giachello, Susana. Asociación de Lucha Contra la Esclerosis Múltiple (ALCEM); Argentina
Artifacts Detection in EEG Signals
No full textResumen no disponibleFil: Quintero-Rincón, Antonio. Instituto Tecnológico de Buenos Aires. Departamento de Bioingeniería; Argentina.Fil: D'Giano, Carlos. Fleni. Centro Integral de Epilepsia y Unidad de Monitoreo de Videoelectroencefalografía; Argentina.Fil: Batatia, Hadj. University of Toulouse. Institut de Recherche en Informatique de Toulouse; Francia
The prevalence of migraine in Argentina: A reappraisal
No full textBackground: Argentina has one of the largest territories in the world, which spreads over a lengthy latitudinal span. Its population is mainly composed of a mixture of South American natives and the descendants of numerous waves of European immigrants. Results from a previous study suggested that the prevalence of migraine in Argentina is the lowest in the region. Here we aimed to reassess the prevalence of migraine in Argentina applying a more sensitive and specific screening tool.
Methods: We conducted a random computer assisted telephonic interview (n= 2500) using the Migraine Screen Questionnaire to evaluate the prevalence of migraine and some of its features among Argentinian adults.
Results: The overall prevalence of migraine was 9.5% (14% in females and 5% in males). Estimated migraine prevalence rates ranged between 6.3% and 12% across different regions. The approximated prevalence of high frequency and chronic migraine were 1.9% and 1.5% of the total population respectively. Consumption of analgesics on 10 or more days per month was reported by 18% of migraine sufferers (≈1.7% of the population).
Conclusions: The prevalence of migraine in Argentina is higher than previously reported. Prevalence rates vary extensively across the territory. Specifically evaluating the determinants of these variations might be a promising avenue of research.Fil: Lisick, Marco. Instituto Conci·Carpinella. Unidad de Neurociencias; Argentina.Fil: Figuerola, María L. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas “José de San Martín”. División de Neurología; Argentina.Fil: Bonamico, Lucas. Fleni. Departamento de Neurología. Clínica del Dolor. Clínica de Cefaleas; Argentina.Fil: Lew, Daniel. CEMIC; Argentina.Fil: Goicochea, María Teresa. Fleni. Departamento de Neurología. Clínica del Dolor. Clínica de Cefaleas; Argentina
Diagnostic accuracy of the UDS 3.0 neuropsychological battery in a cohort with Alzheimer's disease in Colombia
No full textBackground: Alzheimer's disease (AD) is a neurodegenerative disease that causes a gradual loss of cognitive functions and limits daily activities performance. Early diagnosis of AD is essential to start timely treatment. This study aimed to validate the Uniform Data Set neuropsychological battery version 3.0 (UDS 3.0) in a Colombian cohort.
Methods: This study is a cross-sectional type, consecutive, incidental, with 143 persons, divided into two groups: 48 diagnosed AD cases and 95 healthy controls, between the ages of 50 and 80+, and between 1 and 19+ years of education.
Results: The results indicate differences between the control group and the AD group in most battery tests. A significant correlation was found between the Montreal Cognitive Assessment (MoCA), Multilingual Naming Test (MINT), Craft Story, Benson Figure Test, P-word and F-word Phonemic Fluency Test, and their respective reference tests. Cutoff points were found based on the Youden index for each sub-test. The results indicate that all sub-tests are above the reference line of the ROC curve.
Conclusion: The use of the UDS 3.0 in Colombia would help improving clinical diagnostic routes because of its high accuracy and high correlation with tests that measure general impairment; it has good sensitivity and specificity, and it can be a useful tool for AD.Fil: Porto, Maria F. Universidad de la Costa; Colombia.Fil: Benitez-Agudelo, Juan Camilo. Universidad de la Costa; Colombia.Fil: Aguirre-Acevedo, Daniel Camilo. Universidad de Antioquia; Colombia.Fil: Barceló-Martínez, Ernesto. Universidad de la Costa; Colombia.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina
Neurologic complications of rheumatic fever
No full textSydenham chorea, also known as St. Vitus dance, is a major clinical criterion for the diagnosis of acute rheumatic fever. Clinically, it results in a combination of movement disorders and complex neuropsychiatric symptoms. Cardiac damage due to rheumatic fever may also predispose to neurologic complications later in life. Rheumatic heart disease (RHD) is associated with heart remodeling, cardiac arrhythmias, and ischemic stroke. Furthermore, chronically damaged heart valves are predisposed to infection. Septic brain embolism, a known complication of infective endocarditis, may result in brain ischemia, hemorrhage, and spread of the infection to the brain.Fil: Hawkes, Maximiliano Alberto. Fleni. Departamento de Neurología. Servicio de Neurología Vascular; Argentina.Fil: Ameriso, Sebastián Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Vascular; Argentina
Embryoid Bodies-Based Multilineage Differentiation of Human Embryonic Stem Cells Grown on Feeder-Free Conditions
No full textHuman embryonic stem cells (hESCs) can differentiate into any cell lineage (pluripotency potential) derived from the three germ layers: ectoderm, mesoderm, and endoderm. Pluripotency is usually demonstrated in vitro by spontaneous differentiation of hESCs grown on a monolayer of feeder-cells using an embryoid bodies (EBs)-based method. However, currently hESCs are grown mostly using fully defined media in the absence of a feeder layer. Here we describe a EBs-based protocol that allows multilineage differentiation of hESCs and human induced pluripotent stem cells (hiPSCs) grown on feeder-free conditions.Fil: Isaja, Luciana. Fleni. Laboratorios de Investigación Aplicada en Neurociencias; Argentina.Fil: Ferriol-Laffouillere, Sofía Luján. Fleni. Laboratorios de Investigación Aplicada en Neurociencias; Argentina.Fil: Mucci, Sofía. Fleni. Laboratorios de Investigación Aplicada en Neurociencias; Argentina.Fil: Rodríguez-Varela, María Soledad. Fleni. Laboratorios de Investigación Aplicada en Neurociencias; Argentina.Fil: Romorini, Leonardo. Fleni. Laboratorios de Investigación Aplicada en Neurociencias; Argentina
Risk of intracranial haemorrhage and ischaemic stroke after convexity subarachnoid haemorrhage in cerebral amyloid angiopathy: international individual patient data pooled analysis
No full textObjective
To investigate the frequency, time-course and predictors of intracerebral haemorrhage (ICH), recurrent convexity subarachnoid haemorrhage (cSAH), and ischemic stroke after cSAH associated with cerebral amyloid angiopathy (CAA).
Methods
We performed a systematic review and international individual patient-data pooled analysis in patients with cSAH associated with probable or possible CAA diagnosed on baseline MRI using the modified Boston criteria. We used Cox proportional hazards models with a frailty term to account for between-cohort differences.
Results
We included 190 patients (mean age 74.5 years; 45.3% female) from 13 centers with 385 patient-years of follow-up (median 1.4 years). The risks of each outcome (per patient-year) were: ICH 13.2% (95% CI 9.9–17.4); recurrent cSAH 11.1% (95% CI 7.9–15.2); combined ICH, cSAH, or both 21.4% (95% CI 16.7–26.9), ischemic stroke 5.1% (95% CI 3.1–8) and death 8.3% (95% CI 5.6–11.8). In multivariable models, there is evidence that patients with probable CAA (compared to possible CAA) had a higher risk of ICH (HR 8.45, 95% CI 1.13–75.5, p = 0.02) and cSAH (HR 3.66, 95% CI 0.84–15.9, p = 0.08) but not ischemic stroke (HR 0.56, 95% CI 0.17–1.82, p = 0.33) or mortality (HR 0.54, 95% CI 0.16–1.78, p = 0.31).
Conclusions
Patients with cSAH associated with probable or possible CAA have high risk of future ICH and recurrent cSAH. Convexity SAH associated with probable (vs possible) CAA is associated with increased risk of ICH, and cSAH but not ischemic stroke. Our data provide precise risk estimates for key vascular events after cSAH associated with CAA which can inform management decisions.Fil: Hostettler, Isabel Charlotte. National Hospital of Neurology and Neurosurgery; Reino Unido.Fil: Wilson, Duncan. National Hospital of Neurology and Neurosurgery; Reino Unido.Fil: Fiebelkorn, Catherine Arnold. Mayo Clinic; Estados Unidos.Fil: Aum, Diane. Mayo Clinic; Estados -unidos.Fil: Ameriso, Sebastián Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Vascular; Argentina.Fil: Eberbach, Federico. Fleni. Departamento de Neurología. Servicio de Neurología Vascular; Argentina.Fil: Beitzke, Markus. Medical University of Graz; Austria.Fil: Kleinig, Timothy. Royal Adelaide Hospital; Australia.Fil: Phan, Thanh. Monash Health and Stroke and Ageing Research Group; Australia.Fil: Marchina, Sarah. Harvard Medical School; Estados Unidos.Fil: Schneckenburger, Romain. CHU Caen Normandie; Francia.Fil: Carmona-Iragui, María. Universitat Autònoma de Barcelona; España.Fil: Charidimou, Andreas. Massachusetts General Hospital and Harvard Medical School; Estados Unidos.Fil: Mourand, Isabelle. Hôpital Gui-de-Chauliac; Francia.Fil: Parreira, Sara. University of Lisbon; Portugal.Fil: Ambler, Gareth. Department of Statistical Science; Reino Unido.Fil: Rolf Jäger, Hans. University College London; Reino Unido.Fil: Singhal, Shaloo. Monash Health and Stroke and Ageing Research Group; Australia.Fil: Ly, John. Monash Health and Stroke and Ageing Research Group; Australia.Fil: Bruno, Verónica. Fleni. Departamento de Neurología. Servicio de Neurología Vascular; Argentina
Cognitive consequences of COVID-19: results of a cohort study from South America
No full textBackground: Neurological and psychiatric manifestations associated with SARS-CoV-2 infection have been reported throughout the scientific literature. However, studies on post-COVID cognitive impairment in people with no previous cognitive complaint are scarce.
Objective: We aim to investigate the impact of COVID-19 on cognitive functions in adults without cognitive complaints before infection and to study cognitive dysfunction according to disease severity and cognitive risk factors.
Methods: Forty-five post-COVID-19 patients and forty-five controls underwent extensive neuropsychological evaluation, which assessed cognitive domains such as memory, language, attention, executive functions, and visuospatial skills, including psychiatric symptomatology scales. Data were collected on the severity of infection, premorbid medical conditions, and functionality for activities of daily living before and after COVID-19.
Results: Significant differences between groups were found in cognitive composites of memory (p=0.016, Cohen's d= 0.73), attention (p<0.001, Cohen's d=1.2), executive functions (p<0.001, Cohen's d=1.4), and language (p=0.002, Cohen's d=0.87). The change from premorbid to post-infection functioning was significantly different between severity groups (WHODAS, p=0.037). Self-reported anxiety was associated with the presence of cognitive dysfunction in COVID-19 subjects (p=0.043).
Conclusion: Our results suggest that the presence of cognitive symptoms in post-COVID-19 patients may persist for months after disease remission and argue for the inclusion of cognitive assessment as a protocolized stage of the post-COVID examination. Screening measures may not be sufficient to detect cognitive dysfunction in post-COVID-19 patients.Fil: Crivelli, Lucía. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Calandri, Ismael Luis. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Corvalán, Nicolás. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; ArgentinaFil: Carello, María Agostina. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; ArgentinaFil: Keller, Greta. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; ArgentinaFil: Martínez, Carlos. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; ArgentinaFil: Arruabarrena, Micaela. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; ArgentinaFil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina. Universidad de la Costa; Colombia
Different rates of cognitive decline in autosomal dominant and late-onset Alzheimer disease
No full textAs prevention trials advance with autosomal dominant Alzheimer disease (ADAD) participants, understanding the similarities and differences between ADAD and "sporadic" late-onset AD (LOAD) is critical to determine generalizability of findings between these cohorts. Cognitive trajectories of ADAD mutation carriers (MCs) and autopsy-confirmed LOAD individuals were compared to address this question. Longitudinal rates of change on cognitive measures were compared in ADAD MCs (n = 310) and autopsy-confirmed LOAD participants (n = 163) before and after symptom onset (estimated/observed). LOAD participants declined more rapidly in the presymptomatic (preclinical) period and performed more poorly at symptom onset than ADAD participants on a cognitive composite. After symptom onset, however, the younger ADAD MCs declined more rapidly. The similar but not identical cognitive trajectories (declining but at different rates) for ADAD and LOAD suggest common AD pathologies but with some differences.Fil: Buckles, Virginia D. Washington University School of Medicine; Estados Unidos.Fil: Xiong, Chengjie. Washington University School of Medicine; Estados Unidos.Fil: Bateman, Randall J. Washington University School of Medicine; Estados Unidos.Fil: Hassenstab, Jason. Washington University School of Medicine; Estados Unidos.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Berman, Sarah B. University of Pittsburgh; Estados Unidos.Fil: Chhatwal, Jasmeer P. Massachusetts General Hospital; Estados Unidos.Fil: Danek, Adrian. Klinikum der Universität München; Alemania.Fil: Fagan, Anne M. Washington University School of Medicine; Estados Unidos.Fil: Ghetti, Bernardino. Indiana University School of Medicine; Estados Unidos.Fil: Goate, Alison. Icahn School of Medicine at Mount Sinai; Estados Unidos.Fil: Graff-Radford, Neill. Mayo Clinic; Estados Unidos.Fil: Jucker, Mathias. University of Tuebingen; Alemania.Fil: Levin, Johannes. Munich Cluster of Systems Neurology; Alemania.Fil: Marcus, Daniel S. Washington University School of Medicine; Estados Unidos.Fil: Masters, Colin L. University of Melbourne; Australia.Fil: McCue, Lena. Washington University School of Medicine; Estados Unidos.Fil: McDade, Eric. Washington University School of Medicine; Estados Unidos.Fil: Mori, Hiroshi. Osaka City University Medical School; Japón.Fil: Moulder, Krista L. Washington University School of Medicine; Estados Unidos
Longitudinal Accumulation of Cerebral Microhemorrhages in Dominantly Inherited Alzheimer Disease
Full text linkObjective: To investigate the inherent clinical risks associated with the presence of cerebral microhemorrhages (CMHs) or cerebral microbleeds (CMBs) and characterize individuals at high risk for developing hemorrhagic amyloid-related imaging abnormality (ARIA-H), we evaluated longitudinally families affected by dominantly inherited Alzheimer disease (DIAD).
Methods: Mutation carriers (n=310) and non-carriers (n=201) underwent neuroimaging, including gradient echo MR sequences to detect CMHs, neuropsychological, and clinical assessments. Cross-sectional and longitudinal analyses evaluated relationships between CMHs and neuroimaging and clinical marker of disease.
Results: Three percent of non-carriers and eight percent of carriers developed CMHs primarily located in lobar areas. Carriers with CMHs were older, had higher diastolic blood pressure and Hachinski ischemic scores, and more clinical, cognitive, and motor impairments than those without CMH. APOE-ε4 status was not associated with the prevalence or incidence of CMHs. Prevalent or incident CMHs predicted faster change in clinical dementia rating although not composite cognitive measure, cortical thickness, hippocampal volume, or white matter lesions. Critically, the presence of two or more CMHs was associated with a significant risk for development of additional CMHs over time (8.95±10.04 per year).
Conclusion: Our study highlights factors associated with the development of CMHs in individuals with DIAD. CMHs are a part of the underlying disease process in DIAD and are significantly associated with dementia. This highlights that in participants in treatment trials exposed to drugs, which carry the risk of ARIA-H as a complication, it may be challenging to separate natural incidence of CMHs from drug related CMHs.Fil: Joseph-Mathurin, Nelly. Washington University School of Medicine; Estados Unidos.Fil: Wang, Guoquiao. Washington University School of Medicine; Estados Unidos.Fil: Kantarci, Kejal. Mayo Clinic; Estados Unidos.Fil: Jack, Clifford R. Mayo Clinic; Estados Unidos.Fil: McDade, Eric. Washington University School of Medicine; Estados Unidos.Fil: Hassenstab, Jason. Washington University School of Medicine; Estados Unidos.Fil: Blazey, Tyler M. Washington University School of Medicine; Estados Unidos.Fil: Gordon, Brian A. Washington University School of Medicine; Estados Unidos.Fil: Su, Yi. Banner Alzheimers Institute; Estados Unidos.Fil: Chen, Gengsheng. Washington University School of Medicine; Estados Unidos.Fil: Massoumzadeh, Parinaz. Washington University School of Medicine; Estados Unidos.Fil: Hornbeck, Russ C. Washington University School of Medicine; Estados Unidos.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Ances, Beau M. Washington University School of Medicine; Estados Unidos.Fil: Berman, Sarah B. University of Pittsburgh School of Medicine; Estados Unidos.Fil: Brickman, Adam M. Taub Institute for Research on Alzheimers Disease and the Aging Brain; Estados Unidos.Fil: Brooks, William S. Neuroscience Research Australia; Australia.Fil: Cash, David M. UCL Queen Square Institute of Neurology; Reino Unido.Fil: Chhatwal, Jasmeer P. Massachusetts General Hospital; Estados Unidos