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Living with dementia: increased level of caregiver stress in times of COVID-19
No full textCOVID-19 pandemic in Argentina has affected the care of older adults with dementia deeply. Our objective was to study how the obligatory social isolation affected stress caregiver and burden of care of family members of subjects living with dementia in the community after the initial 4 weeks of quarantine in our setting. We did a questionnaire survey among 80 family caregivers of persons with Alzheimer's disease (AD) or related dementia collected on April 2020. We designed a visual analog scale to test the level of the burden of care. Characteristics of people with dementia and their caregivers were analyzed with descriptive (mean, standard deviation, frequency and percent) and inferential statistics (chi-square test). The sample included older adults (mean age: 80.51 ± 7.65) with different stages of dementia. Family was the primary provider of care in 65%. Overall, COVID-19 confinement increased stress caregiver independently of the dementia stage, but those caring for severe cases had more stress compared to milder forms of the disease. Other findings were that half of the subjects with dementia experienced increased anxiety and that most family members discontinued all sort of cognitive and physical therapies. Family members' main concerns were for severe dementia cases, fear of absence of the paid caregiver during the epidemic, and for mild cases fear of spreading the disease while assisting patients with instrumental activities. A partnership between departments of public health, care workers and families must be planned to guarantee continuity of care during these unique COVID-19 times.Fil: Cohen, Gabriela. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría. Centro de Memoria y Envejecimiento; Argentina.Fil: Russo, María Julieta. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría. Centro de Memoria y Envejecimiento; Argentina.Fil: Campos, Jorge. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría. Centro de Memoria y Envejecimiento; Argentina.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría. Centro de Memoria y Envejecimiento; Argentina
Insular functional alterations in emotional processing of schizophrenia patients revealed by Multivariate Pattern Analysis fMRI
No full textEmotion perception is impaired in schizophrenia patients (SP) and related to reduced social skills performance. There is a remarkable variability across subjects for functional neuroimaging alterations related to this phenomenon. In contrast to the univariate approaches of fMRI, Multivariate Pattern Analysis (MVPA) maintains the within-subject voxel-level variability. The purpose of this study was to assess emotion processing in SP, in previously identified ROIs -i.e. amygdala, hippocampus, insula, and thalamus-, while retaining the functional heterogeneity that may exist between subjects. We evaluated 23 SP and 23 healthy controls (HC). Happy, sad, and neutral faces were presented. A single trial fMRI model was applied. Patterns of activation within each ROI were classified at the subject level. Within each group, stimuli classification scores were tested against random label classification scores. In ROIs with significant results, a whole ROI classification was performed, to test whether en bloc stimuli discrimination was present. A between-group analysis was conducted also. For the classification of stimuli above chance, in the HC results were significant in the left insula in all of the stimuli dichotomies, but were non-significant in SP for happy vs. sad. In whole ROI classification, SP had significant results in bilateral insular cortex for happy vs. neutral. The left amygdala showed diminished stimuli classification scores in SP for sad vs. neutral. In conclusion, MVPA seems useful to study emotional processing in schizophrenia. In SP, either en bloc or no stimuli discrimination was seen in the insula, and reduced stimuli discrimination was seen in the left amygdala.Fil: Drucaroff, Lucas J. Instituto de Neurociencias FLENI-CONICET; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Psiquiatría y Salud Mental; Argentina. Fleni. Servicio de Psiquiatría; Argentina.Fil: Fazzito, Maria Lucía. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Psiquiatría y Salud Mental; Argentina. Fleni. Servicio de Psiquiatría; Argentina.Fil: Castro, Mariana Nair. Instituto de Neurociencias FLENI-CONICET; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Psiquiatría y Salud Mental; Argentina.Fil: Nemeroff, Charles B. University of Texas at Austin. Dell Medical School. Department of Psychiatry; Estados Unidos.Fil: Guinjoan, Salvador Martín. Instituto de Neurociencias FLENI-CONICET; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Psiquiatría y Salud Mental; Argentina. Fleni. Servicio de Psiquiatría; Argentina.Fil: Villarreal, Mirta Fabiana. Instituto de Neurociencias FLENI-CONICET; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Física; Argentina
Consensus recommendations for family planning and pregnancy in multiple sclerosis in argentina
No full textBackground: Multiple sclerosis (MS) is the most common chronic immune-mediated neurological disorder in young adults, more frequently found in women than in men. Therefore, pregnancy-related issues have become an object of concern for MS professionals and patients. The aim of this work was to review the existing data to develop the first Argentine consensus for family planning and pregnancy in MS patients.
Methods: A panel of expert neurologists from Argentina engaged in the diagnosis and care of MS patients met both virtually and in person during 2019 to carry out a consensus recommendation for family planning and pregnancy in MS. To achieve consensus, the procedure of the "formal consensus-RAND/UCLA method" was used.
Results: Recommendations were established based on published evidence and expert opinion focusing on pre-pregnancy counseling, pregnancy, and postpartum issues.
Conclusion: The recommendations of these consensus guidelines are intended to optimize the management and treatment of MS patients during their reproductive age in Argentina.Fil: Gaitán, María Inés. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.Fil: Ysrraelit, María Célica. Fleni. Departamento de Neurología; Argentina.Fil: Fiol, Marcela Paula. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.Fil: Liguori, Nora Fernández. Hospital Universitario Sanatorio Güemes; Argentina. Hospital Enrique Tornú. Sección Neurología; Argentina.Fil: Alonso, Ricardo. Hospital Universitario Sanatorio Güemes; Argentina. Hospital Dr. J. M. Ramos Mejía. Centro Universitario de Esclerosis Múltiple; Argentina.Fil: Pinheiro, Amelia Alves. Hospital San Martín; Argentina.Fil: Balbuena Aguirre, María Eugenia. Hospital de Clínicas “José de San Martín”. Servicio de Neurología. Sección de Neuroinmunologia y Enfermedades Desmielinizantes; Argentina.Fil: Barboza, Andrés. Hospital Central de Mendoza; Argentina.Fil: Bestoso, Santiago. Hospital Escuela Corrientes. Servicio Neurología; Argentina.Fil: Burgos, Marcos. Hospital San Bernardo; Argentina.Fil: Cáceres, Fernando. Institute of Neuroscience Buenos Aires; Argentina.Fil: Carnero Contentti, Edgar. Hospital Alemán. Department of Neuroscience - Neuroimmunology Unit; Argentina.Fil: Carrá, Adriana. Fundación Favaloro/INECO; Argentina. Hospital Británico. MS Section; Argentina.Fil: Cristiano, Edgardo. Centro de Esclerosis Múltiple de Buenos Aires; Argentina.Fil: Curbelo, María Celeste. Hospital Británico. MS Section; Argentina.Fil: Deri, Norma. Centro de Investigaciones Diabaid; Argentina. Hospital Fernández de Buenos Aires; Argentina.Fil: Garcea, Orlando. Hospital Dr. J. M. Ramos Mejía. Centro Universitario de Esclerosis Múltiple; Argentina.Fil: Halfon, Mario Javier. Hospital Británico de Buenos Aires; Argentina.Fil: Hryb, Javier Pablo. Hospital Carlos G. Durand. Servicio de Neurología; Argentina.Fil: Jacobo, Miguel. Red Integral Asistencial al Paciente con EM; Argentina
Statistical Model-Based Classification to Detect Patient-Specific Spike-and-Wave in EEG Signals
No full textSpike-and-wave discharge (SWD) pattern detection in electroencephalography (EEG) is a crucial signal processing problem in epilepsy applications. It is particularly important for overcoming time-consuming, difficult, and error-prone manual analysis of long-term EEG recordings. This paper presents a new method to detect SWD, with a low computational complexity making it easily trained with data from standard medical protocols. Precisely, EEG signals are divided into time segments for which the continuous Morlet 1-D wavelet decomposition is computed. The generalized Gaussian distribution (GGD) is fitted to the resulting coefficients and their variance and median are calculated. Next, a k-nearest neighbors (k-NN) classifier is trained to detect the spike-and-wave patterns, using the scale parameter of the GGD in addition to the variance and the median. Experiments were conducted using EEG signals from six human patients. Precisely, 106 spike-and-wave and 106 non-spike-and-wave signals were used for training, and 96 other segments for testing. The proposed SWD classification method achieved 95% sensitivity (True positive rate), 87% specificity (True Negative Rate), and 92% accuracy. These promising results set the path for new research to study the causes underlying the so-called absence epilepsy in long-term EEG recordings.Fil: Quintero Rincón, Antonio. Universidad Católica de Buenos Aires; Argentina. Fleni. Centro Integral de Epilepsia y Unidad de Monitoreo de Videoelectroencefalografía; Argentina.Fil: Muro, Valeria L. Fleni. Centro Integral de Epilepsia y Unidad de Monitoreo de Videoelectroencefalografía; Argentina.Fil: D'Giano, Jorge. Fleni. Centro Integral de Epilepsia y Unidad de Monitoreo de Videoelectroencefalografía; Argentina.Fil: Prendes, Jorge. IRIT-INPT-ENSEEIHT; Francia.Fil: Batatia, Hadj. Heriot-Watt Universit. MACS School; Emiratos Árabes Unidos
Anti-Ma2-associated encephalitis
No full textFil: Ruiz Yanzi, María Agustina. Fleni. Departamento de Neurología; Argentina.Fil: Bensi, Catalina. Fleni. Departamento de Neurología; Argentina
Utility of a Screening Test (MoCa) to Predict Amyloid Physiopathology in Mild Cognitive Impairment
No full textIntroduction: The MoCa (Montreal Cognitive Assessment) Screening test has become relevant in recent years in the screening of patients with Mild Cognitive Impairment (MCI). It is important to seek and study simple and reliable tools in clinical practices that correlate with biological markers that have been used to predict conversion from MCI to AD. Objective: To analyze the MOCA and its cognitive sub-scores and the relationship with Amyloid pathophysiology in Alzheimer’s Disease. Methodology: 32 patients with MCI were studied, they were separated according positive (n: 20) and negative (n: 12) underlying amyloid pathology. The patients performed a extensive cognitive assessment that included MoCa Test. Results: MoCa Total Scores showed significantly different results between groups (p <0.001) as well as the Memory Score (MoCa MIS), the Executive (MoCa EIS), the Attentional Score (MoCa AIS)) (p < 0.001) and the Orientation Score (MoCa OIS)) (p < 0.05) with worse performance of patients with amyloid pathophysiology. Score of MoCa a cut-off point of < 24 was established, since the diagnostic sensitivity at this point was 83% and the specificity 70%. Conclusions: The MoCa is a useful tool to differentiate biomarker status in MCI. Future studies should study this tool in the prodromal phases of the disease.Fil: Clarens, María Florencia. 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: Helou, María Belen. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Martín, María Eugenia. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Chrem Méndez, Patricio Alexis. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Crivelli, Lucía. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina
Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification
Get PDFPrimary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromosome 21q21.3 and identified bi-allelic variants in JAM2. JAM2 encodes for the junctional-adhesion-molecule-2, a key tight-junction protein in blood-brain-barrier permeability. We show that JAM2 variants lead to reduction of JAM2 mRNA expression and absence of JAM2 protein in patient's fibroblasts, consistent with a loss-of-function mechanism. We show that the human phenotype is replicated in the jam2 complete knockout mouse (jam2 KO). Furthermore, neuropathology of jam2 KO mouse showed prominent vacuolation in the cerebral cortex, thalamus, and cerebellum and particularly widespread vacuolation in the midbrain with reactive astrogliosis and neuronal density reduction. The regions of the human brain affected on neuroimaging are similar to the affected brain areas in the myorg PFBC null mouse. Along with JAM3 and OCLN, JAM2 is the third tight-junction gene in which bi-allelic variants are associated with brain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the movement of solutes through the paracellular spaces in the neurovascular unit is a key mechanism in CNS calcification.Fil: Schottlaender, Lucia V. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido. UCL Great Ormond Street Institute of Child Health. Dubowitz Neuromuscular Centre; Reino Unido. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fleni. Departamento de Neurología; Argentina.Fil: Abeti, Rosella. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido.Fil: Jaunmuktane, Zane. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido. University College London Hospitals NHS Foundation Trust. The National Hospital for Neurology and Neurosurgery. Division of Neuropathology; Reino Unido.Fil: Macmillan, Carol. University of Chicago. Department of Pediatrics; Estados Unidos.Fil: Chelban, Viorica. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: O'Callaghan, Benjamin. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: McKinley, John. Dublin Neurological Institute at the Mater Misericordiae University Hospital. Department of Neurology; Irlanda. Royal Victoria Hospital. Regional Neurosciences Centre; Reino Unido.Fil: Maroofian, Reza. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Efthymiou, Stephanie. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Athanasiou-Fragkouli, Alkyoni. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Forbes, Raeburn. Craigavon Area Hospital. Neurology Centre. Southern HSC Trust; Reino Unido.Fil: Soutar, Marc P M. UCL Queen Square Institute of Neurology. Department of Neurodegenerative Disease; Reino Unido.Fil: Livingston, John H. The Leeds Teaching Hospitals NHS Trust. Paediatric Neurology; Reino Unido.Fil: Kalmar, Bernardett. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Swayne, Orlando. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido. The National Hospital for Neurology and Neurosurgery; Reino Unido.Fil: Hotton, Gary. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido. The National Hospital for Neurology and Neurosurgery; Reino Unido.Fil: SYNAPS Study Group. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Pittman, Alan. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Launchbury, Francesca. UCL Queen Square Institute of Neurology. Department of Neurodegenerative Disease; Reino Unido.Fil: Mendes de Oliveira, João Ricardo. Universidade Federal de Pernambuco. Departamento de Neuropsiquiatria; Brasil.Fil: de Grandis, Maria. Aix-Marseille University, Inserm, CNRS, Institut Paoli-Calmettes; Francia.Fil: Richard-Loendt, Angela. UCL Queen Square Institute of Neurology. Department of Neurodegenerative Disease; Reino Unido.Fil: Althonayan, Juri. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido.Fil: McDonnell, Gavin. Royal Victoria Hospital. Regional Neurosciences Centre; Reino Unido.Fil: Carr, Aisling. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido. The National Hospital for Neurology and Neurosurgery; Reino Unido.Fil: Khan, Suliman. CENTOGENE AG; Alemania.Fil: Beetz, Christian. CENTOGENE AG; Alemania.Fil: Bisgin, Atil. Çukurova University. Medical Genetics Department of Medical Faculty & AGENTEM (Adana Genetic Diseases Diagnosis and Treatment Center); Turquía.Fil: Bozdogan, Sevcan Tug. Çukurova University. Medical Genetics Department of Medical Faculty & AGENTEM (Adana Genetic Diseases Diagnosis and Treatment Center); Turquía.Fil: Begtrup, Amber. GeneDx; Estados Unidos.Fil: Torti, Erin. GeneDx; Estados Unidos.Fil: Greensmith, Linda. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido.Fil: Giunti, Paola. UCL Queen Square Institute of Neurology. Department of Clinical and Movement Neurosciences; Reino Unido.Fil: Morrison, Patrick J. Centre for Cancer Research and Cell Biology; Reino Unido.Fil: Brandner, Sebastian. Division of Neuropathology, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust; Reino Unido.Fil: Aurrand-Lions, Michel. Aix-Marseille University, Inserm, CNRS, Institut Paoli-Calmettes; Francia.Fil: Houlden, Henry. UCL Queen Square Institute of Neurology. Department of Neuromuscular Diseases; Reino Unido. The National Hospital for Neurology and Neurosurgery; Reino Unido. The National Hospital for Neurology and Neurosurgery. Neurogenetics Laboratory and Clinical Service; Reino Unido
Covid-19: Relationship between angiotensin-converting enzyme 2, cardiovascular system and host immune response
No full textLa enfermedad por coronavirus 2019 (COVID-19) provoca el síndrome respiratorio agudo severo por coronavirus 2
(SARS-CoV-2), pudiendo ser particularmente perjudicial para los pacientes con enfermedad cardiovascular (ECV)
subyacente, y siendo una causa de morbilidad y mortalidad significativas en todo el mundo. El virus infecta las células
huésped a través de los receptores de la enzima convertidora de la angiotensina 2 (ECA2) y su internalización del
complejo en dicha célula. ACE2 es un componente enzimático clave del sistema renina-angiotensina-aldosterona
(SRAA), degradando angiotensina (Ang) II, un péptido con múltiples acciones que promueven ECV, y generando
Ang-(1-7), que antagoniza los efectos de Ang II. Además, la evidencia experimental sugiere que el bloqueo de
SRAA por los inhibidores de la ECA y los antagonistas de los receptores de tipo 1 de Ang II, aumentan la ECA2
que, en parte, contribuye al beneficio de estos pacientes. Este virus lleva a una neumopatía, al tiempo que causa
lesiones agudas de miocardio y daño crónico al sistema cardiovascular. Esta lesión miocárdica se presenta en la
fase más severa de COVID-19; pero aún, el mecanismo fisiopatológico de la lesión no fue esclarecido. Por lo
tanto, se debe prestar especial atención a la protección cardiovascular durante el tratamiento para COVID-19. El
síndrome de dificultad respiratoria aguda (SDRA) es una enfermedad clínica de alta mortalidad, y ACE2 tiene un
efecto protector sobre este tipo de lesión pulmonar aguda. La investigación actual muestra que el mal pronóstico
de los pacientes con COVID-19 está relacionado con factores como género masculino, la edad >60 años, las
enfermedades subyacentes: hipertensión, diabetes, ECV, SDRA secundario y otros factores relevantes. Si bien los
datos son limitados, los posibles mecanismos de lesión miocárdica incluyen la entrada viral directa a través del
receptor de membrana de la ECA2 y la toxicidad en las células huésped, la lesión de miocitos relacionada con la
hipoxia y el síndrome de liberación de citoquinas mediado por el sistema inmune, necesitándose más estudios para
esclarecer el mecanismo de cardiotoxicidad y su prevención.
En este artículo se actualiza el conocimiento actual de la biología del SARS-CoV-2 y los posibles mecanismos de
lesión miocárdica debido a toxicidades virales y respuestas inmunes del huésped.Fil: Perrone, Sergio Victor. Fleni. Departamento de Neurología. Servicio de Cardiología; Argentina.Fil: Bevacqua, Raúl J. Hospital General de Agudos Dr. J. M. Ramos Mejía. División Cardiología; Argentina
Psychological distress associated with COVID-19 quarantine: Latent profile analysis, outcome prediction and mediation analysis
No full textBackground: Mental health of the population during COVID-19 quarantine could be at risk. Previous studies in short quarantines, found mood-related and anxiety symptomatology. Here we aimed to characterize the subtypes of psychological distress associated with quarantine, assess its prevalence, explore risk/protective factors, and possible mechanisms.
Methods: Online cross-sectional data (n = 4408) was collected during the Argentine quarantine, between 1st-17th April 2020 along a small replication study (n = 644). Psychological distress clusters were determined using latent profile analysis on a wide-range of symptoms using the complete Brief-Symptom Inventory-53. Multinomial and Elastic-net regression were performed to identify risk/protective factors among trait-measures (Personality and Resilience) and state-measures (COVID-19 related fear and coping-skills).
Results: Three latent-classes defined by symptom severity level were identified. The majority of individuals were classified in the mild (40.9%) and severe classes (41.0%). Participants reported elevated symptoms of Phobic-Anxiety (41.3%), Anxiety (31.8%), Depression (27.5%), General-Distress (27.1%), Obsession-Compulsion (25.1%) and Hostility (13.7%). Logistic-regressions analyses mainly revealed that women, young individuals, having a previous psychiatric diagnosis or trauma, having high levels of trait-neuroticism and COVID-related fear, were those at greater risk of psychological distress. In contrast, adults, being married, exercising, having upper-class income, having high levels of trait-resilience and coping-skills, were the most protected. Mediation analysis, showed that state-measures mediated the association between trait-measures and class-membership.
Conclusions: Quarantine was associated intense psychological distress. Attention should be given to COVID-19-related fear and coping-skills as they act as potential mediators in emotional suffering during quarantine.Fil: Crivelli, Lucía. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Fernández, Rodrigo S. Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE- CONICET); Argentina. Universidad de Buenos Aires.Facultad de Ciencias Exactas y Naturales; Argentina.Fil: Magrath Guimet, Nahuel. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Pedreira, María E. Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE- CONICET); Argentina. Universidad de Buenos Aires.Facultad de Ciencias Exactas y Naturales; Argentina
Microcirugía de las fístulas durales arteriovenosas espinales, más un repaso de la anatomía vascular vertebromedular
No full textIntroducción: la fístula dural arteriovenosa espinal (FDAVE) es una enfermedad vascular rara, de etiología desconocida y frecuentemente subdiagnosticada. El tratamiento puede ser microquirúrgico o endovascular
Material y Método: análisis retrospectivo de una serie de 8 pacientes consecutivos con FDAVE tratados por microcirugía entre 2010 y 2020. Fueron evaluados parámetros como edad, sexo, cuadro clínico pre y postoperatorio medido con las escalas de Aminoff-Logue y Rankin modificada. Los estudios diagnósticos con RMN (Resonancia Magnética Nuclear), ARM (Angio Resonancia Magnética) y ADM (Angiografía Digital Medular) se utilizaron para determinar nivel lesional y resultados quirúrgicos.
Resultados: fueron operados 8 pacientes (7 masculinos y 1 femenino) con un promedio de edad de 58 años. El tiempo de evolución del cuadro clínico al diagnóstico fue menor a 12 meses salvo un caso de 32 meses. Las FDAVE fueron localizadas en: 6 a nivel dorsal entre D6 y D12, una en L2 y la última en S1 (5 derechas y 3 izquierdas) . La arteria de Adamkiewicz se identificó en: 4 casos en L1, 2 en D12, 1 en D10 y un caso en D7 (6 izquierdas y 2 derechas). De los 8 pacientes operados, 3 fueron embolizados previamente. La evolución postoperatoria del cuadro neurológico fue: 2 de 8 permanecieron estables y 6 de 8 mejoraron uno o más puntos en la escala de Rankin modificada; no hubo complicaciones en el postoperatorio. Todos los pacientes mejoraron las imágenes en RMN diferida y la ADM luego de los 6 meses fue negativa. El seguimiento promedio fue de 48 meses con un rango de 11 a 116 meses, ningún paciente presentó recidiva de la FDAVE.
Conclusiones: El tratamiento quirúrgico de las FDAVE es un método muy eficaz, de baja morbilidad y menor tasa de recurrencia comparado con el tratamiento endovascular.Fil: Mormandi, Rubén. Fleni. Departamento de Neurocirugía; Argentina.Fil: Ruella, Mauro E. Fleni. Departamento de Neurocirugía; Argentina.Fil: Villamil, Facundo. Fleni. Departamento de Neurocirugía; Argentina.Fil: Cervio, Andres Eduardo. Fleni. Departamento de Neurocirugía; Argentina.Fil: Condomí Alcorta, Santiago G. Fleni. Departamento de Neurocirugía; Argentina.Fil: Salvat, Jorge M. Fleni. Departamento de Neurocirugía; Argentina