Circulating autoantibodies against the NR2 peptide of the NMDA receptor are associated with subclinical brain damage in hypertensive patients with other pre-existing conditions for vascular risk.

Arterial hypertension (HT) and other vascular pre-existing conditions (PEC) generate asymptomatic brain damage which increases the occurrence of stroke and cognitive decline. The aim of this work was to explore if serum antibodies against the NR2 subunit of the NMDA receptor (NR2Ab) could predict subclinical brain damage (SBD) in hypertensive patients with PEC. Forty seven neurologically asymptomatic hypertensive subjects were classified according to the number of PEC (retinopathy, overweight/obesity, diabetes mellitus and dyslipidemia). NR2A/B Ab were measured in serum employing an ELISA method. 3.0-T Brain MRI imaging was performed, and visual ratings of white matter hyperintensities (WMH) and counts of dilated Virchow-Robin spaces (DVRS) and lacunes were obtained. Brain atrophy was evaluated with cortical thickness measurements and linear measures. Higher levels of NR2Ab were associated with more severe periventricular WMH (PWMH), more DVRS and more severe SBD; while greater frontal interhemispheric fissure width (IHFW), as a linear measure of frontal atrophy, was inversely related with NR2Ab. Overall and regional cortical thickness were not significantly associated with NR2 Ab. A multivariate analyses showed that IHFW and PWMH were the only variables independently associated with serum NR2Ab concentration. ROC analysis revealed that NR2Ab (cutoff: 1.7ng/ml) predicted PWMH with a sensitivity and specificity of 65% and 87% respectively. CONCLUSIONS: Serum NR2Ab levels may reflect SBD in HT subjects with PEC, especially in younger populations at risk, where age-related cortical atrophy has not yet been fully established.

[Cognitive diagnosis of cerebrovascular disease by event related potentials: anatomical sources that generate P300]. / Diagnóstico cognitivo en la enfermedad cerebrovascular mediante potenciales relacionados con eventos: fuentes anatómicas generadoras de la P300.

INTRODUCTION: Cerebrovascular disease causes different cognitive alterations. There is a need to develop tools that are capable of diagnosing them. One of them could be event related potentials. These provide an indicator of cognitive processing in real time. PATIENTS AND METHODS: A study was conducted of 10 patients with cerebral infarction in the frontal region and 10 paired healthy controls. Evaluation of the patients was performed a week after the stroke. A continuous performance test was applied to both groups together with the recording of the electrical activity in the brain in order to obtain the P300 component. The results were submitted to the non-parametric Student's t test, and the Bayesian model averaging method (BMAM) was employed to calculate the sources generating the electrical activity recorded on the electroencephalogram. RESULTS: Patients displayed significantly poorer performances compared to the healthy controls in the attention test. The BMAM showed that the P300 component was related to the right hand temporal structures in healthy controls, whereas the left temporoparietal regions were also involved in the patients. CONCLUSIONS: These findings indicate the existence of subclinical disorders affecting sustained attention and that they can only be detected by very sensitive tools; furthermore, they also have implications for the brain circuits regulating sustained attention and the P300 component.

Diagnóstico cognitivo en la enfermedad cerebrovascular mediante potenciales relacionados con eventos: fuentes anatómicas generadoras de la P300 / Cognitive diagnosis of cerebrovascular disease by event-related potentials: anatomical sources that generate p300

Introducción. La enfermedad cerebrovascular causa alteraciones cognitivas disímiles. Es preciso desarrollar herramientas capaces de diagnosticarlas, y una de ellas podría ser los potenciales relacionados con eventos. Éstos brindan un indicador en tiempo real del procesamiento cognitivo. Pacientes y métodos. Se estudiaron 10 pacientes con infarto cerebral en la región frontal y 10 controles sanos pareados. La evaluación de los pacientes se realizó una semana después de presentar el infarto. A ambos grupos se les aplicó un test de ejecución continua asociado al registro de la actividad eléctrica cerebral para la obtención del componente P300. Los resultados obtenidos se sometieron a la prueba no paramétrica t de Student, y el electroencefalograma, al método de promediación de modelos bayesianos (MPMB) para el cálculo de las fuentes generadoras de la actividad eléctrica registrada. Resultados. Los pacientes tuvieron ejecuciones significativamente más pobres que los controles sanos en la prueba de atención. El MPMB mostró que el componente P300 se relaciona con las estructuras temporales derechas en los controles sanos, mientras que en los pacientes se suman las zonas temporoparietales izquierdas. Conclusiones. Estos resultados indican la existencia de alteraciones subclínicas de la atención sostenida, y que sólo herramientas más sensibles pueden detectarlas; además, tienen implicaciones para los circuitos cerebrales reguladores de la atención sostenida y del componente P300 (AU)

Introduction. Cerebrovascular disease causes different cognitive alterations. There is a need to develop tools that are capable of diagnosing them. One of them could be event-related potentials. These provide an indicator of cognitive processing in real time. Patients and methods. A study was conducted of 10 patients with cerebral infarction in the frontal region and 10 paired healthy controls. Evaluation of the patients was performed a week after the stroke. A continuous performance test was applied to both groups together with the recording of the electrical activity in the brain in order to obtain the P300 component. The results were submitted to the non-parametric Student’s t test, and the Bayesian model averaging method (BMAM) was employed to calculate the sources generating the electrical activity recorded on the electroencephalogram. Results. Patients displayed significantly poorer performances compared to the healthy controls in the attention test. The BMAM showed that the P300 component was related to the right-hand temporal structures in healthy controls, whereas the left temporoparietal regions were also involved in the patients. Conclusions. These findings indicate the existence of subclinical disorders affecting sustained attention and that they can only be detected by very sensitive tools; furthermore, they also have implications for the brain circuits regulating sustained attention and the P300 component (AU)

[Some considerations about the possible pathological mechanisms at work in antiphospholipid syndrome and stroke]. / Algunas consideraciones acerca de los posibles mecanismos patológicos en el síndrome antifosfolípidos e ictus.

INTRODUCTION AND DEVELOPMENT: Over the last two decades antiphospholipid syndrome (APS) has started to be recognized from the association of apparently anionic phospholipid-specific antibodies with thrombosis, thrombocytopenia and recurrent foetal losses. This syndrome affects patients with systemic lupus erythematosus and is considered to be an important cause of thromboembolic disease. Antiphospholipid antibodies are serum immunoglobulins that react with negatively charged phospholipids, albeit directly or by means of a cofactor, affect the coagulation system, and promote thrombosis. Recent research has been directed towards gaining an understanding of the mechanisms by which these antibodies are able to play a direct role in the pathophysiology of thrombosis, and the extent to which certain risk factors, such as smoking, high blood pressure, lipid disorders and so on, exert an influence over the expression of phospholipids in the cerebral endothelium. CONCLUSION: These antibodies have no single mechanism of action; different authors have described different pathological mechanisms, which help us to understand the heterogeneous clinical manifestations of APS.

Algunas consideraciones acerca de los posibles mecanismos patológicos en el síndrome antifosfolípidos e ictus / Some considerations about the possible pathological mechanisms at work in antiphospholipid syndrome and stroke

Introducción y desarrollo. En las dos últimas décadas ha comenzado a reconocerse el síndrome antifosfolípidos (SAP) por la asociación de anticuerpos con una aparente especificidad por fosfolípidos aniónicos con trombosis, trombocitopenia y pérdidas fetales recurrentes. Este síndrome afecta a pacientes con lupus eritematoso sistémico y se considera una causa importante de enfermedad tromboembólica. Los anticuerpos antifosfolípidos son inmunoglobulinas del suero que reaccionan con fosfolípidos cargados negativamente, ya sea directamente o a través de un cofactor, afectan el sistema de la coagulación y promueven la trombosis. Algunas investigaciones recientes se han encaminado a comprender los mecanismos por los que estos anticuerpos pueden desempeñar un papel directo en la fisiopatología de la trombosis, y cómo pueden influir determinados factores de riesgo como el tabaquismo, la hipertensión arterial, la hiperlipidemia, etc., sobre la expresión de los fosfolípidos en el endotelio cerebral. Conclusión. No existe un mecanismo único de acción de estos anticuerpos; diversos autores han descrito diferentes mecanismos patológicos, los cuales ayudan a comprender las heterogéneas manifestaciones clínicas del SAP (AU)

Introduction and development. Over the last two decades antiphospholipid syndrome (APS) has started to be recognized from the association of apparently anionic phospholipid-specific antibodies with thrombosis, thrombocytopenia and recurrent foetal losses. This syndrome affects patients with systemic lupus erythematosus and is considered to be an important cause of thromboembolic disease. Antiphospholipid antibodies are serum immunoglobulins that react with negatively charged phospholipids, albeit directly or by means of a cofactor, affect the coagulation system, and promote thrombosis. Recent research has been directed towards gaining an understanding of the mechanisms by which these antibodies are able to play a direct role in the pathophysiology of thrombosis, and the extent to which certain risk factors, such as smoking, high blood pressure, lipid disorders and so on, exert an influence over the expression of phospholipids in the cerebral endothelium. Conclusion. These antibodies have no single mechanism of action; different authors have described different pathological mechanisms, which help us to understand the heterogeneous clinical manifestations of APS (AU)

[Specific alterations in attention in the early stages of Parkinson's disease]. / Alteraciones específicas de la atención en estadios tempranos de la Enfermedad de Parkinson.

INTRODUCTION: The cognitive disorders presented by patients with Parkinson s disease (PD) have drawn attention to the role played by the basal ganglia in cognition. It has been suggested that through a system of cortico subcortical circuits they monitor the work done by the frontal regions by guiding the anterior and posterior attentional systems, whose functioning is necessary for the so called executive functions to be carried out. PATIENTS AND METHODS: We studied 10 patients with PD in developmental stages I and II according to the scale of Hoehn and Yahr, and 10 healthy paired controls. All of them were administered a test for simple sustained attention, complex sustained attention and attentional shift. RESULTS: In the simple sustained attention task there were no significant differences between groups. In the complex sustained attention test the patients committed more mistakes, and in the attentional shift task they committed more omissions and there was a significant increase in reaction time. CONCLUSIONS: Even in the early stages of the disease, patients suffering from Parkinson present cognitive disorders. These are concentrated in the detection and evaluation of new information, in the capability to shift attention between different spatial regions in a flexible manner and in choosing, inhibiting and activating motor programmes. In order to detect these alterations more sensitive and complex tests must be used.

Alteraciones específicas de la atención en estadios tempranos de la enfermedad de Parkinson / Specific alterations in attention in the early stages of Parkinson´s disease

Introducción. Los trastornos cognitivos que presentan los pacientes con enfermedad de Parkinson (EP) han llamado la atención sobre la función de los ganglios basales en la cognición. Se ha propuesto que monitorizan el trabajo de las regiones frontales mediante un sistema de circuitos cortico subcorticales, al guiar a los sistemas atencionales anterior y posterior, cuyo funcionamiento se necesita para el desarrollo de las llamadas funciones ejecutivas. Pacientes y métodos. Se estudiaron 10 pacientes con EP en estadios evolutivos I y II según la escala de Hoehn yYahr y 10 controles sanos pareados. A todos se les aplicó una prueba de atención sostenida simple, atención sostenida compleja y de cambio atencional. Resultados. En la prueba de atención sostenida simple no hubo diferencias significativas entre los grupos. En la de atención sostenida compleja los pacientes cometieron una mayor cantidad de errores, y en la de cambio atencional cometieron más omisiones y aumentaron significativamente su tiempo de reacción. Conclusiones. Los pacientes parkinsonianos que se encuentran en estadios tempranos de la enfermedad presentan alteraciones cognitivas. Éstas se concentran en la detección y evaluación de nueva información, en la posibilidad de cambiar de manera flexible la atención entre regiones espaciales diferentes y en elegir, inhibir y activar programas motores. Para detectar estas alteraciones se precisa de pruebas más sensibles y complejas (AU)