Cognitive outcomes following functional neurosurgery in refractory OCD patients: a systematic review.

Neurosurgery is a therapeutic option for patients with refractory obsessive-compulsive disorder who do not respond to previous treatments. Although its efficacy in reducing clinical symptomatology has been proven, few studies have analyzed its effects at the cognitive level. The aim of this systematic review was to describe the cognitive outcomes of functional neurosurgery in patients that went through capsulotomies or cingulotomies. PubMed, Medline, Scopus, PsycInfo, PsyArticles, and Web of Knowledge were searched for studies reporting cognitive outcomes in refractory obsessive-compulsive patients after capsulotomies and cingulotomies. The risk of bias was assessed with the Assessment Tool for Before-After (Pre-Post) Studies With No Control Group tool; 13 studies met inclusion criteria, including 205 refractory obsessive-compulsive disorder patients for both surgical procedures. Results showed a substantial number of studies that did report significant cognitive improvement after surgery, being this improvement specially related to memory and executive functions. The second-most frequent finding is the maintenance of cognitive performance (nor improvement or worsening). From a neuropsychological point of view, this outcome might be considered a success, given that it is accompanied by amelioration of obsessive-compulsive symptoms. Subtle cognitive adverse effects have also been reported. Neurosurgery procedures appear to be safe from a cognitive point of view. Methodological issues must be improved to draw clearer conclusions, but capsulotomies and cingulotomies constitute an effective alternative treatment for refractory obsessive-compulsive disorder patients.

Evolution of cognitive impairment after a traumatic brain injury: is there any improvement after controlling the practice effect? / Evolución de las alteraciones cognitivas tras un traumatismo craneoencefálico: ¿hay mejoría tras controlar el efecto de la práctica?

INTRODUCTION: The importance of knowing the pattern of evolution of cognitive deficits in the first months after a traumatic brain injury (TBI) has encouraged the development of numerous longitudinal studies. However, the results of most of them should be taken with caution due to the lack of adequate control of practice effects that can lead to overestimating the genuine recovery of cognitive processes. AIM: To describe the cognitive changes between the acute and subacute phases of the TBI controlling the effect of the practice. PATIENTS AND METHODS: Twenty-two patients were assessed in two different time points after TBI (immediately and after six months) using the following tests: Trail Making Test (A, B, B/A, B-A), Stroop Test (W, C, CW, interference), Digit Symbol-Coding, Symbol Search, Digits Forward and Backward, Verbal Fluency and Short-term Memory. To control for the practice effects, a transformation of the scores was performed applying the procedure proposed by Calamia et al. RESULTS. Before controlling the practice effects, the scores of all tests improved (p > 0.001). However, afterward, the improvement remained only in the Trail Making Test-B, B/A and B-A, Digit Symbol-Coding, Symbol Search, Stroop CW and Digits Backward. CONCLUSIONS: The lack of control of practice effects in longitudinal studies can generate misleading interpretations about the evolution of cognitive deficits. The pattern of recovery after a TBI varies depending on the cognitive process.

TITLE: Evolución de las alteraciones cognitivas tras un traumatismo craneoencefálico: ¿hay mejoría tras controlar el efecto de la práctica?Introducción. La importancia de conocer el patrón de evolución de los déficits cognitivos en los primeros meses tras un traumatismo craneoencefálico (TCE) ha fomentado el desarrollo de numerosos estudios longitudinales. Sin embargo, los resultados de la mayoría de ellos deberían tomarse con cautela debido a la falta de un control adecuado del efecto de la práctica, que puede llevar a sobreestimar la recuperación genuina de los procesos cognitivos. Objetivo. Describir los cambios cognitivos entre las fases aguda y subaguda del TCE controlando el efecto de la práctica. Pacientes y métodos. Veintidós pacientes realizaron dos evaluaciones neuropsicológicas tras el TCE (inmediata y tras seis meses) mediante los siguientes tests: Trail Making Test (A, B, B/A y B-A), test de Stroop (P, C, PC e interferencia), clave de números, búsqueda de símbolos, dígitos directos e inversos, fluidez verbal y memoria inmediata. Para controlar el efecto de la práctica se realizó una transformación de las puntuaciones aplicando el procedimiento propuesto por Calamia et al. Resultados. Antes de controlar el efecto de la práctica, se evidenció una mejoría en las puntuaciones de todos los tests (p > 0,001). Sin embargo, tras él, la mejoría permaneció sólo en el Trail Making Test-B, B/A y B-A, la clave de números, la búsqueda de símbolos, el test de Stroop PC y los dígitos inversos. Conclusiones. La falta de control del efecto de la práctica en estudios longitudinales puede generar interpretaciones erróneas sobre el perfil de evolución de los déficits cognitivos. El patrón de recuperación tras un TCE varía en función del proceso cognitivo.

Brain disease, connectivity, plasticity and cognitive therapy: A neurological view of mental disorders. / Enfermedad cerebral, conectividad, plasticidad y terapia cognitiva. Una visión neurológica del trastorno mental.

INTRODUCTION: Our conception of the mind-brain relationship has evolved from the traditional idea of dualism to current evidence that mental functions result from brain activity. This paradigm shift, combined with recent advances in neuroimaging, has led to a novel definition of brain functioning in terms of structural and functional connectivity. The purpose of this literature review is to describe the relationship between connectivity, brain lesions, cerebral plasticity, and functional recovery. DEVELOPMENT: Assuming that brain function results from the organisation of the entire brain in networks, brain dysfunction would be a consequence of altered brain network connectivity. According to this approach, cognitive and behavioural impairment following brain damage result from disrupted functional organisation of brain networks. However, the dynamic and versatile nature of these circuits makes recovering brain function possible. Cerebral plasticity allows for functional reorganisation leading to recovery, whether spontaneous or resulting from cognitive therapy, after brain disease. CONCLUSIONS: Current knowledge of brain connectivity and cerebral plasticity provides new insights into normal brain functioning, the mechanisms of brain damage, and functional recovery, which in turn serve as the foundations of cognitive therapy.

Enfermedad cerebral, conectividad, plasticidad y terapia cognitiva. Una visión neurológica del trastorno mental / Brain disease, connectivity, plasticity and cognitive therapy: A neurological view of mental disorders

INTRODUCCIÓN: La relación entre mente y cerebro ha evolucionado desde el clásico dualismo hasta los conocimientos actuales que ponen de manifiesto que las funciones mentales son el resultado de la actividad cerebral. Este cambio de paradigma, junto con los recientes avances en diferentes técnicas de neuroimagen, ha dado lugar a una novedosa concepción del funcionamiento cerebral en términos de conectividad estructural y funcional. El objetivo del presente trabajo es describir la relación entre conectividad, lesión cerebral, plasticidad cerebral y recuperación funcional. DESARROLLO: Si la función cerebral surge de la organización en red del cerebro como un todo, la disfunción cerebral se puede producir por una alteración en la conexión de estas redes. Así, a partir del modelo conectivista, los trastornos cognitivos y del comportamiento que aparecen tras una afección cerebral se describen como consecuencia de una alteración en la organización funcional de las redes cerebrales. Sin embargo, la pérdida de funciones puede ser recuperada gracias a la capacidad de los circuitos de ser dinámicos y versátiles. La plasticidad cerebral permite una reorganización funcional que llevará a una recuperación, espontánea o potenciada con terapia cognitiva, después de algún tipo de enfermedad cerebral. CONCLUSIONES: El conocimiento de la conectividad y la plasticidad cerebrales proporciona una nueva perspectiva desde la que entender el funcionamiento cerebral en condiciones normales, los mecanismos del daño cerebral y los de la recuperación funcional, constituyendo las bases para el desarrollo de la terapia cognitiva

INTRODUCTION: Our conception of the mind-brain relationship has evolved from the traditional idea of dualism to current evidence that mental functions result from brain activity. This paradigm shift, combined with recent advances in neuroimaging, has led to a novel definition of brain functioning in terms of structural and functional connectivity. The purpose of this literature review is to describe the relationship between connectivity, brain lesions, cerebral plasticity, and functional recovery. DEVELOPMENT: Assuming that brain function results from the organisation of the entire brain in networks, brain dysfunction would be a consequence of altered brain network connectivity. According to this approach, cognitive and behavioural impairment following brain damage result from disrupted functional organisation of brain networks. However, the dynamic and versatile nature of these circuits makes recovering brain function possible. Cerebral plasticity allows for functional reorganisation leading to recovery, whether spontaneous or resulting from cognitive therapy, after brain disease. CONCLUSIONS: Current knowledge of brain connectivity and cerebral plasticity provides new insights into normal brain functioning, the mechanisms of brain damage, and functional recovery, which in turn serve as the foundations of cognitive therapy

[Processing speed in relapsing-remitting multiple sclerosis: the role played by the depressive symptoms]. / Velocidad de procesamiento en la esclerosis multiple remitente recurrente: el papel de los sintomas depresivos.

INTRODUCTION: Reduced speed of information processing seems to characterize neuropsychological performance in multiple sclerosis (MS) patients. However, the impact in speed of information processing of depressive symptoms, that are highly prevalent in this population, has not been precisely defined yet due to the presence of some methodological limitations in most preceding studies. SUBJECTS AND METHODS: 42 MS remittent recurrent patients, 20 with depressive symptoms (BDI > 13), and 22 without, were compared to 24 healthy controls in neuropsychological tasks of speed of processing (SDMT, Stroop, TMT y PASAT-BNB). RESULTS: MS patients without depressive symptoms performed significantly worse than healthy controls the Stroop (W, C and WC), and the PASAT-BNB (execution time) tests. MS patients with depressive symptoms performed significantly worse than healthy controls the Stroop (W, C and WC), SDMT, TMT (A, B and B-A), and the PASAT-BNB (execution time and errors) tests. MS patients with depressive symptoms performed significantly worse than MS patients without depressive symptoms the SDMT, TMT (A, B and B-A), and the PASAT-BNB (execution time) tests. CONCLUSIONS: MS impact was not generalized in neuropsychological performance of patients. Depressive symptoms seem to play and important role determining the speed deficit. While MS reduced speed of information processing, depressive symptoms were associated to specific cognitive deficit different from speed ones.

[HIV-1 neuropathogenesis: therapeutic strategies against neuronal loss induced by gp120/Tat glycoprotein in the central nervous system]. / Neuropatogenesis inducida por el virus del sida: estrategias terapeuticas frente a la neurodegeneracion inducida por la glucoproteina gp120/Tat en el sistema nervioso central.

Neuroinflammation is a key process in the neuropathogenesis of AIDS virus since as a result of the aberrant activation of the chemokine receptors (CXCR4, CX3CR1 and CR5) produces proinflammatory cytokine release by infected cells, increases microglial neurotoxicity and generates lipoperoxides and reactive oxygen species (ROS) that eventually damage the neuron. Moreover, the neurotoxin Tat produces dendritic loss by interacting with the low-density lipoprotein receptor (LRP) and also overstimulates N-methyl D-aspartate receptors (NMDA). Furthermore, the aberrant interaction of glycoprotein gp120 with the CXCR4 chemokine receptor causes caspase-3-dependent apoptosis (ceramide is also released) activating apoptotic proteins (p53 and retinoblastoma), which are part of the neurotoxic mechanisms associated to neuronal dysfunction in neuroAIDS. Similarly, gliosis/microglial activation and the release of neurotoxic factors by infected monocytes with elevated amounts of certain chemokines in the cerebrospinal fluid (MCP-1 and fractalkine, among others) contribute to the neuropathogenesis of HIV-1. Alpha-synuclein and beta amyloid deposits have also been detected in post mortem brains of seropositives patients. In addition, there are studies have detected several systemic markers related with the degenerative effects of the virus and its neurotoxins on the central nervous system; such as osteopontin, CD163 and fractalkine, among others. Lastly, clinical trials have been conducted using protective strategies related that attempt to inhibit apoptotic proteins (GSK-3 beta), microglial activation inhibitors (minocycline), antioxidants (selegiline) or trophic factors (IGF-1, growth hormone or erythropoietin). These trials have shown that their treatments are beneficial and complementary to treat complications of HIV/AIDS.