Thalamic nuclear abnormalities as a contributory factor in sudden cardiac deaths among patients with schizophrenia

Patients with schizophrenia have a two- to three-fold increased risk of premature death as compared to patients without this disease. It has been established that patients with schizophrenia are at a high risk of developing cardiovascular disease. Moreover, an important issue that has not yet been explored is a possible existence of a "cerebral" focus that could trigger sudden cardiac death in patients with schizophrenia. Along these lines, several structural and functional alterations in the thalamic complex are evident in patients with schizophrenia and have been correlated with the symptoms manifested by these patients. With regard to abnormalities on the cellular and molecular level, previous studies have shown that schizophrenic patients have fewer neuronal projections from the thalamus to the prefrontal cortex as well as a reduced number of neurons, a reduced volume of either the entire thalamus or its subnuclei, and abnormal glutamate signaling. According to the glutamate hypothesis of schizophrenia, hypofunctional corticostriatal and striatothalamic projections are directly involved in the pathophysiology of the disease. Animal and post-mortem studies have provided a large amount of evidence that links the sudden unexpected death in epilepsy (SUDEP) that occurs in patients with schizophrenia and epilepsy to thalamic changes. Based on the results of these prior studies, it is clear that further research regarding the relationship between the thalamus and sudden cardiac death is of vital importance.

Aproximaciones al lóbulo frontal: una mirada hacia la rehabilitación / Approaches to frontal lobes: a look toward the rehabilitation

La región prefrontal es la estructura más directamente relacionada con el funcionamiento ejecutivo, cognoscitivo y conductual. Es una estructura que es especialmente vulnerable a lesiones cerebrales inducidas como traumas craneoencefálicos, accidentes cerebrovasculares, tumores, trastornos neurodegenerativos y por trastornos del neurodesarrollo. Éstas dejan como secuelas alteración en la capacidad de inhibición, fallas en programación, déficit en memoria operativa y ordenamiento temporal, cambios en conducta social, pseudodepresión, apatía, pérdida de la motivación e iniciativa y dificultad para la inhibición de sus respuestas. La intervención en esta población genera retos para los profesionales de salud quienes han de mantener habilidades personales y profesionales que proyecten en el paciente confianza y efectiva adhesión al tratamiento.

The prefrontal region is the most directly structure related to executive functioning, cognitive and behavioral. Is a structure that is particularly vulnerable to brain damage induced as cephalic trauma, cerebrovascular accidents, tumors, neurodegenerative disorders and neurodevelopmental disorders. These make alterations as sequelae of inhibition in the ability, faulty programming, and working memory deficits in temporal order, changes in social behavior, pseudodepression, apathy, loss of motivation and initiative and difficulty inhibiting their responses. The intervention in this population creates challenges for health professionals who maintain personal and professional skills that project in the patient the trust and effective adherence to treatment.

Modelos neurocognitivos en la esquizofrenia: rol del córtex prefrontal / Neurocognitive models of schizophrenia: the prefrontal cortex role

Los modelos neurocognitivos han dado lugar a un importante avance en la comprensión de diversos desórdenes mentales tales como la esquizofrenia (EQZ). En ese contexto, la disfunción del córtex prefrontal (CPF) es un hallazgo central para explicar su sintomatología. Se ha observado que los niveles anormales de activación de la CPF, así como disfunciones en la conectividad con otras estructuras cerebrales, juegan un importante rol en la delimitación de la enfermedad. Material y Métodos: A través de una revisión teórica, empírica y clínica se describirán cinco aproximaciones neurocognitivas de la esquizofrenia. Conclusiones: Aunque la etiología de la EQZ es probablemente múltiple, un desorden de la interconectividad neuronal, y especialmente de la CPF explican un amplio espectro de su sintomatología.

Introduction: Neurocognitive models gave place to an important improvement in our understanding of several mental disorders such as schizophrenia. In this context, Prefrontal cortex (PFC) dysfunction is an essential variable for its symptomatology account. It has been observed that abnormal level of PFC activation, as well as connectivity dysfunctions with other cerebral structures, play a central role in the delimitation of the disease. Materials and Methods: Through a theoretical, empirical, and clinical review, five neurocognitive approach of schizophrenia will be described. Conclusion: Although schizophrenia etiology is probably multiple, neural interconnectivity disorders and specially those related to PFC, explain a broad range of its symptoms.

Effects of acute prenatal exposure to ethanol on the postnatal morphology of the prefrontal cortex in wistar rats

Prenatal exposure to ethanol is frequently associated with micronecephaly, hypomyelinization, delayed cell migration, and impaired neuronal and glial maturation in the offspring. The mechanism by which ethanol induces its effects on the development of the nervous system is still not fully understood. In this study, the influence of acute prenatal exposure to ethanol on the prefrontal cortex cells of rats were examined. Three doses of ethanol (3g/kg of body weight) were administered intraperitoneally to pregnant female rats on the 12th day of pregnacy, at 8 hours intervals. Control rats received the same treatment but with a saline solution. Cells in the synthesis phase (S) of the cell cycle were labeled with bromodeoxyuridine. Six controls and 12 ethanol-treated neonates were sacrificed on the 8th day of postnatal life. The distance between nuclear cores in immunohistochemically labeled cells was determined by image analysis. Control rats had a normal neocortex, with six layers in the prefrontal region. Rats treated with ethanol showed ectopia of pyramidal neurons in layers I and II, heterotopia in the basal area of the prefrontal fissure, and a decrease in cellular density in layers I and VI of the cerebral prefrontal cortex. These alterations could help to explain some of the dysfunctions reported in patients with fetal alcohol syndrome.