Search

Knowledge of the neurobiological and neurochemical bases of many pathological processes in the brain is of overwhelming importance in orienting and modulating the therapy, monitoring the patient and maintaining the affected brain functions at least at an optimal level. The neurochemistry and neurobiology of autism still have serious unexplained and insufficiently studied gaps. In its essence, autism is a neurobiological or neurogenetic condition with the involvement of several organs or systems, although the central nervous system is predominant. There is significant evidence to support the hypothesis that autism spectrum disorder (ASD) is largely a disorder of the association cortex and its neural connectivity. The association cortex refers to regions of the cerebral cortex involved in integrating sensory information, linking it to memory and cognition, and enabling complex behaviors such as social interaction and communication areas that are often impacted by autism. Intracortical connectivity also seems to be disturbed. The pathophysiology of autism spectrum disorder is multifactorial, involving a complex interplay of environmental, immunological, genetic and epigenetic factors. These elements likely interact early in the development, influencing both neuroanatomical and neurochemical processes in the central nervous system. While researchers have identified several neurochemical pathways associated with ASD, how these pathways interact to cause the core symptoms of autism – such as social communication deficits, restricted interests, and repetitive behaviors – remains incompletely understood. The impact on parents, on social life, and the adaptation or maladaptation of the autistic person to the gradual demands of society are delicate aspects that require an indepth study, a lot of patience and dedication of the specialized and nonspecialized personnel who come into contact with an autistic child. [ABSTRACT FROM AUTHOR]

Encephalitis with anti-NMDA receptor antibodies is one of the most common autoimmune encephalitis, after acute demyelinating encephalitis. Recent data from the specialized literature bring attention to a series of hypothetical mechanisms regarding the causes of the symptoms of encephalitis with anti-NMDA receptor antibodies. Beyond these, the acute psychosis that can occur is associated with the presence in the blood and cerebrospinal fluid of antibodies directed at the NR1a subunit of the NMDA receptor, which causes a slowing of the activity of neurons at this level. Behavioral, mood and cognitive disorders can be the cause of reversible atrophy predominantly in the frontotemporal area, where NMDA receptors are densely distributed. [ABSTRACT FROM AUTHOR]

Institutionalized children often suffer from a vulnerability and neglect that can affect their lives throughout its course, leaving even the sequelae that imprint them and a certain delay in their hormonal, physical and emotional-behavioural development. The environment from which these children come, the family particularities and the nature of the institutionalization, are decisive factors that exert their action and impact in time, often leaving irreversible wounds with a sufficiently visible imprint on the adult life. This article is intended for the analysis of some retroactive findings, observed in institutionalized children aged between 2 and 8 years, findings from more special points of view that have not been the subject of many publications found in the literature. Thus, are described particularities of behavior during institutionalization as well as "post-institutional syndrome", cerebral impairments at the neurobiological and neurogenetic level, delays and deviations in the development of the intellect and, subsequently, their integration into society. [ABSTRACT FROM AUTHOR]