HIV-1 infection and its impact on the HPA axis, cytokines, and cognition

Immediately after infection, Human immunodeficiency virus, type 1 (HIV-1) enters the central nervous system (CNS) and is localized in highest concentration in the hippocampus and basal ganglia. Since these areas are associated with HPA axis and autonomic activities as well as cognition, it has been hypothesized that these functions will be impacted adversely in HIV-1 infection. In the treatment of HIV infection, although the highly potent antiretroviral (HAART) drugs have been effective in reducing peripheral viral load and prolonging life expectancy, these drugs do not cross the blood-brain barrier in therapeutic concentrations. Therefore, it has been proposed that the beneficial effects of HAART on the CNS will be limited. Our investigations on seropositive individuals, showing hypo-reactivity of the autonomic system and HPA axis activity suggest that HIV-1 infection is a model of chronic stress. Furthermore, an elevated baseline TNF-alpha level as well as its increased reactivity to an alpha-adrenergic challenge among HIV-1+ individuals, may lead to additional neurodegeneration. It is proposed that the effects of HIV-1 infection on the brain will have implications for neurocognitive and mental health functioning in seropositive individuals even in patients undergoing HAART therapy. These outcomes may result in the need to develop facilities for long term "care-giving".     

Central nervous system complications of sickle cell disease in children: an overview.

Complications involving the central nervous system are among the most devastating manifestations of sickle cell disease. Although overt stroke occurs in 1 in 10 children with Hemoglobin SS, "silent cerebral infarcts" are even more frequent. Both are associated with significant neuropsychological deficits. The end result of these effects on the CNS often is diminished school performance. The use of transcranial Doppler ultrasonography screening allows the identification of patients at high risk for clinical stroke as well as stroke prevention by chronic transfusion. However, definitive prophylaxis and treatment for most CNS complications of sickle cell disease have yet to be determined.     

Central Nervous System Complications of Sickle Cell Disease in Children: An Overview

Complications involving the central nervous system are among the most devastating manifestations of sickle cell disease. Although overt stroke occurs in 1 in 10 children with Hemoglobin SS, “silent cerebral infarcts” are even more frequent. Both are associated with significant neuropsychological deficits. The end result of these effects on the CNS often is diminished school performance. The use of transcranial Doppler ultrasonography screening allows the identification of patients at high risk for clinical stroke as well as stroke prevention by chronic transfusion. However, definitive prophylaxis and treatment for most CNS complications of sickle cell disease have yet to be determined.     

Neuropsychological Functioning and Antiretroviral Treatment in HIV/AIDS: A Review

This article presents a review of studies that have investigated the neuropsychological effects of antiretroviral treatment (ART) for HIV-1 infection. It provides a brief overview of the era of monotherapy, dual-therapy, and an extended overview of the current era of combination antiretroviral therapy (CART). This review highlights that while CART has had a dramatic effect on the incidence and the severity of HIV-associated neurocognitive disorders (HAND), HAND, in its mild form, still remains prevalent. New causes of this sustained prevalence are poor CNS penetration of some antiretroviral agents, drug resistance, poor adherence, potential neurotoxicity, co-morbidities such as the long-term CART side effects in relation to cardio-vascular disease, and chronic HIV brain infection that may facilitate the expression of new forms of neurodegenerative processes. The review emphasizes the need to address methodological limitations of published studies and the need for large and representative cross-disciplinary longitudinal investigations across the HIV illness span.     

Dementia and the Neurovirulence of HIV-1

Infection with human immunodeficiency virus type 1 (HIV-1) leads rapidly to infection of the brain and subsequent neuropsychological impairment, including subclinical impairment, minor cognitive-motor disorder, and HIV-1-associated dementia (HAD). This article reviews HAD and the factors involved in its pathogenesis; the effectiveness of antiretroviral therapy; the prevalence of HIV-1 and subtypes; and the role of chemokines and cytokines as the capstones associated with neuropathology due to inflammation.     

Theory-Driven Interventions in Psychoneuroimmunology and HIV-1 Infection

Psychoneuroimmunology (PNI) is a rapidly evolving multidisciplinary field founded on the premise that psychosocial factors, the central nervous system, and the immune system are intimately linked. Following publication of scientific evidence supporting this link, a number of animal and human studies have been published, both inside and outside the area of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome. These studies support the existence of bidirectional feedback mechanisms operating between the brain and the immune system. To date, however, there is no all-encompassing model that predicts individual differences in the relationship among psychosocial factors, immunologic measures, and clinical disease progression in HIV type 1 (HIV-1) infection. This variability in human response has been explained by a number of cofactors (host as well as environmental) that appear to accelerate the course of the disease. Since psychosocial factors are highly amenable to behavioral interventions, several models for intervention research have been proposed to evaluate whether such interventions can enhance immune functioning, thereby curtailing disease progression. Examination of these interventions in the context of PNI and HIV-1 infection, however, is rather limited. Therefore, researchers and clinicians must not only consider conceptualizations and paradigms in this area of research, but also focus on empirically testable, theory-driven models that allow for the unique characteristics of individual patients.     

Central and autonomic nervous system integration in emotion

Emotions involve physiological responses that are regulated by the brain. The present paper reviews the empirical literature on central nervous system (CNS) and autonomic nervous system (ANS) concomitants of emotional states, with a focus on studies that simultaneously assessed CNS and ANS activity. The reviewed data support two primary conclusions: (1) numerous cortical and subcortical regions show co-occurring activity with ANS responses in emotion, and (2) there may be reversed asymmetries on cortical and subcortical levels with respect to CNS/ANS interrelations. These observations are interpreted in terms of a model of neurovisceral integration in emotion, and directions for future research are presented.     

The Strelau Temperament Inventory-revised (STI-R): Theoretical considerations and scale development

The development of a revised Strelau Temperament Inventory (STI-R) is reported. It is assumed that the STI-R provides a measure of the basic central nervous system (CNS) properties (strength of excitation, strength of inhibition, and mobility of the CNS) as understood by Pavlov. On the basis of a series of studies, the development of the final forms of the revised STI has undergone several steps. The following forms have been elaborated: (1) a 252-item pilot form of the STI-R; (2) a 166-item STI-R with ‘yes’ and ‘no’ answer format; (3) a short form (84 items) of the STI-R (STI-RS) with ‘yes’ and ‘no’ answer format; (4) a 166-item STI-R with a 4-point Likert scale; and (5) an 84-item STI-RS with a 4-point rating scale. The psychometric characteristics of the consecutive versions of the revised STI improved from step to step, and in general these characteristics are judged as being satisfactory. Especially recommended by the authors are versions (4) and (5), which have, among other things, the highest reliability scores. They are regarded as the final forms of the STI-R and STI-RS.     

Visual prediction: psychophysics and neurophysiology of compensation for time delays

A necessary consequence of the nature of neural transmission systems is that as change in the physical state of a time-varying event takes place, delays produce error between the instantaneous registered state and the external state. Another source of delay is the transmission of internal motor commands to muscles and the inertia of the musculoskeletal system. How does the central nervous system compensate for these pervasive delays? Although it has been argued that delay compensation occurs late in the motor planning stages, even the earliest visual processes, such as phototransduction, contribute significantly to delays. I argue that compensation is not an exclusive property of the motor system, but rather, is a pervasive feature of the central nervous system (CNS) organization. Although the motor planning system may contain a highly flexible compensation mechanism, accounting not just for delays but also variability in delays (e.g., those resulting from variations in luminance contrast, internal body temperature, muscle fatigue, etc.), visual mechanisms also contribute to compensation. Previous suggestions of this notion of "visual prediction" led to a lively debate producing re-examination of previous arguments, new analyses, and review of the experiments presented here. Understanding visual prediction will inform our theories of sensory processes and visual perception, and will impact our notion of visual awareness.     

HIV Infection and the Central Nervous System: A Primer

The purpose of this brief review is to prepare readers who may be unfamiliar with Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome (HIV/AIDS) and the rapidly accumulating changes in the epidemic by providing an introduction to HIV disease and its treatment. The general concepts presented here will facilitate understanding of the papers in this issue on HIV-associated neurocognitive disorders (HAND). Toward that end, we briefly review the biology of HIV and how it causes disease in its human host, its epidemiology, and how antiretroviral treatments are targeted to interfere with the molecular biology that allows the virus to reproduce. Finally, we describe what is known about how HIV injures the nervous system, leading to HAND, and discuss potential strategies for preventing or treating the effects of HIV on the nervous system.     

Extended spider cognition

There is a tension between the conception of cognition as a central nervous system (CNS) process and a view of cognition as extending towards the body or the contiguous environment. The centralised conception requires large or complex nervous systems to cope with complex environments. Conversely, the extended conception involves the outsourcing of information processing to the body or environment, thus making fewer demands on the processing power of the CNS. The evolution of extended cognition should be particularly favoured among small, generalist predators such as spiders, and here, we review the literature to evaluate the fit of empirical data with these contrasting models of cognition. Spiders do not seem to be cognitively limited, displaying a large diversity of learning processes, from habituation to contextual learning, including a sense of numerosity. To tease apart the central from the extended cognition, we apply the mutual manipulability criterion, testing the existence of reciprocal causal links between the putative elements of the system. We conclude that the web threads and configurations are integral parts of the cognitive systems. The extension of cognition to the web helps to explain some puzzling features of spider behaviour and seems to promote evolvability within the group, enhancing innovation through cognitive connectivity to variable habitat features. Graded changes in relative brain size could also be explained by outsourcing information processing to environmental features. More generally, niche-constructed structures emerge as prime candidates for extending animal cognition, generating the selective pressures that help to shape the evolving cognitive system.     

Adrenergic pharmacology: focus on the central nervous system

Norepinephrine and epinephrine are involved in the control of several important functions of the central nervous system (CNS), including sleep, arousal, mood, appetite, and autonomic outflow. Catecholamines control these functions through activation of a family of adrenergic receptors (ARs). The ARs are divided into three subfamilies (alpha1, alpha2, and beta) based on their pharmacologic properties, signaling mechanisms, and structure. ARs in the CNS are targets for several therapeutic agents used in the treatment of depression, obesity, hypertension, and other diseases. Not much is known, however, about the role of specific AR subtypes in the actions of these drugs. In this paper, we provide an overview of adrenergic pharmacology in the CNS, focusing on the pharmacologic properties of subtype-selective AR agonists and antagonists, the accessibility of these drugs to the CNS, and the distribution of ARs in different areas of the brain.     

Service in the Gulf War and Significant Health Problems: Focus on the Central Nervous System

The consensus of several studies on health among Gulf War (GW)-deployed veterans is that they have elevated symptom complaints. Central nervous system (CNS) symptoms among these veterans have been assessed in several investigations. Studies have disagreed as to whether there are neuropsychological deficits in GW-deployed veterans relative to controls. When differences between these groups have been found, they have often been attributed to stress or psychiatric factors, although exposures to neurotoxic substances present in the GW theatre have also been indicted as possible explanations. A review of the existing literature as well as the 5 papers contained in this issue of Journal of Psychopathology and Behavioral Assessment suggests that the neuropsychological and health symptom sequelae of GW zone service are multidetermined and cannot easily be explained on the basis of simplistic models of causation. Psychological, historical, and exposure parameters must be considered in the scientific evaluation of this problem.     

HIV-1 Infection, Neuroendocrine Abnormalities, and Clinical Outcomes

Different lines of evidence suggest that human immunodeficiency virus type 1 (HIV-1) infection is complicated by a variety of adverse effects on neuroendocrine systems. Soon after the discovery of HIV-1, reports began to appear suggesting that a number of neurotransmitter and neuroendocrine activities were negatively impacted by this infection. In 1987 it was observed that fine-needle aspiration of the lung in patients with acquired immunodeficiency syndrome resulted in syncopal reactions. Subsequently, an abnormality in the autonomic nervous system was reported in these patients. However, investigations in this area have remained limited due to the assumption that HIV-1-mediated activation of various endocrine systems was related to the major life stressor of living with a fatal disease. Evidence accumulated over the years has indicated, instead, that there are various other mechanisms in addition to life stressors that also play an important role in negatively impacting the neuroendocrine systems in this infection. This article examines various developments that have taken place in this area in order to provide avenues for future research.     

Tardive dyskinesia and perceptual dysfunction

There is equivocal evidence for a relationship between neuroleptic-induced tardive dyskinesia and central nervous system (CNS) dysfunction. Using the Bender-Gestalt test as the dependent measure, we hypothesized that a group of chronic schizophrenic patients with tardive dyskinesia would show more perceptual dysfunction than those without. Our results supported this hypothesis. CNS dysfunction is discussed in terms of a possible predisposition to tardive dyskinesia.     

Applications of gene targeting technology to mental retardation and developmental disability research

The human and mouse genome projects elucidated the sequence and position map of innumerous genes expressed in the central nervous system (CNS), advancing our ability to manipulate these sequences and create models to investigate regulation of gene expression and function. In this article, we reviewed gene targeting methodologies with emphasis on applications to CNS development and neurodevelopmental disorders.     

功能性胃肠病的发病机制

功能性胃肠病（functional gastrointestinal disorders,FGIDs）是一类常见的消化道疾病,近几年其发病率有明显增高的趋势。以往认为FGIDs主要是由胃肠道动力障碍所引起,但近几年随着人们对这类疾病认识的进一步深入,发现其与内脏感觉、炎症、肠神经系统（ENS）甚至中枢神经系统（CNS）调节功能等因素有关。因此,明确FGIDs的病因和发病机制成为对其进行针对性治疗的突破口。     

BDNF serum levels in subjects developing or not post-traumatic stress disorder after trauma exposure

Post-traumatic stress disorder (PTSD) is a syndrome resulting from exposure to a severe traumatic event that poses threatened death or injury and produces intense fear and helplessness. The neural structures implicated in PTSD development belong to the limbic system, an important region for emotional processing. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that serves as survival factor for selected populations of central nervous system (CNS) neurons and plays a role in the limbic system by regulating synaptic plasticity, memory processes and behavior. Impaired BDNF production in the brain can lead to a variety of CNS dysfunctions including symptoms associated with PTSD. However, so far fewer studies have investigated this neurotrophin in patients with PTSD. Furthermore, given the multiple role of BDNF in various CNS disorders, it cannot be excluded that traumatic events per se may influence neurotrophin levels, without a direct association to the PTSD syndrome.     

Parallel between antianxiety and cardiovascular effects of chlordiazepoxide in genetically nervous dogs

There is evidence that cardiac arrhythmias are partially of CNS origin, and that certain drugs affect arrhythmia, both positively and negatively, through CNS action. We hypothesized and confirmed that chlordiazepoxide diminished the well-established incidence of arrhythmias (A-V blocks and nodal escapes) in five nervous pointer dogs. It is known that this drug normalizes behavior and aids in the bar-pressing performance of nervous dogs. Nervous dogs tend to have low heart rates (HRs) while normals have higher HRs. Chlordiazepoxide increased HRs in our five nervous dogs, and we postulated that HR increase would be less or none in normals. This was confirmed in a later study of five normals. A further study of eight normal dogs and eight nervous dogs essentially reproduced these findings, suggesting the possibility that the slow heart rates and the behavioral abnormality have a common basis, expected to be some CNS biochemical lesion.     

Effects of early noise exposure on hippocampal-dependent behaviors during adolescence in male rats: influence of different housing conditions

Animal Cognition - Central nervous system (CNS) development is a very complex process that can be altered by environmental stimuli such as noise, which can generate long-term auditory and/or...