1,721,222 research outputs found
Schizophrenia and bipolar disorder: The road from similarities and clinical heterogeneity to neurobiological types
Although diagnosis is a central issue in medical care, in psychiatry its value is still controversial. The function of diagnosis is to indicate treatments and to help clinicians take better care of patients. The fundamental role of diagnosis is to predict outcome and prognosis. To date serious concern persists regarding the clinical utility and predictive validity of the diagnosis system in psychiatry, which is at the most syndromal. Schizophrenia and bipolar disorder, which nosologists consider two distinct disorders, are the most discussed psychiatric illnesses. Recent findings in different fields of psychiatric research, such as neuroimaging, neuropathology, neuroimmunology, neuropsychology and genetics, have led to other conceptualizations. Individuals with schizophrenia or bipolar disorder vary greatly with regard to symptoms, illness course, treatment response, cognitive and functional impairment and biological correlates. In fact, it is possible to find heterogeneous correlates even within the same syndrome, i.e., from one stage of the disorder to another. Thus, it is possible to identify different subsyndromes, which share some clinical and neurobiological characteristics. The main goal of modern psychiatry is to ovethrow these barriers and to obtain a better understanding of the biological profiles underlying heterogeneous clinical features and thus reduce the variance and lead to a homogeneous definition. The translational research model, which connects the basic neuroscience research field with clinical experience in psychiatry, aims to investigate different neurobiological features of syndromes and of the shared neurobiological features between two syndromes. In fact, this approach should help us to better understand the neurobiological pathways underlying clinical entities, and even to distinguish different, more homogeneous, diagnostic subtypes
Effects of psychostimulants on neurotrophins implications for psychostimulant-induced neurotoxicity.
It is well documented that psychostimulants may alter neuronal function and neurotransmission in the brain. Although the mechanism of psychostimulants is still unknown, it is known that these substances increase extracellular level of several neurotransmitters including dopamine (DA), serotonin, and norepinephrine by competing with monoamine transporters and can induce physical tolerance and dependence. In addition to this, recent findings also suggest that psychostimulants may damage brain neurons through mechanisms that are still under investigation. In the recent years, it has been demonstrated that almost all psychostimulants are able to affect a class of proteins, called neurotrophins, in the peripheral and central nervous system (CNS). Neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), have relevant action on neurons involved in psychostimulant action, such as DA and serotonergic neurons, and can play dual roles: first, in neuronal survival and death, and, second, in activity-dependent plasticity. In this review, we will focalize on the effects of psychostimulants on this class of proteins, which may be implicated, at least in part, in the mechanism of the psychostimulant-induced neurotoxicity. Moreover, since altered neurotrophins may participate in the pathogenesis of psychiatric disorders and psychiatric disorders are common in drug users, one plausible hypothesis is that psychostimulants can cause psychosis through interfering with neurotrophins synthesis and utilization by CNS neurons
Macro- and micro-structural cerebellar and cortical characteristics of cognitive empathy towards fictional characters in healthy individuals
Few investigations have analyzed the neuroanatomical substrate of empathic capacities in healthy subjects, and most of them have neglected the potential involvement of cerebellar structures. The main aim of the present study was to investigate the associations between bilateral cerebellar macro- and micro-structural measures and levels of cognitive and affective trait empathy (measured by Interpersonal Reactivity Index, IRI) in a sample of 70 healthy subjects of both sexes. We also estimated morphometric variations of cerebral Gray Matter structures, to ascertain whether the potential empathy-related peculiarities in cerebellar areas were accompanied by structural differences in other cerebral regions. At macro-structural level, the volumetric differences were analyzed by Voxel-Based Morphometry (VBM)- and Region of Interest (ROI)-based approaches, and at a micro-structural level, we analyzed Diffusion Tensor Imaging (DTI) data, focusing in particular on Mean Diffusivity and Fractional Anisotropy. Fantasy IRI-subscale was found to be positively associated with volumes in right cerebellar Crus 2 and pars triangularis of inferior frontal gyrus. The here described morphological variations of cerebellar Crus 2 and pars triangularis allow to extend the traditional cortico-centric view of cognitive empathy to the cerebellar regions and indicate that in empathizing with fictional characters the cerebellar and frontal areas are co-recruited
Fronto-thalamic volumetry markers of somatic delusions and hallucinations in schizophrenia
Although the psychotic phenomena of schizophrenia have been extensively investigated, somatic delusions and hallucinations have seldom been reported and their mechanisms are substantially unexplored. Here, we aimed to identify the brain structural correlates of somatic psychotic phenomena using combined volumetry and diffusivity structural neuroimaging techniques. Seventy-five individuals with a DSM-IV-TR diagnosis of schizophrenia and 75 healthy controls (HC) underwent a comprehensive clinical assessment, a high-resolution T1-weighted magnetic resonance imaging and a diffusion tensor imaging protocol using a 3T MRI scanner. Voxel-based volumetry and mean diffusivity (MD) of gray matter (GM) and fractional anisotropy (FA) of white matter (WM) of the whole brain were calculated for each subject. Reduced left fronto-insular GM volume was found in patients with somatic delusions compared with patients without somatic delusions and HC. Increased GM volume was found in the bilateral thalami, primarily in the right ventral-anterior thalamic nucleus projecting to the prefrontal-temporal cortices and the bilateral pars triangularis of the inferior frontal lobe, of patients with somatic hallucinations and HC compared with patients without somatic hallucinations. No differences emerged in GM MD and in WM FA between patients with and without psychotic somatic phenomena (i.e. delusions or hallucinations). These findings provide the first evidence that a frontal-thalamic structural perturbation mediates somatic psychotic phenomena in schizophrenia. © 2012 Elsevier Ireland Ltd
Brain microstructure of subclinical apathy phenomenology in healthy individuals
Although apathy has been extensively studied in relation to neuropsychiatric disorders, it is still unclear whether, in healthy people, it should be considered as a physiological phenomenon or whether it is a risk factor for progression to clinical disturbances. Here, we investigated subclinical apathy phenomenology and its brain microstructural correlates in healthy individuals. We submitted 72 participants to a comprehensive clinical assessment, a high-resolution structural MRI and a diffusion tensor imaging scan protocol. Data of individual microstructural (mean diffusivity and fractional anisotropy) variations were processed across genders in relation to the Apathy Rating Scale score. In females, subclinical apathy phenomenology was associated with microstructural variation of the bilateral thalami, the anterior thalamic radiation, the forceps major, and the corona radiate. These are white matter areas mostly connecting the thalami to the frontal and occipital cortices, regions that are known to be implicated in the expression of apathy in clinical samples. No significant relationship with brain microstructure was found in males who showed a positive correlation between subclinical apathy and somatic phenomenology of depression. In conclusion, our results show that in healthy individuals subclinical apathy phenomenology is associated with different mechanisms across genders, and raise the issue about whether brain microstructural changes associated with subclinical apathy in healthy females could be a precocious marker useful in the prediction of progression to more severe apathetic condition
Hippocampal multimodal structural changes and subclinical depression in healthy individuals
Several neuroimaging studies report reduced hippocampal volume in depressed patients. However, it is still unclear if hippocampal changes in healthy individuals can be considered a risk factor for progression to clinical depression. Here, we investigated subclinical depression and its hippocampal correlates in a non-clinical sample of healthy individuals, with particular regard to gender differences
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The unbalanced reorganization of weaker functional connections induces the altered brain network topology in schizophrenia
Abstract Network neuroscience shed some light on the functional and structural modifications occurring to the brain associated with the phenomenology of schizophrenia. In particular, resting-state functional networks have helped our understanding of the illness by highlighting the global and local alterations within the cerebral organization. We investigated the robustness of the brain functional architecture in 44 medicated schizophrenic patients and 40 healthy comparators through an advanced network analysis of resting-state functional magnetic resonance imaging data. The networks in patients showed more resistance to disconnection than in healthy controls, with an evident discrepancy between the two groups in the node degree distribution computed along a percolation process. Despite a substantial similarity of the basal functional organization between the two groups, the expected hierarchy of healthy brains' modular organization is crumbled in schizophrenia, showing a peculiar arrangement of the functional connections, characterized by several topologically equivalent backbones. Thus, the manifold nature of the functional organization’s basal scheme, together with its altered hierarchical modularity, may be crucial in the pathogenesis of schizophrenia. This result fits the disconnection hypothesis that describes schizophrenia as a brain disorder characterized by an abnormal functional integration among brain regions
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