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Sani G.,University of Rome La Sapienza | Sani G.,Centro Lucio Bini | Sani G.,Neuropsychiatry Laboratory | Napoletano F.,University of Rome La Sapienza | And 10 more authors.
Psychotherapy and Psychosomatics | Year: 2014

Background: Mixed depression (MxD) is narrowly defined in the DSM-IV and somewhat broader in the DSM-5, although both exclude psychomotor agitation as a diagnostic criterion. This article proposes a clinical description for defining MxD, which emphasizes psychomotor excitation. Methods: Two hundred and nineteen consecutive outpatients were diagnosed with an MxD episode using criteria proposed by Koukopoulos et al. [Acta Psychiatr Scand 2007;115(suppl 433):50-57]; we here report their clinical features and antidepressant-related effects. Results: The most frequent MxD symptoms were: psychic agitation or inner tension (97%), absence of retardation (82%), dramatic description of suffering or weeping spells (53%), talkativeness (49%), and racing or crowded thoughts (48%). MxD was associated with antidepressants in 50.7% of patients, with similar frequency for tricyclic antidepressants (45%) versus selective serotonin reuptake inhibitors (38.5%). Positive predictors of antidepressant-associated MxD were bipolar disorder type II diagnosis, higher index depression severity, and higher age at index episode. Antipsychotic or no treatment was protective against antidepressant-associated MxD. Conclusions: MxD, defined as depression with excitatory symptoms, can be clinically identified, is common, occurs in both unipolar depression and bipolar disorder, and is frequently associated with antidepressant use. If replicated, this view of MxD could be considered a valid alternative to the DSM-5 criteria for depression with mixed features. © 2014 S. Karger AG, Basel.

Koukopoulos A.,Centro Lucio Bini | Sani G.,Centro Lucio Bini | Sani G.,University of Rome La Sapienza | Sani G.,Neuropsychiatry Laboratory
Acta Psychiatrica Scandinavica | Year: 2014

Objective: To review the DSM-5 proposed criteria for mixed depression in light of robust and consistent historical and scientific evidence. Method: An extensive historical search, a systematic review of the papers used by DSM-5 as reference papers, and a PubMed search were performed. Results: As Hippocrates, depressive mixed states have been described as conditions of intense psychic suffering, consisting of depressed mood, inner tension, restlessness, and aimless psychomotor agitation. In DSM-5, new criteria are proposed for a mixed features specifier, as part of depression either in major depressive disorder (MDD) or bipolar disorder. Those criteria require, as diagnostically specific, manic/hypomanic symptoms that are the least common kinds of symptoms that actually arise in depressive mixed states. The DSM-5 proposal is based, almost entirely, on a speculative wish to avoid 'overlapping' manic and depressive symptoms. Mixed states are, in fact, nothing but overlapping manic and depressive symptoms. Conclusion: In this article, we review the psychopathology and research on mixed depressive states, and try to demonstrate that the DSM-5 proposal has weak scientific basis and does not identify a large number of mixed depressive states. This may be harmful because of the different treatment required by these conditions. © 2013 John Wiley & Sons A/S.

Piras F.,Neuropsychiatry Laboratory | Chiapponi C.,Neuropsychiatry Laboratory | Girardi P.,University of Rome La Sapienza | Caltagirone C.,Neuropsychiatry Laboratory | And 2 more authors.
Cortex | Year: 2015

The most widely accepted model of obsessive-compulsive disorder (OCD) assumes brain abnormalities in the "affective circuit", mainly consisting of volume reduction in the medial orbitofrontal, anterior cingulate and temporolimbic cortices, and tissue expansion in the striatum and thalamus. The advent of whole-brain, voxel-based morphometry (VBM) has provided increasing evidence that regions outside the "affective" orbitofronto-striatal circuit are involved in OCD. Nevertheless, potential confounds from the different image analysis methods, as well as other factors, such as patients' medication and comorbidity status, may limit generalization of results.In the present paper, we systematically reviewed the whole-brain VBM literature on OCD by focussing specifically on degree of consistency between studies, extent to which findings have been replicated and interrelation between clinical variables and OCD anatomy, a potentially crucial factor that has been systematically examined only in a limited number of studies. The PubMed database was searched through February 2012. A total of 156 studies were identified; 18 of them fulfilled the inclusion/exclusion criteria and included 511 patients and 504 controls. Results support the notion that the brain alterations responsible for OCD are represented at the network level, and that widespread structural abnormalities may contribute to neurobiological vulnerability to OCD. Apart from defects in regions within the classic "affective" circuit, volume reduction of the cortical source of the dorsolateral (DL) prefronto-striatal "executive" circuit (dorsomedial, DL, ventrolateral and frontopolar prefrontal cortices), and of reciprocally connected regions (temporo-parieto-occipital associative areas) is consistently described in OCD patients. Moreover, increased volume of the internal capsule and reduced frontal and parietal white matter volumes may account for altered anatomical connectivity in fronto-subcortical circuitry. Morphometric changes in both "affective" and "executive" parallel the disease clinical course, being at the same time responsible for variation in symptom severity. Thus, OCD mechanisms involve a more widespread network of cerebral dysfunctions than previously thought, which may explain the heterogeneity in clinical manifestations and symptom severity. © 2013 Elsevier Ltd.

Iorio M.,Neuropsychiatry Laboratory | Spalletta G.,Neuropsychiatry Laboratory | Chiapponi C.,Neuropsychiatry Laboratory | Luccichenti G.,Istituto di Ricovero e Cura a Carattere Scientifico Santa Lucia Foundation | And 5 more authors.
Frontiers in Aging Neuroscience | Year: 2013

White matter hyperintensities (WMH) are brain areas of increased signal on T2-weighted or fluid-attenuated inverse recovery magnetic resonance imaging (MRI) scans. In this study we present a new semi-automated method to measure WMH load that is based on the segmentation of the intensity histogram of fluid-attenuated inversion recovery images. Thirty patients with mild cognitive impairment with variable WMH load were enrolled. The semi-automated WMH segmentation included removal of non-brain tissue, spatial normalization, removal of cerebellum and brain stem, spatial filtering, thresholding to segment probable WMH, manual editing for correction of false positives and negatives, generation of WMH map, and volumetric estimation of the WMH load. Accuracy was quantitatively evaluated by comparing semi-automated and manual WMH segmentations performed by two independent raters. Differences between the two procedures were assessed using Student's t-tests and similarity was evaluated using linear regression model and Dice similarity coefficient (DSC). The volumes of the manual and semi-automated segmentations did not statistically differ (t-value = -1.79, DF = 29, p = 0.839 for rater 1; t-value = 1.113, DF = 29, p = 0.2749 for rater 2), were highly correlated [R2 = 0.921, F(1,29) = 155.54, p < 0.0001 for rater 1; R2 = 0.935, F(1,29) = 402.709, p < 0.0001 for rater 2] and showed a very strong spatial similarity (mean DSC = 0.78, for rater 1 and 0.77 for rater 2). In conclusion, our semi-automated method to measure the load of WMH is highly reliable and could represent a good tool that could be easily implemented in routinely neuroimaging analyses to map clinical consequences of WMH. © 2013 Iorio, Spalletta, Chiapponi, Luccichenti, Cacciari, Orfei, Caltagirone and Piras.

Spalletta G.,Neuropsychiatry Laboratory | Piras F.,Neuropsychiatry Laboratory | Caltagirone C.,Neuropsychiatry Laboratory | Caltagirone C.,University of Rome Tor Vergata | Orfei M.D.,Neuropsychiatry Laboratory
Human Brain Mapping | Year: 2014

Lack of insight into illness is a multidimensional phenomenon that has relevant implications on clinical course and therapy compliance. Here, we focused on metacognitive insight in schizophrenia, that is, the ability to monitor one's changes in state of mind and sensations, with the aim of investigating its neuroanatomical, psychopathological, and neuropsychological correlates. Fifty-seven consecutive patients with Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision) diagnosis of schizophrenia were administered the Insight Scale, and comprehensive psychopathological and neuropsychological batteries. They underwent a high-resolution T1-weighted magnetic resonance imaging investigation. Gray matter (GM) and white matter (WM) volumes were analyzed on a voxel-by-voxel basis using Statistical Parametric Mapping 8. Reduced metacognitive insight was related to reduced GM volumes in the left ventrolateral prefrontal cortex, right dorsolateral prefrontal cortex and insula, and bilateral premotor area and putamen. Further, it was related to reduced WM volumes of the right superior longitudinal fasciculum, left corona radiata, left forceps minor, and bilateral cingulum. Increased metacognitive insight was related to increased depression severity and attentional control impairment, while the latter was related to increased GM volumes in brain areas linked to metacognitive insight. Results of this study suggest that prefrontal GM and WM bundles, all implied in cognitive control and self-reflection, may be the neuroanatomical correlates of metacognitive insight in schizophrenia. Further, higher metacognitive insight is hypothesized to be a risk factor for depression which may subsequently impair attention. This line of research may provide the basis for the development of cognitive interventions aimed at improving self-monitoring and compliance to treatment. © 2014 Wiley Periodicals, Inc.

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