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A growing importance has been placed on the recognition and supervision of non-motor features of Parkinson's disease (PD). Depression has been estimated to affect one in three individuals with PD and can lead to worse health outcomes and decreased quality of life. Anxiety, apathy and anhedonia further complicate PD outcomes. In this double-blind, placebo-controlled trial, participants (individuals with mild to moderate PD; n = 24) were randomly assigned to treatment (800 mg/d docosahexaenoic acid (DHA) and 290 mg/d eicosapentaenoic acid, a precursor to DHA) or placebo (an equicaloric amount of corn oil). Treatment duration was 6 months. Treatment had no statistically significant effect on rate of change on either Unified Parkinson's Disease Rating Scale or Hoehn-Yahr Scale score. However, 75% of DHA-treated patients, reduced Hamilton Rating Scale for Depression total score by at least 50%, compared with only 25% into the placebo group. At the end of the six-month study, DHA integration reduced the depressive symptoms.

Background/Aims: Dopamine is an important neurotransmitter involved in the pathophysiology of depression and anhedonia. Dopamine transporters (DAT) may play a crucial role in the pathophysiology of dopaminergic transmission. We investigated the relationship between striatal DAT availability and depression, pointing out possible correlations with anhedonia and treatment outcomes. Methods: Ten depressed patients with anhedonia, 10 depressed patients without anhedonia and 20 healthy controls underwent single photon emission computed tomography using 123I-FP-CIT [123I-N-ω-fluoropropyl-carbomethoxy-3β-(4-iodophenyl)tropane]. Psychometric measures included the Snaith-Hamilton Pleasure Scale and the Hamilton Depression Rating Scale. A further assessment of DAT availability was performed in the 10 patients with marked anhedonia after a 3-month pharmacological treatment. Results: Depressed patients with and without anhedonia showed significantly lower 123I-FP-CIT binding ratios in the bilateral striatum, caudate and putamen. No significant changes were detected after treatment in the 10 patients with marked anhedonia. When considering clinical outcomes, subjects with remission of depression showed a significant reduction of 123I-FP-CIT binding ratios in all regions at baseline, but after treatment no differences were found any longer. Conclusions: We suppose that a hypofunction of the striatal dopaminergic system may be a ‘state' feature of a depressive condition as a whole rather than anhedonia itself. On the other hand, some anhedonic features mainly represent an enduring trait that persists independently of mood state.

Repetitive transcranial magnetic stimulation (rTMS) of human motor cortex can produce long-lasting changes in the excitability of excitatory and inhibitory neuronal networks. The effects of rTMS depend critically on stimulus frequency. The aim of our present study was to compare the effects of different rTMS protocols. We compared the aftereffects of 6 different rTMS protocols [paired associative stimulation at interstimulus intervals of 25 (PAS25) and 10 ms (PAS10); theta burst stimulation delivered as continuous (cTBS) or intermittent delivery pattern (iTBS); 1- and 5-Hz rTMS] on the excitability of stimulated and contralateral motor cortex in 10 healthy subjects. A pronounced increase of cortical excitability, evaluated by measuring the amplitude of motor evoked potentials (MEPs), was produced by iTBS (+56%) and PAS25 (+45%). Five-hertz rTMS did not produce a significant increase of MEPs. A pronounced decrease of cortical excitability was produced by PAS10 (−31%), cTBS (−29%), and 1-Hz rTMS (−20%). Short-interval intracortical inhibition was suppressed by PAS10. Cortical silent period duration was increased by 1-Hz stimulation. No significant effect was observed in the contralateral hemisphere. Head-to-head comparison of the different protocols enabled us to identify the most effective paradigms for modulating the excitatory and inhibitory circuits activated by TMS.

Alzheimer's disease (AD) is a degenerative disorder characterized by a decreased regional cerebral blood flow (CBF). It is most likely that a reduction in CBF could displace a pathway leading to AD genesis, in so far neuron death explains a sustained reduction in the supply of oxygen, glucose, and nutrients. Nevertheless, the concept of secondary CBF deficiency cannot explain the critical stages of early memory loss while, on the other hand, the picture of progressive ischemia due to primary CBF decline sheds light on the course of AD in a most persuasive manner. The concept of primary CBF deficiency is even more strengthened by the lack of correlation between degree of dementia and amount of CBF. Vascular abnormalities, frequently observed to co-occur with AD, might play a critical role in the initiation and aggravation of AD pathology given that the elimination of amyloid-β (Aβ) through a vascular route is an important brain Aβ clearance mechanism and its failure leads to formation of vascular amyloidosis and dense-core plaques. The goal of this review is to provide scientists comprehensive knowledge of the state-of the art influence vascular damage and reduced perfusion have on the final development of AD and to hopefully stimulate more research in this area of neuroscience.

Ketamine is a non-competitive N-methyl-D: -aspartate (NMDA) receptor antagonist which interferes with the action of excitatory amino acids (EAAs) including glutamate and aspartate. The use of ketamine at subanaesthetic doses has increased because of its psychotomimetic properties. However, long-term ketamine abuse may interfere with memory processes and inhibit the induction of long-term potentiation (LTP) in the hippocampus, an effect probably mediated by its NMDA antagonist action. Neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) serve as survival factors for selected populations of central nervous system neurons, including cholinergic and dopaminergic neurons. In addition, neurotrophins, particularly BDNF, may regulate LTP in the hippocampus and influence synaptic plasticity.The purpose of this study was to test the hypothesis that ketamine use in humans is associated with altered serum levels of neurotrophins.We measured by enzyme-linked immunosorbent assay the NGF and BDNF serum levels in two groups of subjects: frequent ketamine users and healthy subjects.Our data show that BDNF serum levels were increased in chronic ketamine users as compared to healthy subjects, while NGF levels were not affected by ketamine use.These findings suggest that chronic ketamine intake is associated with increases in BDNF serum levels in humans. Other studies are needed to explore the pharmacological and molecular mechanism by which ketamine, and/or other NMDA antagonists, may induce modification in the production and utilization of BDNF and alter normal brain function.

Objectives: A “disconnectivity model” of schizophrenia has been proposed, but it is still unclear if white matter abnormalities are associated with gray matter changes and if they may be the anatomic substrate of cognitive impairment, which is a core symptom of the disorder. The first objective was to detect if white matter microstructure alterations in schizophrenia are associated with or independent of gray matter change, using an optimized method for white matter (Tract-Based Spatial Statistics) and gray matter analyses (whole-brain voxel-wise approach). The second objective was to identify the neuropsychological correlates of white matter abnormalities in the schizophrenic group, using a comprehensive neuropsychological battery. Methods: In this case-control study 43 schizophrenic patients and 43 healthy volunteers were consecutively enrolled and matched for age and gender. Results: Fractional anisotropy reduction was found in 6 fronto-temporal clusters (corrected p-valuesb0.05)inschizophrenicgroupincomparisonwithhealthyvolunteers,and3clustersshowed fractional anisotropy increase (corrected p-values b0.05). Two of the clusters showing reduced fractional anisotropy were associated with reduced gray matter density in neuroanatomically-related regions in schizophrenic subjects (p-values ranging from 0.001 to 0.026). Executive, constructionalpraxis, and working memory deficits were significant predictors of fractional anisotropy reduction in 4 clusters in the schizophrenic group (p-values ranging from b0.0001 to 0.0017). Conclusions: Ourdatasupportthedisconnectivityhypothesisinschizophrenia,enlighteningalink between reduced fronto-temporal connectivity and “frontal” cognitive deficits. Reduced gray matterdensitymaybeinvolvedprimarilyinthepathogenesisofsomeofthesedisconnectedareas.

"Punding" is a stereotypical motor behavior characterized by an intense fascination with repetitive handling and examining of objects. Since its first description in amphetamine and cocaine addicts, data on punding has only derived from studies performed in patients with Parkinson's disease (PD). Punding is classifiable as the most severe form of Repetitive Reward-Seeking Behaviours (RRSB) syndromes. The aim of this study was to investigate the occurrence and phenomelogy of RRSB acutely induced by cocaine in order to determine the prevalence, severity and distinctive features discriminating "punders" from "non-punders". A consecutive sample of 50 cocaine addicts received a clinical psychiatric interview. RRSB diagnosis and severity were assessed using a modified version of a previous published questionnaire designed to identify punding in patients with PD. In the present series, 38% of the cocaine addicts met the proposed diagnostic criteria for a RRSB and 8% were considered punders. Subjects with vs. without RRSB did not differ in terms of sex ratio, age, education, occupation, predisposing habits, duration of cocaine use, hours of sleep, comorbid psychiatric disorders, and concomitant use of other drugs. These results and the observation that in the majority of cases RRSB started soon after first drug intake, strongly suggest that an underlying unknown predisposition led to the development of these behaviors. In conclusion, RRSB and punding is much more common than has been described previously and the resultant social disability is often overlooked.

Premenstrual dysphoric disorder (PMDD) is a complex clinical syndrome that is notoriously difficult to treat. The purpose of the present study was to provide preliminary data on the effectiveness of duloxetine in PMDD.Fifty-five women with PMDD were treated with a 60 mg/day dosage of duloxetine for two menstrual cycles. Responses were assessed at first and second treatment cycle.Outcome measures included a visual analogue scale, the Zung Self-rating Scale for Depression, the Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale and the Clinical Global Impressions Scale.Fifty patients completed the trial. All had significant improvement of depression and anxiety and response, defined as a 50% decrease in daily symptom scores, occurred in 39 (78%) patients. The effects of active treatment were marked by the first active cycle of menstruation.Duloxetine 60 mg/day was effective in reducing PMDD symptoms and generally well tolerated. Limitations of the study were open-label design and lack of placebo control. However, the results appeared to be strong and consistent across measures. Adverse events (nausea, insomnia, poor appetite) were low. Further studies are needed to confirm these results.

This study aimed to test the effectiveness of an individualized, integrated, day-care treatment programme for the acute phase of "difficult-to-treat depression" (DTD) in a sample of bipolar and unipolar subjects with a complex co-morbidity pattern.A total of 291 patients meeting criteria for DTD were consecutively recruited. All participants underwent a 12-week day-care intervention including individual psychological support and group psycho-education. Subjects were assessed for depressive symptom severity by the 21-item Hamilton Depression Rating Scale (HDRS) at the baseline (T0) and after 4 (T1) and 12 (T2) weeks of treatment. A repeated measures general linear model was performed to test for interactive effects among variables.An overall significant improvement was detected in the majority of cases (F = 138.6, p0.0001). Responders reported lower rates of personality disorders and higher baseline depressive severity. An interaction between bipolarity and co-morbidity was associated with a poorer outcome (F = 5.9, p = 0.0034). Family involvement was the only significant predictor for symptom improvement (F = 7.9, adjusted p = 0.0025).Our intervention proved to be effective in the treatment of complex and severe forms of depression. Our results on the role of family support require further investigation to better define suitable targets for tailored therapeutic approaches.

Chronic cocaine and heroin users display a variety of central nervous system (CNS) dysfunctions including impaired attention, learning, memory, reaction time, cognitive flexibility, impulse control and selective processing. These findings suggest that these drugs may alter normal brain functions and possibly cause neurotoxicity. Neurotrophins are a class of proteins that serve as survival factors for CNS neurons. In particular, nerve growth factor (NGF) plays an important role in the survival and function of cholinergic neurons while brain-derived neurotrophic factor (BDNF) is involved in synaptic plasticity and in the maintenance of midbrain dopaminergic and cholinergic neurons. In the present study, we measured by enzyme-linked immunosorbent assay (ELISA) the NGF and BDNF levels in serum of three groups of subjects: heroin-dependent patients, cocaine-dependent patients and healthy volunteers. Our goal was to identify possible change in serum neurotrophins in heroin and cocaine users. BDNF was decreased in heroin users whereas NGF was decreased in both heroin and cocaine users. These findings indicate that NGF and BDNF may play a role in the neurotoxicity and addiction induced by these drugs. In view of the neurotrophin hypothesis of schizophrenia the data also suggest that reduced level of neurotrophins may increase the risk of developing psychosis in drug users.

Objective To investigate if different interneuronal circuits in human motor cortex mediate inhibition through different subtypes of the gamma-aminobutyric acid A receptor (GABAAR). Methods Two distinct forms of motor cortical inhibition were measured in 10 healthy subjects by established transcranial magnetic stimulation (TMS) protocols: short interval intracortical inhibition (SICI) and short latency afferent inhibition (SAI). Their modification by a single oral dose of three different positive GABAAR modulators (20 mg of diazepam, 2.5 mg of lorazepam and 10 mg of zolpidem) with different affinity profiles at the various α-subunit bearing subtypes of the GABAAR (diazepam: non-selective, lorazepam: unknown, zolpidem: 10-fold higher affinity to α1- than α2- or α3-subunit bearing GABAARs, no affinity to α5-subunits) was tested in a randomized crossover design. In addition, the sedative drug effects were recorded by a visual analogue scale. Results Diazepam and lorazepam increased SICI, whereas zolpidem did not change SICI. In contrast, diazepam had no effect on SAI, whereas lorazepam and zolpidem decreased SAI. The sedative effects were not different between drugs. Conclusions The dissociating patterns of drug modification of SICI versus SAI strongly suggest that different GABAAR subtypes are involved in SICI and SAI. Significance We provide evidence, for the first time, for a dissociation of effects of diazepam and zolpidem on SAI and confirm the previously reported differential effect of zolpidem and of diazepam and lorazepam on SICI. The differential effects of the three benzodiazepines on SAI and SICI suggest that neuronal circuits in human motor cortex that mediate inhibition through different GABAAR subtypes can be segregated by TMS.

In a cross-comparison study, the Cloninger's Temperament and Character Inventory (TCI) personality profile was administered to 28 probable pathological gamblers (PPGs), 32 nonpathological gamblers (non-PGs), and 65 controls. As a screening device, the validated Italian version of the South Oak Gambling Screen was administered to all subjects. Novelty Seeking (NS) values were higher in PPGs in comparison with both non-PGs (p.05) and controls (p.001). PPGs showed lower Self-Directedness (SD) and Cooperativeness (CO) values with respect to both non-PGs (p.05 and p = .001, respectively) and controls (p.001 and p = .001, respectively). The subsamples of PPGs reporting either a current substance misuse condition or a parental involvement in gambling/substance misuse showed higher NS (p = .01) and lower CO (p = .005) values than the remaining PPGs. A duration of problem gambling in excess of 20 years was associated with lower (p = .001) CO values. Specific temperamental (NS) and character (SD; CO) dimensions differentiated PPGs from both non-PGs and controls; assessment of personality profile with the TCI may identify at-risk social gamblers.

Giovanni Camardese,1 Beniamino Leone,1 Riccardo Serrani,1 Coco Walstra,1 Marco Di Nicola,1 Giacomo Della Marca,2 Pietro Bria,1 Luigi Janiri1 1Institute of Psychiatry and Psychology, 2Institute of Neurology, Catholic University of the Sacred Heart, Rome, Italy Objectives: We investigated the clinical benefits of bright light therapy (BLT) as an adjunct treatment to ongoing psychopharmacotherapy, both in unipolar and bipolar difficult-to-treat depressed (DTD) outpatients.Methods: In an open-label study, 31 depressed outpatients (16 unipolar and 15 bipolar) were included to undergo 3weeks of BLT. Twenty-five completed the treatment and 5-week follow-up.Main outcome measures: Clinical outcomes were evaluated by the Hamilton Depression Rating Scale (HDRS). The Snaith–Hamilton Pleasure Scale and the Depression Retardation Rating Scale were used to assess changes in anhedonia and psychomotor retardation, respectively.Results: The adjunctive BLT seemed to influence the course of the depressive episode, and a statistically significant reduction in HDRS scores was reported since the first week of therapy. The treatment was well-tolerated, and no patients presented clinical signs of (hypo)manic switch during the overall treatment period. At the end of the study (after 5weeks from BLT discontinuation), nine patients (36%, eight unipolar and one bipolar) still showed a treatment response. BLT augmentation also led to a significant improvement of psychomotor retardation.Conclusion: BLT combined with the ongoing pharmacological treatment offers a simple approach, and it might be effective in rapidly ameliorating depressive core symptoms of vulnerable DTD outpatients. These preliminary results need to be confirmed in placebo-controlled, randomized, double-blind clinical trial on larger samples. Keywords: light therapy, unipolar depression, bipolar depression, anhedonia, psychomotor dysfunction&nbsp

Inhibition is of fundamental importance to regulate activity in cortical circuits. Inhibition is mediated through a diversity of different interneurones and γ-aminobutyric acid A receptor (GABAAR) subtypes. Here we employed paired-pulse transcranial magnetic stimulation (TMS) to measure short interval intracortical inhibition (SICI), a GABAAR-mediated inhibition in human motor cortex, to address the question of which GABAAR subtype is responsible for this form of inhibition. It has been shown that classical benzodiazepines (diazepam and lorazepam) have a non-selective affinity profile at different α-subunit-bearing subtypes of the GABAAR while zolpidem has a 10-fold greater affinity to the α1-subunit-bearing GABAAR compared with those bearing the α2- or α3-subunit. We found that, in seven healthy subjects, a single oral dose of 20 mg of diazepam or 2.5 mg of lorazepam significantly increased SICI, whereas 10 mg of zolpidem did not change SICI. This dissociation occurred despite equal sedation by all three drugs, an α1-subunit GABAAR-mediated effect. The findings strongly suggest that SICI is not mediated by the α1-subunit-bearing subtype of the GABAAR but by those bearing either the α2- or α3-subunit. This study represents an attempt by means of TMS to identify GABAAR subtype-specific action at the systems level of human cortex, a highly relevant issue because the different α-subunit-bearing subtypes of the GABAAR are differently involved in benzodiazepine-mediated effects such as sedation, amnesia or anxiolysis, in developmental cortical plasticity, and in neurological disorders such as epilepsy.

Objective A few personality traits are characteristic of pathologic gamblers (PGs), but it is not clear if and how their personality profile differs from that of non-pathologic gamblers (non-PGs). Methods Sixty-five non-clinical subjects, differentiated into non-PGs and PGs with the means of the South Oak Gambling Screen (SOGS) and Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition–Text Revision ( DSM-IV-TR ) criteria, were administered with the Temperament and Character Inventory; their values were compared with those of control subjects (CS). Results Novelty seeking (NS) and self-transcendence (ST) values were higher whereas self-directedness and cooperativeness values were lower in PGs with respect to both non-PGs and CS. A positive correlation was noted between SOGS score and NS ( r = 0.40) and ST ( r = 0.50) values, as well as a significant positive dependence between SOGS score and a family history of gambling ( t = 2.816; P = .007). The subsamples of PGs reporting a parental involvement in gambling showed higher NS than the remaining PGs. Conclusions Specific temperamental and character dimensions, especially NS and ST, differentiated PGs from both non-PGs and CS; the identification of a personality profile at risk for problem gambling may represent an important predictor of outcome and constitute a possible target for specific treatment approaches.

A day hospital setting may provide a good management for suicidal patients. Of 70 subjects admitted for a suicide attempt to the "A. Gemelli" Hospital in Rome, eight (11.4%) dropped out, 62 (88.5%) completed the study, and 15 (24.19%) showed suicidal ideation within 1 year. No patients completed suicide.

Keywords: itching, nodules, pregabalin, prurigoSUMMARYWhat is known and objective: Prurigo nodularis (PN) is achronic skin condition that is difficult to treat. Pregabalin isone of the possible treatments for PN but its safety and effi-cacy are not well defined. We aimed to assess the efficacy ofpregabalin in patients with PN.Methods: Thirty patients (10 men, 20 women; mean age51.6 ± 9.39 years) were treated with pregabalin (75 mg/day) for3 months. Efficacy was classified as (i) successful (disappear-ance of the pruritus and reduction of nodules); (ii) slightimprovement/reduction of the nodules, that is, number and/orflattening, no disappearance of itching; or (iii) unsuccessful.Results: Twenty-three patients (76%) responded successfullyafter 3 months of treatment. There was a statistically signifi-cant difference between visual analogue scale scores beforeand after 1 month treatment period (8AE15 ± 2AE04 and 1AE5±1AE12,respectively; P

Background: The goal of the current meta-analysis was to review and examine in detail the features of cognitive performance in psychotic (MDDP) versus non-psychotic (MDD) major depressive disorder. Methods: An electronic literature search was performed to find studies comparing cognitive performance in MDDP versus MDD. A meta-analysis of broad cognitive domains (processing speed, reasoning/problem solving, verbal learning, visual learning, attention/working memory) and individual cognitive tasks was conducted on all included studies (n = 12). Demographic and clinical features were investigated via meta-regression analysis as moderators of cognitive performance. Results: No difference in socio-demographic and clinical variables was detected between groups. In general, a poorer cognitive performance was detected in MDDP versus MDD subjects (ES = 0.38), with a greater effect size in drug-free patients (ES = 0.69). MDDP patients were more impaired in verbal learning (ES = 0.67), visual learning (ES = 0.62) and processing speed (ES = 0.71) tasks. A significantly poorer performance was also detected in MDDP patients for individual tasks as Trail Making Test A, WAIS-R digit span backward and WAIS-R digit symbol. Age resulted to have a negative effect on tasks involved in working memory performance. Conclusion: In line with previous meta-analyses, our findings seem to support an association between psychosis and cognitive deficits in the context of affective disorders Psychosis during the course of MDD is associated with poorer cognitive performance in some specific cognitive domains, such as visual and verbal learning and executive functions. (C) 2014 Elsevier B.V. All rights reserved. Background The goal of the current meta-analysis was to review and examine in detail the features of cognitive performance in psychotic (MDDP) versus non-psychotic (MDD) major depressive disorder. Methods An electronic literature search was performed to find studies comparing cognitive performance in MDDP versus MDD. A meta-analysis of broad cognitive domains (processing speed, reasoning/problem solving, verbal learning, visual learning, attention/working memory) and individual cognitive tasks was conducted on all included studies (n=12). Demographic and clinical features were investigated via meta-regression analysis as moderators of cognitive performance. Results No difference in socio-demographic and clinical variables was detected between groups. In general, a poorer cognitive performance was detected in MDDP versus MDD subjects (ES=0.38), with a greater effect size in drug-free patients (ES=0.69). MDDP patients were more impaired in verbal learning (ES=0.67), visual learning (ES=0.62) and processing speed (ES=0.71) tasks. A significantly poorer performance was also detected in MDDP patients for individual tasks as Trail Making Test A, WAIS-R digit span backward and WAIS-R digit symbol. Age resulted to have a negative effect on tasks involved in working memory performance. Conclusion In line with previous meta-analyses, our findings seem to support an association between psychosis and cognitive deficits in the context of affective disorders. Psychosis during the course of MDD is associated with poorer cognitive performance in some specific cognitive domains, such as visual and verbal learning and executive functions.

Although the pathophysiology of gambling is unknown, an involvement of midbrain dopaminergic pathway has been hypothesized. In this study, the association between brain-derived neurotrophic factor (BDNF) and pathological gambling was investigated. We measured BDNF serum levels in (1) video players (n = 10); (2) card players (n = 9); (3) mixed players (n = 21; both video and card players) and (4) age-matched controls (n = 18). Mixed players had increased BDNF serum levels as compared to controls and higher South Oaks Gambling Screen score as compared to card or video players. Thus, the data demonstrate that patients affected by severe pathological gambling show enhanced BDNF serum levels.

It has been proposed that deficits in the production and the utilization of brain-derived neurotrophic factor (BDNF) may contribute to the pathogenesis of schizophrenia. At the same time, electroconvulsive shock, an experimental model of electroconvulsive therapy (ECT), has been shown to induce an increase of BDNF protein in brains of animal models. These findings suggest that one putative mechanism of action of ECT is the regulation of BDNF and/or related neurotrophins. In this case report, a 54-year-old man with severe treatment-resistant schizophrenic symptoms was treated with ECT. To evaluate the effect of ECT on BDNF serum levels, we collected a blood sample before each ECT session. During the course of ECT treatment, the paranoid and hallucinatory symptoms gradually improved, whereas BDNF levels increased over time. In addition, there was a general improvement of its positive and negative schizophrenic symptoms and depressive state. In conclusion, this case report further validates the therapeutic efficacy of ECT in schizophrenic patients with inadequate or poor response to traditional treatments. Moreover, ECT therapeutic effect is associated with an increase in BDNF serum levels. Further studies are needed to characterize the relationship between BDNF and ECT in schizophrenic patients.

The recreational drug 'ecstasy'[3,4-methylenedioxymethamphetamine (MDMA)] exerts a potent action on central serotonergic and dopaminergic neurons. These neurons utilize neurotrophins for their survival and function. In order to explore MDMA effects on neurotrophins, we measured by enzyme-linked immunosorbent assay the serum levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in 'ecstasy-addicted', 'ecstasy-addicted with signs of psychosis' and 'healthy' subjects. We found that BDNF serum levels were significantly increased in both groups of 'ecstasy-addicted' as compared with 'healthy subjects', supporting the hypothesis that BDNF is involved in MDMA action.

Antiphospholipid syndrome is a disorder characterised by recurrent venous or arterial thrombosis and/or foetal losses associated with typical laboratory abnormalities. The initial manifestation of anthiphospholipid syndrome can involve many organ systems either singly or in combination. We describe the case of a 62 year old female showing schizophrenia-like symptoms in which further evaluations allowed us to diagnose the antiphospolipid syndrome.

Study Objectives: To evaluate sleep modifi cations induced by chronic benzodiazepine (BDZ) abuse. Methods: Cohort study, comparison of sleep measures between BDZs abusers and controls. Drug Addiction Unit (Institute of Psychiatry) and Unit of Sleep Disorders (Institute of Neurology) of the Catholic University in Rome. Six outpatients affected by chronic BDZ abuse were enrolled, (4 men, 2 women, mean age 53.3 ± 14.8, range: 34-70 years); 55 healthy controls were also enrolled (23 men, 32 women, mean age 54.2 ± 13.0, range: 27-76 years). All patients underwent clinical evaluation, psychometric measures, ambulatory polysomnography, scoring of sleep macrostructure and microstructure (power spectral fastfrequency EEG arousal, cyclic alternating pattern [CAP]), and heart rate variability. Results: BDZ abusers had relevant modifi cation of sleep macrostructure and a marked reduction of fast-frequency EEG arousal in NREM (patients: 6.6 ± 3.7 events/h, controls 13.7 ± 4.9 events/h, U-test: 294, p = 0.002) and REM (patients: 8.4 ± 2.4 events/h, controls 13.3 ± 5.1 events/h, U-test: 264, p = 0.016), and of CAP rate (patients: 15.0 ± 8.6%, controls: 51.2% ± 12.1%, U-test: 325, p < 0.001). Discussion: BDZ abusers have reduction of arousals associated with increased number of nocturnal awakenings and severe impairment of sleep architecture. The effect of chronic BDZ abuse on sleep may be described as a severe impairment of arousal dynamics; the result is the inability to modulate levels of vigilance.

Objective To examine attachment and affective temperament in patients who have been diagnosed with Bipolar Disorder and to investigate possible differences in both variables among Bipolar I Disorder (BD-I), Bipolar II Disorder (BD-II), and cyclothymic patients. Methods Ninety (45 male and 45 female) outpatients with bipolar or cyclothymic disorder between the ages of 18 and 65 years were recruited consecutively between September 2010 and December 2011 at the Bipolar Disorder Unit of the Psychiatry Day Hospital affiliated with the University General Hospital “A. Gemelli” in Rome, Italy. Patients were assessed using the Structured Clinical Interview for DSM-IV, the Hamilton Depression Rating Scale, the Young Mania Rating Scale, the Temperament Evaluation of Memphis, Pisa, and San Diego—auto-questionnaire version, and the Experiences in Close Relationships (ECR) questionnaire applied by trained interviewers. Results The 3 groups of patients differed only on the ECR Anxiety scores with BD-I patients having the highest anxiety levels, followed by the BD-II patients, and the patients with cyclothymic disorder reporting the lowest level of anxiety. Conclusions This finding suggests that bipolar disorder (type I, type II) and cyclothymic/dysthymic temperament are more strongly associated with insecure attachment style as compared to the general population.

The diagnosis of bipolar disorder (BD) is predominantly clinical. Some authors have suggested that BD is underdiagnosed and that many patients, particularly those with major depressive disorder, actually have BD. Some studies have suggested that BD is wrongly diagnosed, probably because of the idea of a "bipolar spectrum." To address this potential overdiagnosis, clinicians should carefully and systematically assess whether symptoms are included in diagnostic criteria and include the individual context of the patient.

The aims of the study were: (1) to study possible associations between temperament, personality dimensions, and psychopathological variables in a clinical sample of euthymic patients with bipolar disorder (BD) and cyclothymia; and (2) to assess how Cloninger's temperament and personality dimensions were associated with affective temperaments. Participants, consisting of 60 patients with BD (type I or II) and cyclothymia in the euthymic phase, completed Akiskal's Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Autoquestionnaire (TEMPS-A), and Cloninger's Temperament and Character Inventory-revised version (TCI-R). The diagnostic groups differed in past hospitalization, for age at onset of the disorder, and on two affective temperaments: the TEMPS-A Hyperthymia, and the TEMPS-A Irritability. There were six significant associations between affective temperaments and Cloninger's personality dimensions, ranging from 0.26 to 0.54. The measures of Akiskal and of Cloninger tap common behavioral features in patients with bipolar disorder and cyclothymia, yet the differences indicate that the two measures are not redundant. BD and cyclothymic patients differed significantly in temperament and personality, differences that may have important implications for treatment.

Epidemiological studies suggest that n-3 polyunsaturated fatty acid (n-3 FA) deficiency is a risk factor for bipolar disorders (BDs). The aim of this study was to determine whether such a deficit does exist in patients with BD and to characterize the overall plasma fatty acid (FA) profile in these patients. Using gas chromatography/mass spectrometry, we measured fasting plasma levels of 15 FAs in 42 patients diagnosed with BD according to DSM-IV criteria and in 57 age- and gender-matched healthy controls. Plasma docosahexaenoic acid (DHA) levels were significantly decreased in bipolar patients (p < 0.001 versus healthy controls). Compared with controls, patients had higher plasma levels of all other FAs, including arachidonic acid (AA, p < 0.001), alpha-linolenic acid (ALA, p < 0.001), and eicosapentaenoic acid (EPA) (p < 0.001). Although in the present study we observed significant DHA deficits in the plasma of bipolar patients our findings do not support the therapeutic use of ALA and/or EPA supplementation. DHA may provide a basis for possible pharmacological intervention in psychiatric disorders at the level of second messengers linked to the phosphatidylinositol cycle. Finally, measurement of FA levels in plasma seems to be more reliable and reproducible than assays of erythrocyte FA content.

Background: Our aim was to study the relationship between hormonal disturbances and psychopathology in Eating Disorders (ED).Methods: Forty-nine women diagnosed as Eating Disorders according to DSM-IV were subjected to control plasma levels of TSH, FT3, FT4, LH, FSH, 17beta-estradiol, prolactin, cortisol, DHEAS, GH and IGF-1. They were also administered by SCL-90R, BAT, DES II questionnaires. We applied multivariate regression models.Results: Our results highlight a statistically significant relation between LH, FSH and prolactin decreased levels, mood and thought disturbances (subscales 3, 5, 7, 8 and 9 of SCL-90r) which are associated to Body Attitude ( BAT total scale) and Dissociative Experiences (DES II total scale). Conclusions: Decreased sexual hormones levels could have a role in ED psychological disturbances, not inquired yet

BACKGROUND: Mixed mood states, even in their sub-threshold forms, may significantly affect the course and outcome of bipolar disorder (BD). AIM: To compare two samples of BD patients presenting a major depressive episode and a sub-threshold mixed state in terms of global functioning, clinical outcome, social adjustment and quality of life during a 1-year follow-up. METHODS: The sample was composed by 90 subjects (Group 1, D) clinically diagnosed with a major depressive episode and 41 patients (Group 2, Mx) for a sub-threshold mixed state. All patients were administered with a pharmacological treatment and evaluated for depressive, anxious and manic symptoms by common rating scales. Further evaluations included a global assessment of severity and functioning, social adjustment and quality of life. All evaluations were performed at baseline and after 1, 3, 6 and 12 months of treatment. RESULTS: The two groups were no different for baseline as well as improvement in global severity and functioning. Though clearly different for symptoms severity, the amount of change of depressive and anxiety symptoms was also no different. Manic symptoms showed instead a trend to persist over time in group 2, whereas a slight increase of manic symptoms was observed in group 1, especially after 6 months of treatment. Moreover, in group 1, some manic symptoms were also detected at the Young Mania Rating Scale (n = 24, 26.6%). Finally, improvement in quality of life and social adjustment was similar in the two groups, though a small trend toward a faster improvement in social adjustment in group 1. CONCLUSIONS: Sub-threshold mixed states have a substantial impact on global functioning, social adjustment and subjective well-being, similarly to that of acute phases, or at least major depression. In particular, mixed features, even in their sub-threshold forms, tend to be persistent over time. Finally, manic symptoms may be still often underestimated in depressive episodes, even in patients for BD.

Our study aims to assess the prevalence of behavioural addictions in an adolescent population, evaluating the effects of gender and age, and to assess the correlations among different behavioural addictions. 2853 high school students were assessed in order to evaluate the prevalence of behavioural addictions such as Pathological Gambling (PG), Compulsive Buying (CB), Exercise Addiction (EA), Internet Addiction (IA), and Work Addiction (WA), in a population of Italian adolescents. The South Oaks Gambling Screen-Revised Adolescent (SOGS-RA), the Compulsive Buying Scale (CBS), the Exercise Addiction Inventory (EAI), the Internet Addiction Test (IAT), and the Work Addiction Risk Test (WART), were compiled anonymously by the students. Overall prevalence was 7.0% for PG, 11.3% for CB, 1.2% for IA, 7.6% for WA, 8.5% for EA. PG and EA were more common among boys, while gender had no effect on the other conditions. CB was more common among younger (

AimHigh-sensitive C-reactive protein (hs-CRP) has been used to assess low-grade immune system activation. In a population-based cohort hs-CRP was associated with functional somatic symptoms (SS), particularly with general and musculoskeletal functional SS clusters.Immune system dysregulation has also been reported in depression that is frequently associated to a high burden of SS.We investigated the correlation between hs-PCR and SS in depressed patients.Methods123 outpatients (M/F = 58/65; mean age 48,6 ± 14,8) during a Major Depressive Episode were recruited at the Institute of Psychiatry of the Catholic University in Rome. Severity of depression was assessed with the HAM-D scale. The somatization factor of the HAM-D (somatic anxiety, gastrointestinal symptoms, general somatic symptoms, hypochondria, weight loss) measured SS burden. A blood sample was collected to determine hs-CRP.ResultsHs-CRP and depression severity were not correlated, while hs-CRP and SS were (r = -0,27; p = 0,001). Patients with higher (> 3) somatizazion factor had significantly lower hs-PCR values compared to patients with lower (≤3) somatization factor (2,47 mg/L ± 4.77 vs. 3.20 mg/L ± 4.44; p = 0,026).ConclusionsIn contrast with the hypothesized cytokine involvement in somatic features of sickness behavior, higher somatic burden correlates with lower immune activation.The role of sickness behavior in experiencing SS and hs-CRP's use as valid indicator of cytokine production remain uncertain. Further studies are necessary, also to explore the relationship between HPA axis dysregulation and immune activation, possibly relevant to the interpretation of our results.

Objectives . To compare two samples of Bipolar (BD) patients presenting “ pure ” (D) and mixed (Mx) depression to assess any difference in terms of clinical outcome, social functioning and quality of life during a 1-year follow-up. Methods . A total of 114 depressed outpatients (HDRS 13) were included. “ Pure ” depressed (D, n 76) were divided from “ mixed ” depressed (Mx, n 38) by the number of concomitant manic symptoms. All patients were evaluated by the Hamilton Depression Rating Scale (HDRS), the Hamilton Anxiety Rating Scale (HARS), the Young Mania Rating Scale (YMRS), the Global Assessment of Functioning (GAF), the Social Adjustment Self-reported Scale (SASS) and the Quality of Life Scale (QoL), at baseline and after 1, 3, 6 and 12 months of treatment. Results . Mx patients were signifi cantly younger at the onset of BD. Manic features persisted signifi cantly higher in Mx than in D patients all over the follow-up period. Axis I comorbidities had a negative impact on the course of social functioning over the medium term period, while Mx patients showed a faster improvement in social adjustment than “ pure ” depressed patients. Conclusions . Mixed features may persist relatively stable throughout a depressive episode, having a negative impact over clinical and functional outcome, but not on social adjustment.

Background and aimHigh, normal or low plasma magnesium (Mg) levels have been observed in depressed patients. The aim of our study was to investigate the relationship of plasma Mg levels with depression severity, specific psychopathological dimensions and treatment outcome.Materials and methods123 outpatients (M/F 60/63; mean age = 48 ± 15) during a Major Depressive Episode (MDE) were recruited. Most of them were affected by “difficult to treat” depression, that includes patients with history of at least two MDE, risk of chronicization and who did not achieve remission in previous treatments.The psychopathological status was assessed using HAM-D, HAM-A, DRRS for psychomotor retardation and SHAPS for anhedonia. HAM-D was repeated at 3 months. A blood sample was collected to determine total plasma Mg levels.ResultsWe observed an association between Mg levels and psychomotor retardation scores (p = 0.045). Moreover, subjects with residual symptoms after treatment (HAM-D at 3 months > 15) have lower starting Mg values compared to treatment-responsive individuals (2.14 ± 0.2 vs. 2.25 ± 0.21, p = 0,039).ConclusionsConflicting data on plasma Mg levels in depression could be due to the isolation of brain Mg compartments from blood Mg compartments. As in a previous study, the association between high Mg levels and psychomotor retardation found in this larger sample strengthens the notion that high Mg levels play a part in the hypoactivity so often observed in depressed patients. Also, low Mg values in patients with poor treatment outcome suggest Mg could have a therapeutic potential in “difficult-to-treat” patients.

In recent years, mobile phone use has become increasingly common among Italian youth, while a growing scientific literature has been identifying the occurrence of a problematic mobile phone use which seems to share some features of other conditions often referred to as behavioural addictions. The study aimed to assess the prevalence of problematic mobile phone use in a population of Italian adolescents and its association with other behavioural addictions. The Mobile Addiction Test (MAT) was administered to 2,790 high school students from Barletta, an Italian town, together with the South Oaks Gambling Screen-Revised for Adolescents (SOGS-RA), the Compulsive Buying Scale (CBS), the Internet Addiction Test (IAT), the Exercise Addiction Inventory (EAI), the Work Addiction Risk Test (WART). MAT scores fitted a Gaussian distribution model. Scores ≥ 17 was found as a cut-off value over which identifying problematic mobile phone users. Overall prevalence of problematic mobile phone use was 6.3%; this condition was associated with other behavioural addictions like compulsive buying. Problematic mobile phone use in adolescence should become a public health issue, and it could be a cause of health problems and social costs.

Introduction There is a lack of studies regarding sexuality and sexual behavior in women with bipolar disorder. The aim of this study is to investigate sexual behavior in women affected by bipolar disorder in order to stimulate interest and debate in this area of care. Methods Sixty women (30 BD I and 30 BD II) consent to participate in the study and were included in the sample. Moreover, sixty female healthy subjects without histories of psychiatric disorders were recruited as normal controls. Patients and healthy subjects were given the Sexual Interest and Sexual Performance Questionnaire, a questionnaire devised to explore various aspects of sexual behavior. Results The results of the present study suggest an increase of sexual interest in patients with BD I as compared both with BD II patients and healthy controls. In women with BD I such increase of interest was detected on some items of section I of the Sexual Interest and Sexual Performance Questionnaire, in particular “Actual Value of Sexuality” and “Implicit Sexual Interest”, which implicitly explore sexual interest without overtly focusing upon sexual problems. Moreover, we observed a higher desired frequency of intercourse in women with BD I than BD II and a higher occurrence of repeated sexual intercourse in women with BD I than BD II. Conclusions The main finding of the present study was an increase of sexual interest in BD I as compared with BD II female patients and normal controls. This result was detected when sexual interest was explored implicitly. Our study is limited by the small size of our subject groups. Further investigations on larger subject samples are needed to better clarify particular aspects of sexual behavior of BD patients.

Comorbid conditions are frequent in Bipolar disorder (BD) and may complicate the treatment and course of illness. We investigated the role of Substance use disorder (SUD), axis II Personality disorders (PD) and continuous personality traits on the medium-term outcome (6 months) of treatment for bipolar depression. One-hundred and thirty-nine BD patients meeting criteria for a depressive episode were included in the study. Fifty-six patients were diagnosed for antecedent SUD and 61 for PD. Personality dimensions were evaluated by the Temperament and Character Inventory (TCI-R). Depressive severity over time was evaluated by the Hamilton Rating Scales for Depression (HAMD). Neither PD nor SUD influenced the outcome of depression, though relapse in SUD was concurrent with a slight worsening of depressive symptoms. Variables independently associated with a poor outcome were a high baseline severity and high scores at the temperamental trait of Harm avoidance. Results did not confirm SUD and PD as complicating factors for the medium-term treatment of depression in BD patients. Though several limitations characterize the present study, neurotic personality traits are supposed to be associated with a slower recovery from depressive symptoms in BD, independently from their initial severity.

Objective In this open, prospective study we aimed to investigate the efficacy, medical safety and practicability of pregabalin in outpatient detoxification of alcohol-dependent patients with mild-to-moderate alcohol withdrawal syndrome (AWS). Craving reduction, improvement of psychiatric symptoms and quality of life were the secondary endpoints. Methods Forty alcohol dependent patients (DSM-IV) were detoxified receiving 200–450 mg of pregabalin. Withdrawal (Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar)) and craving (Visual Analogue Scale (VAS); Obsessive and Compulsive Drinking Scale (OCDS)) rating scales were applied; psychiatric symptoms and quality of life were evaluated using the Symptom Check List-90 Revised (SCL-90-R) and the QL-Index, respectively. Relapsed and abstinent patients in the post-detoxification evaluation have been compared. Results Alcohol withdrawal symptoms and craving for alcohol resulted significantly reduced (p

Introduction The aim of this trial was to compare lorazepam with non-benzodiazepine medications such as pregabalin and tiapride in the treatment of alcohol withdrawal syndrome (AWS). These drugs were chosen for their inhibitorial effects on the hypersecretion of neurotransmitters usually observed in AWS. Craving reduction and improvement of psychiatric symptoms were the secondary end-points. Methods One hundred and ninety subjects affected by current alcohol dependence were considered consecutively: 111 were enrolled and divided into three groups of 37 subjects each. Within a treatment duration of 14 days, medication was given up to the following maximum doses (pregabalin 450 mg/day; tiapride 800 mg/day; lorazepam 10 mg/day). Withdrawal (CIWA-Ar), craving [visual analogue scale (VAS); Obsessive and Compulsive Drinking Scale (OCDS)], psychiatric symptoms [Symptom Check List 90 Revised (SCL-90-R)] and quality of life (QL-index) rating scales were applied. Results On the CIWA-Ar score, all the groups showed a significant reduction between times (P

Slow waves and sleep spindles are the two main oscillations occurring during non-REM sleep. While slow oscillations are primarily generated and modulated by the cortex, sleep spindles are initiated by the thalamic reticular nucleus and regulated by thalamo-reticular and thalamo-cortical circuits. In a recent high-density EEG study, the authors found that 18 medicated schizophrenia patients had reduced sleep spindles, compared with healthy and depressed subjects, during the first non-REM episode. In the present study, the authors investigated whether spindle deficits were present in a larger sample of schizophrenia patients, were consistent across the night, were related to antipsychotic medications, and were suggestive of impairments in specific neuronal circuits.Whole-night high-density EEG recordings were performed in 49 schizophrenia patients, 20 nonschizophrenia patients receiving antipsychotic medication, and 44 healthy subjects. In addition to sleep spindles, several parameters of slow waves were assessed.Schizophrenia patients had whole-night deficits in spindle power (12-16 Hz) and in slow (12-14 Hz) and fast (14-16 Hz) spindle amplitude, duration, number, and integrated activity in the prefrontal, centroparietal, and temporal regions. Integrated spindle activity and spindle number had the largest effect sizes (effect size: ≥ 2.21). In contrast, no slow wave deficits were found in schizophrenia patients.These results indicate that spindle deficits can be reliably established in schizophrenia, are stable across the night, are unlikely to be due to antipsychotic medications, and point to deficits in the thalamic reticular nucleus and thalamo-reticular circuits.

The recreational drug 'ecstasy'[3,4-methylenedioxymethamphetamine (MDMA)] exerts a potent action on central serotonergic and dopaminergic neurons. These neurons utilize neurotrophins for their survival and function. In order to explore MDMA effects on neurotrophins, we measured by enzyme-linked immunosorbent assay the serum levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in 'ecstasy-addicted', 'ecstasy-addicted with signs of psychosis' and 'healthy' subjects. We found that BDNF serum levels were significantly increased in both groups of 'ecstasy-addicted' as compared with 'healthy subjects', supporting the hypothesis that BDNF is involved in MDMA action.

Brain-derived neurotrophic factor (BDNF) gene variants may potentially influence behaviour. In order to test this hypothesis, we investigated the relationship between BDNF Val66Met polymorphism and aggressive behaviour in a population of schizophrenic patients. Our results showed that increased number of BDNF Met alleles was associated with increased aggressive behaviour.

Behavioural addictions (BAs) can be understood as disorders characterized by repetitive occurrence of impulsive and uncontrolled behaviours. Very few studies have investigated their association with mood disorders. The present study was undertaken to determine the prevalence of the main behavioural addictions in a sample of bipolar outpatients in euthymic phase or stabilised by medications and to investigate the role of impulsivity and temperamental and character dimensions.One-hundred-fifty-eight Bipolar Disorder (BD) (DSM-IV) outpatients were assessed with tests designed to screen the main behavioural addictions: pathological gambling (SOGS), compulsive shopping (CBS), sexual (SAST), Internet (IAD), work (WART) and physical exercise (EAI) addictions. TCI-R and BIS-11 were administered to investigate impulsivity and personality dimensions mainly associated with BAs. The clinical sample has been compared with 200 matched healthy control subjects.In bipolar patients, 33% presented at least one BA respect to the 13% of controls. Significantly higher scores at the scales for pathological gambling (p.001), compulsive buying (p.05), sexual (p.001) and work addictions (p.05) have been found. Self-Directness (p=.007) and Cooperativeness (p=.014) scores were significantly lower while impulsivity level was significantly higher (p=.007) in bipolar patients with BA than those without BA.To our knowledge, this is the first study investigating the prevalence of behavioural addictions in BD showing a significant association of these disorders. BAs are more frequent in bipolar patients than in healthy controls and are related to higher impulsivity levels and character immaturity.

Pregabalin (PRE) acts as a presynaptic inhibitor of the release of excessive levels of excitatory neurotransmitters by selectively binding to the α2-δ subunit of voltage-gated calcium channels. In this randomised, double-blind comparison trial with naltrexone (NAL), we aimed to investigate the efficacy of PRE on alcohol drinking indices. Craving reduction and improvement of psychiatric symptoms were the secondary endpoints. Seventy-one alcohol-dependent subjects were detoxified and subsequently randomised into two groups, receiving 50 mg of NAL or 150—450 mg of PRE. Craving (VAS; OCDS), withdrawal (CIWA-Ar) and psychiatric symptoms (SCL-90-R) rating scales were applied. Alcohol drinking indices and craving scores were not significantly different between groups. Compared with NAL, PRE resulted in greater improvement of specific symptoms in the areas of anxiety, hostility and psychoticism, and survival function (duration of abstinence from alcohol). PRE also resulted in better outcome in patients reporting a comorbid psychiatric disorder. Results from this study globally place PRE within the same range of efficacy as that of NAL. The mechanism involved in the efficacy of PRE in relapse prevention could be less related to alcohol craving and more associated with the treatment of the comorbid psychiatric symptomatology.

(1) To measure depressive and dissociative symptoms in a population of patients with Non-Epileptic Seizures (NES, or pseudo-seizures); (2) To compare NES with Epileptic subjects and Normal controls; (3) To try to define a personality profile specific, or typical, of NES patients.30 consecutive patients (21 females and 9 males, mean age 32.9+/-11.7 years) with NES diagnosed on clinical basis and confirmed by video-EEG recording; 30 patients with epilepsy matched for age and sex who had presented at least two seizures in the 12 months prior to the study despite pharmacological treatment; 30 Control subjects, healthy volunteers, matched for age and sex. Psychometric evaluation: Hamilton Rating Scale for Depression (HDRS), Dissociative Experience Scale (DES), Minnesota Multiphasic Personality Inventory-2 (MMPI-2). Groups were compared by means of one-way Analysis of Variance (ANOVA) for independent samples, followed by posthoc Tukey HSD Test, with Bonferroni correction for multiple comparisons.Depressive and dissociative symptoms showed a significantly higher prevalence in the NES group as compared to Epileptics (p0.001) and Controls (p0.001), whereas patients with epilepsy did not differ from Controls. The analysis of the MMPI-2 in NES group showed a general increase in most MMPI-2 T-scores as compared to Epileptics and Controls, rather than a constant elevation (T-score70) of one or more scales. No specific personality profile could be identified for the NES group.Our results are consistent with the hypothesis that depression and dissociative mechanisms are important precursors to the development and expression of NES.

Introduction Bipolar disorder patients (BP) with comorbid Substance Use Disorder (SUD) may present clinical features that could compromise adherence and response to pharmacological treatment. The purpose of this study was to examine clinical and psychopathological features of BP with and without comorbid SUD in a real-world setting. Methods The sample was composed by 131 affective patients. Sixty-five patients were affected by Bipolar Disorder I (BP-I, 49.2%), 29 by Bipolar Disorder II (BP-II, 22.3%) and 37 by Cyclothymic Disorder (CtD, 28.5%), according to DSM-IV. Sixty-six patients were diagnosed for a comorbid SUD. All patients have been submitted to psychometric assessment with Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Rating Scale (HARS), Young Mania Rating Scale (YMRS), Global Assessment Scale (GAS), Social Adjustment Self-reported Scale (SASS), Quality of Life Scale (QoL), at baseline and repeated follow-up periods (1, 3, 6, 12 months). Results BP comorbid for SUD were more likely diagnosed as BP-II and CtD and were less likely to present a moderate–severe manic symptomatology. Furthermore, personality disorders were more frequent in SUD patients than in non-comorbid BP. BP with SUD were not different for primary outcome measure (HDRS, HARS, YMRS, GAS) from non-comorbid BP; however, BP with SUD were significantly more impaired in social functioning (SASS) at any stage of the follow-up and poor functioning increased the risk of relapse in substance use during treatment. Finally, SUD comorbidity did not represent a risk factor for treatment drop-out, while in our sample young age, low treatment dosage and BP-I diagnosis were significantly associated with drop-out. Discussion The primary finding of this work is that BP with comorbid SUD are significantly more compromised in social functioning. Second, these patients were less likely to be diagnosed for BP-I and to present a severe manic symptomatology. Finally, we found that the diagnosis of SUD, but young age, low treatment dosage and BP-I diagnosis to be risk factors for treatment drop-out. Physicians should be alert to these differences in their clinical practice.

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.