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Background: Metacognitive functions play a key role in understanding which psychological variables underlying the personality might lead a person with a severe mental disorder to commit violent acts against others. The aims of this study were to: (a) investigate the differences between patients with poor metacognitive functioning (PM group) and patients with good metacognitive functioning (GM group) in relation to a history of violence; (b) investigate the differences between the two groups in relation to aggressive behavior during a 1-year follow-up; and (c) analyze the predictors of aggressive behavior. Methods: In a prospective cohort study, patients with severe mental disorders with and without a lifetime history of serious violence were assessed with a large set of standardized instruments and were evaluated bi-monthly with MOAS in order to monitor any aggressive behavior. The total sample included 180 patients: 56% outpatients and 44% inpatients, and the majority were male (75%) with a mean age of 44 (± 9.8) years, and half of them had a history of violence. The sample was split into two groups: poor metacognition (PM) group and good metacognition (GM) group, according to MAI evaluation scores. Results: The PM patients reported a history of violence more frequently than GM patients, during the 1-year follow-up, but no differences between groups in aggressive and violent behavior were found. The strongest predictors of aggressive behavior were: borderline and passive-aggressive personality traits and a history of violence, anger, and hostility. The metacognitive functions alone did not predict aggressive behavior, but metacognitive functions interacted with hostility and angry reactions in predicting aggressive behavior. Conclusions: This study led to some important conclusions: (a) some aspects closely related to violence are predictive of aggressive behavior only in patients with poor metacognition, thus good metacognition is a protective factor; (b) poor met

Objective: The relationship between alcohol and substance use and the risk of violence exhibited by patients with mental disorders is under-researched. This prospective cohort study aims to compare patients with severe mental disorders and with different substance use behaviors in terms of sociodemographic and clinical characteristics, hostility, impulsivity and aggressive behaviors. Furthermore, this study aims to assess differences in violent behaviors during a 1-year monitoring follow-up. Methods: A total of 378 participants with severe mental disorders from Italian residential facilities and from four Departments of Mental Health (244 outpatients and 134 residential patients) were enrolled. Participants were categorized as Persons with Current Substance Use, Persons with Former Substance Use and Persons with Non-Substance Use. All these patients underwent a complex multidimensional assessment, including the lifetime and current substance use; a subsample of outpatients was also assessed with a laboratory substance assay including the testing for specific substances. We assessed the differences among these three groups in hostility, impulsivity and aggressive behaviors. Results: The results of the close 1-year monitoring show a significantly higher risk of violence for patients with severe mental disorders Persons with Current Substance Use compared to Persons with Former Substance Use and Persons with Non-Substance Use. Persons with Current Substance Use showed significantly higher scores for irritability, negativism and verbal assault compared to Persons with Non-Substance Use. Persons with Former Substance Use showed significantly higher scores for lifetime history of aggressive behaviors compared with patients with Persons with Non-Substance Use. Conclusion: These findings suggest that patients with comorbid mental illness and substance use disorders should be referred for specific interventions to reduce aggressive behavior and ensure patient well-being and

Ophthalmic surgery in the past few years has made a lot of progress by combining the most advanced laser techniques with the standard procedures for cataract, corneal graft, and the correction of refractive defects such as myopia, hypermetropia, astigmatism, and presbyopia. There is therefore pressing request from advanced and specialist hospital to have laser platforms available (excimer and femto). This chapter deals about the strategy of Tuscany Region (Italy) that, starting from the request of Careggi University Hospital, called a competition designed by its central office ESTAR to satisfy initial specific request but also other possible regional authorities requests with known cost of equipment, disposables, maintenance and key operators for the upcoming 5 years.

The original version of this Article contained errors. In the title of the paper, the word “in” was incorrectly given as “In”. In the original Table 1, cells in column six were not merged correctly and the table has been replaced. Finally, the original Figures 1 and 2 have been replaced with higher resolution images. These errors have now been corrected in the PDF and HTML versions of the Article. The accompanying Supplementary Information file was correct at the time of publication.

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Pathological gambling or gambling disorder has been defined by the DSM-5 as a behavioral addiction. To date, its pathophysiology is not completely understood and there is no FDA-approved treatment for gambling disorders. Glutamate is the principal excitatory neurotransmitter in the nervous system and it has been recently involved in the pathophysiology of addictive behaviors. In this paper, we review the current literature on a class of drugs that act as modulating glutamate system in PG. A total of 19 studies have been included, according to inclusion and exclusion criteria. Clinical trial and case series using glutamatergic drugs (N-acetylcysteine, memantine, amantadine, topiramate, acamprosate, baclofen, gabapentin, pregabalin, and modafinil) will be presented to elucidate the effectiveness on gambling behaviors and on the related clinical dimensions (craving, withdrawal, and cognitive symptoms) in PG patients. The results have been discussed to gain more insight in the pathophysiology and treatment of PG. In conclusion, manipulation of glutamatergic neurotransmission appears to be promising in developing improved therapeutic agents for the treatment of gambling disorders. Further studies are required. Finally, we propose future directions and challenges in this research area.

Bipolar disorders (BDs) and addictions constitute reciprocal risk factors and are best considered under a unitary perspective. The concepts of allostasis and allostatic load (AL) may contribute to the understanding of the complex relationships between BD and addictive behaviors. Allostasis entails the safeguarding of reward function stability by recruitment of changes in the reward and stress system neurocircuitry and it may help to elucidate neurobiological underpinnings of vulnerability to addiction in BD patients. Conceptualizing BD as an illness involving the cumulative build-up of allostatic states, we hypothesize a progressive dysregulation of reward circuits clinically expressed as negative affective states (i.e., anhedonia). Such negative affective states may render BD patients more vulnerable to drug addiction, fostering a very rapid transition from occasional drug use to addiction, through mechanisms of negative reinforcement. The resulting addictive behavior-related ALs, in turn, may contribute to illness progression. This framework could have a heuristic value to enhance research on pathophysiology and treatment of BD and addiction comorbidity.

Anhedonia is present in Parkinson's Disease (PD) as well as in addictive behaviors. Pathological Gambling (PG) and other Impulse Control Disorders (ICDs) have emerged as iatrogenic complications associated with dopamine replacement therapy. We studied 154 PD patients, divided into three groups: 11 with PG, 23 with other ICDs (compulsive buying, hypersexuality, binge eating), 120 without ICDs. All patients underwent a thorough clinical, neuropsychological and psychiatric evaluation. The PG-group, compared to the ICDs-group and PD-controls, reported a significantly higher incidence of anhedonia (45% vs. 9% vs. 14% respectively), higher Snaith-Hamilton Pleasure Scale (SHAPS) scores (2.0±1.3 vs. 1.0±1.1 vs. 1.0±1.2), higher levels of impulsivity traits as measured by the Barratt Impulsiveness Scale (70.0±10.6 vs. 64.8±11 vs. 60.9±9.3) and more severe frontal dysfunctions (Frontal Assessment Battery, FAB: 12.4±4.9 vs. 15.5±1.6 vs. 14.4±3). A model for PG (incorporating anhedonia, impulsivity levels and frontal impairment) is discussed in the context of the pathophysiology of addictive behaviors. The impairment of hedonic capacity, possibly resulting from an underlying neuropsychological dysfunction, might facilitate loss of control over reward-related behavior, thus favoring the shift towards predominantly habit-based compulsive behaviors.

Despite almost a decade of intense research, effective treatment strategies for Pathological Gambling (PG) remain very challenging. This paper details a case report suggesting that the treatment of PG may benefit from the use of the non-specific glutamate blocker amantadine. The drug was well-tolerated and effective, leading to a 43-64% reduction in severity of gambling symptoms (as measured with G-SAS). Our result is discussed in the context of the glutamatergic hypothesis of addiction and in light of previous observations on the potential impact of glutamatergic agents in the treatment of PG. The role of the dopaminergic system, and its interaction with the glutamatergic system, is also explored. Further studies are required to define the true benefits of amantadine for the treatment of PG.

OBJECTIVE: We aimed at evaluating the association between appetite and symptoms of depression and anxiety, cognitive dysfunction, fatigue, and comorbidities in patients on hemodialysis (HD). DESIGN: A cross-sectional study was conducted. SETTING: The study was conducted in an outpatient HD service of a tertiary level academic hospital. PATIENTS: A total of 90 patients on HD were evaluated for appetite (during the past week, how would you rate your appetite?), symptoms of depression (Beck Depression Inventory [BDI]) and anxiety (Hamilton Anxiety Rating Scale [HARS]), cognitive dysfunction (Mini Mental State Examination [MMSE]), and comorbidities (Charlson Comorbidity Index). MAIN OUTCOME MEASURE: Relationship between appetite and symptoms of depression and/or anxiety, cognitive dysfunction, and comorbidities was assessed. RESULTS: In 43 patients, the appetite was very good/good (group 1), in 22, it was fair (group 2), and in 25, it was poor/very poor (group 3). Mean and median BDI were significantly higher in group 3 as well as the percentage of patients with BDI ≥16. Mean and median HARS and the percentage of patients with HARS >13 were significantly higher in group 3. MMSE was significantly lower in group 3 as well as the percentage of patients with MMSE ≤23. Multiple linear regression analysis showed a dependence of appetite by age and BDI (P = .007 and P = .002, respectively). CONCLUSIONS: Anorexia is associated with older age and symptoms of depression in patients on HD.

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.

Background: Little is known about the course of the symptoms of depression/anxiety and the factors predictive of such courses in hemodialysis (HD) patients. This study aimed at evaluating the possible changes of Beck Depression Inventory (BDI) and Hamilton Anxiety Rating Scale (HARS) over time, and factors associated with such changes in HD patients. Methods: We screened 110 patients for study participation. Of these, 30 were excluded because of dialytic vintage <6 months, alcohol/substance abuse, inability to answer to the questionnaires, diagnosis of psychotic or neurological disorders or recent stressful life events. Eighty patients were included in the study and BDI, HARS, Charlson Comorbidity Index, SF-36 Vitality Subscale, Mini-Mental State Examination (MMSE), routine laboratory parameters, C-reactive protein (CRP) and interleukin-6 were measured at baseline. The 18-month course of BDI and HARS was measured in patients with baseline BDI <=14. Results: At baseline, 42 patients had BDI >14 and 38 patients <=14. In patients with BDI <=14, the BDI decreased/remained stable in 19 and increased in 19. Patients with increased BDI had lower baseline MMSE (22.6 ± 2.6 vs. 25.9 ± 2.7, p=0.004) and higher baseline serum CRP (6.07 ± 4.2 vs. 1.64 ± 1.59, p=0.003). At multivariate analysis the relationship between BDI changes and MMSE and serum CRP was statistically significant. In 25 patients, the HARS decreased/remained stable, while in 13 it increased. Characteristics of the 2 groups of patients did not differ significantly. Conclusions: In a meaningful proportion of HD patients, symptoms of depression worsen over time, and CRP and MMSE are independent predictors of such change.

Oxcarbazepine (OXC) is a keto-congener of carbamazepine, which has fewer side effects and drug interactions. However, the efficacy of OXC in treating bipolar disorder is not as well established as that of carbamazepine. This article is a systematic literature review of all studies regarding OXC and bipolar disorders, with particular attention to papers published in the last 6 years. Using the terms 'oxcarbazepine and bipolar disorder', 'oxcarbazepine and mania' or 'oxcarbazepine and bipolar depression', a computer-aided search of MEDLINE for the years 2000-2006 has been conducted. Since its introduction as an antiepileptic drug in early 2000, clinical research regarding the potential role of OXC in the treatment of bipolar disorder remains limited. There is a lack of double-blind, placebo-controlled studies. Studies recently published have small samples of patients, with insufficient follow-up periods and other methodological weaknesses. The efficacy of OXC in bipolar disorder has not been widely studied. Some authors recommend using OXC as monotherapy or as add-on therapy in refractory mania, although results are not conclusive. It is unknown whether OXC has efficacy in the maintenance treatment of bipolar disorder. OXC can be particularly useful as an add-on treatment in bipolar disorder patients for whom previous treatments have failed, or in patients who have difficulty tolerating adequate dosages of standard approved treatments.