The European Insomnia Guideline: An update on the diagnosis and treatment of insomnia 2023.

Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential-diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders, etc.), treatment-resistant insomnia (A) and for other indications (B). Cognitive-behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in-person or digitally (A). When cognitive-behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low-dose sedating antidepressants (B) can be used for the short-term treatment of insomnia (≤ 4 weeks). Longer-term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged-release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive-behavioural therapy for insomnia (B).

Sex differences in psychiatric comorbidity and clinical presentation in youths with conduct disorder.

BACKGROUND: Conduct disorder (CD) rarely occurs alone but is typically accompanied by comorbid psychiatric disorders, which complicates the clinical presentation and treatment of affected youths. The aim of this study was to investigate sex differences in comorbidity pattern in CD and to systematically explore the 'gender paradox' and 'delayed-onset pathway' hypotheses of female CD. METHODS: As part of the FemNAT-CD multisite study, semistructured clinical interviews and rating scales were used to perform a comprehensive phenotypic characterization of 454 girls and 295 boys with CD (9-18 years), compared to 864 sex- and age-matched typically developing controls. RESULTS: Girls with CD exhibited higher rates of current major depression, anxiety disorders, post-traumatic stress disorder and borderline personality disorder, whereas boys with CD had higher rates of current attention-deficit/hyperactivity disorder. In line with the 'gender paradox' hypothesis, relative to boys, girls with CD showed significantly more lifetime psychiatric comorbidities (incl. Alcohol Use Disorder), which were accompanied by more severe CD symptoms. Female and male youths with CD also differed significantly in their CD symptom profiles and distribution of age-of-onset subtypes of CD (i.e. fewer girls with childhood-onset CD). In line with the 'delayed-onset pathway' hypothesis, girls with adolescent-onset CD showed similar levels of dimensional psychopathology like boys with childhood-onset CD, while boys with adolescent-onset CD had the lowest levels of internalizing psychopathology. CONCLUSIONS: Within the largest study of CD in girls performed to date, we found compelling evidence for sex differences in comorbidity patterns and clinical presentation of CD. Our findings further support aspects of the 'gender paradox' and 'delayed-onset pathway' hypotheses by showing that girls with CD had higher rates of comorbid lifetime mental disorders and functional impairments, and they usually developed CD during adolescence. These novel data on sex-specific clinical profiles of CD will be critical in informing intervention and prevention programmes.

Cortisol to Dehydroepiandrosterone Sulphate Ratio and Executive Function in Bipolar Disorder.

INTRODUCTION: Bipolar disorder (BD) is associated with impairment in cognitive domains such as verbal memory and executive functions. Very few studies have assessed dehydroepiandrosterone sulphate (DHEA-S) in BD and its relation to cognitive functioning despite evidence showing its regulatory effects on glucocorticoid action. The aim of our study was to explore the association of cortisol, DHEA-S, and cortisol to DHEA-S ratio with visuospatial memory and executive functioning in BD. METHODS: Cognitive performance of 60 bipolar I patients and 30 healthy subjects was evaluated by using Cambridge Neuropsychological Test Automated Battery tasks targeting visuospatial memory (spatial recognition memory) and executive functions (planning [Stockings of Cambridge; SOC] and attentional set shifting [ID/ED]). Morning serum cortisol and DHEA-S levels were measured in patients. Main effects of cortisol, DHEA-S, and cortisol/DHEA-S ratio for each neurocognitive task were explored in multiple regression analyses correcting for demographic and clinical parameters as well as treatment-related factors (current use of antipsychotic and mood stabilizer medication). RESULTS: Bipolar patients showed poorer performance than healthy subjects in planning and attentional set shifting but not in visuospatial memory. Cortisol to DHEA-S ratio predicted worse performance in planning (SOC). CONCLUSIONS: This is the first study to assess memory and executive function in BD in relation to DHEA-S and cortisol to DHEA-S ratio. We report an association of cortisol to DHEA-S ratio with worse performance in planning in bipolar I patients, which warrants further investigation.

Positive and negative parenting in conduct disorder with high versus low levels of callous-unemotional traits.

Less is known about the relationship between conduct disorder (CD), callous-unemotional (CU) traits, and positive and negative parenting in youth compared to early childhood. We combined traditional univariate analyses with a novel machine learning classifier (Angle-based Generalized Matrix Learning Vector Quantization) to classify youth (N = 756; 9-18 years) into typically developing (TD) or CD groups with or without elevated CU traits (CD/HCU, CD/LCU, respectively) using youth- and parent-reports of parenting behavior. At the group level, both CD/HCU and CD/LCU were associated with high negative and low positive parenting relative to TD. However, only positive parenting differed between the CD/HCU and CD/LCU groups. In classification analyses, performance was best when distinguishing CD/HCU from TD groups and poorest when distinguishing CD/HCU from CD/LCU groups. Positive and negative parenting were both relevant when distinguishing CD/HCU from TD, negative parenting was most relevant when distinguishing between CD/LCU and TD, and positive parenting was most relevant when distinguishing CD/HCU from CD/LCU groups. These findings suggest that while positive parenting distinguishes between CD/HCU and CD/LCU, negative parenting is associated with both CD subtypes. These results highlight the importance of considering multiple parenting behaviors in CD with varying levels of CU traits in late childhood/adolescence.

Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies.

Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [rg ], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (rgs = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.

Genome-wide association study of treatment-resistance in depression and meta-analysis of three independent samples.

BACKGROUND: Treatment-resistant depression (TRD) is the most problematic outcome of depression in terms of functional impairment, suicidal thoughts and decline in physical health.AimsTo investigate the genetic predictors of TRD using a genome-wide approach to contribute to the development of precision medicine. METHOD: A sample recruited by the European Group for the Study of Resistant Depression (GSRD) including 1148 patients with major depressive disorder (MDD) was characterised for the occurrence of TRD (lack of response to at least two adequate antidepressant treatments) and genotyped using the Infinium PsychArray. Three clinically relevant patient groups were considered: TRD, responders and non-responders to the first antidepressant trial, thus outcomes were based on comparisons of these groups. Genetic analyses were performed at the variant, gene and gene-set (i.e. functionally related genes) level. Additive regression models of the outcomes and relevant covariates were used in the GSRD participants and in a fixed-effect meta-analysis performed between GSRD, STAR*D (n = 1316) and GENDEP (n = 761) participants. RESULTS: No individual polymorphism or gene was associated with TRD, although some suggestive signals showed enrichment in cytoskeleton regulation, transcription modulation and calcium signalling. Two gene sets (GO:0043949 and GO:0000183) were associated with TRD versus response and TRD versus response and non-response to the first treatment in the GSRD participants and in the meta-analysis, respectively (corrected P = 0.030 and P = 0.027). CONCLUSIONS: The identified gene sets are involved in cyclic adenosine monophosphate mediated signal and chromatin silencing, two processes previously implicated in antidepressant action. They represent possible biomarkers to implement personalised antidepressant treatments and targets for new antidepressants.Declaration of interestD.S. has received grant/research support from GlaxoSmithKline and Lundbeck; has served as a consultant or on advisory boards for AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Janssen and Lundbeck. S.M. has been a consultant or served on advisory boards for: AstraZeneca, Bristol-Myers Squibb, Forest, Johnson & Johnson, Leo, Lundbeck, Medelink, Neurim, Pierre Fabre, Richter. S.K. has received grant/research support from Eli Lilly, Lundbeck, Bristol-Myers Squibb, GlaxoSmithKline, Organon, Sepracor and Servier; has served as a consultant or on advisory boards for AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Eli Lilly, Lundbeck, Pfizer, Organon, Schwabe, Sepracor, Servier, Janssen and Novartis; and has served on speakers' bureaus for AstraZeneca, Eli Lily, Lundbeck, Schwabe, Sepracor, Servier, Pierre Fabre, Janssen and Neuraxpharm. J.Z. has received grant/research support from Lundbeck, Servier, Brainsway and Pfizer, has served as a consultant or on advisory boards for Servier, Pfizer, Abbott, Lilly, Actelion, AstraZeneca and Roche and has served on speakers' bureaus for Lundbeck, Roch, Lilly, Servier, Pfizer and Abbott. J.M. is a member of the Board of the Lundbeck International Neuroscience Foundation and of Advisory Board of Servier. A.S. is or has been consultant/speaker for: Abbott, AbbVie, Angelini, Astra Zeneca, Clinical Data, Boehringer, Bristol Myers Squibb, Eli Lilly, GlaxoSmithKline, Innovapharma, Italfarmaco, Janssen, Lundbeck, Naurex, Pfizer, Polifarma, Sanofi and Servier. C.M.L. receives research support from RGA UK Services Limited.

Major Depression and the Degree of Suicidality: Results of the European Group for the Study of Resistant Depression (GSRD).

Background: This European multicenter study aimed to elucidate suicidality in major depressive disorder. Previous surveys suggest a prevalence of suicidality in major depressive disorder of ≥50%, but little is known about the association of different degrees of suicidality with socio-demographic, psychosocial, and clinical characteristics. Methods: We stratified 1410 major depressive disorder patients into 3 categories of suicidality based on the Hamilton Rating Scale for Depression item 3 (suicidality) ratings (0=no suicidality; 1-2=mild/moderate suicidality; 3-4=severe suicidality). Chi-squared tests, analyses of covariance, and Spearman correlation analyses were applied for the data analyses. Results: The prevalence rate of suicidality in major depressive disorder amounted to 46.67% (Hamilton Rating Scale for Depression item 3 score ≥1). 53.33% were allocated into the no, 38.44% into the mild/moderate, and 8.23% into the severe suicidality patient group. Due to the stratification of our major depressive disorder patient sample according to different levels of suicidality, we identified some socio-demographic, psychosocial, and clinical variables differentiating from the patient group without suicidality already in presence of mild/moderate suicidality (depressive symptom severity, treatment resistance, psychotic features, add-on medications in general), whereas others separated only when severe suicidality was manifest (inpatient treatment, augmentation with antipsychotics and benzodiazepines, melancholic features, somatic comorbidities). Conclusions: As even mild/moderate suicidality is associated with a failure of achieving treatment response, adequate recognition of this condition should be ensured in the clinical practice.

Clinical and treatment-related predictors of cognition in bipolar disorder: focus on visual paired associative learning.

Bipolar disorder (BD) is associated with impairment in cognitive domains such as verbal memory and executive functions. However, visual paired associative learning (PAL) has been far less researched. Neurocognitive dysfunction in BD patients has been related to several clinical factors, but data on the effect of medication are relatively scarce and inconsistent. The aim of our study was to explore the effect of clinical and treatment-related parameters on executive functions and visual memory/learning, including PAL, in BD. Cognitive performance of 60 bipolar I patients and 30 healthy subjects was evaluated by using CANTAB battery tasks targeting spatial recognition memory, PAL and executive functions (set shifting, planning, inhibitory control). Bipolar patients showed poorer performance in PAL, set shifting, planning and inhibitory control than healthy subjects; however, only differences in PAL and planning survived correction for multiple comparisons. Number of previous manic episodes and illness duration predicted worse performance in set shifting and PAL, respectively, whereas current treatment with valproate predicted better performance in PAL. This is one of the first studies to assess clinical and treatment-related predictors of PAL in BD. We report a possibly beneficial effect of valproate on PAL, which warrants further investigation.

Validating a two-dimensional bipolar spectrum model integrating DSM-5's mixed features specifier for Major Depressive Disorder.

INTRODUCTION: The literature on DSM-5's 'Major Depressive Disorder with lifetime mixed features' (MDD-MF) is limited. This study investigated MDD-MF's potential inclusion into a bipolar spectrum. METHODS: We recruited 287 patients with Bipolar I disorder (BD-I), BD-II, MDD-MF or 'MDD without lifetime mixed features' (MDD-noMF); most (N=280) were stabilized for at least one year on medication. Sixteen validators (clinical features, psychiatric family history, temperament, stabilizing treatment) were compared across groups and subjected to trend analyses. Two discriminant function analyses (DFA; primary and secondary), excluding or including, respectively, treatment-related predictors, explored latent dimensions maximizing between-group discrimination; mahalanobis distances between group 'centroids' were calculated. RESULTS: Eleven validators differed significantly across groups; nine varied monotonically along a bipolar diathesis gradient with significant linear trends; two peaked at MDD-MF and displayed significant quadratic trends. In the primary DFA, apart from a classic bipolarity dimension, correlating with hospitalizations, early age at onset, lifetime psychosis and lower anxious temperament scores, on which groups ranked along a bipolar propensity gradient, a second dimension was also significant, peaking at BD-II and MDD-MF (challenging the classic bipolar ranking), which correlated with lifetime psychiatric comorbidities, suicidality, lower lifetime psychosis rates, female gender, higher cyclothymic and lower depressive temperament scores; MDD-MF was equipoised amidst BD-II and MDD-noMF. After including treatment-related predictors (secondary DFA), discrimination improved overall but BD-II and MDD-MF were closest than any other pair, suggesting similar treatment patterns for these two groups at this naturalistic setting. CONCLUSIONS: To our knowledge, this is the first time a two-dimensional bipolar spectrum based on classic external validators is proposed, fitting the data better than a unidimensional model. Additional predictors are warranted to improve BD-II/MDD-MF discrimination.

Association of 5-HTTLPR Polymorphism with the Nursing Diagnoses and the Achievement of Nursing Outcomes in Patients with Major Depression.

The aim of this study is to investigate whether a 44-base-pair insertion/deletion polymorphism in the upstream regulatory region of the serotonin transporter gene (5-HTTLPR) is associated with the nursing diagnoses and the achievement of the desired nursing outcomes in inpatients with major depression. Thirty five patients were evaluated. The nursing diagnoses of risk for suicide and imbalanced nutrition are reported less often in homozygotes of the high-expressing gene (LA). Carriers of the low-expressing genes (LG or S) have a worse response to interventions which aim to increase low self-esteem, indicating that they may need more intensive care in order to achieve the desired outcome. Genetics in psychiatric nursing could help refine personalized care, however further studies with large sample sizes and multiple gene evaluations are needed.

Mental Health Nursing in Greece: Nursing Diagnoses and Interventions in Major Depression.

The aim of the study was to assess nursing diagnoses and nursing interventions that were accordingly implemented during the care of inpatients with major depression in Greece. Twelve nurses working in three major psychiatric hospitals were recruited. Semi-structured interviews were used and audio-recorded data indicated that risk for suicide, social isolation, low self-esteem, sleep problems, and imbalanced nutrition are the nursing diagnoses most commonly reported. Establishing trust and rapport is the primary intervention, followed by specific interventions according to each diagnosis and the individualized care plan. The findings of the study also highlight the need for nursing training in order to teach nurses initial assessment procedures and appropriate evidence-based intervention techniques.

Use of the Sleep Apnea Scale of the Sleep Disorders Questionnaire (SA-SDQ) in adults with epilepsy.

OBJECTIVE: A growing body of literature supports the importance of sleep comorbidities in epilepsy. The prevalence of obstructive sleep apnea (OSA) in adults with epilepsy exceeds that of the general population, and its presence adversely impacts seizure control in some cases. The Sleep Apnea Scale of the Sleep Disorders Questionnaire (SA-SDQ) is a 12-item screening instrument generally used in clinical research. One prior study suggested modified cutoffs for the prediction of OSA in adults with epilepsy using this instrument. Our purpose was to further investigate the validity of the SA-SDQ in adults with epilepsy. METHODS: Ninety adults with epilepsy who underwent polysomnography (PSG) completed the SA-SDQ. Receiver operating characteristics were constructed to assess optimal sensitivity and specificity for predicting OSA (apnea-hypopnea index [AHI]≥5). RESULTS: Obstructive sleep apnea was diagnosed in 40 (44.4%) subjects. The overall area under the curve for the diagnosis of OSA was 0.771 (0.926 for males, 0.687 for females). For all subjects, a SA-SDQ cutoff score of 25 provided good sensitivity (73%) and specificity (72%) for OSA diagnosis. The same cutoff score provided optimal sensitivity (94%) and specificity (83%) for males, whereas for females, it provided lower sensitivity (55%) and specificity (68%). In females, a cutoff of 24 improved sensitivity (68%) but not specificity (58%). For all subjects with moderate-to-severe OSA (AHI≥15), the area under the curve was 0.766, and the optimal cutoff was 28. SIGNIFICANCE: Our work confirms the validity of the SA-SDQ as a screening instrument for OSA in clinical research involving adults with epilepsy. Further, our findings support the use of cutoffs lower than those applied to the general population and a single cutoff score (25) for predicting any severity of OSA in adults with epilepsy.

Impact of COVID-19 outbreak on subjective sleep during lockdown: relation with resilience characteristics.

The SARS-CoV-2 pandemic had a considerable impact on both the physical and mental health of people. Resilience is a psychological characteristic reflecting the ability to overcome or adapt to difficulties such as adversity, trauma, or extremely stressful situations. People with high resilience have been shown to exhibit lower levels of anxiety, stress and depression when faced with a stressful event. Sleep is particularly sensitive to anxiety and stress. The aim of this study was to investigate the impact of COVID-19 pandemic on sleep quantity, quality, and habits, while considering resilience as a factor. A total of 1260 individuals were recruited through an online survey. The variables that were assessed were socio-demographic, sleep habits and sleep disorders history, the Athens Insomnia Scale (AIS), the 25-item version of the Connor-Davidson Resilience Scale (CD-RISC), and any work/financial consequences during the first COVID-19 lockdown. The results showed that sleep habits during the lockdown changed for many of the participants. Their sleep schedule moving towards earlier or later for 9% and 67% of them, respectively; 38% of the participants were found to suffer from insomnia, based on the AIS score. A higher score on the CD-RISC was associated with better sleep. In conclusion, our study confirmed previous studies identifying quantitative and qualitative changes in sleep during the COVID-19 lockdown. It also expanded on the previous findings by identifying the correlation between sleep and resilience during the stressful period of the COVID-19 lockdown.

Factitious Disorder as a Skin Ulcer: A Case Report.

Dermatitis artefacta (factitious dermatitis) is a dermatological disease of different types; it could appear on various parts of the body. It is associated with severe difficulties, such as psychic distress and negative feelings aroused in healthcare personnel or borderline personality disorder, and the long-term possibility of patient self-harm to create more symptoms, resulting in unnecessary medical procedures. This is a case of a 17-year-old girl who was hospitalized with a skin ulcer on her right ankle that proved to be a factitious disorder. She was experiencing severe symptoms of anxiety, such as feeling nervous, having trouble sleeping and concentrating, and an inability to control worry due to her preparation for university studies. She refused to see a mental health professional since the onset of anxiety symptoms, i.e., the last four months. Patients who present with factitious disorder deliberately create clinical signs of a somatic disease because they need warmth and attention in a medical environment. Symptoms offer no significant benefit, and the pathophysiological mechanisms are mainly psychological. The primary treatment for factitious disorder is psychotherapy while the management of the ulcer requires dermatosurgical treatment.

Fine-mapping genomic loci refines bipolar disorder risk genes.

Bipolar disorder (BD) is a heritable mental illness with complex etiology. While the largest published genome-wide association study identified 64 BD risk loci, the causal SNPs and genes within these loci remain unknown. We applied a suite of statistical and functional fine-mapping methods to these loci, and prioritized 22 likely causal SNPs for BD. We mapped these SNPs to genes, and investigated their likely functional consequences by integrating variant annotations, brain cell-type epigenomic annotations, brain quantitative trait loci, and results from rare variant exome sequencing in BD. Convergent lines of evidence supported the roles of SCN2A, TRANK1, DCLK3, INSYN2B, SYNE1, THSD7A, CACNA1B, TUBBP5, PLCB3, PRDX5, KCNK4, AP001453.3, TRPT1, FKBP2, DNAJC4, RASGRP1, FURIN, FES, YWHAE, DPH1, GSDMB, MED24, THRA, EEF1A2, and KCNQ2 in BD. These represent promising candidates for functional experiments to understand biological mechanisms and therapeutic potential. Additionally, we demonstrated that fine-mapping effect sizes can improve performance and transferability of BD polygenic risk scores across ancestrally diverse populations, and present a high-throughput fine-mapping pipeline (https://github.com/mkoromina/SAFFARI).

Depression and Driving.

We have recently published an article in the International Journal of Environmental Research and Public Health presenting the results of our study on the driving behaviour of patients with depression.1 This is the first study conducted on the Greek population assessing the fitness-to-drive of patients with psychiatric disorders through the use of questionnaires and driving simulator. Similar studies in Greece have only been performed among patients with neurological conditions such as Parkinson's disease and mild cognitive impairment.2,3 The aim of the present communication is to discuss our findings in the light of the Greek law and regulations on driving licensure and on the evaluation of driving ability. The main findings of our study add evidence in this discussion by indicating that patients with depression (N=39) do not differ from controls (N=30) regarding their scores on the self-report questionnaires Driver Stress Inventory and Driver Behaviour Questionnaire. The DSI assesses the propensity to develop stress reactions while driving and consists of subscales for driving aggression, dislike of driving, hazard monitoring, thrill seeking, and proneness to fatigue. The DBQ assesses driving behaviour by the subscales of driving errors, traffic violations, and attention lapses. Driving simulator results showed very few differences between patients and controls in terms of their performance on the three selected driving scenarios. The sole difference found between patients and controls was that the former exhibited lower ability to maintain a stable track of the vehicle (measured as the standard deviation of lateral position) only in the rural road scenario. On the other hand, safety distance from the preceding vehicle was found to be higher in patients than in controls, indicating that patients, possibly aware of their somewhat impaired driving ability, tend to drive more carefully.1 These findings provide a plausible explanation for existing conflicting study results, which do not clearly show depression to be associated with susceptibility to traffic accidents and increased crash risk .4-6 International guidelines do not suggest a blanket restriction on the driving licensure of individuals with psychiatric disorders. Instead, there are recommendations for an approach based on the severity of the disorder, insight, adherence to treatment, level of cognitive impairment, and period of stability.7,8 Regulations in Greece are more restrictive, guided by laws 148/08.08.2016 and 5703/09.12.2021, which define the minimum requirements for licensure in certain medical conditions. A psychiatric examination is requested by internists, upon suspicion of a mental health issue and the psychiatric diagnosis assigns a competence level to the patient ("competent" or "non-competent"). The condition can be re-evaluated upon the patient's request after the lapse of one year from the initial examination; in certain conditions, renewal of driving licensure is permitted after a three-year interval in euthymia for individuals manifesting good functionality and social adjustment, provided that no sedative medication is prescribed. There is a need, therefore, for the Greek government to reconsider the minimum requirements for the licensure of patients with depression and the time intervals for evaluation of driving competence, which are not supported by research evidence. Setting a minimum time restriction of 1 year, unconditionally for all patients, does not seem to contribute to risk reduction, while on the contrary, it reduces patient autonomy and social connectivity, increases stigma, and may result in social exclusion, isolation, and the development of depression.9 Thus, it is important for the law to introduce an individualised approach with pros and cons being weighed per case, based on the existing scientific knowledge regarding the contribution of each disease to the risk of road traffic collisions and the clinical status of the patient at the time of the assessment.

[Epidemiological indicators and correlations of adolescent aggression in an urban student population].

Adolescent aggression has received a wide and longtime attention in scientific research, because of the extent of the phenomenon in this age group and of the negative consequences it inflicts on affected adolescents, and their human environments. The aim of this cross-sectional study was to determine the proportion (of high levels) of aggressive behaviors (physical, verbal, and direct aggression, anger, and hostility) in an urban sample of adolescent students, as well as to investigate associations between the occurrence of these behaviors, and adolescents' characteristics and mental health problems. The sample consisted of 2050 students attending the second grade of 49 random selected High Schools and Senior High Schools of the Regional Unit of the Central Sector of Attica and Piraeus. The Buss- Perry Aggression Questionnaire was administered to measure participants' aggression behaviors, while the Strength and Difficulties Questionnaire was also used to estimate their mental health and behavioral difficulties. Information about adolescents' individual, family, and school characteristics, was also collected. Results of the statistical analysis showed that the occurrence rates of high levels of participants' aggressive behaviors ranged between 2.2 (for total aggression) and 10.5% (for anger). Among individual characteristics, gender (with boys predominating in physical and direct aggression and girls in anger), (older) age, and sports activity (to direct aggression) were related to participants' aggressive behaviors. On the other hand, non-intact family structure and household insecurity food intake were positive correlated with specific aggressive behaviors, while pocket money allowance was positive associated with all of them. Concerning participants' mental health and behavioral issues, conduct problems and hyperactivity/ inattention were positive correlated with all investigated aggressive behaviors. In conclusion, the vast majority of the Central Sector of Attica and Piraeus adolescents did not seem to show high levels of aggressive behaviors (except anger). Nevertheless, considering this study outcomes (such as the "aggressive" burden of older adolescents, the role of family structure and pocket money allowance, as well as the co-occurrence with mental and behavioral problems), further longitudinal study is required to better understand the mechanisms that facilitate adolescent aggression.

Driving Behaviour in Depression Based on Subjective Evaluation and Data from a Driving Simulator.

Road traffic collisions are a major issue for public health. Depression is characterized by mental, emotional and executive dysfunction, which may have an impact on driving behaviour. Patients with depression (N = 39) and healthy controls (N = 30) were asked to complete questionnaires and to drive on a driving simulator in different scenarios. Driving simulator data included speed, safety distance from the preceding vehicle and lateral position. Demographic and medical information, insomnia (Athens Insomnia Scale, AIS), sleepiness (Epworth Sleepiness Scale, ESS), fatigue (Fatigue Severity Scale, FSS), symptoms of sleep apnoea (StopBang Questionnaire) and driving (Driver Stress Inventory, DSI and Driver Behaviour Questionnaire, DBQ) were assessed. Gender and age influenced almost all variables. The group of patients with depression did not differ from controls regarding driving behaviour as assessed through questionnaires; on the driving simulator, patients kept a longer safety distance. Subjective fatigue was positively associated with aggression, dislike of driving, hazard monitoring and violations as assessed by questionnaires. ESS and AIS scores were positively associated with keeping a longer safety distance and with Lateral Position Standard Deviation (LPSD), denoting lower ability to keep a stable position. It seems that, although certain symptoms of depression (insomnia, fatigue and somnolence) may affect driving performance, patients drive more carefully eliminating, thus, their impact.

The potential of biomarkers for diagnosing insomnia: Consensus statement of the WFSBP Task Force on Sleep Disorders.

OBJECTIVES: Thus far, the diagnosis of insomnia is based on purely clinical criteria. Although a broad range of altered physiological parameters has been identified in insomniacs, the evidence to establish their diagnostic usefulness is very limited. Purpose of this WFSBP Task Force consensus paper is to systematically evaluate a series of biomarkers as potential diagnostic tools for insomnia. METHODS: A newly created grading system was used for assessing the validity of various measurements in establishing the diagnosis of insomnia; these measurements originated from relevant studies selected and reviewed by experts. RESULTS: The measurements with the highest diagnostic performance were those derived from psychometric instruments. Biological measurements which emerged as potentially useful diagnostic instruments were polysomnography-derived cyclic alternating pattern, actigraphy, and BDNF levels, followed by heart rate around sleep onset, deficient melatonin rhythm, and certain neuroimaging patterns (mainly for the activity of frontal and pre-frontal cortex, hippocampus and basal ganglia); yet, these findings need replication, as well as establishment of commonly accepted methodology and diagnostic cut-off points. Routine polysomnography, EEG spectral analysis, heart rate variability, skin conductance, thermoregulation, oxygen consumption, HPA axis, and inflammation indices were not shown to be of satisfactory diagnostic value. CONCLUSIONS: Apart from psychometric instruments which are confirmed to be the gold standard in diagnosing insomnia, six biomarkers emerge as being potentially useful for this purpose.

Action initiation and punishment learning differ from childhood to adolescence while reward learning remains stable.

Theoretical and empirical accounts suggest that adolescence is associated with heightened reward learning and impulsivity. Experimental tasks and computational models that can dissociate reward learning from the tendency to initiate actions impulsively (action initiation bias) are thus critical to characterise the mechanisms that drive developmental differences. However, existing work has rarely quantified both learning ability and action initiation, or it has relied on small samples. Here, using computational modelling of a learning task collected from a large sample (N = 742, 9-18 years, 11 countries), we test differences in reward and punishment learning and action initiation from childhood to adolescence. Computational modelling reveals that whilst punishment learning rates increase with age, reward learning remains stable. In parallel, action initiation biases decrease with age. Results are similar when considering pubertal stage instead of chronological age. We conclude that heightened reward responsivity in adolescence can reflect differences in action initiation rather than enhanced reward learning.