A large amount of literature surrounds the differences between dissociative neurological symptom disorder with non-epileptic seizures (DNSD-S) and epilepsy.

To explore the research gap on phenotypic differences between DNSD-S and other psychiatric disorders.

We conducted a case–control study of 1860 patients (620 patients with DNSD-S and 1240 controls with other psychiatric disorders) seen at the South London and Maudsley Hospital NHS Trust between 2007 and 2019.

Compared with the controls, the patients with DNSD-S were more likely to be female (76 v. 47%, P < 0.001), of White ethnicity (77 v. 60%, P < 0.001), married (34 v. 14%, P < 0.001) and living in areas of lower socioeconomic status (−3.79, 95% CI −2.62 to −4.96, P < 0.001). Two peaks for age at diagnosis were observed for DNSD-S: the early 20s and late 40s. After 31 years of age, men's chance of being diagnosed with DNSD-S increased from 19 to 28% (P = 0.009). People with DNSD-S presented more commonly with a history of a neurological episodic or paroxysmal disorder (OR = 12, 95% CI 7.82–20.26), another dissociative disorder (OR = 10, 95% CI 1.64– 65.95) or unclassified signs or symptoms (OR = 4, 95% CI 2.61–6.43). Neither anxiety, depression nor other somatoform disorders predicted subsequent diagnosis of DNSD-S, and controls had a larger proportion of preceding psychiatric diagnoses than patients with DNSD-S (65 v. 49%, P < 0.001).

This is the first study comparing demographic and phenotypic correlates of patients with DNSD-S against a large cohort of psychiatric patients. These data will inform development and drive service needs in psychiatry for people with DNSD-S.

Prevalence and clinical correlates of dissociative symptoms in general, and depersonalization (DP) in particular, in patients with mood disorders have received limited attention in the literature1. Thus, the aim ofour study is to evaluate the association between depersonalization symptoms and mood dimensions in a sample of unipolar (UD) and bipolar (BD) patients.

185 patients (95 BD and 90 UD) in eutimic phase (evaluate with YMRS and HDRS) are assessed with: SCID-P for axis I diagnosis, HDRS, YMRS, MOOD-SR-lifetime version2 and SCI-DER.

through a regression analysis we underline in UD patients that the presence of depersonalization symptoms is significantly associated with the following mood dimensions: psychomotor retardation (p = 0.031; B = 2,197), mixed irritability (p = 0.035; B = 2,137) and social extroversion (p = 0.028; B = -2,229). We found no significat association in the group of BD patients.

In UD patiens, the presence of depersonalization symptoms must carefully consider. Further research are needed to identify specific clinical endophenotypes3.

Impulsivity is a core feature of bipolar disorder (BD). The best definition of impulsivity is the predisposition to have rapid and unplanned reactions to internal and external stimuli without regard to the negative consequences of these actions to the impulsive individual or others. Thus, the aim of our study is to investigate the relationship between impulsivity, panic disorder (PD) comorbidity and panic spectrum symptoms in patients with BD.

247 eutimic patients were assessed with SCID-P, MOOD-SR, PAS-SR. Impulsivity dimension was defined on the basis BIS Scale score (version 11).

A backward stepwise logistic regression in bipolar patients with PAS explained score statistically much higher for impulsivity (pas +6.09 vs pas - 3.88 p < 001) and the difference is statistically significant stratifing for BD. A stepwise linear regression, corrected by age and gender, displayed significantly statistical correlation with impulsivity score and PAS-SR by cut-off 35 (OR = 1.210).

In our sample BD eutimic patients explained score statistically much higher for impulsivity. This data confirm the presence of the trait impulsivity in BD eutimic patients. BD patients with a comorbid anxiety disorder seem to display significant higher levels of impulsivity when compared to patients without an anxiety disorder. Impulsivity was linked with atypical panic like symptoms more with PD diagnosis. Results suggest the presence of specific bipolar disorder endophenotipe. Further neurobiologies studies are needed to elucidate the implications and reasons of this association.

There is a strong association between depersonalization (DP) and panic disorder (PD), as documented by Roth (1960) and later by Cassano (1989)1. In the PD is shown a prevalence of 7.8% to 82.6% from the DP. The aim of our study was to evaluate the association between depersonalization symptoms and PD in a sample of patients with anxiety disorders and mood.

A sample of 310 patiens was assessed with: SCID-P for axis I diagnosis and SCI-DER (structured clinical interview for depersonalization and derealization symptoms, lifetime version)2.

Through a linear regression analysis we underline that, the presence of depersonalization symptoms, irrespective of age, gender and mood disorder, is significantly associated with the PD diagnosis (total score SCI-DER Tot p = 0.001; derealization p = 0.001; somatopsychic depersonalization p = 0.001; autopsychic depersonalization p = 0.003; affective depersonalization p = 0.047).

The presence of depersonalization symptoms must carefully assess in clinical setting and suggest the presence of panic disorder.

The aim of our study is to evaluate, in a sample of bipolar (BD) eutimic patients, the association between depersonalization symptoms, facial emotions expression recognition and affective temperament.

95 bipolar eutimic patients (YMRS< 6 and HDRS< 8), are assessed with: SCID-P, TEMPS, SCI-DER1 e POFA (test of recognitionof facial emotions expression by Ekman e Friesen).

Throught a regression analysis we underline that, independently to panic disorder, the ipertimic temperament is associated with: major recognition of happiness (p < 0.001; β = -4,483) and minor recognition of anger (p = 0.005; β = 3,202) in BD patients with high scores in autopsychic depersonalization domain; major recognition of sadness (p = 0.001; β = -3,944) and minor recognition of anger (p = 0.005; β = 3,181) in BD patients with high scores in affective depersonalization domain. Moreover, the cyclotimic temperament is associated with: major recognition of surprise (p = 0.004; β = -3,233) and happiness (p = 0.044; β = -2,124) in BD patients with high scores in Derealization (DER-TOT); major recognition of surprise (p = 0.001; β = -3,792) and happiness (p = 0.018; β = -2,532) in BD patients with high scores in somatopsychic depersonalization domain.

The presence of depersonalization and derealization symptoms is associated with a selective deficit in the recognition of several emotions. in bipolar patients this selective deficit is dependent of type of affective temperament. Further research is warranted to replicate our clinical observation.

Major depressive disorder (MDD) is moderately heritable, however genome-wide association studies (GWAS) for MDD, as well as for related continuous outcomes, have not shown consistent results. Attempts to elucidate the genetic basis of MDD may be hindered by heterogeneity in diagnosis. The Center for Epidemiological Studies Depression (CES-D) scale provides a widely used tool for measuring depressive symptoms clustered in four different domains which can be combined together into a total score but also can be analysed as separate symptom domains.

We performed a meta-analysis of GWAS of the CES-D symptom clusters. We recruited 12 cohorts with the 20- or 10-item CES-D scale (32 528 persons).

One single nucleotide polymorphism (SNP), rs713224, located near the brain-expressed melatonin receptor (MTNR1A) gene, was associated with the somatic complaints domain of depression symptoms, with borderline genome-wide significance (pdiscovery = 3.82 × 10−8). The SNP was analysed in an additional five cohorts comprising the replication sample (6813 persons). However, the association was not consistent among the replication sample (pdiscovery+replication = 1.10 × 10−6) with evidence of heterogeneity.

Despite the effort to harmonize the phenotypes across cohorts and participants, our study is still underpowered to detect consistent association for depression, even by means of symptom classification. On the contrary, the SNP-based heritability and co-heritability estimation results suggest that a very minor part of the variation could be captured by GWAS, explaining the reason of sparse findings.

Twin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ.

Multivariate familial models were run on data from 1265 individuals aged 6–18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice–delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI).

Significant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41–0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80–87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ.

The aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD.