Empathy refers to the cognitive and emotional reactions of an individual to the experiences of another. Women with premenstrual dysphoric disorder (PMDD) report severe social difficulties during the luteal phase of their menstrual cycle.

This clinical and functional magnetic resonance imaging study aimed to explore affective and cognitive empathy in women with PMDD, during the highly symptomatic luteal phase.

Overall, 32 women with PMDD and 20 healthy controls participated in the study. The neuroimaging data were collected using a highly empathy-engaging movie. First, we characterised the synchrony of neural responses within PMDD and healthy groups, using the inter-individual correlation approach. Next, using network cohesion analysis, we compared connectivity within and between brain networks associated with affective and cognitive empathy between groups, and assessed the association of these network patterns with empathic measures.

A consistent, although complex, picture of empathy abnormalities was found. Patients with PMDD showed decreased neural synchrony in parietal and frontal key nodes of cognitive empathy processing (theory-of-mind network), but higher neural synchrony in the anterior insula and anterior cingulate cortex, a part of the salience network, implicated in affective empathy. Positive correlations between cognitive perspective-taking scores and neural synchrony were found within the theory-of-mind network. Interestingly, during highly emotional moments, the PMDD group showed increased functional connectivity within this network.

Similar to major depression, individuals with PMDD show enhanced affective empathy and reduced cognitive empathy. These findings echo clinical observations reported when women with PMDD have a dysregulated emotional response to negative stimuli.

Resilience has been recently considered one of the possible mechanisms for the association between morningness–eveningness and depression. Meanwhile, anxiety is closely associated with mood disorder, but its association with morningness–eveningness is unclear. Therefore, this study aimed to explore the mediating effects of resilience and anxiety on morningness–eveningness and depression as the possible mechanisms.

This study included patient group and nonpatient group. Patient group consists of 743 patients with mood disorders [Major Depressive Disorder (MDD), 233; Bipolar Disorder I (BDI), 113; Bipolar Disorder II (BDII), 397] whereas nonpatient group consists of 818 individuals without mood disorder. The Composite Scale of Morningness, Connor–Davidson Resilience Scale, Self-Rating Depression Scale, and Beck Anxiety Inventory were used to evaluate morningness–eveningness, resilience, anxiety, and depression, respectively.

Our model provided a good fit for the data. The association between morningness–eveningness and depression symptoms was partially serially mediated by resilience and anxiety in both the patient and nonpatient groups. The patient group exhibited significantly stronger morningness–eveningness toward resilience and anxiety than the nonpatient group. In the indirect effect of morningness–eveningness on depression, group differences exist only through each mediation of resilience and anxiety, not through serial mediation.

Our results expand on the mechanism underlying the association between morningness–eveningness and depression. They highlight the importance of morningness–eveningness modification to increase resilience and the need to consider anxiety jointly in this process.

The aim of this study was to evaluate the impact of a multifaceted intervention to implement an adapted guideline for the management of depression in primary health care.

A hybrid trial was carried out to determine the effect of a multicomponent provider-centred intervention to improve the detection and diagnosis of depression in primary care, as part of the guideline implementation process, and to collect information about barriers and facilitators in a real-world context. Before the multicomponent intervention, a descriptive cross-sectional study was performed to assess the population prevalence of depression in the participating health centres and to detect possible differences. Subsequently, a quasi-experimental two-phase study was carried out with a concurrent control group to assess the impact of the multicomponent intervention on the main outcomes (detection of depression, evaluation of its severity and the use of structured methods to support the diagnosis).

Nine-hundred seventy-four patients took part in the first phase. According to their clinical records, the prevalence of depression ranged from 7.2% to 7.9%, and there were no significant differences between the health centres scheduled to receive the intervention and those in the control group. In the experimental phase, 797 randomly selected participants received the multicomponent intervention. Adjusted multivariable analysis performed before the implementation revealed no significant differences in depression between the experimental and control groups. However, after the intervention, modest but significant differences were observed, which persisted at 1 year after the intervention.

A multicomponent intervention for the implementation of a clinical guideline for the management of depression in primary care produced improvements in the identification of depression and in the degree of severity recorded.

Neuroprogressive models of the trajectory of cognitive dysfunction in patients with bipolar disorder (BD) have been proposed. However, few studies have explored the relationships among clinical characteristics of BD, cognitive dysfunction, and aging.

We conducted a cross-sectional analysis in euthymic participants with the MATRICS Cognitive Consensus Battery, the Trail Making Test B, the Stroop Test, and the Wechsler Test of Adult Reading. Age- and gender-equated control participants without a mental disorder [‘Healthy Controls’ – HC)] were assessed similarly. We compared cognitive performance both globally and in seven domains in four groups: younger BD (age ⩽49 years; n = 70), older BD (age ⩾50 years; n = 48), younger HC (n = 153), and older HC (n = 44). We also compared the BD and HC groups using age as a continuous measure. We controlled for relevant covariates and applied a Bonferroni correction.

Our results support both an early impairment (‘early hit’) model and an accelerated aging model: impairment in attention/vigilance, processing speed, and executive function/working memory were congruent with the accelerated aging hypothesis whereas impairment in verbal memory was congruent with an early impairment model. BD and HC participants exhibited similar age-related decline in reasoning/problem solving and visuospatial memory. There were no age- or diagnosis-related differences in social cognition.

Our findings support that different cognitive domains are affected differently by BD and aging. Longitudinal studies are needed to explore trajectories of cognitive performance in BD across the lifespan.

Idiopathic Intracranial Hypertension (IIH) is a condition characterized by an increase of intracranial pressure (ICP) with no identifiable cause to date. One-half of patients who suffer from IIH have co-morbid mood disorders, such as Major Depressive Disorder (MDD), that can be refractory to pharmacologic treatment. Electroconvulsive Therapy (ECT) is a safe and effective treatment for treatment-refractory mood disorder, but possesses a relative contra-indication for IIH due to its theoretical increase in ICP. Can ECT become the gold-standard treatment modality for mood disorder from IIH?

We aim to synthesize and summarize the state of the literature surrounding the intersection of ECT and IIH. We will present notable findings and propose avenues for future investigation.

We conducted a literature review using PubMed’s search function. Key terms that were queried are as follows: Idiopathic Intracranial Hypertension, Pseudotumor Cerebri, Benign Intracranial Hypertension, Mood Disorder, Major Depressive Disorder, ECT, Electroconvulsive Therapy.

The prevailing theory of IIH and mood disorder centers around HPA axis dysfunction, which has been heavily theorized to be positively impacted with ECT. ECT itself may not increase the ICP, but the anesthesia might. The only two case reports in the literature presented safe and successful use of ECT’s in patients with IIH and MDD.

More data is needed to draw conclusions, as the literature surrounding ECT’s use in patients with IIH remains sparse. Further studies must explore whether ECT’s use in IIH remains effective. Through this, we may understand more about both IIH and ECT itself.

No significant relationships.

Arnold Chiari malformation (ACM), a condition in which a portion of the brain pushes through the opening at the base of the skull, can cause headaches, dizziness, difficulty swallowing, muscle weakness and balance problems. The prevalence in the general population has been estimated at slightly less than 1/1000. The majority of these cases are asymptomatic. Chiari malformations are often detected coincidently among patients who have undergone diagnostic imaging for unrelated reasons. Several cases of psychiatric illness comorbid with ACM type 1 (ACM1) are reported in the literature.

Here we reported a patient with bipolar affective disorder, manic episode with a history of depressive episodes for 2 years comorbid with ACM1.

A 39 year-old-woman,with the history of panic disorder and obsessive compulsive disorder comorbid with depression have been using sertraline 50 mg/day for a year, admitted for decreased need of sleep, grandiosity, increased libido,risky behaviours, rapid speech and agitation. The patient met DSM 5 criteria for a manic episode and was hospitalized. She had a positive history of depression in her family. Her lab work up was unremarkable; including negative urine toxicology. MRI scans, for exclusion of organicity, demonstrated ACM1. Her treatment was started with a regimen of haloperidol 20 mg/day, biperiden 10 mg/day. The treatment was switched to olanzapine 20mg/day upon detection of rigidity. Lithium was added as 900mg/day. Neurosurgery, outpatient control was recommended by neurosurgery.

The patient’s symptoms gradually improved within one week with attainment of euthymic mood.

This case might show that ACM1 could cause abnormal functioning of brain circuits promoting psychiatric symptoms.

No significant relationships.

The potential antidepressant properties of probiotics have been suggested, but their influence on the emotional processes that may underlie this effect is unclear.

Depressed volunteers (n = 71) were recruited into a randomised double-blind, placebo-controlled study to explore the effects of a daily, 4-week intake of a multispecies probiotic or placebo on emotional processing and cognition. Mood, anxiety, positive and negative affect, sleep, salivary cortisol and serum C-reactive peptide (CRP) were assessed before and after supplementation.

Compared with placebo, probiotic intake increased accuracy at identifying faces expressing all emotions (+12%, p < 0.05, total n = 51) and vigilance to neutral faces (mean difference between groups = 12.28 ms ± 6.1, p < 0.05, total n = 51). Probiotic supplementation also reduced reward learning (−9%, p < 0.05, total n = 51), and interference word recall on the auditory verbal learning task (−18%, p < 0.05, total n = 50), but did not affect other aspects of cognitive performance. Although actigraphy revealed a significant group × night-time activity interaction, follow up analysis was not significant (p = 0.094). Supplementation did not alter salivary cortisol or circulating CRP concentrations. Probiotic intake significantly reduced (−50% from baseline, p < 0.05, n = 35) depression scores on the Patient Health Questionnaire-9, but these did not correlate with the changes in emotional processing.

The impartiality to positive and negative emotional stimuli or reward after probiotic supplementation have not been observed with conventional antidepressant therapies. Further studies are required to elucidate the significance of these changes with regard to the mood-improving action of the current probiotic.

The identification of potential biomarkers is crucial to improve the management and treatment of mood disorders. Glycogen synthase kinase-3 (GSK-3) is a multifunctional enzyme with an important role in the etiology of mood disorders. Recent findings suggested GSK-3 as a putative biomarker in mood disorders.

The aims of the study are: - to evaluate GSK3 as potential biomarker for differential diagnosis (MDD and BD); - to analyze the regulation of GSK3 by psychopharmacological treatments.

Patients included fulfill the following criteria: (a) principal diagnosis of MDD or BD (DSM-5); (b) age ≥ 18 years; (c) drug-free for at least 4 weeks before the inclusion. For each patient included a healthy control is enrolled, matched by gender and age. All included subjects at the study entry point (t0) are assessed through: - semistructured clinical interview and clinical rating scales (Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale; Young Mania Rating Scale, Clinical Global Impression) - blood draw, to measure GSK-3 levels Patients with MDD or BD are assessed again after 1 week (T1) and after 2 month (T2) of specific pharmacological treatment.

So far, we enrolled 16 patients and 16 healthy controls. The enrollment is still ongoing.

We expect to find GSK-3 levels differently expressed between healthy controls, patients with DDM and patients with BD. This finding would be crucial as it could contribute to the improvement of differential diagnosis. Moreover, we expect to observe a change in GSK-3 levels after psychopharmacological treatments.

Multiple neuroendocrine disorders can present themselves through diverse psychiatric symptoms. In the case of hypothyroidism it can manifest itself through mood disorders that will require a comprehensive differential diagnosis.

We present a case report and a review of the relevant literature about the relation between mood disorders and hypothyroidism.

We present the case of a 56-year-old man with no prior psychiatric record who concurring with a grieving process, developed a depressed mood, fatigue, decreased daily activity, and home isolation for months of evolution. He was diagnosed of hypothyroidism and treated with levotiroxine. It was necessary to boost hormonal treatment with antidepressant drugs due to the persistence of the symptoms after the resolution of the hormonal deficit.

The relationship of depression in patients with overt hypothyroidism is widely recognized. Common alterations to both disorders that could make their diagnosis difficult have been observed: existence of psychomotor slowing, attentional and executive disturbance, anxiety, asthenia, weight gain, depressed mood or bradypsychia among others. In the case of subclinical hypothyroidism, certain neuropsychiatric disorders have been linked without having conclusive evidence.

An early screening of thyroid function at the onset of psychiatric symptoms in individuals without prior psychiatric record is essential in the provision of adequate treatment. Clinical improvement has been seen with hormone replacement therapy alone. However, in up to 10% of patients it becomes insufficient, being necessary to complete it with antidepressant drugs for the complete resolution of the condition.

The outbreak of COVID-19 has disrupted the lives of countless people worldwide. The pandemic has imposed a sense of uncertainty and anxiety, as the world could not predict or prepare for this crisis. It is important to study risk factors, including employment, marital status, and pre-existing medical or psychiatric conditions to effectively handle this pandemic’s mental health impact.

We aim to evaluate factors contributing to the suicides and mood disorders during the coronavirus pandemic.

We examined MeSH terms “COVID-19” in the context of “Mood Disorders,” “Suicide,” “Suicidal Ideation,” “Assisted or Suicide, Attempted or Suicide,” “Risk Factors.” We identified eight case studies for the qualitative synthesis per the PRISMA guidelines, searching Medline, PubMed, PubMed Central, and PsychInfo databases until August 2020.

We identified that the population of all age groups and sex are at risk of stress and mental illness due to the pandemic. Several factors are attributed to the increased risk of mood disorders and suicide. Not having pre-existing psychiatric or medical condition is not a protective factor, since suicide was attempted or committed due to external factors such as economic and social.

The pandemic has increased the risk of mood disorder and suicides in the population. Focus should be on the behavioral and psychological first aid to curb stress.

Since the first reporting of ketamine’s antidepressant effects in 2000, there has been growing public interest in this novel rapid-acting treatment for depression despite its abuse potential. Online media is an increasingly popular way for the general public to source information. Our objective was to examine how online news outlets have portrayed ketamine as an antidepressant by ascertaining the volume and content of relevant articles and trends over time.

In this semi-quantitative study, we identified articles regarding ketamine’s use in depression from the 30 most popular English-language online news-generating sources over 18 years (2000–2017). Articles were then blindly assessed by 2 independent raters, who analysed the texts by quantifying the presence/absence of 12 content items.

We identified 97 articles, the number of which has increased since the first online news report in 2006. Most (69%) came from the USA and nearly all correctly stated the indications for ketamine. About half of the most recent articles mentioned abuse potential and 27% of articles referred to risks of unregulated use of ketamine. Just under 20% of articles referred to the lack of evidence regarding direct comparisons between ketamine and other currently available antidepressants. There was no difference in the overall level of detail within the articles during the study time period.

Online news media articles have been generally positive about ketamine for treating depression but need to be interpreted with caution as many of them did not discuss negative aspects of ketamine and made unsubstantiated claims about ketamine.

Few studies have examined whether UK military veterans are at an increased risk of dementia. We explored the risk of dementia in Scottish military veterans aged up to 73 years in comparison with people who have never served.

Retrospective cohort study of 78 000 veterans and 253 000 people with no record of service, matched for age, sex and area of residence, with up to 37 years follow-up, using Cox proportional hazard analysis to compare risk of dementia in veterans and non-veterans, overall and by subgroup.

Dementia was recorded in 0.2% of both veterans and non-veterans overall, Cox proportional hazard ratio 0.98, 95% confidence interval (CI) 0.82–1.19, p = 0.879 (landmark age: 50 years), with no difference for men but increased risk in veteran women and Early Service Leavers. Post-traumatic stress disorder (PTSD) was associated with a higher risk of dementia in both veterans and non-veterans, although possibly to a lesser degree in veterans. A history of mood disorder was strongly associated with developing dementia, greater in veterans than in non-veterans, odds ratio 1.54, 95% CI 1.01–2.35, p = 0.045.

There was no evidence to suggest that military service increased the risk of dementia, although this may change as the cohort ages. The well-documented association with PTSD shows no evidence of being stronger in veterans; by contrast, the association of mood disorder with dementia is much stronger in veterans. Healthcare providers should carefully assess the cognitive status of older veterans presenting with depressive illness in order to identify early dementia and ensure optimum management.

Systemic inflammation has been linked with mood disorder and cognitive impairment. The extent of this relationship remains uncertain, with the effects of serum inflammatory biomarkers compared to genetic predisposition toward inflammation yet to be clearly established.

We investigated the magnitude of associations between C-reactive protein (CRP) measures, lifetime history of bipolar disorder or major depression, and cognitive function (reaction time and visuospatial memory) in 84,268 UK Biobank participants. CRP was measured in serum and a polygenic risk score for CRP was calculated, based on a published genome-wide association study. Multiple regression models adjusted for sociodemographic and clinical confounders.

Increased serum CRP was significantly associated with mood disorder history (Kruskal–Wallis H = 196.06, p < 0.001, η2 = 0.002) but increased polygenic risk for CRP was not (F = 0.668, p = 0.648, η2 < 0.001). Compared to the lowest quintile, the highest serum CRP quintile was significantly associated with both negative and positive differences in cognitive performance (fully adjusted models: reaction time B = −0.030, 95% CI = −0.052, −0.008; visuospatial memory B = 0.066, 95% CI = 0.042, 0.089). More severe mood disorder categories were significantly associated with worse cognitive performance and this was not moderated by serum or genetic CRP level.

In this large cohort study, we found that measured inflammation was associated with mood disorder history, but genetic predisposition to inflammation was not. The association between mood disorder and worse cognitive performance was very small and did not vary by CRP level. The inconsistent relationship between CRP measures and cognitive performance warrants further study.

(1) To delineate whether cognitive flexibility and inhibitory ability are neurocognitive markers of passive suicidal ideation (PSI), an early stage of suicide risk in depression and (2) to determine whether PSI is associated with volumetric differences in regions of the prefrontal cortex (PFC) in middle-aged and older adults with depression.

Cross-sectional study.

University medical school.

Forty community-dwelling middle-aged and older adults with depression from a larger study of depression and anxiety (NIMH R01 MH091342-05 PI: O’Hara).

Psychiatric measures were assessed for the presence of a DSM-5 depressive disorder and PSI. A neurocognitive battery assessed cognitive flexibility, inhibitory ability, as well as other neurocognitive domains.

The PSI group (n = 18) performed significantly worse on cognitive flexibility and inhibitory ability, but not on other neurocognitive tasks, compared to the group without PSI (n = 22). The group with PSI had larger left mid-frontal gyri (MFG) than the no-PSI group. There was no association between cognitive flexibility/inhibitory ability and left MFG volume.

Findings implicate a neurocognitive signature of PSI: poorer cognitive flexibility and poor inhibitory ability not better accounted for by other domains of cognitive dysfunction and not associated with volumetric differences in the left MFG. This suggests that there are two specific but independent risk factors of PSI in middle- and older-aged adults.