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Type 2 diabetes mellitus (T2DM) is a common metabolic disorder with various medical and psychological adverse effects. Well-being in patients with T2DM is often compromised. The aim of the present study was to investigate clinicodemographic predictors of well-being in patients with T2DM with no known psychiatric history and explore the mediatory role of undiagnosed anxiety and depression. We recruited 175 outpatients with T2DM (54.3% males, aged 34-79 (mean 59.9) years) followed-up at the Diabetes Center of the General Hospital of Nikaia-Peiraeus in Athens. Patients included had no severe diabetes-related complications or known psychiatric history. Well-being was measured with the Mental Health Continuum Short-Form (MHC-SF), a novel 14-item tool measuring the emotional (EWB), social (SWB) and psychological (PWB) dimensions of well-being, as well as a total score of well-being (WBT). Hospital Anxiety and Depression Scale (HADS) was used for screening for undiagnosed anxiety (HADS-A) and depression (HADS-D). Patients' demographics, Body Mass Index (BMI), glycemic control (HbA1c), T2DM duration, comorbid hypertension or dyslipidemia and type of antidiabetic medication were investigated as predictors of well-being or its dimensions in stepwise linear regression models, also including or excluding HADS-A and HADS-D. Mediational effects of HADS-A and HADS-D were explored in structural equation models through path analyses. Results showed that 21.1% of participants had comorbid depression (HADS-D≥11) and 5.1% comorbid anxiety disorder (HADS-A≥11). In the models without HADS, higher WBT as well as EWB and PWB were significantly predicted by lower HbA1c (all p=0.001) and lower BMI (p=0.015, 0.019 and 0.030, respectively). After being included in the model, HADS-A and HADS-D significantly predicted WBT and every dimension of well-being, but the effects of HbA1c and BMI were no longer statistically significant. In path analyses, the indirect effects of HbA1c and BMI on well-being via HADS-D were statistically significant, while the direct and indirect effects via HADS-A were not. Therefore, the effects of HbA1c and BMI on EWB, PWB and WBT were completely mediated by HADS-D. Concludingly, this is the first study using MHC-SF to measure well-being in patients with T2DM. High levels of undiagnosed depression were recorded, in agreement with other studies. Depression was predicted by HbA1c and BMI and finally predicted well-being. Undiagnosed depression fully explained the effects of HbA1c and BMI on well-being. The interplay of glycemic control and positive mental health should be further investigated.

Social distancing restrictions in the COVID-19 pandemic may have had adverse effects on older adults' mental health. Whereby the impact on mood is well-described, less is known about psychotic symptoms. The aim of this study was to compare characteristics associated with psychotic symptoms during the first UK lockdown and a pre-pandemic comparison period.In this retrospective observational study we analysed anonymised records from patients referred to mental health services for older adults in South London in the 16-week period of the UK lockdown starting in March 2020, and in the comparable pre-pandemic period in 2019. We used logistic regression models to compare the associations of different patient characteristics with increased odds of presenting with any psychotic symptom (defined as hallucinations and/or delusion), hallucinations, or delusions, during lockdown and the corresponding pre-pandemic period.1991 referrals were identified. There were fewer referrals during lockdown but a higher proportion of presentations with any psychotic symptom (48.7% vs. 42.8%, p = 0.018), particularly hallucinations (41.0% vs. 27.8%, p 0.001). Patients of non-White ethnicity (adjusted odds ratio (OR): 1.83; 95% confidence interval (CI): 1.13-2.99) and patients with dementia (adjusted OR: 3.09; 95% CI: 1.91-4.99) were more likely to be referred with psychotic symptoms during lockdown. While a weaker association between dementia and psychotic symptoms was found in the pre-COVID period (adjusted OR: 1.55; 95% CI: 1.19-2.03), interaction terms indicated higher odds of patients of non-White ethnicity or dementia to present with psychosis during the lockdown period.During lockdown, referrals to mental health services for adults decreased, but contained a higher proportion with psychotic symptoms. The stronger association with psychotic symptoms in non-White ethnic groups and patients with dementia during lockdown suggests that barriers in accessing care might have increased during the COVID-19 pandemic.

The ongoing coronavirus disease 2019 (COVID-19) pandemic has had a widespread impact on individuals' mental health through indirect psychological and social mechanisms, related to factors such as fear of infection or death, social isolation, lack of social support and financial instability. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has also been associated with the development or recurrence of neuropsychiatric symptoms, both during the acute phase, as well as during the post-acute 'long-COVID' phase. In addition to the COVID-19 survivors with a mental health history that are at a high risk of experiencing a range of neuropsychiatric symptoms following resolution of acute COVID-19, there is accumulating evidence that a diagnosis of COVID-19 may also be associated with new-onset neuropsychiatric morbidity among survivors without pre-existing mental health disorders. In particular, studies investigating the incidence of post-acute neuropsychiatric sequelae, based mostly on retrospective cohort study designs and data from national health registries, have reported the development of new-onset manifestations, including depression, anxiety, psychotic symptoms, sleep disturbances and fatigue. Nevertheless, when COVID-19 survivors were compared with SARS-CoV-2-negative controls and especially survivors of other disorders (such as influenza), the findings regarding the risk of incident neuropsychiatric manifestations varied among studies. While there is evidence of an association between SARS-CoV-2 infection and the subsequent occurrence of new-onset neuropsychiatric symptoms, especially among patients with increased disease severity, further research using methodological approaches less susceptible to confounding bias is required to establish causal relationships.

The coronavirus disease‑2019 (COVID‑19) pandemic, caused by the new coronavirus SARS‑CoV‑2, has spread around the globe with unprecedented consequences for the health of millions of people. While the pandemic is still in progress, with new incidents being reported every day, the resilience of the global society is constantly being challenged. Under these circumstances, the future seems uncertain. SARS‑CoV‑2 coronavirus has spread panic among civilians and insecurity at all socio‑political and economic levels, dramatically disrupting everyday life, global economy, international travel and trade. The disease has also been linked to the onset of depression in many individuals due to the extreme restriction measures that have been taken for the prevention of the rapid spreading of COVID‑19. First, the socio‑economic, political and psychological implications of the COVID‑19 pandemic were explored. Substantial evidence is provided for the consequences of the pandemic on all aspects of everyday life, while at the same time we unravel the role and the pursuits of national regimes during this unforeseen situation. The second goal of this review is related to the scientific aspect of the pandemic. Hence, we explain why SARS‑CoV‑2 is not a so‑called 'invisible enemy', and also attempt to give insight regarding the origin of the virus, in an effort to reject the conspiracy theories that have arisen during the pandemic. Finally, rational strategies were investigated for successful vaccine development. We are optimistic that this review will complement the knowledge of specialized scientists and inform non‑specialized readers on basic scientific questions, and also on the social and economic implications of the COVID‑19 pandemic.

Aims Depression is an important issue in heart failure (HF). The study investigated whole-brain and regional brain glucose metabolism in HF patients and its association with depression comorbidity. Methods and results Twenty-nine hospitalized patients with symptomatic systolic HF (left ventricular ejection fraction 0.93) or 'real' (≤0.93) depression. Conclusion Heart failure patients with more severe disease showed whole-brain and regional brain hypometabolism in 18 F-FDG PET/CT. Depressed HF patients (Beck Depression Inventory score >13) exhibited different metabolic patterns that could be used to differentiate between 'epiphenomenal' and 'real' depression. Namely, presence of whole-brain hypometabolism suggested 'epiphenomenal' depression, whereas absence suggested 'real' depression. Presence of significant relative regional brain hypometabolism enhanced the likelihood of 'real' depression diagnosis.

A 15-year-old female former gymnast with a history of pectus excavatum was reviewed due to unexplained paraparesis and urinary incontinence since age 10. Symptoms were commenced with intolerable upper back pain and development of a soft mass at the sacrum that remitted spontaneously. Brain and whole spine MRI imaging and blood and CSF testing were normal. The combination of skeletal, neurological, and bladder symptoms with normal lumbar MRI and abnormal urodynamic and neurophysiological studies led to the clinical suspicion of occult tethered cord syndrome (oTCS). Surgical cord "untethering" was performed leading to remarkable postoperative clinical improvement. oTCS is a recently defined functional disorder of the spinal cord due to fixation (tethering) of the conus medullaris by inelastic elements that may lead to severe neurological impairment. High clinical suspicion is required as oTCS is a treatable spinal cord disorder.

COVID-19 has caused unprecedented societal turmoil, triggering a rapid, still ongoing, transformation of healthcare provision on a global level. In this new landscape, it is highly important to acknowledge the challenges this pandemic poses on the care of the particularly vulnerable cancer patients and the subsequent psychosocial impact on them. We have outlined our clinical experience in managing patients with gastrointestinal, hematological, gynaecological, dermatological, neurological, thyroid, lung and paediatric cancers in the COVID-19 era and have reviewed the emerging literature around barriers to care of oncology patients and how this crisis affects them. Moreover, evolving treatment strategies and novel ways of addressing the needs of oncology patients in the new context of the pandemic are discussed.

COVID-19 pandemic has caused a global public health emergency resulting in unprecedented individual and societal fear and anxiety. The stress surrounding this biothreat appears to have clinical implications in all aspects of medicine, both in mental and physical health spheres. The impact of COVID-19 related anxiety in Cardiology, Paediatrics, Oncology, Dermatology, Neurology and Mental Health and how it affects treatments is discussed. Moreover, the need for introducing novel communication and therapeutic approaches is highlighted in the new landscape of the COVID-19 era.

There is accumulating evidence in the literature indicating that a number of patients with coronavirus disease 2019 (COVID-19) may experience a range of neuropsychiatric symptoms, persisting or even presenting following the resolution of acute COVID-19. Among the neuropsychiatric manifestations more frequently associated with 'long COVID' are depression, anxiety, post-traumatic stress disorder, sleep disturbances, fatigue and cognitive deficits, that can potentially be debilitating and negatively affect patients' wellbeing, albeit in the majority of cases symptoms tend to improve over time. Despite variations in results obtained from studies using different methodological approaches to define 'long COVID' syndrome, the most widely accepted factors associated with a higher risk of developing neuropsychiatric manifestations include the severity of foregoing COVID-19, the female sex, the presence of comorbidities, a history of mental health disease and an elevation in the levels of inflammatory markers, albeit further research is required to establish causal associations. To date, the pathophysiological mechanisms implicated in neuropsychiatric manifestations of 'long COVID' remain only partially elucidated, while the role of the indirect effects of the COVID-19 pandemic, such as social isolation and uncertainty concerning social, financial and health recovery post-COVID, have also been highlighted. Given the alarming effects of 'long-COVID', interdisciplinary cooperation for the early identification of patients who are at a high risk of persistent neuropsychiatric presentations, beyond COVID-19 recovery, is crucial to ensure that appropriate integrated physical and mental health support is provided, with the aim of mitigating the risks of long-term disability at a societal and individual level.

Since the outbreak of the coronavirus 2019 (COVID-19) pandemic, there has been widespread concern that social isolation, financial stress, depression, limited or variable access to health care services and other pandemic-related stressors may contribute to an increase in suicidal behaviors. In patients who have recovered from COVID-19, an increased risk of developing suicidal behaviors may be noted, while post-COVID syndrome comprises another potential risk factor contributing to increased suicidal behaviors. Despite the initial alarming predictions for an increase in suicide rates due to the COVID-19 pandemic, the majority of published studies to date suggest that experienced difficulties and distress do not inevitably translate into an increased number of suicide-related deaths, at least not in the short-term. Nevertheless, the long-term mental health effects of the COVID-19 pandemic have yet to be unfolded and are likely to remain for a long period of time. Suicide prevention and measures aiming at promoting well-being and mitigating the effects of COVID-19 on mental health, particularly among vulnerable groups, should thus be a priority for healthcare professionals and policymakers amidst the evolving COVID-19 pandemic.

BackgroundEvidence suggests that environmental factors not only increase psychosis liability but also influence the prognosis and outcomes of psychotic disorders. We investigated temporal and cross-sectional associations of a weighted score of cumulative environmental liability for schizophrenia – the exposome score for schizophrenia (ES-SCZ) – with functioning in first-episode psychosis (FEP).MethodsData were derived from the baseline and 1-month assessments of the Athens FEP Research Study that enrolled 225 individuals with FEP. The Global Assessment of Functioning (GAF) and the Personal and Social Performance Scale (PSP) were used to measure social, occupational, and psychological functioning. The ES-SCZ was calculated based on the previously validated method.ResultsES-SCZ was associated with the total scores of GAF and PSP at baseline and 1-month assessments. These findings remained significant when accounting for several associated alternative explanatory variables, including other environmental factors (obstetric complications, migration, ethnic minority), clinical characteristics (duration of untreated psychosis, symptom severity, previous antipsychotic use), and family history of psychosis, demonstrating that the association between ES-SCZ and functioning is over and above other risk factors and cannot be explained by symptom severity alone. Functioning improved from baseline to 1-month assessment, but no significant ES-SCZ-by-time interaction was found on functioning, indicating that functioning changes were not contingent on ES-SCZ.ConclusionsOur findings suggest that rather than a predictor of functional improvement, ES-SCZ represents a stable severity indicator that captures poor functioning in early psychosis. Environmental risk loading for schizophrenia (ES-SCZ) can be beneficial for clinical characterization and incorporated into transdiagnostic staging models.

Accumulating evidence points toward a very high prevalence of prolonged neurological symptoms among coronavirus disease 2019 (COVID-19) survivors. To date, there are no solidified criteria for ‘long-COVID’ diagnosis. Nevertheless, ‘long-COVID’ is conceptualized as a multi-organ disorder with a wide spectrum of clinical manifestations that may be indicative of underlying pulmonary, cardiovascular, endocrine, hematologic, renal, gastrointestinal, dermatologic, immunological, psychiatric, or neurological disease. Involvement of the central or peripheral nervous system is noted in more than one-third of patients with antecedent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, while an approximately threefold higher incidence of neurological symptoms is recorded in observational studies including patient-reported data. The most frequent neurological manifestations of ‘long-COVID’ encompass fatigue; ‘brain fog’; headache; cognitive impairment; sleep, mood, smell, or taste disorders; myalgias; sensorimotor deficits; and dysautonomia. Although very limited evidence exists to date on the pathophysiological mechanisms implicated in the manifestation of ‘long-COVID’, neuroinflammatory and oxidative stress processes are thought to prevail in propagating neurological ‘long-COVID’ sequelae. In this narrative review, we sought to present a comprehensive overview of our current understanding of clinical features, risk factors, and pathophysiological processes of neurological ‘long-COVID’ sequelae. Moreover, we propose diagnostic and therapeutic algorithms that may aid in the prompt recognition and management of underlying causes of neurological symptoms that persist beyond the resolution of acute COVID-19. Furthermore, as causal treatments for ‘long-COVID’ are currently unavailable, we propose therapeutic approaches for symptom-oriented management of neurological ‘long-COVID’ symptoms. In addition, we emphasize that collaborative research initiatives are urgently needed to expedite the development of preventive and therapeutic strategies for neurological ‘long-COVID’ sequelae.

Among different proposed pathophysiological mechanisms, redox imbalance has been suggested to be a potential contributor in the pathogenesis of schizophrenia. DJ-1 is a redox-sensitive protein that has been shown to have neuroprotective function in the brain in Parkinson's disease and other neurodegenerative diseases. However, a role for DJ-1 in schizophrenia is unknown. Bioinformatic analysis suggested that microRNA (miR)-203a-3p could target the 3' untranslated region (UTR) of DJ-1. In whole blood and blood-derived exosomes of 11 first episode antipsychotic naïve schizophrenia patients, DJ-1 protein and mRNA demonstrated decreased DJ-1 mRNA and protein and increased miR203a-3p levels compared to healthy controls. In whole blood, antipsychotic monotherapy with olanzapine for 6 weeks increased DJ-1 and attenuated miR203a-3p levels, whereas in blood derived exosomes, olanzapine returned DJ-1 and miR203a-3p to levels seen healthy controls. Consistent with this finding, we showed that human umbilical vein endothelial cells (HUVACs) transfected with a DJ-1-3' UTR luciferase reporter construct displayed reduced gene expression when subjected to the oxidative stressor H

The current study aimed to assess the possibility of an association between first and second generation antipsychotic medication and raised eosinophil count. A total of 22 in-patients at the psychiatric unit of the University General Hospital ‘Attikon’, a tertiary hospital, were included in the present study. Patients had received antipsychotic monotherapy and did not have any co-morbidities or require additional treatments. Patients were monitored weekly and their eosinophil count was assessed. One-way ANOVA and summary measures analysis were applied to study the effect of time and medication type on the absolute eosinophil concentration (or relative percentage) for each patient. The differences in mean eosinophil concentrations or relative percentage by patient and time were also assessed. An increase in the absolute concentration and the relative percentage of eosinophils over time was observed in patients receiving Olanzapine, Haloperidol and Aripiprazole. However, there was no difference between individual medications. In conclusion, antipsychotics may be associated with increased eosinophil count over time; however, larger studies involving more patients and a longer follow-up are required to reach a definitive conclusion.

Lay abstract Hypertension, or high blood pressure, is considered the leading cause of cardiovascular death and disability and is usually treated with medication to lower blood pressure and by making changes to the dietary habits of the patient. Lack of sleep is also a potential risk factor for high blood pressure. However, results on this matter have been contradictory so far. We investigated the relationship between sleep characteristics with high blood pressure in a representative Greek population using self-reported questionnaires. Our study revealed that short sleep duration, excessive daytime sleepiness, insomnia, poor sleep quality and high risk of obstructive sleep apnea are associated with increased prevalence of hypertension among younger and middle-aged adults, affecting everyone equally, regardless of sex. Thus, early medical or cognitive behavioral interventions that improve sleep might be necessary in order to reduce high blood pressure and consequently risk of other diseases of the heart and blood vessels.

COVID-19 pandemic has undoubtedly disrupted the well-established, traditional structure of medical education. Τhe new limitations of physical presence have accelerated the development of an online learning environment, comprising both of asynchronous and synchronous distance education, and the introduction of novel ways of student assessment. At the same time, this prolonged crisis had serious implications on the lives of medical students including their psychological well-being and the impact on their academic trajectories. The new reality has, on many occasions, triggered the ‘acting up’ of medical students as frontline healthcare staff, which has been perceived by many of them as a positive learning and contributing experience, and has led to a variety of responses from the educational institutions. All things considered, the urgency for rapid and novel adaptations to the new circumstances has functioned as a springboard for remarkable innovations in medical education,including the promotion of a more “evidence-based” approach.

Objectives: Increasingly, older populations in the United Kingdom and other well-resourced settings are ethnically diverse. Despite a concern that the prevalence of dementia is expected to rise, very little is known about the association of ethnicity and dementia among aging older adults. The current study aimed to compare ethnic group differences in symptom profile, functioning and pharmacotherapy at dementia diagnosis. Design: Cross-sectional study of patient characteristics at the point of dementia diagnosis. Setting and Participants: In total, 12,154 patients aged 65 years or older diagnosed with dementia in Southeast London between 2007 and 2015. Methods: Data were extracted from the Clinical Record Interactive Search system, which provides anonymized access to the electronic health records of a large mental healthcare provider in Southeast London. Patients from ethnic minority backgrounds were compared with white British individuals on mental and physical well-being, functional scales and medications prescribed at dementia diagnosis, as well as subtype of dementia documented anywhere in the record. Results: Compared with white British patients, Black African and Black Caribbean patients were more likely to present with psychotic symptoms and were less likely to have an antidepressant prescribed; white Irish patients had higher rates of substance/alcohol use and depressive symptoms were more prevalent in South Asian patients; all ethnic minority groups had higher odds of polypharmacy; and vascular dementia diagnoses were more common in Black and Irish ethnic minority groups. Conclusions and Implications: At dementia diagnosis, there are substantial differences in noncognitive mental health symptoms and pharmacotherapy across ethnic minority groups and compared with the white British majority population. Some of these differences might reflect access/treatment inequalities or implicit unconscious bias related to ethnicity, influencing both. They need to be taken into consideration to optimize pathways into care and personalize assessment and management.

Background Motor signs in patients with dementia are associated with a higher risk of cognitive decline, institutionalisation, death and increased health care costs, but prevalences differ between studies. The aims of this study were to employ a natural language processing pipeline to detect motor signs in a patient cohort in routine care; to explore which other difficulties occur co-morbid to motor signs; and whether these, as a group and individually, predict adverse outcomes. Methods A cohort of 11,106 patients with dementia in Alzheimer's disease, vascular dementia or a combination was assembled from a large dementia care health records database in Southeast London. A natural language processing algorithm was devised in order to establish the presence of motor signs (bradykinesia, Parkinsonian gait, rigidity, tremor) recorded around the time of dementia diagnosis. We examined the co-morbidity profile of patients with these symptoms and used Cox regression models to analyse associations with survival and hospitalisation, adjusting for twenty-four potential confounders. Results Less than 10% of patients were recorded to display any motor sign, and tremor was most frequently detected. Presence of motor signs was associated with younger age at diagnosis, neuropsychiatric symptoms, poor physical health and higher prescribing of psychotropics. Rigidity was independently associated with a 23% increased mortality risk after adjustment for confounders (p = 0.014). A non-significant trend for a 15% higher risk of hospitalisation was detected in those with a recorded Parkinsonian gait (p = 0.094). Conclusions With the exception of tremor, motor signs appear to be under-recorded in routine care. They are part of a complex clinical picture and often accompanied by neuropsychiatric and functional difficulties, and thereby associated with adverse outcomes. This underlines the need to establish structured examinations in routine clinical practice via easy-to-use tools.

Background/Introduction Depression comorbidity is an important issue in heart failure (HF) disease. Results from the recent prospective randomized trial MOOD-HF did not provide a rationale for the indiscriminate use of antidepressants in depressed HF patients. Purpose The study investigated whole-brain and regional-brain glucose metabolism in HF patients with 18F-FDG PET/CT and its association with depression comorbidity. Methods Twenty-nine hospitalized patients with symptomatic systolic HF disease (LVEF Results HF patients had lower average whole-brain SUVmean (3.90±1.49 vs 5.10±1.35, p=0.001), average regional-brain SUVmean (4.57±2.31 vs 9.96±3.58, p Whole-brain SUVmean had a statistically significant correlation to patient age (r=−0.39, p=0.031), NYHA class (p=0.027), LVEF in the major group of 21 NYHA III-IV patients (p=0.018), diabetes comorbidity (p=0.001), creatinine levels (r=−0.49, p=0.005) and depression (r=−0.36, p=0.049). Regional-brain SUVmean was correlated to whole-brain SUVmean (r=0.53, p=0.002) and depression (r=0.46, p=0.011). The standardized SUVmean, in particular, was found to be a robust index that could differentiate HF patients with “epiphenomenal” (>0.93) or “real” (≤0.93) depression. Conclusion HF patients with more severe disease showed whole-brain and regional-brain hypometabolism in 18F-FDG PET/CT scan, which is consistent with impaired cerebral perfusion. Depressed HF patients (Beck Depression Inventory score >13) exhibited different metabolic patterns that could be used to differentiate between “epiphenomenal” and “real” depression. Namely, presence of whole-brain hypometabolism suggested “epiphenomenal” depression. Absence of whole-brain hypometabolism suggested “real” depression. When the pattern of whole-brain hypometabolism included significant relative, depression-related regional hypometabolism (standardized SUVmean ≤0.93), “real” depression was the most likely diagnosis. The distinction is important, as different types of comorbid depression suggest different treatment approach. Summarizing figure Funding Acknowledgement Type of funding source: None

Stress induced (Takotsubo) cardiomyopathy (TC) represents an acute heart failure syndrome triggered by physical or emotional stressors. COVID-19 pandemic has caused an unprecedented health crisis resulting in fear, distress and anxiety, with emerging cardiovascular implications. COVID-19 related stress can act as potential trigger for TC. We present a case of an elderly female who developed TC due to stress surrounding COVID-19.

As the focus of the COVID-19 crisis is gradually taken away from emergency healthcare needs, increased attention is warranted on the psychological impact of the pandemic on a global level. Existing guidance on managing the COVID-19 related distress needs to be better informed by upcoming larger-scale research. Applying e-Health can be useful in dealing with the immediate psychological needs, while developing strategies to identify vulnerable populations and shifting the provision of mental health and social care to community services need to be prioritised when looking at the future. Focusing on global mental health during this universal crisis is an opportunity for promoting a more compassionate and less discriminating society.

Research has shown that socio-demographic profile and psychopathology symptoms are related to levels of happiness in old age. The aims of this cross-sectional study were: 1) to investigate the effect of recent stressful life events and socio-demographic factors on psychopathological symptoms in elderly residents in mountain regions of Crete, Greece and 2) to explore the mechanism which underlies the relationship between socio-demographic factors and psychopathological symptoms, with levels of happiness in old age. To this end, we used the nine psychopathology dimensions of symptoms as defined in the Symptom Checklist-90-R (SCL-90), while the Holmes and Rahe stress inventory was administered to quantify the stressful life events. A sample of 205 elderly men and women (age=77.1±6.7 years) living in 10 remote rural and isolated villages participated in this study. Data was collected through questionnaires completed upon individual meetings with each participant, with the interviewer's assistance. Each questionnaire included the two aforesaid scales alongside questions on individual socio-demographic characteristics. Analysis of variance was applied to detect socio-demographic factors that have a significant effect on specific psychopathological symptoms. Then, path analysis was applied to quantify the direct and indirect effect of the selected socio-demographic factors on happiness levels. Stressful life events were found to have no statistically significant effect on the presence of specific symptoms (somatization, psychoticism, anxiety) in elderly adults. Furthermore, certain socio-demographic factors (marital status, smoking, family income and social activity) were found to influence happiness, which varied according to the level of psycho-emotional tension. The results suggest that somatization, psychoticism, and phobic anxiety symptoms are psychic reactions independent of recent stressful life events. Our study,despite its regional character, may contribute in the development of appropriate clinical assessment tools and interventions, helping primary care practitioners to approach elderly people living in remote villages in a more appropriate and holistic manner, improving thereby the effectiveness of their interventions.

In light of the unprecedented public health crisis of the COVID-19 pandemic, it is highly important to acknowledge the psychological impact of this mounting threat on healthcare professionals. Previous experience from smaller scale epidemics and emerging literature around COVID-19 show that the unparalleled amount of stress that healthcare workers are dealing with, is associated with increased psychological morbidities. We have depicted the psychological burden that the COVID-19 pandemic has posed on healthcare professionals in Greece and have reviewed the literature around the effect of previous epidemics on frontline healthcare staff. Moreover, we discuss potential triggers and the need for measures to minimise the psychological pressure on those at the frontline against this biothreat.

Background. Bilateral femoral neuropathy is an uncommon complication of various surgical and nonsurgical procedures, such as pelvic/abdominal surgery or vaginal delivery. Case Report. We report a case of a 41-year-old male who was found unresponsive against the wall in a “lithotomy-type” position with both knees flexed at approximately 90 degrees and both hips flexed and externally rotated at approximately 90 and 60 degrees, respectively, 24–48 hours after a drug overdose (combination of dihydrocodeine, paracetamol, diazepam, and amitriptyline). During his recovery, he complained of severe bilateral proximal lower limb weakness and bilateral distal lower limb pain and allodynia. His symptoms were initially attributed to critical illness myopathy/neuropathy (CIMN). However, thorough clinical and neurophysiological evaluation revealed that his symptoms were due to severe bilateral femoral neuropathies. Conclusions. To our knowledge, this is the first reported case of bilateral femoral nerve palsy due to prolonged posturing in a “lithotomy-type” position in the context of a drug overdose.

A 15-year-old female former gymnast with a history of pectus excavatum was reviewed due to unexplained paraparesis and urinary incontinence since age 10. Symptoms were commenced with intolerable upper back pain and development of a soft mass at the sacrum that remitted spontaneously. Brain and whole spine MRI imaging and blood and CSF testing were normal. The combination of skeletal, neurological, and bladder symptoms with normal lumbar MRI and abnormal urodynamic and neurophysiological studies led to the clinical suspicion of occult tethered cord syndrome (oTCS). Surgical cord “untethering” was performed leading to remarkable postoperative clinical improvement. oTCS is a recently defined functional disorder of the spinal cord due to fixation (tethering) of the conus medullaris by inelastic elements that may lead to severe neurological impairment. High clinical suspicion is required as oTCS is a treatable spinal cord disorder.

There is increasing evidence to suggest an association between depression and inflammation, with patients suffering from immune mediated-disorders exhibiting higher levels of depression. Inflammation in depression is a potential target for the development of novel treatment strategies. The present study presents a clinical case in which a patient with an underlying inflammatory condition acutely developed a severe depressive episode resulting in a sudden, dramatic change in their clinical picture. This case, with no similar case reports being in the literature thus far, at least to the best of our knowledge, highlights the increasing consideration that there may be a causative role between neuro-inflammation and depression. This study reports the case of a 40-year-old male with acute lymphoblastic leukaemia (ALL) and no previous psychiatric history, who developed an acute onset of a severe depressive episode in the context of the immune-mediated graft-versus-host disease (GVHD). GVHD is a complication of allogeneic hematopoietic cell transplantation, which the patient had undergone, for the treatment of his ALL. The rapid onset of depression could be explained by the neuroinflammatory processes occurring in GVHD. This provides a clinical example for the possible role of the immune system in depression, and clinicians should be aware of this association.

Introduction/Background Based largely on data from retrospective studies it has been postulated that chemotherapy has an aggravating effect on the cognitive function of breast cancer patients. Potential individual factors related to the effect of chemotherapy on cognitive function have been indicated, such as age-related cognitive dysfunction and stress. Elderly patients differ from non-elderly for higher cognitive related comorbidities, such as dementia, as well as for lower stress levels, indicating that chemobrain may affect differentially these two age groups. The aim of this review is to investigate the effect of stress and chemotherapy on the cognitive dysfunction and identify any potential age-related differences in breast cancer patients treated with adjuvant chemotherapy. Methodology A systematic review of the literature was carried out on Medline, Scopus and Web of Science. The inclusion criteria were original articles published in peer-reviewed journals, elderly and non-elderly patients with breast cancer, reporting on stress and at least one cognitive parameter pre- and/or post-treatment. Results Eight studies met the preset criteria and were further analyzed. 1253 women participated, of whom 800 breast cancer patients treated with surgery only, systemic treatment only, or both. Although all studies included a non-elderly breast cancer patient subpopulation, just two of the studies included patients over 65 years of age. All studies indicated a statistically significant association of stress with various domains of cognitive dysfunction in patients compared to controls, as shown by either self-completed questionnaires, neuropsychological testing or both. Age over 60 was linked to fewer cognitive difficulties mediated by lower levels of stress. Conclusion The evidence supports the association of stress with cognitive deficits in breast cancer patients, regardless of the type of cancer-related treatment. Therefore, stress should be addressed appropriately. Further research is needed to investigate the correlation of stress with cognitive function in elderly patients with breast cancer. Disclosure Nothing to disclose

Introduction/Background Stress, self-esteem and self-rated health are important parameters which have been extensively studied in breast cancer research. However, the correlations between these variables and the proportion of patients experiencing different stress and self-esteem levels are foggy. The aim of this study was to search for correlations between perceived stress, self-esteem and Self-Rated Health (SRH), as well as for their relationship with sociodemographic parameters in breast cancer patients treated with chemotherapy. Methodology The data were collected from 100 patients with breast cancer. Sociodemographic variables, the Perceived Stress Scale (PSS), a 1–5 Lickert scale measuring SRH and the Rosenberg Self-esteem Scale (RSES) were administrated. Pearson9s correlation, Independent Sample9s t-test and ANOVA were utilized. Differences in RSES and PSS levels were presented using proportions based on indicated cut-offs. Results The majority of patients were found to have normal self-esteem (72%), while a high proportion experienced low (38.4%) and mild perceived stress (34.3%). Severe stress was experienced only by 8.1% of the participants. The PSS and RSES scores were inversely correlated (P=0.005), while income satisfaction was positively correlated with SRH (P=0.000) and RSES (P=0.006), and inversely to PSS scores (P=0.033). There were also significant inverse associations between BMI and RSES (P=0.016) and between the number of children and PSS (P= 0.002). Higher PSS (P=0.032) and SRH (P=0.008) scores were recorded for those cohabitating. Finally, there was a significant association between smoking and SRH (P=0.021). Conclusion Only a minority of the participants experienced severe stress, while most of them had normal self-esteem levels. Stress was inversely associated with self-esteem, having more children and a higher income. No relationship between SRH and stress was observed. Future research on the identification of related parameters and the development of interventional programs to address stress should be intensified. Disclosure Nothing to disclose

Background: Clozapine is a second-generation antipsychotic drug used in treatment-resistant schizophrenia. Fever induced by clozapine is a rather frequent side-effect which usually occurs in the first 4 weeks of treatment. Despite its effectiveness, there are potentially life-threatening adverse effects, such as cardiotoxicity. Case Report: We present the case of a 31- year-old caucasian male with refractory schizophrenia who developed benign fever, increase of C-reactive protein and high troponin levels, without presenting any other signs to myocarditis, on the 13th day under clozapine treatment, which declined progressively upon discontinuation of the drug. Discussion: This case hints at the presence of initially subclinical cardiotoxicity as an underlying factor in patients developing fever. Conclusion: Taking advantage of more sensitive methods for measuring troponin, clinicians would be promptly aware of this possible side-effect. This would allow for significant reduction of the risk of cardiac dysfunction, further attained by carefully monitoring the patient.

Schizophrenia (SZ) and cancer (Ca) have a broad spectrum of clinical phenotypes and a complex biological background, implicating a large number of genetic and epigenetic factors. SZ is a chronic neurodevelopmental disorder signified by an increase in the expression of apoptotic molecular signals, whereas Ca is conversely characterized by an increase in appropriate molecular signaling that stimulates uncontrolled cell proliferation. The rather low risk of developing Ca in patients suffering from SZ is a hypothesis that is still under debate. Recent evidence has indicated that microRNAs (miRNAs or miRs), a large group of small non‑coding oligonoucleotides, may play a significant role in the development of Ca and major psychiatric disorders, such as SZ, bipolar disorder, autism spectrum disorders, suicidality and depression, through their interference with the expression of multiple genes. For instance, the possible role of let‑7, miR‑98 and miR‑183 as biomarkers for Ca and SZ was investigated in our previous research studies. Therefore, further investigations on the expression profiles of these regulatory, small RNA molecules and the molecular pathways through which they exert their control may provide a plausible explanation as to whether there is a correlation between psychiatric disorders and low risk of developing Ca.

Immunological abnormalities have been implicated in schizophrenia. On the other hand, antipsychotics may exert immunomodulatory effects, by triggering pro-inflammatory and anti-inflammatory agents through complex homeostatic mechanisms, which seem to be implicated in medication responsiveness and in the presence or not of adverse effects. There is evidence that olanzapine, a second generation antipsychotic, may increase synapse formation and neurogenesis through alterations in the levels of cytokines and neurotrophic factors. In the present study, we recruited 14 drug-naive inpatients with first-episode schizophrenia (male:female ratio, 7:7) with a mean age of 26.5 years. The positive and negative syndrome scale (PANSS) scores and serum levels of a broad spectrum of cytokines and of brain-derived neurotrophic factor (BDNF) were recorded twice, once at baseline prior to the initiation of olanzapine treatment and 8 weeks later, once the dose of olanzapine had stabilized. Subsequently, the associations between the PANSS scores and the measured markers were examined. Correlation analyses revealed that follow-up PANSSnegative positively correlated with baseline interleukin (IL)-6 (ρ=0.685, P=0.007) and baseline IL-27 levels (ρ=0.785, P=0.001). Furthermore, the percentage change in PANSSnegative [(PANSS-follow-up - PANSS-baseline)/PANSS-baseline; ΔPANSSnegative%)] positively correlated with baseline IL-27 (ρ=0.785, P=0.001) and baseline IL-6 levels (ρ=0.685, P=0.007). Finally, linear regression revealed that follow-up PANSSnegative was associated with baseline IL-27 (R2=0.301, P=0.042), ΔPANSSnegative% was associated with baseline IL-6 (R2=0.301, P=0.042) and baseline IL-27 levels (R2=0.446, P=0.009). Thus, these findings indicate that IL-27 and IL-6 may be trait markers in patients being administered olanzapine monotherapy at the onset of schizophrenia. However, further studies are warranted in order to replicate these associations and to confirm their potential use as biomarkers of treatment effectiveness and safety, as well as to explore novel immunomodulatory strategies for the treatment of schizophrenia.

Background & Objective: Neuroinflammation has been proposed as a major mechanism in schizophrenic disorder. Specifically, an increase in the inflammatory response in the central nervous system is capable of activating microglial cells, leading to the release of pro-inflammatory cytokines and thus activating apoptotic signaling. An increase in apoptosis may underlie a potential role of immune neuropathology in the etiopathogenesis of schizophrenia and specifically, the onset of the disorder. We analyzed in whole blood, levels of S100B, the receptor for advanced glycation end products (RAGE) and the apoptotic marker Fas Ligand in a sample of 13 first episode of schizophrenia twice at baseline before the initiation of any antipsychotic medication (A) and 6 weeks later following an antipsychotic monotherapy with olanzapine (B) and in a sample of 10 healthy controls. The S100B, RAGE and Fas Ligand showed statistically significant differences before and after treatment; the S100B measurements yielded a p-value of 0.004 while the soluble RAGE and Fas Ligand measurements yielded a p=0.03, and p=0.04 respectively. The differences between cases and controls were not statistically significant for all measurements, with the only exception being the S100B values where both samples A and B showed significantly higher values than the controls with p=8.5x10-8 and p=2.9x10-10 respectively. Conclusion: The levels of S100B, RAGE, and Fas Ligand of drug-naive first episode psychosis patients with schizophrenia were significantly higher than that of the same medicated first episode psychosis patients, indicating that an increase of apoptotic signaling is present at the onset of schizophrenia and is also associated with treatment progress.

Background: Volumetric studies examining brain structure in depression subtypes are limited and inconclusive. The aim of the current study was to compare the volumes of brain regions previously implicated in depression among patients with melancholic major depressive disorder (MDD), patients with psychotic MDD and normal controls. Methods: Twenty two patients with melancholic MDD, 17 with psychotic MDD and 18 normal controls were included in the study. Hippocampal (HV), amygdala (AV), anterior (ASCV) and posterior (PSCV) subgenual cortex volumes were measured on magnetic resonance volumetric images. Results: There were no volumetric differences between patients with melancholic and psychotic subgroups. We identified larger AVs and smaller left ASCVs in both patient groups compared to controls with medium to large effect sizes. Regression analysis revealed that AVs were predicted by the presence of depression, late depression-onset, insomnia and left hippocampal tail volume in patients, but not in controls. There were no differences in HVs, right ASCVs and PSCVs across the 3 groups. Limitations: Small sample size, a possible inclusion of paracingulate gyrus in ASCV and PSCV tracings, significant differences in education level and medication status are discussed as limitations. Conclusions: Diagnostically delineated melancholic and psychotic MDD patients do not differ in medial temporal and cingulate volumes. However, significant volumetric differences were detected between both patient-groups and controls.

Evidence suggests that hippocampal volumetric abnormalities are present in first-episode schizophrenia. The hippocampus contains the highest brain levels of neurotrophic factors, which are major determinants of neuronal plasticity. Brain-derived neurotrophic factor (BDNF) influences neuronal survival, differentiation, synaptogenesis, and maintenance and is also correlated with neuronal activation in the hippocampus. BDNF is also involved in the development and modulation of dopaminergic-related systems. Alterations of serum BDNF levels have been shown in a number of studies with first episode patients with schizophrenia, probably reflecting an association between BDNF and the pathogenesis of the disorder. In the present study we investigated the correlation between serum BDNF levels and hippocampal volumes in a sample of first episode drug-naïve patients with schizophrenia (FEP) and healthy control subjects. We found that hippocampal volume (HV) was decreased in FEP patients. Corrected right HV of FEP patients were significantly smaller compared to corrected right HVs of healthy subjects. The serum BDNF levels in the sample of FEP patients was significantly reduced compared to the healthy subjects. A significant positive association was found between serum BDNF and the corrected right HV in the group of patients such that the smaller the HV, the more reduced the serum BDNF levels. (Pearson r=0.452, p=0.045). Our findings indicate that low serum BDNF levels are associated with reduction in HV at the onset of schizophrenia and may further support the theory of a neuroprogressive-neurotoxic reaction associated with the onset of psychosis.

Background and aim: Mental health legislation varies considerably from one country to the other. This study aims to describe the characteristics of the individuals who are brought in by the police for psychiatric assessment and the police involvement in this procedure in Greece. Method: Prospective study of the incident books of the police departments throughout Greece concerning involuntary psychiatric admissions. These books were completed by the police officers who brought the individuals for involuntary psychiatric examination. Results: In total, 2,038 involuntary assessments were evaluated and examined in relationship to the demographic characteristics of the examined individuals. The main findings are as follows. Males were more often assessed (69%) at a younger age than females ( p < 0.001). The majority of the assessments led to involuntary admission (87.5%). Immigrant status did not lead to increased involuntary commitment. The chance for involuntary admission was greater for younger Greek nationals offering resistance. An unexpected finding is that police officers were unnecessarily present in almost half of the mental health assessments (49.4%). Conclusion: The psychiatrists in Greece who perform mental health assessments under the Greek Mental Health Law admit the majority of individuals. They also accept the presence of a police officer during the assessment more often than expected. This issue needs immediate addressing by means of better training and support of psychiatrists.

Brain-derived neurotrophic factor signals and dopaminergic function in the brain are strongly associated, and research on BDNF in schizophrenia may enhance our insights on the pathophysiological mechanisms of this disease. In the present study we aimed to investigate the possible association between serum BDNF levels and schizophrenic relapses and the possible differential effects of treatment with typical and atypical antipsychotics on serum BDNF levels in the same group of patients. We measured serum BDNF levels in 47 patients with schizophrenia during a relapse and again 6 weeks after administration of antipsychotic treatment (14 on risperidone, 18 on haloperidol, 10 on olanzapine and five on amisulpride) and in 44 healthy volunteers. Patients with schizophrenia showed reduced serum BDNF levels in relation to healthy volunteers at study entry. No significant differences were revealed in BDNF serum levels after 6 weeks of antipsychotic treatment in the patients compared to their own levels at study entry. However, serum BDNF was significantly increased in the subgroup receiving olanzapine compared to the other antipsychotics. Our findings may indicate a differential effect of olanzapine on BDNF levels compared to haloperidol, risperidone, and amisulpride.