OBJECTIVES To evaluate in a group of physicians the relation between burnout, demographic or job characteristics, anxiety, and immune variables. METHODS Seventy one physicians of all grades were recruited among different departments to a cross sectional survey. The Maslach burnout inventory, scales of emotional exhaustion, depersonalisation, and personal accomplishment, the trait scale of anxiety inventory (STAI-Y2), and a questionnaire on personal and professional characteristics were administered. The immune profile included quantitative (number (%) of lymphocytes and subsets) and functional (natural killer cytotoxicity) measures. RESULTS With a model of stepwise multiple regression analysis, emotional exhaustion was significantly affected by both personal (marital, sex) and job characteristics (qualification, working activity), whereas only patient contact explained a portion of variation in depersonalisation. Furthermore, trait anxiety was found to predict the Maslach burnout inventory scores. After correction for potential confounders, physicians who scored high levels of personal accomplishment showed significantly higher numbers of total lymphocytes, T cells (CD3), T helper cells (CD4), and T suppressor cells (CD8) than those who scored low levels. No other correlation was found between burnout and immune variables. CONCLUSIONS In our group of relatively young physicians a high degree of personal accomplishment was associated with an increase in the number of peripheral lymphocytes, particularly T subsets. The meaning of this is not clear, although it could be speculated that to evaluate oneself positively, particularly with regard to work with patients in the health services, might help to stimulate the immune system. By contrast, there is no evidence that to work hard, to feel tired from work, and to have a cynical reaction towards patient care is related to immunosuppression.

The main focus of Coronavirus disease 2019 (COVID-19) infection is pulmonary complications through virus-related neurological manifestations, ranging from mild to severe, such as encephalitis, cerebral thrombosis, neurocognitive (dementia-like) syndrome, and delirium. The hospital screening procedures for quickly recognizing neurological manifestations of COVID-19 are often complicated by other coexisting symptoms and can be obscured by the deep sedation procedures required for critically ill patients. Here, we present two different case-reports of COVID-19 patients, describing neurological complications, diagnostic imaging such as olfactory bulb damage (a mild and unclear underestimated complication) and a severe and sudden thrombotic stroke complicated with hemorrhage with a low-level cytokine storm and respiratory symptom resolution. We discuss the possible mechanisms of virus entrance, together with the causes of COVID-19-related encephalitis, olfactory bulb damage, ischemic stroke, and intracranial hemorrhage.