key: cord-0846022-ii8s0hmo authors: Faria, I.; Carneiro, M.; Carla, S. title: P.0431 SARS-CoV-2 neuropsychiatric pathogenic mechanisms – a case report of delirium with psychotic symptoms as sole manifestation in SARS-CoV-2 positive patient date: 2021-12-30 journal: Eur Neuropsychopharmacol DOI: 10.1016/j.euroneuro.2021.10.404 sha: e40dbf45a3bac5d3ce79a0ac66a924210fde6233 doc_id: 846022 cord_uid: ii8s0hmo Background: SARS-CoV-2 is a severe acute respiratory syndrome which generates a wide spectrum of clinical presentations. Fever, gastrointestinal and upper respiratory symptoms are among the most common initial manifestations reported [1]. However, neuropsychiatric symptoms are also frequent, and in some cases, these can remain as sole manifestation of the infection [2]. We report a case of a 53-year-old woman with delirium with psychotic component, concomitant with SARS-CoV-2 infection, with no other associated symptoms. We aim to discuss the mechanisms through which SARS-CoV-2 affects the Central Nervous System (CNS), highlighting the heightened possibility of such occurrence, even in the absence of risk factors for neurological disease. Methods: Description of a clinical case and review of the literature on the subject. Results: E., a married 53-year-old woman with no background of medical illness, was brought to the psychiatric emergency room for a case of disorganized behavior with acute onset. Mental state evaluation revealed altered level of conscienciousness, distractibility, incoherent speech, poorly structured persecutory delusional beliefs, auditory hallucinations and sleep maintenance insomnia. Clinical history and examination revealed no other neurological as well as gastrointestinal and respiratory symptoms or signs. Diagnosis of delirium was confirmed using Confusion Assessment Method (CAM) Diagnostic Algorithm. Laboratory investigation revealed leukocytosis and elevation of creatinine-kinase and lactate-dehydrogenase. Electroencephalogram exhibited an unspecific grade 1/5 encephalopathy. No significant changes were found in chest X-ray, brain CT-scan or lumbar puncture. Hospitalization was proposed, aiming diagnostic investigation and clinical stabilization. According to institutional norms at the time, prior screening for SARS-CoV-2 was performed, with the RT-PCR test result coming positive. Cerebral spine fluid was not tested for SARS-CoV-2. E. was medicated with olanzapine 5mg id and was discharged eight days later, fully recovered from her neuropsychiatric symptoms, and exhibiting no other clinical manifestations of SARS-CoV-2 in the meantime. Conclusions: We report the case of a delirium as a sole manifestation of SARS-CoV-2 infection. The presence of symptoms such as delusional beliefs and hallucinations should be interpreted as features of delirium manifestation, instead of a SARS-CoV-2-induced psychosis [3]. Direct and indirect mechanisms of SARS-CoV-2 CNS disturbance have been proposed in scientific literature, such as neuronal invasion and cytokine storm, respectively [4]. In our case, implication of SARS-CoV-2 in delirium etiology is suggested by the temporal relationship between the two and the absence of other possible causes found for this clinical presentation. E.’s absence of risk factors for delirium (such as old age or other medical conditions), as well as the absence of any other symptomatology during the course of this disease, both suggest that SARS-CoV-2 poses a particular risk of CNS damage when compared to other respiratory viruses. Thus, in current pandemic times, the sheer presence of delirium should encourage screening of a SARS-CoV-2 infection, even in the absence of other symptoms [1]. Further studies are needed to understand the mechanisms by which SARS-CoV-2 infection affects the CNS. No conflict of interest Background: SARS-CoV-2 is a severe acute respiratory syndrome which generates a wide spectrum of clinical presentations. Fever, gastrointestinal and upper respiratory symptoms are among the most common initial manifestations reported [1] . However, neuropsychiatric symptoms are also frequent, and in some cases, these can remain as sole manifestation of the infection [2] . We report a case of a 53-yearold woman with delirium with psychotic component, concomitant with SARS-CoV-2 infection, with no other associated symptoms. We aim to discuss the mechanisms through which SARS-CoV-2 affects the Central Nervous System (CNS), highlighting the heightened possibility of such occurrence, even in the absence of risk factors for neurological disease. Methods: Description of a clinical case and review of the literature on the subject. Results: E., a married 53-year-old woman with no background of medical illness, was brought to the psychiatric emergency room for a case of disorganized behavior with acute onset. Mental state evaluation revealed altered level of conscienciousness, distractibility, incoherent speech, poorly structured persecutory delusional beliefs, auditory hallucinations and sleep maintenance insomnia. Clinical history and examination revealed no other neurological as well as gastrointestinal and respiratory symptoms or signs. Diagnosis of delirium was confirmed using Confusion Assessment Method (CAM) Diagnostic Algorithm. Laboratory investigation revealed leukocytosis and elevation of creatinine-kinase and lactate-dehydrogenase. Electroencephalogram exhibited an unspecific grade 1/5 encephalopathy. No significant changes were found in chest Xray, brain CT-scan or lumbar puncture. Hospitalization was proposed, aiming diagnostic investigation and clinical stabilization. According to institutional norms at the time, prior screening for SARS-CoV-2 was performed, with the RT-PCR test result coming positive. Cerebral spine fluid was not tested for SARS-CoV-2. E. was medicated with olanzapine 5mg id and was discharged eight days later, fully recovered from her neuropsychiatric symptoms, and exhibiting no other clinical manifestations of SARS-CoV-2 in the meantime. Conclusions : We report the case of a delirium as a sole manifestation of SARS-CoV-2 infection. The presence of symptoms such as delusional beliefs and hallucinations should be interpreted as features of delirium manifestation, instead of a SARS-CoV-2-induced psychosis [3] . Direct and indirect mechanisms of SARS-CoV-2 CNS disturbance have been proposed in scientific literature, such as neuronal invasion and cytokine storm, respectively [4] . In our case, implication of SARS-CoV-2 in delirium etiology is suggested by the temporal relationship between the two and the absence of other possible causes found for this clinical presentation. E.'s absence of risk factors for delirium (such as old age or other medical conditions), as well as the absence of any other symptomatology during the course of this disease, both suggest that SARS-CoV-2 poses a particular risk of CNS damage when compared to other respiratory viruses. Thus, in current pandemic times, the sheer presence of delirium should encourage screening of a SARS-CoV-2 infection, even in the absence of other symptoms [1] . Further studies are needed to understand the mechanisms by which SARS-CoV-2 infection affects the CNS. Background: Later life depression symptomatology differs from that seen in younger adults and the underlying pathology may also differ. The evidence for neuroinflammation playing a role in depression causation is building in younger adults. Aging has been associated with higher levels of plasma pro-inflammatory cytokines. Depression has been identified as a potentially modifiable risk factor for the development of dementia, but whether it is a risk factor or an early sign of a developing dementia remains unclear. Neuroinflammation is increasingly recognised as a key part of Alzheimer's Disease neuropathology. Depression has been shown in several cohorts from midlife onwards to affect performance on cognitive tests, but the mechanism of this and whether it is merely a state effect is unknown. It is possible that depression may exert its effect on increased risk of dementia via increased neuroinflammation. Aims To investigate the link between depression, inflammation and dementia. We hypothesised that recurrent depression has adverse effects on performance in cognitive tests in middle to older age and that this effect is modified by anti-inflammatory medication. Methods: We identified UK based cohort studies available via Dementia Platforms UK which included individuals aged over 50, medical history, details of prescribed medications, results from detailed cognitive testing and had used reliable measures to assess depression. No specific ethical approval was required for this secondary analysis of existing data. In this abstract we report our results for UK Biobank which administered bespoke, non-standardised cognitive tasks. Individuals with recurrent depression had at least episodes of depression and had sought treatment. Controls had no history of depression. The presence/absence of inflammatory illness was assessed using a standardised list of inflammatory conditions. Individuals with dementia, chronic neurological conditions and chronic psychotic disorders were excluded. A range of possible confounders e.g. age, gender, BMI, smok- Elevated C-Reactive Protein Levels, Psychological Distress, and Depression in 73 131 Individuals Low serum IL-10 concentrations and loss of regulatory association between IL-6 and IL-10 in adults with major depression Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression P.310 Patients with major depressive disorder have lower cerebral serotonin 4 receptor binding than healthy controls The Center for Integrated Molecular Brain Imaging (Cimbi) database A Unique Presentation of Delirium in a Patient with Otherwise Asymptomatic COVID -19 Delirium in COVID-19: epidemiology and clinical correlations in a large group of patients admitted to an academic hospital COVID-19 and psychosis risk: Real or delusional concern? Delirium in COVID-19: A case series and exploration of potential mechanisms for central nervous system involvement Is neuroinflammation the missing link between depression and dementia? 3 University of Toronto and Women's College Hospital, Department of Psychiatry