Cognitive and psychiatric symptoms are frequently reported after SARS-CoV-2 infection, but their interplay has been only partially explored. We investigated frequency and severity of psychiatric symptoms in patients with persistent cognitive complaints after COVID-19.

We conducted a cross-sectional study. Neurologists assessed 101 patients reporting cognitive symptoms after COVID-19. Patients were invited to fill a screening battery with self-reported psychometric scales (Depression Anxiety Stress Scales-21, Impact of Event Scale-Revised, Insomnia Severity Index). Patients scoring above validated cut-offs in ≥1 scale were referred to psychiatrists who administered the Mini-International Neuropsychiatric Interview (M.I.N.I.), Hamilton Anxiety (HAM-A), and Hamilton Depression (HAM-D) rating scales and asked to complete the Personality Inventory for DSM-5-Brief Form (PID-5-BF).

Out of the 57 referred patients, 38 (64.4%) accepted to undergo the psychiatric examination. Among these, 18 (47.4%) were diagnosed with adjustment disorder (23.7%), anxiety disorder (10.5%), major depressive disorder (7.9%), and post-traumatic stress disorder (2.6%). Pharmacologic treatment before post-COVID condition (present in 12 patients, 31.6%) was associated with a score above cut-off on the HAM-A and HAM-D scales. A longer duration of untreated psychiatric illness after COVID-19 was associated with worse scores on the same scales. Patients with a higher PID-5-BF total score had a higher probability of receiving a psychiatric diagnosis.

Almost half of patients with post-COVID-19 conditions reporting cognitive symptoms were found to suffer from a psychiatric condition after psychiatric evaluation. The application of a psychiatric screening in a population suffering from long-term effects of COVID-19 can lead to early diagnosis and timely treatment.

Individuals who have recovered from the acute stage of SARS-CoV-2 infection may be at risk of developing post-COVID-19 condition (PCC), characterised by a spectrum of persisting, non-specific, and functionally impairing symptoms across multiple organ systems. Obesity has been implicated as a risk factor for PCC, mediated by chronic systemic inflammation. The foregoing has also been separately reported to mediate cognitive dysfunction in PCC.

This is a post-hoc analysis of a randomised, double-blinded, placebo-controlled clinical trial evaluating vortioxetine treatment for cognitive impairments in persons with PCC who received vortioxetine or placebo for eight weeks. This analysis comprises baseline data, examining the impact of BMI on cognitive functioning measured by the Digit Symbol Substitution Test (DSST) and Trails Making Tests (TMT)-A/B, as well as inflammation, via serum c-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).

Complete data from 70 participants were statistically analysed and adjusted for age and sex. BMI was negatively correlated with performance on the DSST (β = −0.003, p = 0.047), TMT-A (β = −0.006, p = 0.025), and TMT-B (β = −0.006, p = 0.002). BMI was positively correlated with serum CRP (unstandardized β = 0.193, standardized β = 0.612, p < 0.001) and ESR (β = 0.039, p < 0.001) levels.

We observed a significant negative correlation between BMI and cognitive functioning, and a significant positive correlation between BMI and inflammation in persons with PCC, suggesting a bidirectional interplay between BMI, PCC, and cognitive function; individuals with an elevated BMI may be at a greater risk of developing PCC and/or presenting with greater cognitive deficits mediated by chronic systemic inflammation.