Considering the mechanisms capable of causing brain alterations in COVID-19, we aimed to study the occurrence of cognitive abnormalities in the months following hospital discharge. We recruited 38 (aged 22–74 years; 27 males) patients hospitalized for complications of SARS-CoV-2 infection in nonintensive COVID units. Participants underwent neuropsychological testing about 5 months after hospital discharge. Of all patients, 42.1% had processing speed deficits, while 26.3% showed delayed verbal recall deficits. Twenty-one percent presented with deficits in both processing speed and verbal memory. Bivariate analysis revealed a positive correlation between the lowest arterial oxygen partial pressure (PaO2) to fractional inspired oxygen (FiO2) (P/F) ratio during hospitalization and verbal memory consolidation performance (SRT-LTS score, r = 0.404, p = 0.027), as well as a positive correlation between SpO2 levels upon hospital arrival and delayed verbal recall performance (SRT-D score, rs = 0.373, p = 0.042). Acute respiratory distress syndrome (ARDS) during hospitalization was associated with worse verbal memory performance (ARDS vs. no ARDS: SRT-LTS mean score = 30.63 ± 13.33 vs. 44.50 ± 13.16, p = 0.007; SRT-D mean score = 5.95 ± 2.56 vs. 8.10 ± 2.62, p = 0.029). Cognitive abnormalities can frequently be found in COVID-19 patients 5 months after hospital discharge. Increased fatigability, deficits of concentration and memory, and overall decreased cognitive speed months after hospital discharge can interfere with work and daily activities.

Background and purpose Cognitive dysfunction has been observed following recovery from COVID‐19. To the best of our knowledge, however, no study has assessed the progression of cognitive impairment after 1 year. The aim was to assess cognitive functioning at 1 year from hospital discharge, and eventual associations with specific clinical variables. Methods Seventy‐six patients (aged 22–74 years) who had been hospitalized for COVID‐19 were recruited. Patients received neuropsychological assessments at 5 ( n = 76) and 12 months ( n = 53) from hospital discharge. Results Over half (63.2%) of the patients had deficits in at least one test at 5 months. Compared to the assessment at 5 months, verbal memory, attention and processing speed improved significantly after 1 year (all p < 0.05), whereas visuospatial memory did not (all p > 0.500). The most affected domains after 1 year were processing speed (28.3%) and long‐term visuospatial (18.1%) and verbal (15.1%) memory. Lower PaO 2 /FiO 2 ratios in the acute phase were associated with worse verbal long‐term memory ( p = 0.029) and visuospatial learning ( p = 0.041) at 5 months. Worse visuospatial long‐term memory at 5 months was associated with hyposmia ( p = 0.020) and dysgeusia ( p = 0.037). Conclusion Our study expands the results from previous studies showing that cognitive impairment can still be observed after 1 year. Patients with severe COVID‐19 should receive periodic cognitive follow‐up evaluations, as cognitive deficits in recovered patients could have social and occupational implications.

Emerging evidence indicates that the etiologic agent responsible for coronavirus disease 2019 (COVID-19), can cause neurological complications. COVID-19 may induce cognitive impairment through multiple mechanisms. The aim of the present study was to describe the possible neuropsychological and metabolic neuroimaging consequences of COVID-19 12 months after patients’ hospital discharge. We retrospectively recruited 7 patients (age [mean ± SD] = 56 years ± 12.39, 4 men) who had been hospitalized for COVID-19 with persistent neuropsychological deficits 12 months after hospital discharge. All patients underwent cognitive assessment and brain ( 18 F-FDG) PET/CT, and one also underwent 18 F-amyloid PET/CT. Of the seven patients studied, four had normal glucose metabolism in the brain. Three patients showed various brain hypometabolism patterns: (1) unilateral left temporal mesial area hypometabolism; (2) pontine involvement; and (3) bilateral prefrontal area abnormalities with asymmetric parietal impairment. The patient who showed the most widespread glucose hypometabolism in the brain underwent an 18 F-amyloid PET/CT to assess the presence of Aβ plaques. This examination showed significant Aβ deposition in the superior and middle frontal cortex, and in the posterior cingulate cortex extending mildly in the rostral and caudal anterior cingulate areas. Although some other reports have already suggested that brain hypometabolism may be associated with cognitive impairment at shorter intervals from SarsCov-2 infection, our study is the first to assess cognitive functions, brain metabolic activity and in a patient also amyloid PET one year after COVID-19, demonstrating that cerebral effects of COVID-19 can largely outlast the acute phase of the disease and even be followed by amyloid deposition.

Background and aimsMany recent studies have shown increasing evidence connecting COVID-19 infection with acute thrombotic events, and in particular with ischemic strokes. There are several theories regarding this association, such as alterations in lipid metabolism or platelet aggregation, injury of the endothelial cells, or massive cytokine release, leading to cytokine storm and hyper coagulation. The biological and social consequences of this infection can also lead to psychiatric afflictions, most frequently anxiety and depression being described. This study aims to highlight the possible connections between COVID-19 infection, depression, and ischemic stroke. MethodsWe observed the case of a 48-year-old patient who presented with left hemibody paresthesia and motor deficit on the left side of the body. Two months prior, he presented a COVID-19 infection, followed by a major depressive episode. Clinical, neurological, and neuroimaging examinations were performed to establish the diagnostic. We also analyzed the existing risk factors and possible etiologies. The patient had a history of hypertension, hypercholesterolemia, obesity, and smoking. ResultsFollowing investigations, the diagnosis of acute ischemic thalamic stroke was established. Although there have been more risk factors identified, a causative event that led to the decompensation of these conditions was searched. The post-COVID-19 infection status and recent depression episode represent reasonable presumptive causal factors. ConclusionsThe relation between the acute ischemic thalamic stroke, previous COVID-19 infection, and subsequent depressive episode was considered to be plausible.