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Objective: To characterize the cognitive profile of long COVID-19 subjects and its possible association with clinical symptoms, emotional disturbance, biomarkers, and disease severity. Methods: We performed a single-center cross-sectional cohort study. Subjects between 20 and 60 years old with confirmed COVID-19 infection were included. The assessment was performed 6 months following hospital or ambulatory discharge. Excluded were those with prior neurocognitive impairment and severe neurological/neuropsychiatric disorders. Demographic and laboratory data were extracted from medical records. Results: Altogether, 108 participants were included, 64 were male (59.25%), and the mean age was 49.10 years. The patients were classified into four groups: non-hospitalized (NH, n = 10), hospitalized without Intensive Care Unit (ICU) or oxygen therapy (HOSPI, n = 21), hospitalized without ICU but with oxygen therapy (OXY, n = 56), and ICU (ICU, n = 21) patients. In total, 38 (35.18%) reported Subjective Cognitive Complaints (SCC). No differences were found considering illness severity between groups. Females had more persistent clinical symptoms and SCC than males. Persistent dyspnea and headache were associated with higher scores in anxiety and depression. Persistent fatigue, anxiety, and depression were associated with worse overall cognition. Conclusions: No cognitive impairment was found regarding the severity of post-COVID-19 infection. SCC was not associated with a worse cognitive performance, but with higher anxiety and depression. Persistent clinical symptoms were frequent independent of illness severity. Fatigue, anxiety, and depression were linked to poorer cognitive function. Tests for attention, processing speed, and executive function were the most sensitive in detecting cognitive changes in these patients. [ABSTRACT FROM AUTHOR]

The presence of neurological symptoms within the clinical range of COVID-19 disease infection has increased. This paper presents the situation of a 45-year-old man having the medical antecedent diabetes mellitus, who presented to the emergency department with fever, headache, and respiratory symptoms, nine days following vaccination with the Ad26.COV2-S COVID-19 vaccine. The patient tested positive for SARS-CoV-2 based on nasal polymerase chain reaction (RT-PCR). Two weeks after the presentation, he developed Tolosa–Hunt Syndrome, an autoimmune phenomenon, with painful left ophthalmoplegia. Significant improvement was seen in terms of his discomfort; however, ptosis and ocular mobility improved only moderately after treatment with intravenous methylprednisolone, and the patient was discharged on a new insulin regimen. The patient returned after four weeks and the neurological exam results showed significant signs of right hemiparesis, mixed aphasia, incomplete left ophthalmoplegia, severe headache, and agitation; after a few days, the patient experienced a depressed level of consciousness and coma. The patient's clinical condition worsened and, unfortunately, he died. MRI brain images revealed multiple ischemic strokes, meningitis, infectious vasculitis, and hemorrhagic encephalitis, which are all serious complications of COVID-19. [ABSTRACT FROM AUTHOR]

Since the outbreak of the SARS-CoV-2 pandemic, olfactory disorders have been reported as a frequent symptom of COVID-19; however, its pathogenesis is still debated. The aim of this review is to summarize the current understanding of the pathogenesis of smell impairment in the course of COVID-19 and to highlight potential avenues for future research on this issue. Several theories have been proposed to explain the pathogenesis of COVID-19-related anosmia, including nasal obstruction and rhinorrhea, oedema of the olfactory cleft mucosa, olfactory epithelial damage either within the olfactory receptor cells or the supporting non-neural cells (either direct or immune-mediated), damage to the olfactory bulb, and impairment of the central olfactory pathways. Although the pathogenesis of COVID-19-related anosmia is still not fully elucidated, it appears to be mainly due to sensorineural damage, with infection of the olfactory epithelium support cells via the ACE1 receptor and disruption of the OE caused by immense inflammatory reaction, and possibly with direct olfactory sensory neurons infection mediated by the NRP-1 receptor. Involvement of the higher olfactory pathways and a conductive component of olfactory disorders, as well as genetic factors, may also be considered. [ABSTRACT FROM AUTHOR]

In the first months of the COVID-19 pandemic, several research studies focused on understanding the damage to the respiratory and circulatory systems. However, the evidence of neurological manifestations as part of the clinical spectrum of the disease has increased. The aim of this retrospective study was to determine the potential association of neurological disorders with concomitant COVID-19 infection. We reviewed 101 patients (mean age, 70.05 years; 62.37% men) diagnosed with different neurological disorders and COVID-19 who were referred to the Department of Neurology between March 2020 and May 2021. The protocol included demographic, clinical, and neuroimagistic features, biochemical evaluation data, and prognosis. In the first group of patients with non-severe COVID-19 infection (<50% lung damage), we enrolled 75 cases (mean age, 69.13 years; 65.33% men), and the second group, with 26 patients (mean age, 72.69 years; 53.84% men), developed severe COVID-19 infection (>50% lung damage). Severe COVID-19 infection was significantly correlated with an increased highly sensitive C-reactive protein level (hsCRP) (p < 0.05), lactate dehydrogenase level (LDH) (p < 0.05), erythrocyte sedimentation rate (ESR) (p < 0.05), D-dimer (p < 0.05), fibrinogen level (p < 0.05), and blood glucose (p < 0.05) when compared to the first group. These biochemical parameters were increased in both groups, but the levels were much higher in the second group. Headaches (72.27%) and dizziness (14.85%) were present in the early stage of infection. Cerebrovascular events were also reported: ischemic stroke (48% vs. 57.69%; p < 0.05), cerebral hemorrhage (4.95%), and cerebral venous sinus thrombosis (1.98%). Encephalitis (1.98%) and Guillain–Barré Syndrome (1.98%) were found but less frequently. Cranial nerve abnormalities were statistically more common in the non-severe group: anosmia (32% vs. 26.92%; p < 0.05), dysgeusia/ageusia (48% vs. 42.30%; p < 0.05), impaired eye movement (1.33% vs. 0%), and facial nerve palsy (2.66% vs. 0%). Seizures (13.33% vs. 11.53%; p < 0.05) and a depressed level of consciousness (31.68%) occurred commonly. We detected the neuropsychiatric symptoms of anxiety (23.76%) and depression (14.85%). Mortality was increased in both groups but was much higher in the second group (46.15% vs. 21.33%). Neurological complications during COVID-19 infection are common in hospitalized patients, but the mechanism of these complications is not fully understood, representing a continuous challenge for neurologists. [ABSTRACT FROM AUTHOR]

We performed a systematic literature review of neuroimaging, predominantly focusing on magnetic resonance imaging (MRI) findings associated with neurological manifestations of coronavirus disease-2019 (COVID-19). We screened articles from PubMed, Google Scholar and Scopus, looking for reports that would potentially have neuroimaging findings in patients with COVID-19. Data analysis was performed with patient-based data based on the availability of clinical characteristics and outcomes for each individual patient from the studies. Chi square and Wilcoxon rank-sum tests were used to report COVID-19 severity and outcomes based on neurological imaging indicators and pathophysiology. A total of 171 patients with COVID-19 having neurological complications, from 134 studies, were identified in our review. The most common neuroimaging finding was ischemic stroke (62, 36.2%) cases, followed by CNS inflammatory disorder (44, 25.7%), and hemorrhagic stroke (41, 24.0%). Around 51% of all the fatal COVID-19 cases had an ischemic stroke. Among patients with ischemic stroke, the mean age of those who suffered from COVID-19 infection was 57.5 years (SD = 15.4) whereas it was 50.7 years (SD = 15.1) among those without stroke/other diagnosis. Fatality was more common in patients with ischemic stroke compared to those with other diagnosis (40% vs. 22%, p = 0.011). The most frequently published neuroimaging findings in patients with COVID-19 were ischemic stroke, CNS inflammatory disorder, and hemorrhagic disorder. In those studies, ischemic stroke was associated with fatality, and was more frequently seen in older patients. Based on our findings, early usage of MRI in COVID-19 patients may be recommended. [ABSTRACT FROM AUTHOR]

Predicting the functional recovery of patients with severe neurological condition due to coronavirus disease 2019 (COVID-19) is a challenging task. Only limited outcome data are available, the pathophysiology is poorly understood, and the time-course of recovery is still largely unknown. Here, we report the case of a patient with COVID-19 associated encephalitis presenting as a prolonged state of unresponsiveness for two months, who finally fully recovered consciousness, functional communication, and autonomy after immunotherapy. In a multimodal approach, a high-density resting state EEG revealed a rich brain activity in spite of a severe clinical presentation. Using our previously validated algorithms, we could predict a possible improvement of consciousness in this patient. This case report illustrates the value of a multimodal approach capitalizing on advanced brain-imaging and bedside electrophysiology techniques to improve prognosis accuracy in this complex and new aetiology. [ABSTRACT FROM AUTHOR]