Background: More than one-third of COVID-19 patients present neurological symptoms ranging from anosmia to stroke and encephalopathy. Furthermore, pre-existing neurological conditions may require special treatment and may be associated with worse outcomes. Notwithstanding, the role of neurologists in COVID-19 is probably underrecognized. Objective: The aim of this study was to report the reasons for requesting neurological consultations by internists and intensivists in a COVID-19-dedicated hospital. Methods: This retrospective study was carried out at Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Brazil, a 900-bed COVID-19 dedicated center (including 300 intensive care unit beds). COVID-19 diagnosis was confirmed by SARS-CoV-2-RT-PCR in nasal swabs. All inpatient neurology consultations between March 23rd and May 23rd, 2020 were analyzed. Neurologists performed the neurological exam, assessed all available data to diagnose the neurological condition, and requested additional tests deemed necessary. Difficult diagnoses were established in consensus meetings. After diagnosis, neurologists were involved in the treatment. Results: Neurological consultations were requested for 89 out of 1,208 (7.4%) inpatient COVID admissions during that period. Main neurological diagnoses included: encephalopathy (44.4%), stroke (16.7%), previous neurological diseases (9.0%), seizures (9.0%), neuromuscular disorders (5.6%), other acute brain lesions (3.4%), and other mild nonspecific symptoms (11.2%). Conclusions: Most neurological consultations in a COVID-19-dedicated hospital were requested for severe conditions that could have an impact on the outcome. First-line doctors should be able to recognize neurological symptoms; neurologists are important members of the medical team in COVID-19 hospital care.

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Objective - To describe the clinical, neurological, neuroimaging and cerebrospinal fluid (CSF) findings associated with encephalopathy in patients admitted to a COVID-19 tertiary reference center. Methods - We retrospectively reviewed records of consecutive patients with COVID-19 evaluated by a consulting neurology team from March 30, 2020 through May 15, 2020. Results - Fifty-five patients with confirmed SARS-CoV-2 were included, 43 of whom showed encephalopathy, and were further divided into mild, moderate and severe encephalopathy groups. Nineteen patients (44%) had undergone mechanical ventilation and received intravenous sedatives. Eleven (26%) patients were on dialysis. Laboratory markers of COVID-19 severity were very common in encephalopathy patients, but did not correlate with the severity of encephalopathy. Thirty-nine patients underwent neuroimaging studies, which showed mostly non-specific changes. One patient showed lesions possibly related to CNS demyelination. Four had suffered an acute stroke. SARS-CoV-2 was detected by RT-PCR in only one of 21 CSF samples. Two CSF samples showed elevated white blood cell count and all were negative for oligoclonal bands. In our case series the severity of encephalopathy correlated with higher probability of death during hospitalization (OR = 5.5 for each increment in the degree of encephalopathy, from absent (0) to mild (1), moderate (2) or severe (3), p<0.001). Conclusion - In our consecutive series with 43 encephalopathy cases, neuroimaging and CSF analysis did not support the role of direct viral CNS invasion or CNS inflammation as the cause of encephalopathy.

Background The cerebellum has not been extensively studied in the setting of Alzheimer’s disease (AD). As the disease progresses, the cerebellum is one of the last brain regions to accumulate β‐amyloid (βA) deposits usually as diffuse plaques. However, distinct morphologies are described in the cerebellum in early‐onset Alzheimer’s disease (EOAD). Method To investigate the presence of βA deposits in the cerebellum, we analyzed brain sections immunostained with βA antibody (4G8) of 46 individuals with cognitive impairment and neuropathological diagnosis of AD. Of them, cerebellum sections of 19 individuals with Thal phase 5 were evaluated regarding the distribution and morphology of the βA deposits. All cases are from the Biobank for Aging studies of the University of São Paulo. AD‐type pathology was scored using the Braak and Braak staging, CERAD criteria and the Thal phase system. Diagnosis of AD required at least intermediate AD neuropathological changes. Presence of cognitive impairment (CI) was evaluated according to the Clinical Dementia Rating Scale (CDR>0,5). Result Cerebellar βA pathology was found in 19 cases (41%). Higher frequency of amyloid pathology was observed in the group of individuals who developed CI before 65 years of age (87%). In this group of individuals, focal deposits such as compact plaques were more frequently observed than the typical diffuse deposits often seen in molecular layer. Additionally, EOAD individuals had more involvement of Purkinje cell, and granular cell layers than in the molecular layer. Amyloid angiopathy with capillary involvement was observed in the cerebellum of 3 individuals. Of them, only one had EOAD, but all had two APOE ε4 genes. Conclusion The βA cerebellar involvement can be influenced by the patient’s age, particularly in EOAD cases. These changes observed in the cerebellum may reflect a different vulnerability pattern of βA pathology in individuals with early‐onset AD.