ABSTRACT
Neuropsychiatric disorders associated with coronavirus infections emerged with the coronavirus disease 2019 (COVID-19) pandemic. We describe the clinical, laboratory and radiological features of a patient who presented, after recent COVID-19, two rare neuropsychiatric manifestations: a brief psychotic break followed by severe bilateral peripheral facial palsy.
ABSTRACT
BACKGROUND: COVID-19, a disease caused by SARS-CoV-2, manifests with headache, both in the acute phase and as a post-infection symptom, which may be refractory to usual analgesics. OBJECTIVES: Investigate the therapeutic response of refractory COVID or post-COVID headache to indomethacin. METHODS: This was an observational, retrospective, open and uncontrolled. A sample of 37 patients diagnosed with COVID-19 presenting headache during the acute phase or after the resolution of the disease, with refractoriness to the usual symptomatic medication was treated with indomethacin. RESULTS: Of the 37 patients (24 women and 13 men), 29 were migraineurs and 8 had no previous history of headache. The average age was 40.4 ± 9.4 years, ranging from 19 to 65 years. In 26 (70.3%) patients, the onset of headache occurred within 72 h, and in 11 (29.7%), after 10 days of positivity for Sars-CoV-2. After treatment with indomethacin, 36 patients reported greater than 50% headache relief from the third day and 5 became asymptomatic on the fifth day. CONCLUSIONS: In patients with migraine or no prior history of headache who present with refractory COVID or post-COVID headache to common analgesics, anti-inflammatory drugs, and/or triptans, indomethacin should be considered a therapeutic option.
Subject(s)
COVID-19 , Adult , Analgesics , COVID-19/complications , Female , Headache/drug therapy , Headache/etiology , Humans , Indomethacin/therapeutic use , Male , Middle Aged , Retrospective Studies , SARS-CoV-2ABSTRACT
COVID-19 is a disease caused by SARS-CoV-2 and was initially considered to cause serious damage to the respiratory system. Over time, it has been found to affect other organs due to its ability to bind to the ACE2 receptor (type 2 angiotensin-converting enzyme), which can be found in various tissues, including the central nervous system. In addition, a large formation of pro-inflammatory cytokines responsible for various lesions was observed during the evolution of this disease. Our objective was to demonstrate the molecular mechanisms involved in the infection that may demonstrate the relationship between COVID-19 and the development of depressive conditions. Based on the main medical databases (LiLacs, SciELO, Bireme, Scopus, EBSCO, and PubMed) and using the terms 'coronavirus infections' AND 'Inflammation' AND 'depression' AND 'cytokines', we conducted an integrative review of articles published in 2020. Considering this stage of Covid-19 and the inflammatory component of depression, this review showed a relationship between these two conditions based on common pathophysiological mechanisms indicating possible depressive disorders in surviving patients, especially in the most severe cases. The role of inflammatory cytokines and the presence of ACE-2 receptors on the cell surface appear to be the common pathophysiological mechanism between COVID-19 and depression.