Purpose Of Review: To describe the presentation, etiologies, and suggested management of post-acute COVID-19 neuropsychiatric symptoms.
Recent Findings: Over 30% of patients hospitalized with COVID-19 may exhibit cognitive impairment, depression, and anxiety that persist for months after discharge. These symptoms are even more common in patients who required intensive care for severe effects of the virus. In addition to the pandemic-related psychological stress, multiple biological mechanisms have been proposed to understand the neuropsychiatric symptoms observed with COVID-19. Given limited research regarding effective interventions, we recommend pharmacologic and behavioral strategies with established evidence in other medically-ill populations. Long-term, neuropsychiatric complications of COVID-19 are common and consequential. Because these are likely to co-occur with other medical problems, patients recovering from COVID-19 are best managed in clinics with highly coordinated care across disciplines and medical specialties. Future research is needed to inform appropriate interventions.
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http://dx.doi.org/10.1007/s11920-021-01237-9 | DOI Listing |
Eur J Case Rep Intern Med
December 2024
Internal Medicine, Dubai Health, Dubai, United Arab Emirates.
Background: Hemophagocytic lymphohistiocytosis (HLH), is characterized by systemic uncontrolled inflammation resulting from immune dysregulation secondary to various triggers, including genetics, infections, autoimmune diseases, and malignancies. Macrophage activation syndrome (MAS) is an immune dysregulation phenomenon, in which an underlying rheumatological disease is present. We report a rare, interesting case of a middle-aged female, with a systemic lupus erythematosus (SLE) flare complicated by macrophage activation syndrome (MAS), in which tuberculous meningitis (TBM) was the identified trigger.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
August 2024
Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011.
Methylenetetrahydrofolate reductase (MTHFR) deficiency is a rare autosomal recessive genetic disorder caused by mutations in the gene, leading to a variety of clinical manifestations. In October 2022, the Second Xiangya Hospital of Central South University admitted a 21-year-old male patient with neuropsychiatric disorders, presenting primarily with cognitive decline, limb tremors, abnormal mental and behavioral symptoms, seizures, and gait disturbances. These symptoms had gradually developed over 5 years, worsening significantly in the past year.
View Article and Find Full Text PDFPediatr Infect Dis J
December 2024
From the Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Introduction: Central nervous system (CNS) infections represent some of the most critical pediatric health challenges, characterized by high mortality rates and a notable risk of long-term complications. Despite their significance, standardized guidelines for endocrinological follow-up of CNS infection survivors are lacking, leading to reliance on the expertise of individual centers and clinicians.
Materials And Methods: Prospective monocentric observational study conducted at the Fondazione Policlinico Universitario Agostino Gemelli in Rome, Italy.
Sci Rep
January 2025
Department of Radiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Cognitive impairment (CI) frequently occurs in patients with systemic lupus erythematosus (SLE) and may result from neuroinflammation processes and neurovascular changes in the brain. The cerebral hemodynamics underlying SLE with CI (SLE-CI) remain unclear. 97 patients with SLE and 51 heathy controls (HCs) matched for age and gender underwent MRI.
View Article and Find Full Text PDFHepatol Commun
December 2024
Macquarie Medicine School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia.
Background: HE is a neuropsychiatric complication of liver disease characterized by systemic elevation in ammonia and proinflammatory cytokines. These neurotoxins cross the blood-brain barrier and cause neuroinflammation, which can activate the kynurenine pathway (KP). This results in dysregulated production of neuroactive KP metabolites, such as quinolinic acid, which is known to cause astrocyte and neuronal death.
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