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Many of the symptoms experienced by individuals with Long Covid are similar to those of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is also considered to be a postinfectious syndrome caused by a variety of infectious agents. Notably, the majority were never hospitalized during their acute COVID-19 illness, reflecting mild initial disease. Many people who experience neurologic symptoms that linger after acute COVID-19 are less than 50 years old and were healthy and active prior to infection.

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These syndromes often include predominant neurologic and psychiatric symptoms, such as difficulty with memory, concentration, and ability to accomplish everyday tasks, frequent headaches, alterations in skin sensation, autonomic dysfunction, intractable fatigue, and in severe cases, delusions and paranoia. Since early in the COVID-19 pandemic, patients have described lingering syndromes following acute infection, now called Long Covid. Additionally, high-field magnetic resonance examination of brain tissue demonstrates microvascular damage in structures plausibly related to neurologic manifestations of COVID-19, consistent with endothelial activation and widespread vascular injury observed in other organs ( 4). It is plausible that subtle forms of generalized vascular dysfunction, including thrombotic microangiopathy (microscopic blood clots) in the brain, may lead to neurological symptoms even in the absence of clinically apparent stroke. Indeed, system-wide vascular dysfunction can characterize severe acute COVID-19 and has the potential to contribute to manifestations of organ system failure and systemic inflammation in those most severely ill ( 12). Increases in blood markers of vascular inflammation as well as thrombosis and infarction in other tissues can also be found in patients with COVID-19 and stroke, suggesting that endothelial inflammation and coagulopathy contribute to these events ( 11). Overt cerebrovascular events during acute COVID-19 often occur in those with vulnerabilities to vascular disease (such as advanced age and cardiac disease). However, when infrequently detected, infected cells in human brain lack surrounding clusters of inflammatory cells, suggesting that SARS-CoV-2 presence in the CNS does not incite classic viral encephalitis.ĭoes widespread vascular dysfunction contribute to nervous system complications of COVID-19? Acute COVID-19 is associated with heightened risk of stroke compared with influenza illness of similar severity, even after correcting for stroke risk factors ( 10). Many had systemic or metabolic derangements prior to death that may contribute to pathology in a nonspecific way. Direct examination of autopsy brain tissue has caveats-those who died with acute COVID-19 had severe disease that may not be representative of the majority of those infected with SARS-CoV-2. Indeed, histopathological studies of brain tissue from patients who died with acute COVID-19 reveal only limited detection of SARS-CoV-2 nucleic acid or viral protein in the brain ( 3, 4), consistent with findings in CSF from live patients.

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Instead, the preponderance of evidence from CSF and brain tissue suggests that immune activation and inflammation within the CNS is the primary driver of neurologic disease in acute COVID-19. There is an urgent need to understand the pathophysiology of these disorders and develop disease-modifying therapies.ĭespite early speculation that SARS-CoV-2 may enter the central nervous system (CNS) via migration through the nasal cavity and the olfactory pathway or trafficking across the blood-brain barrier, analysis of cerebrospinal fluid (CSF) from living patients with neuropsychiatric manifestations has almost uniformly failed to detect viral RNA by reverse transcription polymerase chain reaction. With millions of individuals affected, nervous system complications pose public health challenges for rehabilitation and recovery and for disruptions in the workforce due to loss of functional capacity. It is uncertain whether unforeseen neurological consequences may develop years after initial infection. The pathophysiological mechanisms are not well understood, although evidence primarily implicates immune dysfunction, including nonspecific neuroinflammation and antineural autoimmune dysregulation. Even young people with mild initial disease can develop acute COVID-19 and Long Covid neuropsychiatric syndromes. Furthermore, maladies such as impaired concentration, headache, sensory disturbances, depression, and even psychosis may persist for months after infection, as part of a constellation of symptoms now called Long Covid. Although severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is considered a respiratory pathogen, myriad neurologic complications-including confusion, stroke, and neuromuscular disorders-manifest during acute COVID-19.