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The GHOST-CAP mnemonic can be easily implemented at the bedside and covers key aspects of management for patients with acute brain injury; others are included in the FAST-HUG or in specific protocols. Multimodal invasive neuromonitoring may be required to optimize target ranges and therapeutic decisions in individual patients. We believe this concept could encourage teamwork and improve quality-of-care.


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Increasing evidence suggests that infection with Sars-CoV-2 causes neurological deficits in a substantial proportion of affected patients. While these symptoms arise acutely during the course of infection, less is known about the possible long-term consequences for the brain. Severely affected COVID-19 cases experience high levels of proinflammatory cytokines and acute respiratory dysfunction and often require assisted ventilation. All these factors have been suggested to cause cognitive decline. Pathogenetically, this may result from direct negative effects of the immune reaction, acceleration or aggravation of pre-existing cognitive deficits, or de novo induction of a neurodegenerative disease. This article summarizes the current understanding of neurological symptoms of COVID-19 and hypothesizes that affected patients may be at higher risk of developing cognitive decline after overcoming the primary COVID-19 infection. A structured prospective evaluation should analyze the likelihood, time course, and severity of cognitive impairment following the COVID-19 pandemic.


There are at least four possible pathogenic mechanisms that may account for the detrimental effect of COVID-19 on the CNS: (1) direct viral encephalitis, (2) systemic inflammation, (3) peripheral organ dysfunction (liver, kidney, lung), and (4) cerebrovascular changes. In most cases, however, neurological manifestations of COVID-19 may arise from a combination of the above.


Any one or a combination of these mechanisms put COVID-19 survivors at risk for developing long-term neurological consequences, either by aggravating a pre-existing neurological disorder or by initiating a new disorder. This concern is supported by findings that show that one third of patients at the time of discharge have evidence of cognitive impairment and motor deficits [2]. This is particularly relevant because overall COVID-19 clinically affects the elderly most severely [10]. There is a large overlap of the age range when people typically develop neurodegenerative or cerebrovascular disease and the age of risk for the most several COVID-19 infections. This overlap argues that there is a compelling need for prospective neurological surveillance and care.


COVID-19 is associated with a severe innate immune response and sustained rise of systemic cytokine levels. Importantly, this innate immune response has been suggested to drive and predict mortality and severity [11]. Cytokines and related inflammatory mediators found to be elevated include interleukin-1β, interleukin-2, interleukin-2 receptor, interleukin-4, interleukin-10, interleukin-18, interferon-γ, C-reactive protein, granulocyte colony-stimulating factor, interferon-γ, CXCL10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumor necrosis factor-α [10, 12]. Concomitantly, most patients show signs of T cell exhaustion with lower lymphocyte counts. The fact that systemic inflammation has been shown to promote cognitive decline and neurodegenerative disease makes it likely that COVID-19 survivors will experience neurodegeneration in the following years [13, 14]. Of note, cytokine levels can predict the subsequent occurrence of hippocampal atrophy in patients that experience severe seps




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