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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 sepsis [15]. In keeping with this, the most frequent clinical presentation of COVID-19 is the development of acute respiratory distress syndrome (ARDS) [16], the latter being, along with chronic ventilation, highly associated with subsequent cognitive decline, executive dysfunction, and reduced quality of life, often persisting months and years after hospital discharge [17] reviewed in [18]. The causative role of systemic inflammatory damage to the brain is further supported by the fact that none of the cerebrospinal fluid samples investigated in the study by Helms et al. found evidence for a direct presence of SARS-CoV-2 in the cerebrospinal fluid [2]. That being said, one should not ignore the potential importance of the single case report of direct viral infiltration of the brain and viral encephalitis, either by hematogenous or neuronal retrograde dissemination [19].

This conclusion is based on not only epidemiological evidence but also on experiments that showed that systemic, NLRP3 inflammasome-mediated inflammation adversely affects beneficial immune functions in the brain and thereby causes the pathological accumulation of neurodegeneration-associated peptides such as fibrillar amyloid-β [24]. Thus, both peripheral and central induction of the NLRP3 inflammasome can directly induce or aggravate neurodegenerative processes that lead to functional impairment in AD [25] or strongly contribute to the spreading of pathology and thus the progression of the disease [26]. The recent finding showing that NLRP3-driven and interleukin-1β-mediated modulation of phosphokinases and phosphatases largely accounts for the pathological formation of neurofibrillary tangles in murine models of tauopathy raises the concern that COVID-19 patients are likely to experience an induction or strong aggravation of neurodegenerative processes [27].

Our research community draws from and informs multiple disciplines, including neuroscience, medicine, engineering, psychology, education and law. The discoveries that arise from these collaborations will transform our understanding of the human brain, provide novel treatments for brain disorders, and promote brain health throughout the lifespan. And the creative, cross-disciplinary mindset we foster in our trainees is cultivating the next generation of neuroscience research.

While the epidemic of Coronavirus disease 2019 (COVID-19) continues to spread globally, more and more evidences are collected about the presence of neurological manifestations and symptoms associated with it. A systematic review has been performed of papers published until 5 April 2020. 29 papers related to neurological manifestations associated with COVID-19 were examined. The results show presence of central and peripheral nervous system manifestations related to coronavirus. Neurological manifestations, or NeuroCOVID, are part of the COVID-19 clinical picture, but questions remain regarding the frequency and severity of CNS symptoms, the mechanism of action underlying neurological symptoms, and the relationship of symptoms with the course and severity of COVID-19. Further clinical, epidemiological, and basic science research is urgently needed to understand and address neurological sequalae of COVID-19. Concomitant risk factors or determinants (e.g. demographic factors, comorbidities, or available biomarkers) that may predispose a person with COVID-19 to neurological manifestations also need to be identified. The review shows that although more and more papers are reporting neurological manifestations associated with COVID-19; however, many items remain unclear and this uncertainty calls for a global action that requires close coordination and open-data sharing between hospitals, academic institutions and the fast establishment of harmonised research priorities and research consortia to face the NeuroCOVID-19 complications.

Reports are emerging from China and Italy and increasingly from several countries of neurological symptoms associated with SARS-CoV-2, which may be worsening clinical pictures, respiratory outcomes and mortality rates in patients with COVID-19. While most coronaviruses cause mild respiratory illness, it is well known that many beta-coronaviruses have nervous system involvement [1]. Sharing similar genetic traits with MERS and SARS [2, 3] as well as a common host cell entry receptor with SARS [4], SARS-CoV-2 may also demonstrate neurotropism via possible invasion through the cribriform plate, olfactory nerve, thalamus and brainstem resulting in suppression of central cardiorespiratory drive [5]. Reports from China describe neurological symptoms in COVID-19 patients with one retrospective case series from Wuhan, China showing 78 of 214 patients (36%) with neurological manifestations [6,7,8]. Observations from Italy have confirmed Chinese data noting a high number of patients with hyposmia, anosmia and varying patterns of possibly centrally mediated symptoms including respiratory manifestations. In the evolving pandemic, healthcare professionals, therefore, need to recognize and address neurological consequences. We summarized the available knowledge to guide further research, clinical surveillance and management protocols.

We searched papers published in English by 5 April 2020 using PubMed. Search terms relating to COVID-19 (including COVID*, novel coronavirus, nCoV*, *CoV-2, or *CoV2) in titles and abstracts were crossed with terms relating to neurological symptoms or neurotropism including (neurolog*, nervous, dizz*, delirium, encephal*, cereb*, headache, hyposmia, *geusia, hypopsia, myalgia, neurotrop*, or neuroinv*) in full texts. The search resulted in 198 papers, with 154 unique results retrieved, of which 122 were excluded on title/abstract screen and four were excluded on full text screen. Exclusion was based on topic, outcomes covered, and full text unavailability. 29 papers related to neurological manifestations associated with COVID-19 were examined.

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