Intravenous immunoglobulins for treatment of severe COVID-19-related acute encephalopathy

Huo, Shufan; Ferse, Caroline; Bösl, Fabian; Reincke, S. Momsen; Enghard, Philipp; Hinrichs, Carl; Treskatsch, Sascha; Angermair, Stefan; Audebert, Heinrich J.; Ploner, Christoph J.; Endres, Matthias; Prüß, Harald; Franke, Christiana; Scheibe, Franziska

doi:10.1007/s00415-022-11152-5

Cited by 7 publications

(4 citation statements)

References 14 publications

(15 reference statements)

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“…Briefly, this indicates that systemic inflammation induced by type I Interferons perturbates CNS homeostasis on a cellular and molecular level, potentially explaining neurocognitive disturbances in patients with severe COVID-19. This could also support the idea of treating patients with severe systemic infection-induced encephalopathy with immune modulators such as intravenous immunoglobulins, which showed a positive effect in small case series 118,119 as they are known to inhibit with interferons 120 .…”

Section: Discussionmentioning

confidence: 59%

The central nervous system’s proteogenomic and spatial imprint upon systemic viral infections with SARS-CoV-2

Radke

Meinhardt

Aschman

et al. 2023

Preprint

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In COVID-19 neurological alterations are noticed during the systemic viral infection. Various pathophysiological mechanisms on the central nervous system (CNS) have been suggested in the past two years, including the viral neurotropism hypothesis. Nevertheless, neurological complications can also occur independent of neurotropism and at different stages of the disease and may be persistent. Previous autopsy studies of the CNS from patients with severe COVID-19 show infiltration of macrophages and T lymphocytes, especially in the perivascular regions as well as pronounced microglial activation, but without signs of viral encephalitis. However, there is an ongoing debate about long-term changes and cytotoxic effects in the CNS due to the systemic inflammation. Here, we show the brain-specific host response during and after COVID-19. We profile single-nucleus transcriptomes and proteomes of brainstem tissue from deceased COVID-19 patients who underwent rapid autopsy. We detect a disease phase-dependent inflammatory type-I interferon response in acute COVID-19 cases. Integrating single-nucleus RNA sequencing and spatial transcriptomics, we could localize two patterns of reaction to severe systemic inflammation. One neuronal with direct focus on cranial nerve nuclei and one diffusely affecting the whole brainstem, the latter reflecting a bystander effect that spreads throughout the vascular unit and alters the transcriptional state of oligodendrocytes, microglia and astrocytes. Our results indicate that even without persistence of SARS-CoV-2 in the CNS, the tissue activates highly protective mechanisms, which also cause functional disturbances that may explain the neurological symptoms of COVID-19, triggered by strong systemic type-I IFN signatures in the periphery.

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Section: Discussionmentioning

confidence: 59%

The central nervous system’s proteogenomic and spatial imprint upon systemic viral infections with SARS-CoV-2

Radke

Meinhardt

Aschman

et al. 2023

Preprint

Self Cite

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“…Management of encephalopathy includes dealing with contributing factors such as hypoxia, electrolyte imbalance, and sepsis. Anecdotal reports suggest that intravenous immunoglobulin (IVIg) might have a role in management, thus supporting a neuroinflammatory pathophysiological mechanism 72. The effects of IVIg are pleiotropic, and include binding to Fc receptors on macrophages and microglia, as well suppression of inflammation mediated by cytokines and chemokines.…”

Section: Neurological Syndromesmentioning

confidence: 99%

“…Anecdotal reports suggest that intravenous immunoglobulin (IVIg) might have a role in management, thus supporting a neuroinflammatory pathophysiological mechanism. 72 The effects of IVIg are pleiotropic, and include binding to Fc receptors on macrophages and microglia, as well suppression of inflammation mediated by cytokines and chemokines. Encephalopathy in covid-19 is associated with a greater risk of death within 30 days, poorer functional outcome, and risk of a dementia at six months.…”

Section: Neurological Syndromes Encephalopathymentioning

confidence: 99%

Pathophysiology, diagnosis, and management of neuroinflammation in covid-19

Brown,

Benjamin,

Lunn

et al. 2023

BMJ

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Although neurological complications of SARS-CoV-2 infection are relatively rare, their potential long term morbidity and mortality have a significant impact, given the large numbers of infected patients. Covid-19 is now in the differential diagnosis of a number of common neurological syndromes including encephalopathy, encephalitis, acute demyelinating encephalomyelitis, stroke, and Guillain-Barré syndrome. Physicians should be aware of the pathophysiology underlying these presentations to diagnose and treat patients rapidly and appropriately. Although good evidence has been found for neurovirulence, the neuroinvasive and neurotropic potential of SARS-CoV-2 is limited. The pathophysiology of most complications is immune mediated and vascular, or both. A significant proportion of patients have developed long covid, which can include neuropsychiatric presentations. The mechanisms of long covid remain unclear. The longer term consequences of infection with covid-19 on the brain, particularly in terms of neurodegeneration, will only become apparent with time and long term follow-up.

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“…These changes reflect damage to the white matter or small brain hemorrhages, often linked to the effects of severe COVID-19 or its treatments (Singh et al, 2022;Rachel et al, 2023). Another unusual finding, cytotoxic lesions in the splenium of the corpus callosum, has been reported in some cases, potentially resulting from cytokinemediated glutamate release (Hosp et al, 2021;Huo et al, 2022;Rachel et al, 2023).…”

Section: The Cytokine-based Hypothesismentioning

confidence: 99%

COVID-19-associated encephalopathy: connection between neuroinflammation and microbiota-gut-brain axis

Duve,

Petakh,

Kamyshnyi

2024

Front. Microbiol.

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While neurological complications of COVID-19, such as encephalopathy, are relatively rare, their potential significant impact on long-term morbidity is substantial, especially given the large number of infected patients. Two proposed hypotheses for the pathogenesis of this condition are hypoxia and the uncontrolled release of proinflammatory cytokines. The gut microbiota plays an important role in regulating immune homeostasis and overall gut health, including its effects on brain health through various pathways collectively termed the gut–brain axis. Recent studies have shown that COVID-19 patients exhibit gut dysbiosis, but how this dysbiosis can affect inflammation in the central nervous system (CNS) remains unclear. In this context, we discuss how dysbiosis could contribute to neuroinflammation and provide recent data on the features of neuroinflammation in COVID-19 patients.

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Intravenous immunoglobulins for treatment of severe COVID-19-related acute encephalopathy

Cited by 7 publications

References 14 publications

The central nervous system’s proteogenomic and spatial imprint upon systemic viral infections with SARS-CoV-2

The central nervous system’s proteogenomic and spatial imprint upon systemic viral infections with SARS-CoV-2

Pathophysiology, diagnosis, and management of neuroinflammation in covid-19

COVID-19-associated encephalopathy: connection between neuroinflammation and microbiota-gut-brain axis

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