Stellate ganglion block reduces symptoms of Long COVID: A case series

Liu, Luke D.; Duricka, Deborah

doi:10.1016/j.jneuroim.2021.577784

Cited by 58 publications

(92 citation statements)

References 32 publications

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“…In this context review and further study of empirical or anecdotally successful ME/CFS therapies that target glia, such as minocycline ( Plane et al, 2010 ; Miwa, 2021 ; Numata, 2021 ), aripiprazole ( Segnitz et al, 2009 ; Yoneyama et al, 2014 ; Crosby et al, 2021 ), low dose naltrexone ( Cabanas et al, 2021 ), ketogenic diet ( Cossington et al, 2019 ), ketamine ( Chang et al, 2009 ), vagal stimulation ( Clancy et al, 2014 ; Meneses et al, 2016 ; Rodriguez et al, 2020 ; Namgung et al, 2022 ), and noninvasive transcranial neurostimulation ( Gómez et al, 2021 ; Sabel et al, 2021 ; Workman et al, 2021 ) may be informative. Therapies that indirectly affect the innate CNS immune response, including staphylococcal vaccine ( Zachrisson et al, 2002 , 2004 ), Bacillus Calmette–Guérin (BCG) vaccine ( Blok et al, 2015 ; Sánchez-Ramón et al, 2018 ), rintatolimod ( Strayer et al, 2020 ) and stellate ganglion block should also be considered ( Lipov et al, 2020 ; Liu and Duricka, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

Renz‐Polster

Tremblay

Bienzle

et al. 2022

Front. Cell. Neurosci.

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Although myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has a specific and distinctive profile of clinical features, the disease remains an enigma because causal explanation of the pathobiological matrix is lacking. Several potential disease mechanisms have been identified, including immune abnormalities, inflammatory activation, mitochondrial alterations, endothelial and muscular disturbances, cardiovascular anomalies, and dysfunction of the peripheral and central nervous systems. Yet, it remains unclear whether and how these pathways may be related and orchestrated. Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes). We will test this hypothesis by reviewing, in reference to the current literature, the two most salient and widely accepted features of ME/CFS, and by investigating how these might be linked to dysfunctional neuroglia. From this review we conclude that the multifaceted pathobiology of ME/CFS may be attributable in a unifying manner to neuroglial dysfunction. Because the two key features – post exertional malaise and decreased cerebral blood flow – are also recognized in a subset of patients with post-acute sequelae COVID, we suggest that our findings may also be pertinent to this entity.

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Section: Discussionmentioning

confidence: 99%

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

Renz‐Polster

Tremblay

Bienzle

et al. 2022

Front. Cell. Neurosci.

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“…Post-infectious syndromes also occur after other viral infections [25][26][27][28][29][30] and are known since decades. They partly result in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) [11,25,26,[30][31][32][33], which is closely connected to long COVID. Symptoms of long COVID range from fatigue, tiredness, muscle weakness, joint and muscle pain, cognitive impairments ('brain fog'), depression and anxiety, dyspnoea, chest pain and tightness, cough, loss of taste and smell, headache, cardiac symptoms, insomnia, diarrhoea and more [1,2,11,13,14,19,[34][35][36].…”

Section: Introductionmentioning

confidence: 99%

The Adaptive Force as potential biomechanical parameter in the recovery process of patients with long COVID

Schaefer¹,

Bittmann²

2022

Preprint

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Neuromuscular symptoms in long COVID patients are common. Since adequate diagnostics are still missing, investigating muscle function might be beneficial. The holding capacity (maximal isometric Adaptive Force; AFisomax) was previously suggested to be especially vulnerable for impairments. This longitudinal, non-clinical study aimed to investigate the AF in long COVID patients in recovery process. AF parameters of elbow/hip flexors were assessed in 17 patients at three timepoints (pre: long COVID state, post: immediately after first treatment, end: recovery) by an objectified manual muscle test. The tester applied an increasing force on the limb of the patient, who had to resist isometrically for as long as possible. The intensity of 13 common symptoms were queried. At pre, patients started to lengthen their muscles at ~50% of the maximal AF (AFmax), which was then reached during eccentric motion, indicating unstable adaptation. At post and end, AFisomax increased significantly to ~99% and 100% of AFmax, respectively, reflecting stable adaptation. AFmax was statistically similar for all three timepoints. Symptoms intensity decreased significantly from pre to end. In conclusion, maximal holding capacity seems to be impaired in long COVID patients and increases with substantial health improvement. AFisomax might be a suitable sensitive functional parameter to assess long COVID patients and to support therapy process.

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“…Animal studies have demonstrated attenuation of acute lung injury following this approach [38]. Similarly, human long COVID-19 symptoms have been significantly improved after a similar intervention [39] . These observations may indicate a central theme across these disease states as applied to COVID-19 that the central stress response systems with LC_NE/SNS axis overactivation is a main driver for the immunopathology observed in COVID-19 pneumonia [31] [33].…”

Section: Sars-cov2 Imbalance Central Stress Response System In Vulner...mentioning

confidence: 96%

Modulation of the Central Stress Response System to Prevent Complications of COVID-19 ‘Dam and Wall Concept’

Hyoju¹

2022

Preprint

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We are in amidst of COVID-19 pandemic. Since Dec 2019, severe acute respiratory corona virus (SAR-CoV-2) has infected more than half a billion people killing nearly 7 million people worldwide. Now the BA.5 variant of SARS-CoV-2 is causing mayhem and driving the global surge. Epidemiologist are aware of the fact that this virus is capable of escaping immunity and likely to infect the same person multiple times despite adequate vaccination status. Elderly people of age more than 60 years and those with underlying health conditions are considered as high-risk who are likely to suffer complications and death. While it is tempting to frame complications and mortality from COVID-19 as a simple matter of too much of a virulent virus in too weak of a host, much more is at play here. Framing the pathophysiology of COVID-19 in the context of the Chrousos and Gold model of the central stress response system can shed insight into its complex pathogenesis. Understanding the mechanisms by which pharmacologic modulation of the central stress response system via administration of clonidine and/or dexamethasone may offer an explanation as to why a viral pathogen can be well tolerated and cleared by one host while inflaming and killing another.

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Stellate ganglion block reduces symptoms of Long COVID: A case series

Cited by 58 publications

References 32 publications

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

The Adaptive Force as potential biomechanical parameter in the recovery process of patients with long COVID

Modulation of the Central Stress Response System to Prevent Complications of COVID-19 ‘Dam and Wall Concept’

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