Regulation of acute reflectory hyperinflammation in viral and other diseases by means of stellate ganglion block. A conceptual view with a focus on Covid-19

Abstract

Whereas the autonomic nervous system (ANS) and the immune system used to be assigned separate functions, it has now become clear that the ANS and the immune system (and thereby inflammatory cascades) work closely together. During an acute immune response (e. g., in viral infection like Covid-19) the ANS and the immune system establish a fast interaction resulting in "physiological" inflammation. Based on our knowledge of the modulation of inflammation by the ANS we propose that a reflectory malfunction of the ANS with hyperactivity of the sympathetic nervous system (SNS) may be involved in the generation of acute hyperinflammation. We believe that sympathetic hyperactivity triggers a hyperresponsiveness of the immune system ("cytokine storm") with consecutive tissue damage. These reflectory neuroimmunological and inflammatory cascades constitute a general reaction principle of the organism under the leadership of the ANS and does not only occur in viral infections, although Covid-19 is a typical current example therefore. Within the overreaction several interdependent pathological positive feedback loops can be detected in which the SNS plays an important part. Consequently, there is a chance to regulate the hyperinflammation by influencing the SNS. This can be achieved by a stellate ganglion block (SGB) with local anesthetics, temporarily disrupting the pathological positive feedback loops. Thereafter, the complex neuroimmune system has the chance to reorganize itself. Previous clinical and experimental data have confirmed a favorable outcome in hyperinflammation (including pneumonia) after SGB (measurable e. g. by a reduction in proinflammatory cytokines).

The Influence of Modern Neurophysiology on the Previous Definitions of “Segment” and “Interference Field” in Neural Therapy

“…The following interactions between the autonomic nervous system and the immune system [25, 27, 35] show the problems of “segment limitation” – which concern most diseases; after all, these are general principles [66].…”

“…Rather, an "interference field" can act as a neuromodulatory trigger at any point in the organism and trigger corresponding subsequent reactions (sensitization processes, neuroplastic changes). Modified from Fischer et al [66]. using the term "extended segment" in 1998 [5].…”

“…On the one hand, the sympathetic nervous system influences immunological processes; on the other hand, it can cause and maintain inflammation [25,35,38,[64][65][66].…”

“…Then, an infection or a neuromodulatory trigger can lead to such neural overactivity with an exces-Engel/Barop/Giebel/Ludin/Fischer sive immune response (e.g., cytokine storm) and hyperinflammation [66]. This in turn is consistent with Speranski's experiments in 1950 [74]: He called the preload "first strike" and an additional load such as an infection or dental interference field (neuromodulatory trigger) "second strike" [66]. Preloads include i.a.…”

Association of Cardiac Autonomic Responses with Clinical Outcomes of Myasthenia Gravis: Short-Term Analysis of the Heart-Rate and Blood Pressure Variability

“…Most of them are characterized as a consequence of cholinergic deficits. Both the chronic inflammatory process and the presence of cross-reactivity between muscle and ganglionic AChR antibodies have been considered crucially involved in the etiology of autonomic neuropathy [11,12]. However, it still remains unknown whether the presence of subclinical ANS dysfunction is, to some extent, due to parallel progression of muscle weakness and/or a consequence of MG treatment.…”