Characterization of sympathicotonia in [LC] and healthy controls using long-term electrodermal activity EDA follow-up, 2025, Mustonen+

[SNT Gatchaman]

Characterization of sympathicotonia in post-covid condition long covid and healthy controls using long-term electrodermal activity EDA follow-up

Spoiler: Authors

Timo Mustonen; Pasi Kytölä; Hanna Lantto; Erika Lager; Velina Vangelova-Korpinen; Hélène Virrantaus; Aleksandra Sulg; Sanna Stålnacke; Tatiana Posharina; Ritva Luukkonen; Arja Uusitalo; Päivi Piirilä; Mari Kanerva

PURPOSE
After SARS-CoV-2 infection, some patients develop post-COVID condition (PCC), often associated with sympathicotonia. This study aimed to characterize sympathicotonia in PCC patients using a novel long-term electrodermal activity (EDA) analysis via a smart ring and evaluate its clinical applicability.

METHODS
Seventeen PCC patients were recruited from a Long Covid outpatient clinic, and 18 healthy controls volunteered. PCC patients were divided based on self-reported symptoms into those with or without sympathicotonia. A 14-day EDA monitoring was conducted. Sympathetic nervous system (SNS) activity was expressed as a double normalized index of electrodermal activity (DNE), with higher levels indicating higher SNS activity. Orthostatic tests were performed to identify orthostatic sympathicotonia. DNE levels, representing EDA, were compared to self-reported and orthostatic sympathicotonia.

RESULTS
DNE levels did not differ between PCC patients with (N = 12) or without (N = 5) self-reported sympathicotonia or compared with nonsympathetic controls. When dividing all participants by orthostatic test results, DNE levels were lower during day (08:00–14:00; p < 0.05) but higher during late night (00:00–02:00; p < 0.05) in those with orthostatic sympathicotonia (N = 21) compared to those without (N = 14), with the 24-h comparison significant (p = 0.022). Among PCC patients, DNE levels were higher in orthostatic nonsympathicotonic (N = 7) than orthostatic sympathicotonic (N = 10) during morning (09:00–12:00; p < 0.05), with the 24-h comparison significant (p = 0.044).

CONCLUSION
Self-reported symptoms did not distinguish sympathicotonia. However, individuals with orthostatic test-identified sympathicotonia had heightened EDA, indicating increased sympathetic activity, particularly during late night. PCC was not identifiable by EDA. Long-term EDA monitoring may provide an objective tool for detecting sympathicotonia independently of self-reported symptoms.

Web | DOI | PDF | Clinical Physiology and Functional Imaging | Open Access

 

[SNT Gatchaman]

Arguably this paper should be in the psychosomatic subforum. I've posted here due to the physiology data. Finnish team with a mixture of author affiliations: some clinical physiology, Department of Internal Medicine and Rehabilitation; but also Faculty of Social Sciences, Outpatient Clinic for Persistent Symptom Rehabilitation, and a reference to The Wellbeing Services County of Southwest Finland which could be anything.

From Wikipedia —

Sympathicotonia is a stimulated condition of the sympathetic nervous system, marked by vascular spasm elevated blood pressure, and goose bumps.

Heightened sympathetic nervous system activity is also linked to various mental health disorders such as, anxiety disorders and post-traumatic stress disorder (PTSD). It is suggested that the overactivation of the SNS results in the increased severity of PTSD symptoms. In accordance with disorders like hypertension and cardiovascular disease mentioned above, PTSD is also linked with the increased risk of developing mentioned diseases, further correlating the link between these disorders and the SNS.

On the BPS aspects, from the paper —

As known, the sympathetic nervous system (SNS) is activated during stress, leading to increased sweat production and enhanced electrical conductance of the skin. This physiological response results in heightened skin moisture content, which subsequently enhances the electrical conductivity of the skin's outer layer. EDA changes, therefore, serve as an indicator of SNS activity.

Sympathicotonia is considered a physiological phenomenon that can occur even in healthy individuals as part of normal autonomic regulation. However, prolonged or excessive sympathetic activation has been implicated in various autonomic dysfunctions. Several studies on PCC have reported increased sympathetic activity, dysautonomia or postural orthostatic tachycardia syndrome (POTS)‐like condition. Saunders et al. (2023) propose a biopsychosocial model for explaining PCC, suggesting that in the presence of predisposing factors, COVID‐19 infection may trigger the brain's stress systems, leading to sympathetic activation and changes in hormonal and inflammatory regulation. Prolongation of these changes has been hypothesized to cause sensitization of the central nervous system, contributing to the persistence of the symptoms.

Saunders et al is this opinion piece A new paradigm is needed to explain long COVID (2023)

Spoiler: Which if you remember was written by

Link:

My name is Chloe Saunders. I am interested in nature, philosophy, and holistic ways to help people reconnect with their bodies after stress or trauma. I am a Psychiatry Registrar taking three years out of clinical training in Edinburgh to work on a PhD project in Aarhus, Denmark.​

Our clinical observations suggest that sympathicotonia may represent an inherent personal trait or autonomic sensitivity rather than a pathological condition.

Subjective factors, such as altered interoception or anxiety related to PCC symptoms, may have influenced the self‐reporting during outpatient visits. Patients may also have been particularly aware of PCC symptoms as presented by the media during and immediately after the years of the COVID‐19 pandemic, which could have influenced their self‐reports. Furthermore, the present results suggest that sympathicotonia may be very common and not necessarily associated with any disease conditions.

Despite evaluating sudomotor activity, the paper does not mention or reference small fibre neuropathy.

This is their conclusion —

Self‐reported presence or absence of sympathicotonia did not correspond to sympathicotonia detected objectively by orthostatic testing or measured using the new DNE‐based electrodermal activity method in either PCC patients or control subjects. However, in individuals with orthostatic sympathicotonia, DNE values were elevated during the late night, consistent with electrodermal sympathicotonia. The DNE analysis did not distinguish PCC patients from controls. Nevertheless, the results suggest that the DNE index is a useful objective method for detecting sympathicotonia in both healthy subjects and PCC patients, even in cases where individuals do not subjectively perceive symptoms related to increased autonomic nervous activity.

 

[ScoutB]

Reading this is a funny rollercoaster ride of learning about a new condition, sympathicotonia, and then by the end being more confused about what exactly it is than when I started.

Electrodermal activity does seem potentially interesting though, I wonder why it has only been looked at by psychology types, at least according to wiki. They mention there that

The traditional theory of EDA holds that skin resistance varies with the state of sweat glands in the skin [...] But the theory associating sweat and EDA was already debated decades ago since individuals without sweat glands have an EDA signal.

(whoever wrote this article didn't quite manage wikipedia's usual style). Were you thinking that the changes seen elsewhere in LC tissue electron microscopy might have affected the EDA / DNE levels?

 

[Trish]

Is this the same as the lie detector test?