Pharmacopsychiatry 2020; 53(02): 82-83
DOI: 10.1055/s-0039-3402997
P2 Biomarker
Georg Thieme Verlag KG Stuttgart · New York

Investigation of cross-section area of the vagus nerve, heart rate variability and inflammatory markers in major depression

FM Schmidt
1   Universitätsklinikum Leipzig, Germany
,
D Wozniak
1   Universitätsklinikum Leipzig, Germany
,
JO Pelz
1   Universitätsklinikum Leipzig, Germany
,
E Scheller
1   Universitätsklinikum Leipzig, Germany
,
E Boettcher
1   Universitätsklinikum Leipzig, Germany
,
L Schreiber
1   Universitätsklinikum Leipzig, Germany
› Institutsangaben
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Publikationsverlauf

Publikationsdatum:
24. Februar 2020 (online)

 
 

    Introduction Major depression (MD) is a common affective disorder characterized by a low-grade inflammation as well as affections of the autonomous nervous system (ANS). The imbalance between the sympathetic and parasympathetic ANS may result in disruptions of the heart rate variability (HRV) as well as vegetative dysfunctions which are characterized by palpitations, impairment of sleep, appetite and gastrointestinal functioning. Affections of the vagus nerve (VN) could substantially participate in the pro-inflammatory state as well as the impairment of the ANS, as observed in Parkinsonʼs Disease, in which the cross-section area of the VN is reduced.

    To elucidate the role of the VN in MD, the research project focuses on the first-time ultrasonographic assessment of the VN in a cohort of depressed versus non-depressed subjects. Further, the association between the VN and the HRV, markers of inflammation and the presence of autonomous dysfunction and depressiveness shall be explored.

    Methods This trial is a naturalistic cross-sectional study for which 120 subjects (MD = 60, controls = 60) shall be enrolled. The measurements include the high-resolution ultrasonography of the cross-section area of both VN, determination of serum levels of inflammatory markers (IL-1/6/10, INF-g, TNF-a, Indoleamine 2,3-Desoxygenase), HRV measures, as well as electrophysiological (ProSiCard) and questionnaire-based assessment of ANS dysfunction and symptom load of MD.

    Results and Conclusion This study could participate in understanding the neurobiological pathogenesis of MD and could provide a link between inflammation, neurophysiological alterations and the clinical picture for which the VN could be a key mediator.


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