1Doctoral Student, Faculty of Medicine, Public Health, and Nursing, Gadjah Mada University, Indonesia. Email: santiyuliani051@gmail.com
2Department of Neurology, Faculty of Medicine, Public Health, and Nursing, Gadjah Mada University, Indonesia. Email: srisutarni086@gmail.com
3Department of Psychiatry, Faculty of Medicine, Public Health, and Nursing, Gadjah Mada University, Indonesia. Email: carlamarchira141@gmail.com, irwan.supriyantogg@gmail.com
Norepinephrine (NE) dysregulation and sympathetic overactivity are central mechanisms underlying major chronic internal medicine conditions, including hypertension, diabetes mellitus, chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), and heart failure. Neurofeedback has emerged as a potential non-pharmacological intervention capable of modulating cortical rhythms and influencing autonomic balance. This narrative review explores the mechanistic relationship between neurofeedback and NE pathways relevant to chronic diseases. Evidence indicates that neurofeedback can alter cortical oscillations, particularly increasing alpha and alpha–theta activity and reducing high beta rhythms, which may influence locus coeruleus (LC) firing and downstream NE activity. Neurofeedback has also been associated with improved heart rate variability, reduced sympathetic tone, and decreased stress reactivity, suggesting effects on autonomic and HPA axis regulation. While direct measurements of NE modulation remain scarce, current findings support the plausibility of indirect effects. Further clinical studies incorporating NE biomarkers and disease-specific outcomes are required to clarify neurofeedback's therapeutic relevance.
Keywords: Neurofeedback; Norepinephrine; Locus coeruleus; Autonomic dysfunction; Chronic disease.
How to cite this article: Yuliani S, Sutarni S, Marchira CR, Supriyanto I. Neurofeedback-Driven Modulation Of Norepinephrine Activity In Chronic Internal Medicine Conditions: A Narrative Review. Int J Drug Deliv Technol. 2026;16(15s): 880-889. DOI: 10.25258/ijddt.16.15s.98
Source of support: Nil.
Conflict of interest: None