Management of Neuroinflammation in a Child Using Systemic Bioregulation Methods: A Case Report
Abstract
Neuroinflammation is a complex, dynamic immune-inflammatory response of central nervous system tissues to various factors (infections, toxins, injuries, or metabolic disturbances). Neuroinflammation in childhood is often chronic. The key components of this process are: Microglia and astrocyte activation, impaired blood-brain barrier permeability, oxidative stress Research in 2024–2025 links 60–80% of ASD and ADHD cases to low-grade neuroinflammation. Currently, there is no single “universal” treatment protocol for neuroinflammation in medicine, as it is a pathophysiological process, not a diagnosis.Our 3-year-old, 7-month-old patient presented with increased excitability, sleep disturbances, severe sensory deterioration, frequent colds, and constant flatulence. We monitored this with NSE (neuron-specific enolase), a marker of neuronal damage.Traditional therapeutic strategies focus on symptomatic management or aggressive immunosuppression, which can lead to side effects and a high drug burden on the developing organism.Instead of aggressive immunosuppression, systemic bioregulatory medicine was used, and the following medications were prescribed orally: Traumeel S®, Lymphomyosot N ®, Mucosa compositum ®, Nux vomica-Homaccord and Quercetin.A rapid improvement in behavior, sleep, and cognitive function was observed, and flatulence disappeared.NSE dynamics: Baseline: 48.08 ng/ml. Day 10: 19.5 ng/ml. Day 20: 9.88 ng/ml.Treatment of neuroinflammation with bioregulatory drugs provides the body with multi-target modulation of the inflammatory response, stimulates detoxification of the intercellular matrix and restores the integrity of biological barriers, without side effects, in a short time.In this case, chronic low-grade neuroinflammation, presumably of viral etiology, and intestinal dysbiosis were present. Treatment was carried out exclusively with bioregulatory drugs. By using only bioregulatory drugs, we observe a rapid improvement in the patient's condition, in addition to a decrease in the level of neuron-specific enolase (NSE) in the blood. The central diagnostic tool in this case is the neuron-specific enolase (NSE) level, which was 48.08 ng/ml (with a normal range of up to 17 ng/ml), almost three times higher than the upper reference limit. According to scientific data, such a significant increase in NSE reliably indicates impaired neuronal membrane integrity and active destruction of nerve tissue. In the context of childhood, this indicates ongoing neuroinflammation, which interferes with normal synaptogenesis and myelination. We would like to draw attention to the fact that within 21 days (3 weeks), all the patient's symptoms that had been bothering him disappeared, such as sleep disturbances, behavioral and cognitive functions, logoneurosis, pronounced flatulence, loose stools, and the NSE level also decreased from 48.08 ng/ml to 9.88 ng/ml. It can be concluded that the Bioregulatory Approach has proven its effectiveness as a tool for precisely tuning the immune response. This not only helps alleviate ongoing inflammation but also creates conditions for full neuroregeneration and the realization of the child's genetic potential. In the context of the growing number of neurospecific diseases, the integration of bioregulation methods is a strategic necessity for maintaining the intellectual health of the younger generation. In summary, it can be concluded that modern pediatrics is on the threshold of a shift in the therapeutic focus of cognitive and behavioral disorders. Neuroinflammation is no longer viewed as a hypothetical process; it is now a clinically verifiable diagnosis requiring in-depth interdisciplinary analysis.
Fields of Study & Subjects
Neuroinflammation and Neurodegeneration Mechanisms
Complementary and Alternative Medicine Studies
Traumatic Brain Injury and Neurovascular Disturbances
Publication details
- Journal / source
- Figshare
- Publication date
- 1 January 2026
- Language
- EN
- Document type
- Preprint