Sepsis is a life-threatening condition resulting from an inflammatory overreaction that is induced by an infectious factor, which leads to multi-organ failure. Sepsis-associated encephalopathy (SAE) is a common complication of sepsis that can lead to acute cognitive and consciousness disorders, and no strict diagnostic criteria have been created for the complication thus far. The etiopathology of SAE is not fully understood, but plausible mechanisms include neuroinflammation, blood–brain barrier disruption, altered cerebral microcirculation, alterations in neurotransmission, changes in calcium homeostasis, and oxidative stress. SAE may also lead to long-term consequences such as dementia and post-traumatic stress disorder. This review aims to provide a comprehensive summary of substances with neuroprotective properties that have the potential to offer neuroprotection in the treatment of SAE. An extensive literature search was conducted, extracting 71 articles that cover a range of substances, including plant-derived drugs, peptides, monoclonal antibodies, and other commonly used drugs. This review may provide valuable insights for clinicians and researchers working in the field of sepsis and SAE and contribute to the development of new treatment options for this challenging condition.

Traumatic brain injury (TBI) is a disease resulting from external physical forces acting against the head, leading to transient or chronic damage to brain tissue. Primary brain injury is an immediate and, therefore, rather irreversible effect of trauma, while secondary brain injury results from a complex cascade of pathological processes, among which oxidative stress and neuroinflammation are the most prominent. As TBI is a significant cause of mortality and chronic disability, with high social costs all over the world, any form of therapy that may mitigate trauma-evoked brain damage is desirable. Melatonin, a sleep–wake-cycle-regulating neurohormone, exerts strong antioxidant and anti-inflammatory effects and is well tolerated when used as a drug. Due to these properties, it is very reasonable to consider melatonin as a potential therapeutic molecule for TBI treatment. This review summarizes data from in vitro studies, animal models, and clinical trials that focus on the usage of melatonin in TBI.

Glucagon-like peptide-1 Receptor Agonists (GLP-1 RAs) have been one of the most discussed issues in medicine for the past few years. Initially dedicated to patients with type 2 diabetes mellitus (T2DM), the medicine turned out to be an effective weight-loss treatment for people beyond this population. Whereas their beneficial somatic and metabolic effect are beyond doubt, their possible psychiatric adverse reactions have raised concerns. Eating disorders (EDs) are among the mental illnesses whose number is increasing worldwide. Thus, this review aims to summarize the status of knowledge on the correlation between the popularity of GLP-1 RAs and EDs. The conclusions are not unequivocal, pointing out that GLP-1 ARs have the potential to be an effective therapeutic option in some cases of Eds, but if used inappropriately, may increase morbidity of eating disorders.

Postconcussion syndrome (PCS) is one of the leading complications that may appear in patients after mild head trauma. Every day, thousands of people, regardless of age, gender, and race, are diagnosed in emergency departments due to head injuries. Traumatic Brain Injury (TBI) is a significant public health problem, impacting an estimated 1.5 million people in the United States and up to 69 million people worldwide each year, with 80% of these cases being mild. An analysis of the available research and a systematic review were conducted to search for a solution to predicting the occurrence of postconcussion syndrome. Particular biomarkers that can be examined upon admission to the emergency department after head injury were found as possible predictive factors of PCS development. Setting one unequivocal definition of PCS is still a challenge that causes inconsistent results. Neuron Specific Enolase (NSE), Glial Fibrillary Acidic Protein (GFAP), Ubiquitin C-terminal Hydrolase-L1 (UCH-L1), Serum Protein 100 B (s100B), and tau protein are found to be the best predictors of PCS development. The presence of all mentioned biomarkers is confirmed in severe TBI. All mentioned biomarkers are used as predictors of PCS. A combined examination of NSE, GFAP, UCH-1, S100B, and tau protein should be performed to detect mTBI and predict the development of PCS.

Background/Objectives: Over the last two decades, there has been a substantial change in the understanding of post-traumatic hypopituitarism (PTHP), which is no longer regarded as a marginal phenomenon. Clinical manifestations of pituitary hormone deficiency are frequently nonspecific, with fatigue and cognitive dysfunction predominating. Given that head injuries currently constitute a global burden for healthcare systems, the aim of the present study was to determine whether self-reported post-mild traumatic brain injury (mTBI) symptoms that may indicate hypopituitarism reflect true pituitary insufficiency or are attributable to other hormonal aberrations. The study aimed to assess the relationship between self-reported symptoms of PTHP and hormonal test results following mTBI. Setting: Patients were recruited from a tertiary trauma center Emergency Department (ED) in northern Poland from January 2023 to October 2025. Participants: The participants were adult (18 > y.o.) individuals with mTBI who met the inclusion criteria. Design: This was a prospective cohort study. During their post-head injury admission to the ED, patients had a blood sample taken. The procedure was repeated consecutively after 3, 6 and 12 months. After 6 and 12 months, patients were asked to complete a questionnaire. Methods: Pituitary and thyroid hormones were measured using the chemiluminescence immunoassay method and the heterogenous immunochemiluminescence method. The questionnaire used, Questionnaire for the Assessment of Symptoms of Anterior Pituitary Insufficiency in Patients After Mild Traumatic Brain Injury (mTBI) Hospitalized in the Emergency Department, was designed for the purposes of this study. Results: Self-reported symptoms suggestive of anterior pituitary dysfunction following mTBI were not confirmed by laboratory assessment of pituitary hormones. However, after 6 months, a statistically significant correlation was found between the number of reported symptoms and prolactin levels (ρ = 0.730; p = 0.0013), whereas after 12 months a downward trend in free triiodothyronine (fT3) levels was observed compared with the baseline. Conclusions: Persistent symptoms reported by patients following mTBI at 6 and 12 months, particularly fatigue and impaired concentration, showed statistical associations with prolactin levels at 6 months and lower fT3 levels at 12 months. These findings reflect correlations identified in the statistical analysis and do not support inferences regarding causality or the presence of true PTHP.

Background/Objectives: In recent years, the perception of mild traumatic brain injury (mTBI) has significantly changed, which implies the need to revise the approach towards post-injury monitoring. Since post-concussion symptoms may overlap with manifestations of neuroendocrine dysfunction, we investigated whether thyroid hormone measurements may provide complementary information to neuron-specific enolase (NSE), a commonly used biomarker of neuronal injury by assessing the association between NSE and thyroid hormone levels following mTBI and to explore potential neuroendocrine alterations during a 12-month follow-up period. Methods: We conducted a prospective cohort study. Participants, adults aged ≥18 years with mTBI meeting the inclusion criteria, were recruited from a tertiary trauma center emergency department (ED) in northern Poland from January 2023 to October 2025. During their post-head injury admission to the ED, patients had a blood sample taken and were asked to complete online questionnaires. The procedure was repeated after 3, 6 and 12 months. The NSE, pituitary and thyroid hormones were measured using a chemiluminescence immunoassay method (CLIA). The questionnaires used in the study were: Rivermead Post-Concussion Symptoms Questionnaire (RPQ), Hospital Anxiety and Depression Scale (HADS) and Pittsburgh Sleep Quality Index (PSQI) and the Polish validation of EQ-5D-5L. Results: Higher NSE levels were associated with lower fT3 levels at 3 months post injury. No significant association was found at 6- and 12-month follow up. Conclusions: In patients with persistently elevated NSE levels three months after mTBI, reduced fT3 concentrations were observed. Although exploratory, these findings suggest a potential link between neuronal injury biomarkers and post-traumatic neuroendocrine responses, supporting further investigation of multi-marker approaches for post-mTBI monitoring.