This review explores the maternal gut microbiome’s role in shaping neonatal neurodevelopmental outcomes following perinatal asphyxia (PA), a leading cause of infant mortality and disability with limited therapeutic options beyond hypothermia. We synthesized current evidence on microbiome-mediated neuroprotective mechanisms against hypoxic-ischemic brain injury. The maternal microbiome influences fetal development through bioactive metabolites (short-chain fatty acids, indole derivatives) that cross the placental barrier, bacterial antigen regulation, and infant microbiome colonization. These pathways activate multiple protective mechanisms: anti-inflammatory signaling via NF-κB suppression and regulatory T cell expansion; antioxidant defenses through Nrf2 activation; neural repair via BDNF upregulation and neurogenesis; and oxytocin system modulation. Animal models demonstrate that maternal dysbiosis from high-fat diet or antibiotics exacerbates PA-induced brain damage, increasing inflammatory markers and hippocampal injury. Conversely, probiotic supplementation, dietary fiber, and specific interventions (omega-3, resveratrol) reduce neuroinflammation and oxidative injury. Human studies link maternal dysbiosis-associated conditions (obesity, gestational diabetes) with adverse pregnancy outcomes, though direct clinical evidence for PA severity remains limited. Understanding the maternal microbiome-fetal brain axis opens therapeutic avenues, including prenatal probiotics, dietary modifications, and targeted metabolite supplementation to prevent or mitigate PA-related neurological sequelae, potentially complementing existing neuroprotective strategies.

The reactivity of an electroencephalogram (EEG) to external stimuli is impaired in comatose patients showing burst-suppression (BS) patterns following hypoxic–ischemic brain injury (HIBI). We explored the reactivity of BS induced by isoflurane in rat models of HIBI and controls using intermittent photic stimulation (IPS) delivered to one eye. The relative time spent in suppression referred to as the suppression ratio (SR) was measured on the contralateral fronto-occipital cortical EEG channel. The BS reactivity (BSR) was defined as the decrease in the SR during IPS from the baseline before stimulation (SR_PRE). We found that BSR increased with SR_PRE. To standardize by anesthetic depth, we derived the BSR index (BSRi) as BSR divided by SR_PRE. We found that the BSRi was decreased at 3 days after transient global cerebral ischemia in rats, which is a model of brain injury after cardiac arrest. The BSRi was also reduced 2 months after experimental perinatal asphyxia in rats, a model of birth asphyxia, which is a frequent neonatal complication in humans. Furthermore, Oxytocin attenuated BSRi impairment, consistent with a neuroprotective effect in this model. Our data suggest that the BSRi is a promising translational marker in HIBI which should be considered in future neuroprotection studies.

Infections represent the most common complication occurring during the evolution of the severely burned patient, hence requiring closer study and targeted result analysis. The fungal infections are one of the most aggressive types of existing infections, their opportunistic character enabling them to cause invasive infections, ultimately leading to a higher morbidity and a higher rate of mortality. The present study focuses on the presence of Candida spp. in 19 out of a total of 70 patients admitted to the Critical Care Burn Unit in the Clinical Emergency Hospital Bucharest, between 01.01.2019-31.12.2019. No other fungal species, besides Candida spp., were identified in this patient lot. The aim of this study was to analyze the risk factors and the dynamics of the biological parameters of the patients presenting Candida spp. infections, in order to determine how these contribute to the prognostic and final outcome of these patients. We can conclude that a precise diagnostic and prompt treatment can make a significant difference in the outcome of severely burnt patients presenting with a fungal infection.

Background/Objectives: Birth asphyxia is a frequent neonatal complication in humans. Its outcome is variable, and the factors underlying this variability remain incompletely understood. Maternal gut microbiome impairment has been proposed as one factor that may influence offspring neurodevelopment, especially when the immature brain is exposed to additional vulnerability such as perinatal asphyxia (PA). Building on our previous maternal microbiome disruption model and on our prior observation that electroencephalography (EEG) reactivity to photic stimulation under deep anesthesia detects functional impairment two months after PA, we assessed whether this reactivity was further impaired after prolonged gestational antibiotic administration and whether probiotics modulated this effect. Methods: Wistar dams received antibiotics, probiotics, antibiotics with probiotics, or control treatment, and offspring underwent PA. Adult EEG reactivity to photic stimulation was assessed during chloral hydrate-induced burst suppression. Burst count reactivity (BCR) was used as the primary event-based readout of stimulus-evoked burst recruitment and was compared with the suppression-ratio-based burst-suppression reactivity index (BSRi). Results: Burst suppression remained reactive to photic stimulation in all groups. BCR was lower after gestational antibiotic treatment than in controls. The magnitude of the effect was attenuated by probiotics coadministration. BSRi showed the same overall pattern. Conclusions: Prolonged gestational antibiotic exposure increased the severity of perinatal asphyxia as measured by EEG reactivity in the adult offspring. The converging BCR and BSRi results support burst-suppression reactivity as a functional neurophysiological readout in this PA model and support further methodological development of EEG reactivity measures for translational studies of hypoxic–ischemic brain injury.

Prolonged gestational antibiotic exposure was previously reported to impair EEG reactivity in adult offspring after perinatal asphyxia. It remained unclear to what extent the effect depended on perinatal insult. We assessed adult EEG reactivity after uncomplicated birth using the same gestational treatment paradigm. Pregnant Wistar rats received antibiotics (AB), probiotics (P), combined treatment (AB&P), or control (C). Adult offspring (AB: 5; P: 8; AB&P: 7; C: 9; 14 males) underwent intermittent photic stimulation during chloral-hydrate-induced EEG burst suppression. Reactivity to 60 s stimulation was quantified in 180 s trials using burst count reactivity (BCR) and the burst-suppression reactivity index (BSRi). After baseline burst count filtering, 200 trials were retained across groups. BCR did not differ significantly between groups. No multiplicity-corrected pairwise comparison identified a specific treatment-associated difference in BCR or BSRi. Mixed-effects models accounting for repeated trials likewise showed no significant overall group effect. Our small cohort did not provide evidence for a long-term effect of gestational antibiotic or probiotic exposure following uncomplicated birth. Together with the previous report, we suggest that gestational antibiotic administration could impair resilience to perinatal asphyxia at an exposure level without a readily detectable effect after uncomplicated birth.

During deep anesthesia, the EEG becomes discontinuous. Burst-suppression is often an intended target during deep sedation or medically induced coma. Within this state, anesthetic depth is commonly monitored by the suppression ratio (SR), which expresses the fraction of time spent in suppression. However, accumulating evidence suggests that SR remains reactive to external stimulation. We tested whether ambient music commonly played in operating theaters alters the SR in male Wistar rats under sevoflurane, chloral hydrate, or isoflurane anesthesia. To this end, the first 60 s of the Stayin’ Alive audio track by the Bee Gees were played to examine auditory-induced burst-suppression reactivity in an experimental model previously established for intermittent photic stimulation. SR and the burst-suppression reactivity index (BSRi, derived as the decrease in SR during stimulation normalized to pre-stimulation SR) were measured in repeated trials. Auditory stimulation transiently decreased SR under all three anesthetics. This was associated with an increase in the rate of burst occurrence without increased burst duration. The BSRi changes depended on the anesthetic type, comparable to photic stimulation. Our experimental data suggest that the suppression ratio used to monitor targeted burst-suppression reflects both anesthetic depth and the level of ambient stimulation. Ambient sound in the operating theater or intensive care settings could influence EEG-based measures used for anesthesia monitoring.