Dopamine/BDNF loss underscores narcosis cognitive impairment in divers: a proof of concept in a dry condition.

PURPOSE: Divers can experience cognitive impairment due to inert gas narcosis (IGN) at depth. Brain-derived neurotrophic factor (BDNF) rules neuronal connectivity/metabolism to maintain cognitive function and protect tissues against oxidative stress (OxS). Dopamine and glutamate enhance BDNF bioavailability. Thus, we hypothesized that lower circulating BDNF levels (via lessened dopamine and/or glutamate release) underpin IGN in divers, while testing if BDNF loss is associated with increased OxS. METHODS: To mimic IGN, we administered a deep narcosis test via a dry dive test (DDT) at 48 msw in a multiplace hyperbaric chamber to six well-trained divers. We collected: (1) saliva samples before DDT (T0), 25 msw (descending, T1), 48 msw (depth, T2), 25 msw (ascending, T3), 10 min after decompression (T4) to dopamine and/or reactive oxygen species (ROS) levels; (2) blood and urine samples at T0 and T4 for OxS too. We administered cognitive tests at T0, T2, and re-evaluated the divers at T4. RESULTS: At 48 msw, all subjects experienced IGN, as revealed by the cognitive test failure. Dopamine and total antioxidant capacity (TAC) reached a nadir at T2 when ROS emission was maximal. At decompression (T4), a marked drop of BDNF/glutamate content was evidenced, coinciding with a persisting decline in dopamine and cognitive capacity. CONCLUSIONS: Divers encounter IGN at - 48 msw, exhibiting a marked loss in circulating dopamine levels, likely accounting for BDNF-dependent impairment of mental capacity and heightened OxS. The decline in dopamine and BDNF appears to persist at decompression; thus, boosting dopamine/BDNF signaling via pharmacological or other intervention types might attenuate IGN in deep dives.

Effect of mild hyperbaric oxygen therapy on children diagnosed with autism.

INTRODUCTION: Hyperbaric oxygen (HBO2) therapy is emerging internationally as the primary treatment modality for inflammatory pathways related to neurological disorders. Currently, literature concerning its effectiveness in autistic children is limited. Using neurocognitive tests and clinical-diagnostic evaluations, this study evaluates the clinical, cognitive and behavioral effects of HBO2 on children diagnosed with autism. METHODS: An experimental HBO2 group (EXP: F = 1; M = 7; mean age: 7 ± 2.33; years) and a control non-HBO2 group of autistic children (CTRL: F = 2; M= 5; mean age: 6.6 ± 2.7 years) correctly completed the Aberrant Behavior Checklist-Community (ABC) before HBO2 (T0), after 40 sessions of HBO2 (T1), and one month after the end of treatments (T2). Additionally, the experimental HBO2 group was evaluated with the Childhood Autism Rating Scale at T0 and T2. RESULTS: Total ABC score was lower at T2 (mean ± SD: 50.38 ± 18.55; p ⟨ 0.001) compared to scores obtained at T0 (mean ± SD: 57.5 ± 19.01). Similarly, in the control group the total ABC score differed statistically (p ⟨ 0.05) between T0 (103.6 ± 20.38) and (T2: 59 ± 25.25). CONCLUSION: Despite the improvements reported in both groups, our results do not support the utility of HBO2 in children diagnosed with autism..