The use of oxygen mixture and closed circuit apparatus in diving augments the risk of central nervous system oxygen toxicity (CNS O2T); it is known that the pattern of electroencephalogram (EEG) changes during saturation dives1. In fact breathing oxygen at various depths, especially between 8 and 18 m seawater (msw), can increase the toxicity of oxygen on central nervous system. The aim of this study was to investigate and define the possible alterations of cerebral activity dur- ing a prolonged hyperbaric oxygen exposure and decompression compared to a baseline activity. The EEG was recorded inside the hyperbaric chamber by a Holter apparatus equipped with Bluetooth technology (Ates Medica Device, Italy; Electrical Geodesic, Inc, USA). A 32-channel EEG was recorded with a Bluetooth system in 11 subjects. A 20-minute EEG recording was carried out under three different conditions: breathing air inside a hyperbaric chamber at sea level (1 ATA); breathing O2 at 18 m (2.8 ATA); during decompression (rate of descent and ascent 9 m/min; overall time 60 minutes). EEG data were analyzed using fast Fourier transform. Relative power was estimated for delta (1-4 Hz), theta (5-7 Hz), alpha (8-12 Hz), beta1 (13-15 Hz), and beta2 (15-30 Hz) frequency ranges. The relative power and statistical tests were represented using topographic maps2: one map for each band in the air condition (1- 20 minutes) and 7 maps for O2 and decompression conditions indicating the intervals of analysis (1, 2, 5, 8, 10-12, 15-17, and 18-20 minutes). While breathing oxygen, brain activity shows an early fast delta decrease in the posterior regions with a synchronous and significant increase of alpha in the same regions (post hoc paired sample 2-tailed t test with Bonferroni correction, P < .05). During decompression, the delta relative power decrease, compared to baseline, is uniformly distributed over the cerebral cortex until minute 8. At minute 10-12 this decrease is principally localized in the posterior regions. The EEG power in alpha activity is maximal in the same posterior regions during the first 2 minutes of decompression and only returns to baseline after 20 minutes. The findings (ie, a decrease of delta and an increase of alpha activity) showed an opposite behaviour compared to hypoxia condition. Decrease in delta activity observed during oxygen breathing would be a sign of reduced performance of cortical inhibitory mechanisms. Thus, it is possible to detect an increase in alpha activity in the central regions where this activity is normally very low. Results may be relevant in order to establish a reference point in future studies on O2 sensitive patients who reported problems during oxygen diving. Acknowledgments This study has been funded by a grant SMD L-023: Rilevazioni elettrofisiologiche in immersione; Cap. 1322, Italian Ministry of Defense, Direzione Generale della Sanità Militare, 2010. References 1. Pastena L, et al. Aviat Space Environ Med. 1999;70:270-276. 2. Formaggio E, et al. J Neuroeng Rehabil. 2013. doi:10.1186/1743-0003-10-24. 3. Papadelis C, et al. Clin Neurophysiol. 2007;118:31-52.
Quantitative EEG during hyperbaric oxygen breathing in professional divers.
STORTI, Silvia Francesca;
2013-01-01
Abstract
The use of oxygen mixture and closed circuit apparatus in diving augments the risk of central nervous system oxygen toxicity (CNS O2T); it is known that the pattern of electroencephalogram (EEG) changes during saturation dives1. In fact breathing oxygen at various depths, especially between 8 and 18 m seawater (msw), can increase the toxicity of oxygen on central nervous system. The aim of this study was to investigate and define the possible alterations of cerebral activity dur- ing a prolonged hyperbaric oxygen exposure and decompression compared to a baseline activity. The EEG was recorded inside the hyperbaric chamber by a Holter apparatus equipped with Bluetooth technology (Ates Medica Device, Italy; Electrical Geodesic, Inc, USA). A 32-channel EEG was recorded with a Bluetooth system in 11 subjects. A 20-minute EEG recording was carried out under three different conditions: breathing air inside a hyperbaric chamber at sea level (1 ATA); breathing O2 at 18 m (2.8 ATA); during decompression (rate of descent and ascent 9 m/min; overall time 60 minutes). EEG data were analyzed using fast Fourier transform. Relative power was estimated for delta (1-4 Hz), theta (5-7 Hz), alpha (8-12 Hz), beta1 (13-15 Hz), and beta2 (15-30 Hz) frequency ranges. The relative power and statistical tests were represented using topographic maps2: one map for each band in the air condition (1- 20 minutes) and 7 maps for O2 and decompression conditions indicating the intervals of analysis (1, 2, 5, 8, 10-12, 15-17, and 18-20 minutes). While breathing oxygen, brain activity shows an early fast delta decrease in the posterior regions with a synchronous and significant increase of alpha in the same regions (post hoc paired sample 2-tailed t test with Bonferroni correction, P < .05). During decompression, the delta relative power decrease, compared to baseline, is uniformly distributed over the cerebral cortex until minute 8. At minute 10-12 this decrease is principally localized in the posterior regions. The EEG power in alpha activity is maximal in the same posterior regions during the first 2 minutes of decompression and only returns to baseline after 20 minutes. The findings (ie, a decrease of delta and an increase of alpha activity) showed an opposite behaviour compared to hypoxia condition. Decrease in delta activity observed during oxygen breathing would be a sign of reduced performance of cortical inhibitory mechanisms. Thus, it is possible to detect an increase in alpha activity in the central regions where this activity is normally very low. Results may be relevant in order to establish a reference point in future studies on O2 sensitive patients who reported problems during oxygen diving. Acknowledgments This study has been funded by a grant SMD L-023: Rilevazioni elettrofisiologiche in immersione; Cap. 1322, Italian Ministry of Defense, Direzione Generale della Sanità Militare, 2010. References 1. Pastena L, et al. Aviat Space Environ Med. 1999;70:270-276. 2. Formaggio E, et al. J Neuroeng Rehabil. 2013. doi:10.1186/1743-0003-10-24. 3. Papadelis C, et al. Clin Neurophysiol. 2007;118:31-52.
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