Division of Pediatric Neurology, Nationwide Children's Hospital, Columbus, OH, USA.
Department of Pediatrics, Nationwide Children's Hospital, Columbus, OH, USA.
Neurogastroenterol Motil. 2018 Mar;30(3). doi: 10.1111/nmo.13220. Epub 2017 Sep 27.
Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery.
Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n = 18) and control subjects (n = 6) without symptoms or hemodynamic changes during tilt-table testing.
Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P = .003) and tachygastria (P = .014) power ratios, while the dominant frequency (P < .001) and the percent normogastria (P = .004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P = .001), tachygastria (P = .005), and normogastria (P = .03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5 ± 122.8 vs 91.2 ± 15.3 pg/mL, P = .012) and epinephrine (434 ± 91.3 vs 48.7 ± 2.5 pg/mL, P = .03), but not norepinephrine (P > .05), also differed with syncope between cases and controls.
The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.
恶心是神经介导性晕厥的常见前驱症状，但将恶心与晕厥联系起来的生物学因素尚未得到研究。我们旨在通过探索倾斜诱导晕厥过程中胃肌电活动和血浆肾上腺素、去甲肾上腺素和加压素浓度的相关变化，来描述倾斜诱导晕厥时的恶心。
比较了倾斜诱导晕厥伴恶心的患者（n=18）和无倾斜试验时症状或血液动力学变化的对照受试者（n=6）的胃电图和血浆激素变化。
在晕厥前的 4 分钟期间，连续胃电图时段显示时间上的慢波胃电（bradygastria）（P=0.003）和快波胃电（tachygastria）（P=0.014）功率比增加，而主导频率（P<0.001）和正常胃电百分比（P=0.004）降低。晕厥导致每个频率范围内的胃电图功率比在病例和对照组之间存在显著差异：慢波胃电（bradygastria）（P=0.001）、快波胃电（tachygastria）（P=0.005）和正常胃电（normogastria）（P=0.03）。恶心总是在胃电图变化之后出现，而恶心缓解总是先于胃电图正常化。与晕厥相关的血浆加压素（676.5±122.8 vs 91.2±15.3 pg/mL，P=0.012）和肾上腺素（434±91.3 vs 48.7±2.5 pg/mL，P=0.03），但去甲肾上腺素（P>0.05）不同。
与倾斜诱导晕厥相关的恶心在时间上与胃电活动变化以及血浆加压素和肾上腺素增加有关。诱导晕厥的生物学机制与幻觉运动等其他实验性恶心模型在生理学上不同，但晕厥伴恶心似乎具有类似的胃电图和激素变化。因此，倾斜诱导晕厥可能是一个有意义的恶心研究实验模型。
