Scientists have long attributed fainting to a sudden restriction of blood flow to the brain.
However, many questions persist: What triggers these spontaneous changes in blood flow? Which brain regions are pivotal in this process?
New findings from research conducted on mice and published in the journal Nature shed light on the intricate mechanisms underlying fainting episodes.
The study suggests that activation of neurons connecting the heart and brain may provoke fainting spells.
“This is the first step in demonstrating that fainting involves more than just reduced blood flow,” remarked Vineet Augustine, an assistant professor of neurobiology at the University of California, San Diego, and a co-author of the study.
“While decreased blood flow is a contributing factor, there are additional neural circuits at play here,” Augustine explained.
“It’s not as straightforward as conventional cardiology textbooks suggest.”
Specifically, the research identified neurons beneath the skull that transmit signals from the heart to the brainstem, leading to a drop in heart rate, blood pressure, and breathing rate.
These physiological changes often characterize reflex syncope, the most common form of fainting triggered by factors like dehydration, blood sight, or prolonged standing.
Dr. Zachary Goldberger, a cardiologist at the University of Wisconsin-Madison School of Medicine and Public Health, who was not involved in the study, expressed optimism about these insights.
“Understanding these potential mechanisms opens doors for future therapies,” he noted. “Previously, we struggled to address this issue effectively.”
The study’s scope excludes fainting caused by severe heart conditions such as extremely slow or rapid heart rhythms, which are less common but more life-threatening, according to Goldberger.
The research initially hypothesized that fainting involved activation of the vagus nerve, a network of neurons connecting the brain to various organs.
This nerve is part of the parasympathetic nervous system, responsible for promoting rest and relaxation.
Scientists believe that during a faint, an exaggerated parasympathetic response leads to excessive slowing of heart rate, blood pressure, and breathing.
To investigate the role of the vagus nerve, researchers examined the internal organs of mice under a microscope.
They pinpointed a specific set of neurons within the vagus nerve that extend from the heart’s lower chambers to the brainstem.
“These neurons have dual branches,” Augustine elaborated. “One branch communicates with the heart, while the other relays signals to the brainstem, creating a functional bridge.”
In experiments, researchers stimulated these neurons in mice using light, triggering fainting-like responses.
“By inserting a small fiber into their brains and delivering brief blue light pulses, we activated these neurons,” described Jonathan Lovelace, a co-author of the study and a staff research associate in Augustine’s lab.
“After a brief period of walking, the mice would suddenly collapse and lie still for a moment before resuming normal activity,” Lovelace added.
The mice exhibited classic signs of human fainting, including decreased blood pressure, heart rate, and breathing, along with dilated pupils and eye rolling.
“We observed a distinct eye-roll phenomenon that closely correlated with the onset of fainting,” Augustine noted.
Furthermore, neuron activation was linked to blood vessel constriction and reduced blood flow from the heart to the brain, additional hallmark features of fainting.
Despite these significant findings, Augustine emphasized the need for further research to understand real-life triggers of vagus nerve pathway activation and to validate findings in humans.
“While prior understanding suggested fainting results from inadequate blood flow to the brain due to heart inefficiencies, this study highlights the complexities involved,” explained Dr. Shamai Grossman, an associate professor of emergency medicine at Harvard Medical School.
Grossman added that most fainting episodes are benign, occurring from trivial causes such as prolonged standing or dehydration.
However, certain individuals, such as beginners playing musical instruments or pregnant women, may experience fainting due to increased chest pressure hindering blood return to the heart.
Despite current limitations in preventing spontaneous fainting, Augustine proposed targeting these identified neurons for potential therapies in the future.
“Manipulating genes involved in the vagus nerve pathway or employing targeted nerve stimulation could hold promise,” he concluded.
