We describe the first direct brain-to-brain interface in humans and present results from experiments involving six different subjects. Our non-invasive interface, demonstrated originally in August 2013, combines electroencephalography (EEG) for recording brain signals with transcranial magnetic stimulation (TMS) for delivering information to the brain. We illustrate our method using a visuomotor task in which two humans must cooperate through direct brain-to-brain communication to achieve a desired goal in a computer game. The brain-to-brain interface detects motor imagery in EEG signals recorded from one subject (the “sender”) and transmits this information over the internet to the motor cortex region of a second subject (the “receiver”). This allows the sender to cause a desired motor response in the receiver (a press on a touchpad) via TMS. We quantify the performance of the brain-to-brain interface in terms of the amount of information transmitted as well as the accuracies attained in (1) decoding the sender’s signals, (2) generating a motor response from the receiver upon stimulation, and (3) achieving the overall goal in the cooperative visuomotor task. Our results provide evidence for a rudimentary form of direct information transmission from one human brain to another using non-invasive means.

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Infants born prematurely, often associated with maternal infection, frequently exhibit breathing instabilities that require resuscitation. We hypothesized that breathing patterns during the first hour of life would be predictive of survival in an animal model of prematurity. Using plethysmography, we measured breathing patterns during the first hour after birth in mice born at term (Term 19.5), delivered prematurely on gestational day 18.5 following administration of low-dose lipopolysaccharide (LPS; 0.14 mg/kg) to pregnant dams (LPS 18.5), or delivered on gestational day 18.7 or 17.5 by caesarian section (C-S 18.5 and C-S 17.5, respectively). Our experimental approach allowed us to dissociate effects caused by inflammation, from effects due to premature birth in the absence of an inflammatory response. C-S 17.5 mice did not survive, whereas mortality was not increased in C-S 18.5 mice. However, in premature pups born at the same gestational age (day 18.5) in response to maternal LPS injection, mortality was significantly increased. Overall, mice that survived had higher birth weights and showed eupneic or gasping activity that was able to transition to normal breathing. Some mice also exhibited a “saw tooth” breathing pattern that was able to transition into eupnea during the first hour of life. In contrast, mice that did not survive showed distinct, large amplitude, long-lasting breaths that occurred at low frequency and did not transition into eupnea. This breathing pattern was only observed during the first hour of life and was more prevalent in LPS 18.5 and C-S 18.5 mice. Indeed, breath tidal volumes were higher in inflammation-induced premature pups than in pups delivered via C-section at equivalent gestational ages, whereas breathing frequencies were low in both LPS-induced and C-section-induced premature pups. We conclude that a breathing pattern characterized by low frequency and large tidal volume is a predictor for the failure to survive, and that these characteristics are more often seen when prematurity occurs in the context of maternal inflammation. Further insights into the mechanisms that generate these breathing patterns and how they transition to normal breathing may facilitate development of novel strategies to manage premature birth in humans.

We used lipopolysaccharide (LPS) to induce cytokine‐mediated inflammation and preterm labor. Dams injected with LPS gave birth on G18.5, one day early. Saline injected dams either gave birth at term (G19.5) or had a c‐section (C‐S) on G18.5. Breathing and cardiac function were then assessed <10 and >60 min. after birth. C‐S preterm and term animals had high survival rates (~94%). LPS preterm animals had low survival rates (43%). Survival corresponded with a fast transition from a low frequency, high tidal volume, long duration ('large') breath pattern to a eupneic pattern. Non‐survivors failed to make the transition. Heart rate was directly related to breathing rate and correlated with survival. However, cardiac activity continued after non‐survivors took their last breath indicating that respiratory, not cardiac, failure was the primary cause of death. A subset of animals that did not transition to a eupneic pattern were administered caffeine. Caffeine improved survival outcomes, however, after an anoxic bout these animals had delayed heart and breathing rate recovery times. In conclusion, LPS‐mediated preterm birth increases mortality rates. This is due to a failure to transition from an initial 'large' respiratory pattern to a eupneic pattern and may correspond with an inability to alter network dynamics when transitioning from a low to high oxygen environment. Grant Funding Source: Supported by Seattle Children's Hospital Inter‐Center Funds