The condition, known medically as Takotsubo syndrome, usually follows the experience of extreme stress, such as that felt after the loss of a loved one. It is marked by an abrupt weakening and bulging of the heart, until it begins to resemble a narrow-necked Japanese octopus trap called a takotsubo. (The doctor who first described the syndrome was Japanese.) Researchers have suspected that the disorder — which mostly strikes women and which, while occasionally fatal, tends to resolve over time — is connected to the brain and its control over how the nervous system handles stress. The sympathetic nervous system revs up the body, including the heart, in response to danger; the parasympathetic system calms things back down; and the limbic system generates and controls emotional responses. The regions of the brain that regulate these systems communicate closely with one another in order to keep basic, autonomic processes, like the beating of our hearts, running smoothly.

A group of Swiss cardiologists wondered if a disruption in the interplay among these systems could be connected to broken-heart syndrome. They recruited 15 volunteers who had survived Takotsubo syndrome within the past few years and another 39 unaffected subjects; neuroscientists then conducted functional M.R.I. scans of each brain. In the healthy volunteers, the parts of the brain associated with the emotions and the sympathetic and parasympathetic nervous systems lit up synchronously, as expected. But the communication among those areas was relatively slight in the Takotsubo survivors. The dimmed neuronal activity was most notable between the brain regions that control the sympathetic and parasympathetic nervous systems; the physiological calming that should occur after stress was apparently less likely to take place.