The UI team decided to test SM and two other amygdala-damaged patients with a well-known internally generated threat. In this case, they asked the participants, all females, to inhale a gas mixture containing 35 percent carbon dioxide, one of the most commonly used experiments in the laboratory for inducing a brief bout of panic that lasts for about 30 seconds to a minute. The patients took one deep breath of the gas, and quickly had the classic panic-stricken response expected from those without brain damage: They gasped for air, their heart rate shot up, they became distressed, and they tried to rip off their inhalation masks. Afterward, they recounted sensations that to them were completely novel, describing them as "panic."
"They were scared for their lives," says first author Justin Feinstein, a clinical neuropsychologist who earned his doctorate at the UI last year.
Wemmie had looked at how mice responded to fear, publishing a paper in the journal Cell in 2009 showing that the amygdala can directly detect carbon dioxide to produce fear. He expected to find the same pattern with humans.
"We were completely surprised when the patients had a panic attack," says Wemmie, also a faculty member in the Iowa Neuroscience Graduate Program.
By contrast, only three of 12 healthy participants panickeda rate similar to adults with no history of panic attacks. Notably, none of the three patients with amygdala damage has a history of panic attacks. The higher rate of carbon dioxide-induced panic in the patients suggests that an intact amygdala may normally inhibit panic.
Interestingly, the amygdala-damaged patients had no fear leading up to the test, unlike the healthy participants, many who began sweating and whose heart rates rose just before inhaling the carbon dioxide. That, of course, was consistent with the notion that the amygdala detec
|Contact: Richard Lewis|
University of Iowa