From Bipolar Darkness, the Empathy to Be a Doctor

      This New York Times article by Elyssa Ely, M.D. (March, 2009) is about scientist Alice Flaherty who, after delivering stillborn twins in 1998 became severely depressed and was eventually diagnosed with bipolar disorder. Instead of becoming consumed in her illness, she uses it to help her patients. Her miracle drug is empathy. The wife of a former patient said this of Dr. Flaherty: “Doctors tend to see patients with an overtone of category. Alice never did. She understood Bill’s depression and his movement problems. But she really understood his needs, appetites, moods, guilts, sadnesses and potential pleasures.”
     It is this sort of empathy that is one of Dr. Flaherty's primary research interests; she studies the underlying neural mechanisms associated with empathy. Specifically, she studies the mirror neuron system in the insula, cingulate and inferior frontal parts of the brain, which have been implicated in feelings of empathy (i.e. they become activated when someone witnesses someone else experiencing emotion).
      This article is fascinating because it highlights the ways in which someone's personal struggles can be the catalyst behind really interesting scientific discoveries. Research sometimes becomes "MEsearch," and that is okay. Dr. Flaherty has the capacity to empathize with others in part due to her personal experiences, which provides evidence that someone's ability to empathize is most likely due to both genetic and environmental factors.The study of empathy is important because it is a feeling that helps us understand others and form meaningful relationships. By elucidating the neural mechanisms involved, we may be able to help people who struggle socially.

Interested in learning more about mirror neurons? Check out this video:
http://www.ted.com/talks/vs_ramachandran_the_neurons_that_shaped_civilization.html

Impairment of prosocial sentiments is associated with frontopolar and septal damage in frontotemporal dementia

    This brain lesion study sought to provide evidence that patients with damage to their frontopolar cortex and septal areas show less prosocial behavior than control participants. Prosocial behavior is defined as behavior that lets us care about others and that causes us to dislike making mistakes (e.g. guit, pity, and embarrassment). Researchers used a moral sentiment task, which consisted of 98 scenarios, each accompanied by a choice of 4 adjectives that the participants had to choose to indicate how the scenario would make them feel (see figure). Behavioral data was recorded (i.e. the participants’ choices to the questions in each of the 98 scenarios), and imaging was acquired with a PET scanner. Behavioral results indicated that participants with lesions to their frontopolar cortex and septal areas showed less prosocial behavior and other critical sentiments than controls, and they showed frontotemporal and subcortical hypometabolism, which was predicted.
    In my opinion, this study’s primary strength was that they ruled out the possibility for an alternative hypothesis, that the relationship between FPC-septal hypometabolism and reduced prosocial sentiments in lesion patients was simply due to overall emotional blunting. Even after controlling for other types of emotions, the relationship between FPC-septal hypometabolism and reduced prosocial sentiments remained robust. I think it is extremely important to study prosocial sentiment because of the role it plays in our everyday functioning and our ability to interact with a multitude of other individuals. Those who lack prosocial behavior (i.e. sociopaths, those with developmental delays like autism, etc.) may lack it because of structural differences in the FPC and septal areas of their brains.


 Moll, J., Zahn, R., de Oliveira-Souza, R., Bramati, I., Krueger, F., Tura, B., Cavanagh, A., Grafman, J. Impairment of prosocial sentiments is associated with frontopolar and septal damage in frontotemporal dementia. Neuroimage 54 (2011), 1735-1742.