Mind, Mood, and Aesthetics.

What comes first: the expression or the emotion? If you smile do you become happy, or are you happy so you then smile? Since Charles Darwin first observed “that even the simulation of an emotion tends to arouse it in our mind,” a large body of evidence has supported the facial-feedback hypothesis, which suggests that the emotion follows the expression. Volunteers forced to smile by placing a pencil in their mouths found cartoons funnier, and those forced to frown rated unpleasant photographs more negatively. But recently, thanks to more advanced neuroimaging capabilities, we are beginning to better understand the mechanism at work. Since Paul Ekman illuminated the impact of facial expressions, we have gained a detailed understanding of how facial muscle movements linked through primitive coupled neural pathways within the amygdala trigger mood and autonomic nervous system manifestations. Those who are sad tend to frown, and those who frown are more likely to be sad. The facial feedback hypothesis today is providing a framework for reevaluating and treating one of the leading causes of disability in the United States (US). Mood disorders, and depression in particular, are highly prevalent in Western society. The National Institute of Mental Health estimates 9.5% of Americans suffer from mood disorders, and in 2012 an estimated 16 million adults aged 18 or older in the US had at least one major depressive episode. This represented 6.9% of all US adults. The lifetime prevalence of depression is 16.2%, and depressive symptoms can be found in 44% of elderly people. Since 1987 there has been a 4-fold increase in the diagnosis of depression, which perhaps not surprisingly coincides with the approval of Prozac (Eli Lilly and Company, Indianapolis, Indiana). More than 10% of the US population is now taking antidepressants, spending 11 billion dollars on the second most commonly prescribed category of medication. Antidepressants though, are not without drawbacks. They must be taken daily to be effective, compliance can be a hurdle, and once started and taken regularly it can be problematic if they are suddenly stopped. Some of the antidepressant medications pose risks, including insomnia, decreased libido, cardiac symptoms, and more. And efficacy, while proven to benefit, many anti-depressants still leave 33% of patients symptomatic, despite multiple drug trials. Could there be a better, more direct, safer, and nonsystemic alternative? Since Finzi first described botulinum toxin A (BtxnA) effects on depression in 2006, multiple double-blind placebocontrolled studies have shown that the injection of BtxnA (Botox; Allergan, Irvine, California; or Dysport; Galderma, Fort Worth, Texas) into the corrugators significantly improves symptoms of depression in those who suffer from major depressive disorders, with remission rates comparing favorably to traditionally prescribed antidepressants. Yes, that is right: Botox/Dysport treats depression with results that rival the most recognized antidepressants. Since BtxnA likely does not directly cause its effects from behind the blood-brain barrier, how does it affect mood? Using the facial-feedback hypothesis as a model, if a frown is inhibited then our ability to be sad is also reduced. But even prior, our ability to perceive negative emotions may also be attenuated. It is widely accepted that when attempting to empathize or understand sadness, whether from a book, movie, or story, we use our facial muscles to initiate a frown, which then prompts a mood of sadness coupled to a limbic system-triggered autonomic nervous system response resulting in the physical manifestations of sadness. This primitively driven behavior operates below our conscious mind. Havas et al showed that following placement of BtxnA in the corrugators, reading, recognition, and