why we need a neuroscience of creativity and psychopathology

frontiersin |  Individuals with a predisposition to mental disorder may utilize different strategies, or they may use familiar strategies in unusual ways, to solve creative tasks. For over a century, knowledge of psychopathological states in the brain has illuminated our knowledge of normal brain states, and that should also be the case with the study of the creative brain. Neuroscience can approach this study in two ways. First, it can identify genetic variations that may underlie both creativity and psychopathology. This molecular biology approach is already underway, with several studies indicating polymorphisms of the DRD2 and DRD4 genes (Reuter et al., 2006; Mayseless et al., 2013), the 5HT2a gene (Ott et al., 2005) and the NRG1 gene (Kéri, 2009) that have been associated with both creativity and certain forms of psychopathology.

Second, brain imaging work can be applied to the study of the cognitive mechanisms that may be commonly shared between creativity and psychopathology. For example, psychologists have long suggested that both schizotypal and highly creative individuals tend to utilize states of cognitive disinhibition to access associations that are ordinarily hidden from conscious awareness (e.g., Kris, 1952; Koestler, 1964; Eysenck, 1995). Research is revealing that indeed both highly creative subjects and subjects who are high in schizotypy demonstrate more disinhibition during creative tasks than less creative or less schizotypal subjects (see Martindale, 1999; Carson et al., 2003; Abraham and Windmann, 2008; Dorfman et al., 2008). However, the neural substrates of cognitive disinhibition, as applied to creativity, need to be further studied.

My colleagues and I have found that cognitive disinhibition (in the form of reduced latent inhibition) combined with very high IQ levels predicts extraordinary creative achievement (Carson et al., 2003). These results have since been replicated (Kéri, 2011). We hypothesized that cognitive disinhibition allows a broadening of stimuli available to consciousness while high IQ affords the cognitive resources to process and manipulate that increased stimuli to form novel and creative ideas without the individual becoming overwhelmed and confused. What we did not test is whether the high creative achievers in our studies exhibited phasic changes in latent inhibition, or whether their reduced inhibition was more trait-like, as is seen in persons at risk for psychosis. Because latent inhibition tasks are compatible with neuroimaging, the study of controlled cognitive disinhibition is one area of potential study for the neuroscience of creativity.

Additional areas of study are suggested by the shared vulnerability model of creativity and psychopathology (Carson, 2011, 2013). The shared vulnerability model suggests that creativity and psychopathology may share genetically-influenced factors that are expressed as either pathology or creativity depending upon the presence or absence of other moderating factors (see Figure 1). The shared vulnerability components that have been identified, in addition to cognitive disinhibition, include novelty salience, neural hyperconnectivity, and emotional lability.