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.
