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work has revealed that patients with schizophrenia exhibit abnormal PFC profiles marked by either lower or inefficient frontal cortex function in response to tasks that require cognitive or affective inhibition (e.g., Perlstein etal, 2003; Koike etal, 2013; Eich etal, 2014), but not perceptual filtering (e.g., Smith et al., 201 1).

Furthermore, a simul- taneous analysis of global anatomical and functional connectivity has revealed both lower structural connectivity and diminished coherence (i.e., either abnormally increased or decreased connec- tions) in functional connectivity among different brain regions in patients diagnosed with schizophrenia, relative to healthy control subjects, that was predictive of symptom severity (Skudlarski et al., 2010).

Similarly, patients with bipolar disorder marked by psy- chotic features have been shown to exhibit significant disruptions in the frontoparietal control network (e.g., Baker et al., 2014). Such neurocognitive abnormalities in these forms of psychopathology may prolong periods of hypofrontality in the patients, thus altering dramatically the quantity of creative output by increasing the gen- erative phase of creative production.

As patients periodically shift to states of higher PFC regulation (e.g., as a result of pharmaco- logical treatment), the likelihood of encountering and identifying particularly viable, high-quality creative ideas increases, due to the overall increased volume of their creative output.

We note that this model is in line with evidence suggesting higher creativity in patients with mild forms or those at risk of these disorders (e.g., Richards and Kinney, 1990; Johnson etal., 2012) and not in those diagnosed with severe cases of psychopathology char- acterized by very limited or non-existent regulatory function.

In brief, too little PFC regulation may significantly impair the quality of creative output, whereas too much PFC regulation may limit the quantity of creative production and, as a result, also hinder the likelihood of generating an idea that would be characterized as highly creative (see also Abraham, in press; Abraham etal., 2007).

CONCLUSION Much of past research on the relationship between psychopathol- ogy and creativity is marred by serious methodological limita- tions, correlational designs, and problematically unidirectional www.f rontiersin .org July 2014 I Volume 5 | Article 835 I 3 Ramey and Chrysikou Psychopathology and creative thought interpretations, the prevalence of which might be attributed to the curiously persistent historical link between creativity and "mad- ness."

Here we propose that, independent of psychopathology, highly productive individuals often produce work of greater qual- ity. As such, an increase in the quantity of one's output positively affects the likelihood of generating those statistically rare acts and achievements identified and celebrated as creative.

We argue that creativity may depend on a dynamic filtering mechanism, the flexibility of which relies on tradeoffs between rule-based (e.g., PFC) and stimulus-based (e.g., sensorimotor or subcortical) brain regions, and which, when influenced by psychopathology, can alter dramatically the quantity — and so quality — of creative output.

REFERENCES Abraham, A. (in press). "Neurocognitive mechanisms underlying creative thinking: Indications from studies of mental illness" in Creativity and Mental Illness, ed. Kaufman (Cambridge University Press). Abraham, A., Windmann, S., McKenna, P., and Giintiirkun, O. (2007).