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1.
Figure 2

Figure 2. From: FRONTOTEMPORAL AND DOPAMINERGIC CONTROL OF IDEA GENERATION AND CREATIVE DRIVE.

A much more common complaint than excessive creative drive is its lack. Is creative block caused by an increase in temporal lobe activity, and creative drive caused by its decrease? Probably not. There seems to be a better correlation between frontal lobe malfunction and creative block (See Fig. 2). Evidence comes from several conditions associated both with frontal lobe dysfunction and with creative block (see Table 1.) Since the frontal and temporal lobes are to a first approximation mutually inhibitory, creative block and pressured output do not usually occur together. They can, however—as in the highly repetitive hypergraphia of some epileptics.

Alice W. Flaherty. J Comp Neurol. ;493(1):147-153.
2.
Figure 1

Figure 1. From: FRONTOTEMPORAL AND DOPAMINERGIC CONTROL OF IDEA GENERATION AND CREATIVE DRIVE.

Dopamine does not merely raise baseline arousal. The focused aspect of creative drive, its high goal-directedness, may be driven by mesolimbic dopaminergic activity (see Fig. 1). Dopamine mediates reward-seeking activity ranging from gambling and cocaine addiction to the appreciation of beautiful faces and music (Aharon et al, 2001; Breiter et al, 2001). It can trigger the drive to communicate (Wintink and Brudzynski, 2001), although too much dopaminergic activity may cause stuttering or coprolalia. High doses of levodopa can cause excessively focused, highly complex motor stereotypies, such as repeatedly disassembling and reassembling one's motorcycle engine (Fernandez and Friedman, 1999). Whereas dopamine agonists can induce hypomania and hallucinations (Peet and Peters, 1995), the dopamine antagonists, generally used as antipsychotics, are notorious for their ability to suppress not only hallucinations and stereotypies but also creativity.

Alice W. Flaherty. J Comp Neurol. ;493(1):147-153.

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