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 ). Evidence comes from several conditions associated both with frontal lobe dysfunction and with creative block (see .) 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.
The first condition linking frontal dysfunction and block is depression. Many techniques, including functional brain imaging and lesion analysis, have demonstrated frontal deficits in depression. During depression, motivation and cognitive flexibility decrease, as do goal-directed activities such as eating and sex. Although creative subjects paradoxically more often have a history of depression than the average, their creative work is not done during their depressions, but in rebound periods of increased energy between depressions (Jamison, 1989
; Flaherty, 2004
When depression is treated, frontal lobe function normalizes on functional imaging (Goldapple et al, 2004
). Creative block usually improves as normal levels of motivation return—with the caveat that side effects such as mood flattening or agitation from antidepressants can be counterproductive. Stimulants can help depression, as well as creativity as described above. Non-pharmacologic treatments of depression such as exercise and phototherapy may help creativity and productivity even in blocked subjects with no signs of depression (Norden and Avery, 1993
; Steinberg et al, 1997
The second frontal lobe condition similar to creative block—especially writer's block—is a lesion in Broca's area. Broca's lesions produce a selective deficit in speech production, in contrast to the speech comprehension problems of Wernicke's aphasia. Although writer's block is not an aphasia or agraphia, it shares with Broca's aphasia such features as painfully retained awareness of speech errors, as well as decreased linguistic output. This awareness causes frustration and depressed mood that further inhibit speech. shows the parallels between Broca's aphasia and block, and Wernicke's aphasia and hypergraphia.
Relation between states of creative drive, aphasias, mood states, and lesion locations.
A third group of conditions, frontal lesions outside Broca's area, can cause depression and decreased speech independent of aphasia. Frontal lobe lesions can cause cognitive deficits such as perseveration that are similar to the dogged and unproductive efforts of blocked writers. Both appear to respond to sudden environmental changes—blocked subjects can escape their mental ruts when distracted by a break from the problem.
Anxiety is a fourth condition that, like depression, shows frontal lobe changes in a number of paradigms (Cannistraro and Rauch, 2003
), and anxiety is highly associated with creative block. Block of this form, which resembles performance anxiety, should respond to antidepressants just as anxiety does. Arousal levels are higher in anxiety than depression, however, and stimulants can be counterproductive. This reflects the Yerkes-Dodson law that task performance is an inverted U-shaped function of arousal level. Anxiety states exceed the ideal arousal for task performance. Task performance has a similar inverted U-shaped relationship to the beneficial cognitive effects of dopamine agonists (Kimberg et al, 2001
Fifth, features of writer's cramp—a focal dystonia that shows changes in sensorimotor and premotor cortex activity (Lehericy et al, 2003
)—suggest that it may be a more motor, posterior frontal analogue of writer's block. Writer's cramp, like block, appears to be induced by highly attended, repetitive, stressed practice of the task. Continued attempts to write often only worsen the cramp, whereas enforced inactivity—like the breaks that help perseveration and block—can sometimes be therapeutic (Byl et al, 1996
Sixth, electromagnetic studies demonstrate that the functioning frontal lobe stimulates creativity. When subjects with high and low creativity are compared, the former have both higher baseline frontal lobe activity and greater frontal increase while performing creative tasks (Carlsson et al, 2000
). There is preliminary evidence that transcranial magnetic stimulation over frontal lobes can increase creativity in normal subjects during both drawing and writing tasks (Snyder et al, 2004
). There are case reports of patients whose creativity increased after receiving subcortical deep brain stimulating electrodes near the nucleus accumbens (Gabriels et al, 2003
; Flaherty et al, In press
). The accumbens' connections to the frontal and temporal lobes, and its role in limbic generation of drives, may help explain this effect.
Relative contributions to creativity from the temporal and frontal lobes may in part reflect the distinction variously described as divergent versus convergent thought, primary versus secondary process thought, or the writing versus editing stages (Flaherty, 2004
). What about relative contributions to idea generation from different frontal subsystems? Lesions of medial prefrontal cortex can produce amotivational, abulic states of decreased creative drive. Dorsolateral prefrontal cortex's importance for working memory and flexible problem solving suggests a greater role in creative skill than in drive. Motor and premotor cortex are probably more necessary for performance than for conception of a creative plan. While lesions of all of these systems would be detrimental to idea generation, orbitofrontal lesions may have a partly opposing effect, as they can produce disinhibition syndromes that at least superficially resemble mania.