More brains and bonkers connection: thinking out of a broken box

We have covered many studies linking creativity with Psychosis and this new study by Manzano et al provides further corroborating evidence.

Dopamine has been linked with psychosis and is now also being increasingly being linked with creativity, especially divergent creativity and thinking style.

Divergent thinking is influenced by dopaminergic function. Reuter [6] found a correlation between divergent thinking (the Inventiveness battery of the Berliner Intelligenz Struktur Test) and polymorphisms of the dopamine D2 receptor gene–DRD2 TAQ IA. Higher creativity scores were observed in carriers of the A1 allele. This polymorphism is unrelated to general intelligence [7], [8], which suggests that it is more specifically related to Glr (“long-term storage and retrieval”). This finding is in line with functional imaging research showing the D2 system to be involved in attentional set shifting and response flexibility, which are important components of divergent thinking [9]. Furthermore, the finding indicates that divergent thinking is related to regional differences in D2 densities, since the DRD2 TAQ IA polymorphism has been shown to modulate D2 binding potential (D2BP) in both striatal [10] and extrastriatal regions [11].

Divergent thinking is traditionally measured using alternate uses test, for eg., in which a familiar object like brick is provided and subjects asked to name novel use for that object. The responses are marked for creativity as per the follwoing criterion:

• Fluency–the number of valid responses;
• Originality–how frequent the participant’s responses were among the responses of the rest of the sample;
• Flexibility–the number of semantic categories produced;
• Switching–the number of shifts between semantic categories;
• and Elaboration–how extensive each response is (if the task involves producing more than single words)

The main findings of the study was that dopamine D2 binding potential (D2BP) receptor density in thalamus correlated negatively with divergent thinking and creativity scores. Here is how the authors interpret the results:

Based on the current findings, we suggest that a lower D2BP in the thalamus may be one factor that facilitates performance on divergent thinking tasks. The thalamus contains the highest levels of dopamine D2 receptors out of all extrastriatal brain regions [33], [45]. Decreased D2BP in the thalamus has been suggested, firstly, to lower thalamic gating thresholds, resulting in decreased filtering and autoregulation of information flow [31] and, secondly, to increase excitation of cortical regions through decreased inhibition of prefrontal pyramidal neurons [46], [47], [48]. The decreased prefrontal signal-to-noise ratio may place networks of cortical neurons in a more labile state, allowing them to more easily switch between representations and process multiple stimuli across a wider association range [49]. This state, which we hereforth will refer to as the “creative bias”, could benefit performance on tasks that involve continuous generation and (re-)combination of mental representations and switching between mind-sets. The creative bias could also explain why the different measures of divergent task performance correlate: A decreased signal-to-noise ratio in thalamus would decrease information gating and possibly increase fluency; decreased signal-to-noise ratio in cortical regions should better enable flexibility and switching between representations; similarly, the associative range should be widened and selectivity should be decreased which might spur originality and elaboration.
Besides carrying benefits related to fluency and switching, the decreased signal-to-noise ratio associated with the creative bias should be disadvantageous in relation to tasks that require high levels of selective attention. Some support for this prediction can be taken from Dorfman [50] who showed that the greater a person’s divergent thinking scores, the slower his or her reaction times were on a negative priming task requiring the inhibition of interfering information. Furthermore, the creative bias may also bring a risk of excessive excitatory signals from the thalamus overwhelming cortical neurotransmission, with ensuing cognitive disorganization and positive symptoms [30]. It is thus tempting to suggest that dopaminergic modulation of neurotransmission mediated through dopamine D2-receptors could be one of the mechanisms which associate creativity with positive psychotic symptoms. Interestingly, positive symptoms are not necessarily related to problems in executive function, at least not to the same extent as negative symptoms [51], which indicates that in the creative individual “blind variation” might be affected without a concomitant decline in “selective retention”. It can be speculated that aberrant thalamic function may promote unusual associations, as well as improved performance on divergent thinking tests in healthy individuals, in the absence of the detrimental effects typically associated with psychiatric disorders. In other words, thinking outside the box might be facilitated by having a somewhat less intact box.

In plain English speak, the same decreased signal-to-noise ratio in perfrontal regions that gives rise to creativity also gives rise to proneness to psychosis. The more the noise that is introduced the greater the chances that the ideas generated by ‘blind variation’ are more creative; if the ‘selective retention’ procedure is also defective or loosened to an extent, it may result in psychopathology and psychosis, while if intact it leads to creativity. Thus while one factor , that of loosening of associations, flexibility and set switching is common to both psychosis and creativity, the defects in selective retention may be the crucial factor that distinguishes brains from bonkers.