Do both psychopathology and creativity result from a labile wake-sleep-dream cycle?

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Background

The idea of association between creativity and mental illness is hardly new. Aristotle saw creativity and madness as a ‘mixture’ whose elements are difficult to disentangle, opining, ‘No excellent soul is exempt from a mixture of madness’. The psychiatric histories of many creative individuals reveal psychopathology. Longitudinal population-based data shows a familial cosegregation of both bipolar disorder and schizophrenia with creativity. Imaging of a creative task demonstrates brain connectivity similar to that seen in schizotypy. Yet despite accumulating evidence, the link between creativity and mental illness is not well understood. Transient dissociations of wake and sleep occur (daydreaming and lucid dreaming). A labile sleep-wake cycle may progress to the ‘mixing’ (or de-differentiation) of the waking, sleeping and dreaming states (W/S/D). There is already interest in a labile W/S/D cycle and dissociative symptoms. We welcome empirical and theoretical contributions on a labile W/S/D cycle as the neurobiological substrate of both creative insight (through remote association of ideas) and mental illness.


Dreaming is hyperassociative. REM dreams associate things which, in wake, would not be seen as connected. Creative insight spots analogies between phenomena previously thought to be dissociated or irrelevant to each other. Therefore, less distinction between W/S/D may foster hyperassociativity and creative insight but progressive invasion of dreaming into wake may engender dissociations, hypnagogia, oneirism, confuso-oneiric state, or crepuscular state. In manic states waking thought, speech and writing can be so associative, they fragment and become incomprehensible. If dream-like associations are taken as real, psychosis may result. Anxiety/fear is the predominant emotion during REM dreaming. Less distinction between W/S/D may result in an enduring de-differentiation which precipitates anxiety disorders, schizotypy or psychosis.


Memory processes continue during sleep, de-differentiation may disrupt these. For example, the partial invasion of the wake state into REM dreaming may impair elaborative encoding, resulting in episodic memory loss. Indeed, creative writers may compensate for disruption to REM dreaming through elaboratively encoding their memories during wake. Sleep spindles integrate new memories into neural networks. The partial invasion of the wake state may disrupt NREM spindle activity. Episodic, rather than semantic, memory loss characterises schizophrenia, and spindle activity is reduced. Therefore, ultimately, the progressive de-differentiation of W/S/D may engender schizophrenia rather than creativity.


Differentiation between W/S/D recruits aminergic, cholinergic and dopaminergic systems. Neuromodulation depends on neuro-membrane structure, poised at the edge of chaos-between solid and liquid states. Such self-organized criticality enables optimal functioning. Creative individuals may be in a super-critical state, hyperassociative but vulnerable because, in such a state, small changes in membrane composition can engender significant, unpredictable neuromodulatory effects. Transmitter complexity in W/S/D implies heterogeneous cognitive and behavioural effects for de-differentiation, accounting for diverse psychopathologies. To understand subsequent psychopathologies, the concepts of self-organizing and autopoiesis (‘self-producing) are significant. Autopoiesis may explain how, when disorganized during psychopathology, reconstitution is attempted, e.g. if REM dreaming is invaded by wake, the REM period may lengthen to compensate. Indeed, the final pathway for bipolar disorder may be an autopoietic reaction to schizophrenia, to restore W/S/D differentiation through alternating aminergic and cholinergic overdrive.

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