Creativity: Nature or Nurture?

Creativity exists as an amalgamation of innate talent and acquirable skills, making it the subject of an enduring and complex debate; is creativity a result of nature or nurture? And why are some people more creative than others? Over the years, lesion studies have provided considerable insight regarding the relationship between brain structures and artistic abilities. Additionally, the ever-growing documentation (and scrutiny) of savant/autistic individuals has created a quest to understand and explain the neurological basis of these findings.

What is creativity?

Caselli (2009) conspicuously defined creativity as ‘an attempt to bridge the gap between what is and what should be’ using original or imaginative ideas. The complexity of this debate arises due to the fact that individuals can express creativity across a multitude of disciplines and at different points along a continuum. Innovative behaviour is not restricted to humans, however what separates us from the rest of the animal kingdom, is our utilisation of art as a communicative system. With respect to this, artistic creativity can therefore be defined as a conscious and cognitive process involving several key phases: preparation, incubation, illumination (eureka moment) and production (Heilman, 2016).

So what do we know about the brain already…?

The brain’s outer membrane, and the image people most typically envisage when they imagine the brain, is the cerebral cortex (or cerebrum), which is separated into four lobes: parietal, occipital, temporal and frontal. A structure termed the corpus callosum facilitates communication between the left and right hemispheres – structures that we now understand to differ in their specialities. Information concerning the integration and understanding of stimuli, analysis, language and serial movements (e.g. throwing) are functions belonging to the left hemisphere. The right side of the brain deals with anything concerning visual stimuli e.g. processing, memory, imagery, colour discrimination, as well as the integration of information from all brain regions (Lusebrink, 2004). Just beneath the cerebrum lies the limbic system – a collection of structures responsible for a number of functions including motivation, behaviour, long-term memory, olfaction and (of particular concern in this article) emotion. Despite it being an extensive complex, for the purpose of this article it can broken down into the following critical components: (1) the thalamus – a relay station for all sensory processes occurring in the brain, (2) the hippocampus – crucial in the formation (but not storage) of long-term memories, (3) amygdala – emotional integration of both the conscious (left side) and non-conscious (right side) variety, (4) basal ganglia – the planning and execution of movement.


Figure 1: the visual pathway from the eye to the brain. Taken from

The visual cortex, found in the occipital lobe, (as shown in figure 1) serves as the final destination for visual information (colour, texture, direction and movement) entering the brain before processing begins. Separation of the visual pathway into two distinct streams, originating in the occipital lobe, forms the basis of the ‘two-stream hypothesis’ and is shown in figure 2. It proposes that form, shape and colour information is received and conveyed to the temporal lobe via the ventral stream, leaving the dorsal stream as the pathway responsible for spatial information travelling to the parietal lobe (Lusebrink, 2004). As the complexity of art increases, recruitment of neurons in the frontal cortex (responsible for higher processing) also increases. Neurons that fire together, wire together’ is a phrase denoting the fact that brain stimulation facilitates brain growth e.g. musicians have been found to have a larger auditory cortex than non-musicians (Heilman, 2016). Nonetheless, this certainty is a source of controversy as it further blurs the boundaries between nature and nurture as explanations for creativity.

Nature or nurture?

The theory of natural selection by Charles Darwin proposes sexual selection as a biological underpinning of art; animals use embellishment and behavioural displays to lure potential sexual partners e.g. peacock’s displaying their tail or the colourful plumage of birds. Such behaviours persisted and evolved with the rise of the Homo sapiens e.g. the use of decorative face paint in African tribes (which is akin to the application of make-up by women in contemporary society). This behaviour highlights many desirable characteristics such as intelligence, creativity and physical aptness that reflect the condition of the brain and body in the flaunting individual (Zaidel, 2010).


Figure 2: the ventral and dorsal visual pathways originating from the occipital lobe. Taken from

Additionally, conclusions drawn from experiments by Reader and Laland (2003) revealed that many birds and non human primates exhibit creativity in the form of cunning and deceptive behaviours, e.g. pigeons teaching each other how to reach food in a difficult place/situation or monkeys rinsing the sand off their sweet potatoes before eating them and passing this on to their relatives. There are many more documented examples of animals using creative methods for survival, leading to an explanation of creativity in humans ‘as an extension of the fundamental biological survival functions’ (Zaidel, 2014) – though this can be extended as an explanation for both sexual and survival functions.

Studying the effects of brain damage, disease or abnormalities can shed some insight into the importance played by specific brain structures or regions. Research concerning savants for example, has been used to try and enhance our understanding of anatomical differences underlying their creative abilities. The term ‘savant’ refers to individuals that possess a constrained yet exceptional level of intellect, in an otherwise defective brain. Savant syndrome can be split into a 50:50 ratio between those who suffer autism and those who have acquired the condition as a result of some form of CNS damage (also known as acquired savant syndrome) (Zaidel, 2014). For example, an interesting MRI study by Treffert (2009) reported the absence of the corpus callosum in the brains of savants that were able to simultaneously scan and interpret two different pages of text. This echoes a fascinating finding by researchers at Cornell University, which found a smaller corpus callosum in writers, musicians and artists (Cox, 2013). Since a component of creativity is considered to be a consequence of the brains’ communicative ability (established previously as the primary role of the corpus callosum), these findings do prove somewhat counterintuitive. Whilst a correlation does not always imply cause and effect, it may be worth looking into this further; perhaps the augmentation of creativity in this way requires that the brain and its hemispheres specialise in a different way by sacrificing efficiency or function in other regions. Of course there is a possibility that multiple factors are at play and that genetic codes have a lot more to answer for. Additionally, lesion studies examining pre and post-damage productivity by artists uncovered the resilience of their skills, regardless of the extent or lateralisation of damage. Artists suffering with dementia and other neurodegenerative diseases display a similar level of resilience even into the later stages of their disease, where a diminished motor activity is what finally stops their art production (Zaidel, 2010). Therefore the extent of the evidence discussed, points towards creativity being an intricate process with no single brain region or pathway playing a dominant role.

Art and emotion: what can art therapy tell us?

Emotion affects almost every aspect of cognition: memory, attention, information processing, etc. (Zaidel, 2010), therefore it is conceivable to propose that art, with the ability to evoke the most powerful of emotions, should have the same effect. A compelling argument states that artistic abilities have evolved as a compensational mechanism allowing the retention of communication in the face of adversity (Zaidel, 2014). This is supported with the emergence of art therapy as a method of treatment for many patients suffering with brain trauma or disease. This technique focuses on how visual and somatosensory information reflect emotions, which in turn affect our experiences, behaviour and thoughts. In this way, art therapy can used to improve emotional and cognitive maturity and has been used to repair damaged cortical pathways. Since all forms of art involve motor movement, victims of stroke, Alzheimer’s disease and schizophrenia were exposed to art therapy in an attempt to activate the basal ganglia – a bridge between motor association and the somatosensory cortices – resulting in a reduction of impairment in these pathways.

The science underlying this therapeutic phenomenon is neuroplasticity – pertaining to the brains’ capacity to reorganise itself in response to injury, disease, new situations or changes in the environment. The success of art therapy is a consequence of its dynamic nature; interaction with art media calls on the activation of sensory, motor and cognitive (interpretation, decision-making, forming internal images) systems (Lusebrink, 2004). Whilst promising, this method remains slightly ambiguous and relatively new. Only time can reveal its efficacy, yet for the sake of this debate it does say a lot about the role of nurture.

So…what can we conclude?

Art is a uniquely human construct that allows us to reflect upon reality as we see it; stylised by our own sense of individuality. Creativity, on the other hand, is subject to influence by both nature and nurture. As already outlined, basic neural underpinnings for creativity can be explained as an evolutionary adaptation for reproduction and survival that grew in complexity as brain anatomy developed. Everyone is innately creative and we use it in our everyday life for a multitude of reasons: negotiations in the workplace, daydreaming, cooking, choosing your clothing and decorating your home. To the contrary, artistic creativity relies very heavily on nurture; an individual’s environment can ease or impede ones artistic faculties.

As Picasso once said:

All children are artists. The problem is trying to stay an artist once one grows up’.

Author: Tiffany Quinn

Edited by: Molly Campbell


Cox, B. (2013). Are some people born creative?. The Guardian. [online] Available at: [Accessed 5 Feb. 2017].


Heilman, K. (2016). Possible Brain Mechanisms of Creativity. Archives of Clinical Neuropsychology, [online] 31(4), pp.285-296. Available at: [Accessed 3 Feb. 2017].


Lusebrink, V. (2004). Art Therapy and the Brain: An Attempt to Understand the Underlying Processes of Art Expression in Therapy. Art Therapy, [online] 21(3), pp.125-135. Available at: [Accessed 1 Feb. 2017].


Roeser, S. (2010). Emotions and risky technologies. 1st ed. Dordrecht: Springer, pp.62-63.


Treffert, D. (2009). The savant syndrome: an extraordinary condition. A synopsis: past, present, future. Philosophical Transactions of the Royal Society B: Biological Sciences, [online] 364(1522), pp.1351-1357. Available at: [Accessed 1 Feb. 2017].


Zaidel, D. (2010). Art and brain: insights from neuropsychology, biology and evolution. Journal of Anatomy, [online] 216(2), pp.177-183. Available at: [Accessed 3 Feb. 2017].


Zaidel, D. (2014). Creativity, brain, and art: biological and neurological considerations. Frontiers in Human Neuroscience, [online] 8. Available at: [Accessed 2 Feb. 2017].




In this blog article I will underline the key pathophysiology surrounding attention deficit hyperactivity disorder: ADHD

Brain pathophysiology

Many of the brain pathophysiological defects of ADHD are linked with that of the prefrontal lobe, an area which plays a large role in cognition. Therefore, it is uncoincidental that the symptoms linked with the disorder include poor concentration, impulsivity and hyperactivity (R.A. Barkley 2003).  With the use of functional neuroimaging techniques such as FMRI and PET scans, we are able to understand differences in the brain function and structure of ADHD patients, the most prominent of which is seen when using structural MRI. Scans have revealed specific areas in subjects with ADHD are smaller than an individual that does not had ADHD. These areas include the prefrontal lobe, caudate, cerebellum and cerebellar vermis (Zang Yu-Feng 2006).  Using a regional homogeneity method to characterise the local synchronisation of spontaneous brain activity in individuals with methylphenidate and those with placebo. It was seen that in those with the placebo the regional homogeneity of activity was decreased in the bilateral dorsolateral prefrontal cortices. Contrastingly regional homogeneity increased in the bilateral sensorimotor and parieto-visual cortices. Furthermore in those with who taken the methylphenidate, the major effect was down regulation in the right parietal cortex. This down regulation was correlated with decreased symptom scores after 8 weeks of acute methylphenidate doses (Li An et al 2012).

Structural connectivity

Diffusion tensor imaging allows for the imaging of axonal connections between brain areas.  The technique relies on the free movement of water molecules where there are no means of restriction. DTI allows for analysis of the white matter tracts of the brain, where it can map the orientation of the axon and the location. From this, we can image and see the specific connection between brain areas (Konrad and Eickhoff 2010).  Decreased fractional anisotropy (FA) in the right supplementary motor area, right anterior limb of internal capsule, right cerebral peduncle, left middle-cerebellar peduncle, and left cerebellum can be seen in children with ADHD. These results were consistent with those seen with MRI.  Fractional anisotropy is most simply the degree of which the water molecule is directionally dependent as a result of cell membranes and myelin sheath, to that which is free moving with Brownian motion. Finding of lower FA in children with ADHD specifically in these areas is intriguing, as the supplementary motor area has a role in planning, initiation, and execution of motor acts. Additionally, the  right frontostriatal circuitry is thought to be important in the development of organisation and planning (Ashtari et al 2004), which could be linked to poor organisational skills displayed. Consequently, they were able to piece to together links between brain regions and behaviour.

In a study exploring the relationship of frontostriatal structure in ADHD children and behaviour, Casey et al (1997) adopted MRI and behavioural tests. A correlation was found between impulse control and volumetric measure of globus pallidus and basal ganglia. Maps of cortical thickness showed ADHD patients to have a thinner cortex in bilateral frontal regions and the right cingulate cortex, in contrast to those without the disorder. There is now substantial evidence amounting to the role of the cerebellar region in ADHD, as the fractional anisotropy of the area is significant in inattention subscale scores (Durston et al 2003).


Genetics accounts for 75% of ADHD cases, as shown by data gathered across four genome-wide association scans investigating the disorder’s heritability. Furthermore, this research placed emphasis on the rarer variants of genes associated with ADHD, such as those coding for DRD4 and DRD5 dopamine receptors (Neale et al 2010).   Further genome-wide association scans show limited overlap  apart with the CDH13. Typically, many of the genes involved are involved in dopaminergic signalling. These include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH. A mutation in the DRD4–7 receptor results in a wide range of behavioural phenotypes, including ADHD symptoms such as split attention (Kebir et al 2009). Furthermore, polymorphisms of this gene show significance in attention sustained performance tasks (Kieling et al 2006) Given the evidence obtained as a result of the study and meta-analysis, is it clear that DRD4 mutations are influential in displaying ”ADHD-like” phenotypes.  Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.


In conclusion, ADHD presents as difficulties in maintaining attention and concentration, but also can affect social aspects. Studies to find clear brain pathologies through imaging techniques have highlighted defects the prefrontal lobe and cerebellum and thus these regional defects are said to contribute to the symptomatic phenotype of the disorder.  There is a clear involvement of biogenic amines, specifically dopamine, with current models showing emphasis on the  mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic systems. Furthermore, abnormalities may exist in other pathways such as glutamatergic, serotonergic or cholinergic neurotransmission.   Genetic studies have shown the significance of specific gene variants in contributing to the disorder, specifically those linked to the G-protein coupled receptors DRD4 and DRD5.  Genetic   and phenotypic heterogeneity amongst individuals could explain differences between genetic studies.  However, these differences may exist in different pathways but present the same phenotypic behavioural traits. Meta-analyses have produced a more reliable result than gene-wide association scanning alone, however, the association found only accounts for a small proportion of the genetics of ADHD. Approaches in neuroimaging genetics and epigenetic studies are being investigated to aid a clearer picture of the genetic component of this disorder.

Author: Liam Read

Editor: Molly Campbell

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ASHTARI, M., KUMRA, S., BHASKAR, S. L., CLARKE, T., THADEN, E., CERVELLIONE, K. L., RHINEWINE, J., KANE, J. M., ADESMAN, A., MILANAIK, R., MAYTAL, J., DIAMOND, A., SZESZKO, P. & ARDEKANI, B. A. 2005. Attention-deficit/hyperactivity disorder: A preliminary diffusion tensor imaging study. Biological Psychiatry, 57, 448-455.

BARKLEY, R. A. 2003. Issues in the diagnosis of attention-deficit/hyperactivity disorder in children. Brain and Development, 25, 77-83.

CASEY, B. J., CASTELLANOS, F. X., GIEDD, J. N., MARSH, W. L., HAMBURGER, S. D., SCHUBERT, A. B., VAUSS, Y. C., VAITUZIS, A. C., DICKSTEIN, D. P., SARFATTI, S. E. & RAPOPORT, J. L. 1997. Implication of Right Frontostriatal Circuitry in Response Inhibition and Attention-Deficit/Hyperactivity Disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 36, 374-383.

KEBIR, O., TABBANE, K., SENGUPTA, S. & JOOBER, R. 2009. Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies. J Psychiatry Neurosci, 34, 88-101.

KONRAD, K. & EICKHOFF, S. B. 2010. Is the ADHD brain wired differently? A review on structural and functional connectivity in attention deficit hyperactivity disorder. Human Brain Mapping, 31, 904-916.

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YU-FENG, Z., YONG, H., CHAO-ZHE, Z., QING-JIU, C., MAN-QIU, S., MENG, L., LI-XIA, T., TIAN-ZI, J. & YU-FENG, W. 2007. Altered baseline brain activity in children with ADHD revealed by resting-state functional MRI. Brain and Development, 29, 83-91.