India Bohanna, PhD – Brain Blogger Health and Science Blog Covering Brain Topics Wed, 30 May 2018 15:00:03 +0000 en-US hourly 1 What is Creativity? Art as a Symptom of Brain Disease Sun, 23 Sep 2012 11:00:40 +0000 We don’t normally associate creativity with brain disease, but a recent paper published in Brain suggests that maybe we should. When we think of someone affected by a serious brain disorder, we imagine deterioration and loss of function, but a surprising new study shows that some people may actually develop artistic talent as a result of their brain disorder, and that in turn, their art can tell us about the nature of their brain disorder.

This recent review by Schott brings together cases of individuals with neurological conditions, who with no previous artistic motivations suddenly become compelled to make art, and the art is good!

The authors describe a case of an epileptic man with no artistic ability who began to suffer recurring epileptic attacks in which he acted aggressively, could not speak or focus his eyes, and acted out of character. During these attacks, the patient began to draw spontaneously and compulsively, and with remarkable skill. In another case, a 68 year-old man had begun to paint at age 56 with the onset of dementia, despite never being interested in art before. In the ten years that passed after the onset of his dementia, his paintings became more and more detailed, colorful, precise and realistic, and he even began to win awards for his art.

Both these cases highlight the importance of context in understanding how art can tell us about brain disorders. The onset of uncharacteristic artistic behavior or the compulsive desire to create art where there has been no desire before might indicate an emerging neurological abnormality. Similarly, in people who already have creative ability, dramatic changes in style (e.g. from abstract to realistic) can indicate the onset or progression of brain dysfunction.

But how can these unusual events tell doctors about the patient’s underlying condition? In these and most other cases of emerging artistry, involvement of the left anterior temporal lobe appears to be crucial. The temporal lobe and frontal brain regions work together and are involved in creativity. Damage or degeneration of temporal regions can release the temporal lobe’s inhibitory influence on the frontal cortex, resulting in enhanced creativity. For example, a magnetic resonance imaging (MRI) scan of the elderly man with dementia revealed severe damage to the temporal lobe, while his frontal brain regions remained intact.

Similarly, an imbalance between left and right hemisphere activity appears to affect creativity. For example, in the case of the epileptic patient, based on his unusual behavior, neurologists deduced that the seizures were originating in the left frontal hemisphere. Depression of the dominant, logical left-brain regions during his seizure had caused the “release” of the more creative right brain, resulting in his unusual artistic ability.

These interesting case studies offer a new perspective on the way we study brain disorders, and challenge our understanding of creativity. The neural networks involved in creativity are delicately balanced. Disruption of this network can lead to the surprising and counter-intuitive emergence of new artistic talent; talent that is regarded by many to be a skill that is learned over years of practice. What makes some people artistically talented and others not? Practice or innate ability? The relevance of the age-old debate, ‘nature versus nurture?’ is brought to the fore by these cases, and points to the emergence of an exciting new, interdisciplinary field of neuroscience research.


Schott GD (2012). Pictures as a neurological tool: lessons from enhanced and emergent artistry in brain disease. Brain : a journal of neurology, 135 (Pt 6), 1947-63 PMID: 22300875

Image via IgorGolovniov / Shutterstock.

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The Neuroscience of Belonging Mon, 17 Sep 2012 11:00:14 +0000 The brain has evolved to respond in predictable ways to threats in the physical environment. Similarly, the brain is attuned to identify and reinforce behaviours that benefit our survival. These threat and reward-related circuits are well described. For example the amygdala, the most well studies threat-related brain region, responds to universally threatening stimuli such as a threat of pain or an approaching tarantula.

But what about more complex, subjective, social stimuli? For example, when a person feels rejected by a friend or partner, what happens in the brain? It is well established that people who have satisfying social relationships and feel cared for and loved by others are more physically healthy and live longer than those who feel socially isolated. In fact, feeling socially connected is protective against a range of conditions such as heart disease and cancer. Despite this, the way perceptions of social connectedness modulate physical health is not known.

A recent research review, published in Nature Neuroscience, suggests that social disconnection may be processed in the brain in the same way as the threat of physical harm. That is, when a person perceives that their relationship with another person is under threat, the brain responds by activating a basic ‘alarm system’. This alarm system sets in motion a range of neurophysiological processes that are the same, whether the threat is physical and in the environment, or perceived and based on individual judgment of a threat to social connectedness. This alarm system includes the amygdala, the anterior cingulate cor­tex and the insula, all of which are known for their roles in both threat- and pain-related processing.

What happens when this alarm system is activated? The sympathetic nervous system and hypothalamic-pituitary-adrenal axis go into overdrive, increasing inflammation and a compromising the immune system. These processes contribute to many diseases such as diabetes, those of aging, and cancer. New evidence suggests that these responses occur in response to perceived social isolation as well to a physical threat of harm.

On the other hand, how does social connectedness improve health? Research shows that being reminded of your social connections activates basic reward-related circuits that are also activated when learning to respond to beneficial environmental cues. Researchers use the example of seeing a picture of a highly supportive romantic partner; when viewing this picture during painful stimuli, people perceive and report less pain. This simultaneously activates reward-related brain regions including the ventromedial prefrontal cortex and the posterior cingulate. This may be the key to how feeling socially connected can lead to better health. Activation of these brain regions is thought to cause the release stress-reducing neuropeptides such as opiods and oxytocin, which boost the immune system and protect the body from damage due to inflammation

This is a new and exciting area of research, and suggests what many people have intuitively known for many years: belonging and feeling cared for are critical to good health.


Eisenberger NI, & Cole SW (2012). Social neuroscience and health: neurophysiological mechanisms linking social ties with physical health. Nature neuroscience, 15 (5), 669-74 PMID: 22504347

Image via Andrey Pavlov / Shutterstock.

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How Does the Brain Recover After Stroke? Wed, 05 Sep 2012 11:00:51 +0000 People who have suffered traumatic brain injury or stroke often have serious, immediate deficits in motor, sensory, and cognitive function. Interestingly however, these functions often recover in the following weeks and months, without apparent reason. Until now, the repair mechanisms behind this spontaneous recovery have been a mystery. A recent study published in Brain demonstrates the ingenious ability of the central nervous system to repair itself after brain injury.

In anesthetised mice, Ueno and colleagues injured the region of the motor cortex that controls movement of the forelimb, in one hemisphere only. This resulted in the loss of forelimb function on one side, measured by behavioural tests that required the mice to walk across a ladder, up a staircase and through a cylinder. Similar to the spontaneous recovery seen in humans, the mice began to recover their motor function after two weeks, with improvement peaking after six weeks.

To try to understand and visualise the neural processes behind this recovery, the authors injected colored tracers into the injured motor cortex, the same cortical region in the opposite, uninjured hemisphere, and the corticospinal tract, which carries signals from the brain to the limbs to generate movement. This allowed the investigators to look at the changes in the brain and corticospinal tract associated with the loss of motor function and subsequent recovery.

Tracing showed that new fibres, originating in the uninjured motor cortex, began to grow and connect with neurons on the opposite, damaged side of the corticospinal tract. New fibres began to form 2 to 4 weeks after injury, with the new axons growing longer, sprouting “branches”, and finally connecting with the neurons involved in forelimb movement on the damaged side.

It was important to find out if this newly rewired pathway was responsible for the recovery in motor function seen in the mice. The authors stimulated the healthy motor cortex using a microstimulator, and recorded muscle activity in the forelimb on the opposite, injured side. When the healthy cortex was stimulated, the muscles on the injured side responded, demonstrating that this rewiring between the brain and spinal cord was indeed responsible for restoring motor function.

The authors also demonstrate the importance of one molecule, brain-derived neurotrophic factor (BDNF) in this rewiring process. BDNF is important for the growth of neurons throughout the brain, and in this experiment BDNF was necessary to induce sprouting and branching in the new pathways, a process essential for the recovery of function. When BDNF production was blocked, the animals did not recover their motor function.

This study demonstrates that the brain is extremely capable at repairing itself, and suggests exciting new possibilities for improving recovery after traumatic brain injury and stroke in humans. Developing treatments that enhance this rewiring, sprouting and branching process may improve the likelihood of recovery for people who have lost cognitive or motor function due to injury.


Ueno M, Hayano Y, Nakagawa H, & Yamashita T (2012). Intraspinal rewiring of the corticospinal tract requires target-derived brain-derived neurotrophic factor and compensates lost function after brain injury. Brain : a journal of neurology, 135 (Pt 4), 1253-67 PMID: 22436236

Image via Evgeny Korshenkov / Shutterstock.

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Cannabis and the Adolescent Brain Sat, 18 Aug 2012 11:00:10 +0000 For some time, people have known that using cannabis during adolescence increases the risk of developing cognitive impairment and mental illness (e.g. depression, anxiety or schizophrenia) later in life. Importantly however, the mechanisms responsible for this vulnerability are not well understood. A new study, published in Brain, shows that long-term cannabis use that starts during adolescence damages the neural pathways connecting brain regions, and that this may cause the later development of cognitive and emotional problems.

The authors used diffusion tensor imaging (DTI), a MRI technique that measures water diffusion, to examine the microstructure of white matter in 59 heavy cannabis users, who used cannabis at least twice a month for three years or longer, as well as 33 non-users. In the human brain, white matter pathways are formed by bundles of axons, which carry the neural signals, and myelin, which coat the axons and speeds up signal transfer. These white matter pathways are crucial for normal brain function as they enable disparate regions of the brain to communicate, and act together.

When the authors investigated white matter microstructure in the cannabis users, they found damage in the white matter pathways of the hippocampus, crucial for memory, and the corpus callosum, which connects the brain’s two hemispheres. Both pathways are critical for normal brain function. The authors suggest that impaired connectivity due to damage in these pathways may be the cause of the cognitive impairment and vulnerability to schizophrenia, depression and anxiety seen in long-term users.

The authors also show an inverse relationship between the amount of white matter damage and the age of first use. That is, participants who started using cannabis younger had more white matter damage and showed poorer brain connectivity. Adolescence is a critical period in the development of white matter in the brain, when the neural connections we rely on in adulthood are being finally formed. The authors point out that white matter cells have cannabinoid receptors (those susceptible to cannabis) during adolescence, which disappear as the brain matures. This new study demonstrates a mechanism that may help explain how cannabis use in adolescence causes long-term changes in brain function. The cannabis users in the study had significantly higher levels of depression and anxiety compared to the non-users.

This important new study suggests that young people’s brains are at risk of white matter injury due to cannabis, and that cannabis exposure during adolescence may permanently damage white matter development. Future research must address the question; can white matter pathways and connectivity recover when a person quits using cannabis?


Zalesky A, Solowij N, Yücel M, Lubman DI, Takagi M, Harding IH, Lorenzetti V, Wang R, Searle K, Pantelis C, & Seal M (2012). Effect of long-term cannabis use on axonal fibre connectivity. Brain : a journal of neurology, 135 (Pt 7), 2245-55 PMID: 22669080

Image via Amihays / Shutterstock.

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