Author Archives: Harry Huang

What’s the Neuroscience Behind the Bouba/Kiki Effect?

(Ramachandran, 2004)

Let’s start off with this famous experiment done by neuroscientist V. S. Ramachandran and Edward Hubbard (Ramachandran and Hubbard, 2001). They asked American college undergraduates and Tamil Speakers in India “which of these shapes is bouba and which is kiki?” What do you think?

Did you pick the right one as “bouba” and the left one as “Kiki”? Yes, your instinct was correct. 95% to 98% of subjects responded the same way as you just did (Ramachandran and Hubbard, 2001). Another group of researchers tested this similar question to toddlers. The finding was that the associations of “kiki” to jagged shapes and “bouba” to rounded shapes were consistent even prior to language development (Maurer et al., 2006). These results suggested that no matter the test subjects were different native languages speakers or very young children, people were always able to make this association.

Ramachandran and Hubbard reasoned that because of the sharp form of the visual shape, subjects tended to map the name “kiki” onto the left figure, and because of the rounded auditory sound, subjects tended to map the name “bouba” onto the right figure (Ramachandran and Hubbard, 2001). Other researchers have proposed that perhaps this effect happened because when you say “bouba”, your mouth makes a more rounded shape, whereas when you say “kiki”, your mouth makes a more angular shape (D’Onofrio, 2014). It has also been suggested that this Bouba-Kiki effect (BK effect) could occur through cognitive mechanisms similar to those that underlie synesthesia (Ramachandran and Hubbard, 2001), the phenomenon in which someone experienced sensation in a particular modality (hearing, for example) when a different modality was stimulated (seeing a particular color, for example). To sum up, one thing that scientists agreed on was that in order for the BK effect to take place, some sort of integration of shapes and sound occurred in the brain (Spence and Deroy, 2013).

All these explanations made sense, right? But after learning about all BK effect in Dr. O’Toole’s class, I was still curious about how and where these integration processes happened in my brain when I selected “bouba” to the right figure and “kiki” to the left figure. To investigate this phenomenon one step further, two neuroscientists from Sorbonne University in Paris published their study using functional Magnetic Resonance Imaging (fMRI) (Peiffer-Smadja and Cohen, 2019).

These researchers had two questions in mind. Question #1: did this integration of shapes and sounds occur at an automatic or a controlled level? In other words, would participants show a BK effect even when no explicit judgment was required on audio-visual matching? Question #2: did this integration take place in our sensory cortices or in our supramodal regions (areas of the brain that have abstract functions to more one type of sensory input)?

In order to test the first question, the researchers designed a task called Implicit Association Test (IAT). The underlying trick is that responses are supposed to be faster and more accurate when concepts are strongly associated. In this case, we would predict that the response to be faster and more accurate whenever “kiki” sounds were paired with spiky shapes (congruent block) than whenever “kiki” sounds were paired with rounded shapes (incongruent block).

For each trial, participants were simultaneously presented with a pseudoword and a shape. The participants in this task were asked to decide if the pseudoword contained the sound “o” or the sound “i”. Then they had to decide if the shape was round or spiky. As anticipated, responses were faster and more accurate in congruent blocks than in incongruent blocks. This experiment was a clever twist to the traditional “BK” experiment. Here, the participants were never explicitly asked about matching the shapes and sounds. Still, the bouba-kiki sound-shape association had an impact on their behavior even when it was irrelevant to the task. The persistence of the BK effect even in this setting suggested that it may came at least in part from automatic perceptual stages of stimulus processing, which was separated from attention and task-related influences. The first mystery was solved.

Next, using fMRI, the authors were looking for which brain regions were activated when the subjects performed implicit BK matching tasks. Participants were simply asked to pay attention to both visual and auditory stimuli when sometimes the pairs were matching (bouba-round) and sometimes the pairs were mismatching (bouba-spiky). They found that cross-modal matching influenced activations in both auditory and visual sensory cortices. Moreover, they found higher activation in the prefrontal cortex to mismatching stimuli than to matching stimuli. Taken together, when the pairs were matching, the visual cortex (where visual information is processed by the brain) and the auditory cortex (where auditory information is processed by the brain) showed more activation. On the contrary, when the pairs were mismatching, prefrontal cortex showed more activation.

(Neuro4Kidz , 2018)
The prefrontal cortex is the front part of the frontal lobe and has been implicated in cognitive behavior planning, personality expression, decision making and social behavior (Yang and Raine, 2009).



(Broda-Bahm, 2013)

So, what could we conclude from these findings? Results indicated that BK matching had an effect on the early stages in sensory processing, while mismatching had an effect on the later stages of supramodal processing. As a follow-up, the authors hypothesized that the crossmodal BK effect perhaps was modulating the executive processes (processes that are necessary for the cognitive control of behavior) in the prefrontal cortex.

Bear in mind that these conclusions should be taken as preliminary findings. The common problem with fMRI study is that a structure active for a task does not mean it is critical for the task. So, the only certain inference we can make from the study is that prefrontal activation is related with part of the integration processes of BK effect. In the scientific literature, mechanisms involved in cross-modal integration is currently not well-understood (Peiffer-Smadja and Cohen, 2019). For hundreds of years, we have been investigating how our brain processes sensory information. And this BK effect perhaps now provides us a unique window to look into how our brain combines all these sensory information and create a coherent picture of how we perceive the world around us.

Works Cited

Broda-Bahm, K. (2013, April 8). Ban the Bullet (From Your Slides). Retrieved from Persuasive Litigator:

Neuro4Kidz . (2018, June 2). Build that Prefrontal Lobe up. Retrieved from Medium:

D’Onofrio A (2014) Phonetic Detail and Dimensionality in Sound-shape Correspondences: Refining the Bouba-Kiki Paradigm. 57:367-393.

Maurer D, Pathman T, Mondloch CJ (2006) The shape of boubas: sound–shape correspondences in toddlers and adults. 9:316-322.

Peiffer-Smadja N, Cohen L (2019) The cerebral bases of the bouba-kiki effect. NeuroImage 186:679-689.

Ramachandran V, Hubbard E (2001) Synaesthesia—A Window Into Perception, Thought and Language.

Ramachandran VS (2004) A brief tour of human consciousness: From impostor poodles to purple numbers. New York, NY, US: Pi Press, an imprint of Pearson Technology Group.

Spence C, Deroy O (2013) How automatic are crossmodal correspondences? Consciousness and Cognition 22:245-260.

Yang Y, Raine A (2009) Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: a meta-analysis. Psychiatry Res 174:81-88.

From Cheese to Brain Structures

Four weeks into the NBB Paris program, I now know my friends in our apartment very well. In our apartment (maybe this applies to the others too), neither neuroscience nor soccer is the most discussed topic. This conversation is by far the most frequent. “What are we getting for dinner?” “I don’t know!” All of us are from different parts of the United States and even different parts of the world, which makes our restaurant selection processes a bit tricky. Nick Maamari, an Emory NBB senior from Dubai, thinks that cheese is the most disgusting food in the world. On the other hand, Daniel Son, a Korean-American student from Portland, Oregon, enjoys eating cheese so much that he bought a slice of gouda cheese from Monoprix on the first day we arrived in Paris.

France is a country known for its cheeses. In 1962, President Charles de Gaulle said, “how can you govern a country which has two hundred and forty-six varieties of cheese?” (Mignon, 1962) Being a neuroscience student, I ask, “what happened in Nick’s brain when he ate these French cheeses?”

Nick: “Eww*1,000”

Daniel: “the more it stinks, the better it tastes!”

Disgust has been identified as a basic emotion since Charles Darwin (Rozin and Fallon, 1987). Like other emotions, disgust has a characteristic facial expression (like the one shown in Nick’s photo), an appropriate action (Nick would definitely leave a restaurant if all available food has cheese), a distinctive physiological manifestation (nausea), and a characteristic feeling state (revulsion) (Rozin and Fallon, 1987). Research has found two brain structures that are considered as neural sites for processing disgust: insular cortex and basal ganglia (Sprengelmeyer, 2007). First, let’s start with some neuroanatomy.

(Byrne & Dafny, Eds.)

The insula cortex (or insula) lies deep within the lateral sulcus (as shown above) and it sits on an island (hence the name insular) covered with frontal, parietal and temporal opercula (“the lid”). It is interconnected with many cortical regions and subcortical structures, placing it at an ideal position to integrate homeostatic information with information about the physical and external environment (Sprengelmeyer, 2007).

(Henkel, 1998)

Basal ganglia is a group of subcortical nuclei responsible primarily for motor control and other roles such as executive functions, reward and emotions (Lanciego et al.). Two major neurodegenerative disorders, Huntington’s disease, and Parkinson’s disease are caused by the hyperactivation or hypoactivation of this structure, respectively (Cepeda et al., 2014). Previous research has identified cases where patients with Huntington’s disease were unable to recognize disgust (Sprengelmeyer et al., 1998).

Numerous research has shown the role of insula and basal ganglia in mediating disgust (Sprengelmeyer, 2007). However, most previous studies have focused on the recognition of facial expressions of disgust. The reason for the lack of research on food aversion is mainly due to a great variation between how each individual perceive what food is disgusting and also due to ethical issues associated with invoking uncomfortable feelings in experiments (Royet et al., 2016). A group of French researchers narrowed down their experimental food to … guess what, cheese (Royet et al., 2016). Cheese is loved by people like Daniel and hated by people like Nick, therefore, making it a great model to study the cerebral processes of food disgust.

In the first part of the study, the authors conducted a survey of the French population (this may be a biased sample and results do not apply to the rest of the world), to evaluate individual preferences for 75 foods and estimate the proportion of individuals who are disgusted by cheese. The authors have found a higher percentage (11.5%) of people disgusted by cheese than by other types of food. Now they have a study sample of individuals expressing a deep disgust for cheese.

The second part of the study involved Functional Magnetic Resonance imaging (fMRI), which is a tool to show activations of brain regions. The participants were asked to begin their experiments in a hunger state (these poor people did not even get a full breakfast) in order to make sure that the results were not biased by different metabolic rates after a meal. The researchers first presented participants in an MRI scanner with both the image and the smell of six different types of cheese and six other control foods. The participants were asked to judge whether the smell and sight of food are pleasant or not and whether they have a strong desire to eat the food.

After analyzing their data, the researchers found that global pallidus and substantia nigra (shown above) of the basal ganglia are more activated in people who dislike cheese. The authors also found that another structure of the basal ganglia, the ventral pallidum was inactivated in individuals disgusted by cheese. These structures are involved in what’s called the “reward pathway” of the brain, which regulates our perception of pleasure and facilitates the reinforcement of a particular behavior (Berridge and Kringelbach, 2015). Taken together, the authors proposed that perhaps a modified version of the pathway for encoding reward was involved when we were presented with food that aroused strong feelings of dislike. Interestingly, the authors did not observe any differences in activation of insula in people who like or dislike cheese.

One thing to keep in mind as you read fMRI studies is that “correlation does not imply causation”. A structure active for a task does not mean it is critical for the task. Also, conclusions made in papers generally involve heavy statistics and morphing all brains of the participants, who of course, have different brain shapes and sizes (Logothetis, 2008). Therefore, research results should be interpreted cautiously.

This study fills in some gaps in the research of disgust, specifically for food. It helps us understand the role of different parts of the basal ganglia in processing disgust. The null finding of insula also supports that insula has more complicated functions than simply processing disgust. A foundation of knowledge on this topic can be applied to a wide variety of eating disorders that affects many people in our lives. I would like to end with my favorite celebrity chef, Gordon Ramsay, who must have his brain structures associated with disgust constantly activated when judging his students’ dishes!

(Schocket, 2017)

Berridge Kent C, Kringelbach Morten L (2015) Pleasure Systems in the Brain. Neuron 86:646-664.

Cepeda C, Murphy KPS, Parent M, Levine MS (2014) The role of dopamine in Huntington’s disease. Prog Brain Res 211:235-254.

Lanciego JL, Luquin N, Obeso JA Functional neuroanatomy of the basal ganglia. Cold Spring Harb Perspect Med 2:a009621-a009621.

Logothetis NK (2008) What we can do and what we cannot do with fMRI. Nature 453:869.

Royet J-P, Meunier D, Torquet N, Mouly A-M, Jiang T (2016) The Neural Bases of Disgust for Cheese: An fMRI Study. 10.

Rozin P, Fallon AE (1987) A perspective on disgust. Psychological Review 94:23-41.

Sprengelmeyer R (2007) The neurology of disgust. Brain 130:1715-1717.

Sprengelmeyer R, Rausch M, Eysel UT, Przuntek H (1998) Neural Structures Associated with Recognition of Facial Expressions of Basic Emotions. Proceedings: Biological Sciences 265:1927-1931.

Byrne, J. H., & Dafny, N. (Eds.). Neuroanatomy Online: An Electronic Laboratory for the Neurosciences. Retrieved from Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston (UTHealth):

Henkel, J. (1998). Parkinson’s Disease: New Treatments Slow Onslaught of Symptoms. FDA Consumer, 17.

Mignon, E. (1962). Les Mots du Général.

Schocket, R. (2017, September 6). This Is The Disgusting Reason Gordon Ramsay Refused To Swim In A Hotel’s Pool. Retrieved from BuzzFeed:

Would Lithium be a Good Treatment for Vincent Van Gogh?

I am not an art enthusiast, but this summer of my junior year in college has brought me closer to the life of perhaps the most famous painter in the history of western art, Vincent van Gogh. Before I traveled to Europe this summer, I watched two recent movies “Loving Vincent” and “At Eternity’s Gate” that were made based on the life of Vincent van Gogh. My summer started in the Netherlands, and I traveled down to Belgium, Paris, and Provence. This route coincidentally followed van Gogh’s path of mental deterioration, which eventually ended with his suicide in 1890 at the age of 37.

Self Portrait (1887), Rijksmuseum, Amsterdam

Van Gogh Self Portrait (1889), Musée d’Orsay, Paris

Garden of the Hospital in Arles (1889), Espace van Gogh, Arles
Van Gogh was committed after the infamous episode of cutting off his left earlobe in December 1888.

The mental state of van Gogh has long been a subject of controversy. Three years ago, mental health doctors and art history experts came together at the Van Gogh Museum in Amsterdam to find a diagnosis for him (Siegal, 2016). (Read more at After having a thorough examination of the medical record of his case as well as personal letters, the doctors failed to come to the conclusion of a single diagnosis. Though there might be more than one illness van Gogh has suffered in his life, most analytics, including American Psychiatrist Dietrich Blumer, agree on that van Gogh has displayed many symptoms of bipolar disorder (Blumer, 2002).

Professor Isabella Perry first assigned van Gogh with a diagnosis of bipolar disease (Perry, 1947). People with bipolar disease have recurrent episodes of elevated mood and depression, together with changes in activity levels (Anderson, Haddad, & Scott, 2012). Van Gogh’s life has been also associated with periods of intense activity and depression (Perry, 1947). Bipolar disease is the 6th leading cause of disability worldwide and has a prevalence of about 1-3% of our general population (Moreira, Van Meter, Genzlinger, & Youngstrom, 2017). This particular psychiatric illness has also been linked with creative accomplishment and many names in the history of creative art. Writers Ernest Hemingway, Virginia Woolf, Composer Robert Schumann, Painter Jackson Pollock and most likely Vincent van Gogh are all among the list (Rothenberg, 2001).

Lithium has been used as the main treatment for bipolar disease for the last sixty or more years (Won & Kim, 2017). Lithium has also been demonstrated to reduce suicide rates and prevent manic episodes in bipolar disease patients (Anderson et al., 2012). However, only one-third of bipolar disorder patients respond to the treatment. Why this treatment works in some patients and does not work in other patients is unknown (Tobe et al., 2017). Although the therapeutic pathways of lithium are complex, through recent research, lithium’s exact mechanism is progressively being clarified. It is becoming more evident that biological systems modulated by lithium are deeply intertwined with biological disruptions associated with bipolar disorder (Won & Kim, 2017).

A recent study published in PNAS used stem cells (cells that can differentiate into other cell types) to unravel lithium’s target and therefore gave the scientists an opportunity to look deeply into the cellular mechanism of bipolar disorder. In this article, the authors have cleverly used lithium, the most common treatment for bipolar disorder, as their “molecular can-opener for prying intracellularly to reveal otherwise inscrutable pathophysiology” in bipolar disorder. They mapped the “lithium-response pathway” which functions to govern the phosphorylation of a protein called CRMP2 involved in the neural network. Normally, the “tug-of-war” between the inactive state (phosphorylated) and active state (non-phosphorylated) is all done physiologically inside our brain. In bipolar disease patients, this “set-point” has gone all wrong. So, the role of lithium is to operate as a “referee” to normalize that set-point (Tobe et al., 2017). Though the “lithium-response pathway” is certainly not a complete picture of bipolar disorder, it helped us to gain significant insights into how lithium modulates our body and alleviate symptoms for patients with the disease.

(Watch Principal Investigator Evan Snyder explains this study)

Psychiatrist Albert Rothenberg argued in his paper that research has shown that lithium treatment has the risk of cognitive impairment and decreased productivity. Another impediment is that many creative people hold the false belief that there is an intrinsic connection between suffering and mental illness. Some believe that tampering with their illness will also destroy their creative talents. And therefore, non-compliance with the doctor’s prescription is fairly common (Rothenberg, 2001). Even if van Gogh had treatment available, whether he would have complied remains questionable.

So, to answer my question raised in the title of this blog post, yes, lithium could have been a useful treatment. But considering the fact that only a third of patients respond to treatments and also the fact that van Gogh had a history of drinking absinthe regularly, lithium would not a magical pill that will fix all the problems with him. By focusing our research on the molecular mechanism of lithium on bipolar disorder, we would be able to map out bipolar disorder in the brain and help these people suffering from this disease. Who knows, the next van Gogh might be among them.


Anderson, I. M., Haddad, P. M., & Scott, J. (2012). Bipolar disorder. 345, e8508. doi:10.1136/bmj.e8508 %J BMJ : British Medical Journal

Blumer, D. (2002). The Illness of Vincent van Gogh (Vol. 159).

Moreira, A. L. R., Van Meter, A., Genzlinger, J., & Youngstrom, E. A. (2017). Review and Meta-Analysis of Epidemiologic Studies of Adult Bipolar Disorder. The Journal of clinical psychiatry, 78(9), e1259-e1269. doi:10.4088/jcp.16r11165

Perry, I. H. (1947). VINCENT VAN GOGH’S ILLNESS: A Case Record. Bulletin of the History of Medicine, 21(2), 146-172.

Rothenberg, A. J. P. Q. (2001). Bipolar Illness, Creativity, and Treatment. 72(2), 131-147. doi:10.1023/a:1010367525951

Tobe, B. T. D., Crain, A. M., Winquist, A. M., Calabrese, B., Makihara, H., Zhao, W.-n., . . . Snyder, E. Y. (2017). Probing the lithium-response pathway in hiPSCs implicates the phosphoregulatory set-point for a cytoskeletal modulator in bipolar pathogenesis. 114(22), E4462-E4471. doi:10.1073/pnas.1700111114 %J Proceedings of the National Academy of Sciences

Won, E., & Kim, Y.-K. (2017). An Oldie but Goodie: Lithium in the Treatment of Bipolar Disorder through Neuroprotective and Neurotrophic Mechanisms. 18(12), 2679.

What Happens to Olivier Giroud’s Brain after He Broke my Heart?

On Wednesday night, along with some friends, I went to the Mazet bar in the 6th Arrondissement of Paris to watch some soccer.

The Mozet (61 Rue Saint-André des Arts, 75006 Paris)

It was the night of Europa League final and two rivalries from London, Arsenal and Chelsea were facing each other. Being a huge Arsenal fan since middle school, I was very nervous about the game. Olivier Giroud, a French footballer who plays as a forward for Chelsea broke the deadlock after half time by scoring a header that ultimately led to Chelsea winning the Europa League this season. At the end of the game, I felt disappointed and miserable looking at the scoreboard, Chelsea 4 – 1 Arsenal.

Embed from Getty Images

As an amateur soccer player myself, I know in order to score such a header, both power and precision during the impact with the ball are crucial. Though it may seem effortless when a professional footballer heads the ball, it is in fact quite painful for a non-athlete like me who do not know how to control a header well. Being a neuroscience student, this got me thinking that perhaps there are some negative consequences to the brains as these professional soccer players head the ball almost every single day, both on-pitch and off-pitch.

I first heard about Chronic Traumatic Encephalopathy (CTE) in the 2015 movie starring Will Smith as Dr. Bennet Omalu. Dr. Omalu first found CTE in American football players when he performed an autopsy on former Pittsburgh Steelers center Mike Webster in 2002 (Omalu et al., 2005).

This disease has been observed in athletes with a history of repetitive brain trauma and symptoms include memory disturbances, behavioral and personality changes, parkinsonism and speech and gait abnormalities (McKee et al., 2009). Currently, CTE has been associated with several pathological hallmarks. One of them is neurofibrillary tangles of tau deposition, which is as a marker of Alzheimer’s Disease (McKee et al., 2009). In other words, the protein tau becomes abnormal and is now unable to carry out its normal job to facilitate forming microtubules (Kadavath et al., 2015), the “conveyor belt” of nerve cells.

So, does heading in soccer lead to this disease? This is a tough question to answer. The main reason is that CTE does not have a definite diagnosis prior to autopsy. Therefore, there is a very limited study sample to test this question and we have to rely heavily on case studies. One famous case was Brazilian captain and two-times FIFA world cup winner, Hilderaldo Bellini. With no history of concussion, he died at the age of 83 and examination by the doctor revealed widespread CTE (Grinberg et al., 2016).

Bellini has a statue at the entrance of Maracanã, one of the most important soccer stadiums in the world. Rio de Janeiro, Brazil

One neuroimaging study has identified thinning of the cerebral cortex in former professional soccer players when compared against former non-contact athletes. The cerebral cortex is the outer layer of neural tissue of our brain and is involved heavily in memory, attention, perception, etc. (Penfield & Rasmussen, 1950). The authors have also found that thinning of the cortex was tied to how many times the players have headed the ball in their career. Cortical thinning was also related to a decrease in cognitive performance and hence concluded that maybe these “sub-concussive head impact” of headings in soccer are not so good at all (Koerte et al., 2016). However, one thing to note is that a self-report survey was used to obtain a rough estimate of how many times the players headed the ball in their career. As a result, the exact forces and the exact frequency of heading the ball were not considered (Koerte et al., 2016).

Prof Henrik Zetterberg is a world-leading expert in developing biomarkers for Alzheimer’s disease and whom my lab at Emory had the honor to collaborate in several studies. He did a study to look at the evidence in neurochemical fluctuations immediately after study participants head the balls. Results demonstrate that headings in soccer do not have a short-term biochemical sign of neuronal injury.  They have further suggested that the effect of heading in soccer seems to be quite different from that caused by head punches in boxing (Zetterberg et al., 2007).

After looking at a case study, an imaging study, and a neurochemical study, it seems that both positive and negative findings exist. A review of the current scientific literature demonstrates that the effects of heading the ball and connection to CTE remain inconclusive (Grinberg et al., 2016). Though there is evidence of a relationship between heading and abnormal brain structure, most data is still preliminary (Rodrigues, Lasmar, & Caramelli, 2016). As for now, it is not yet the right time to think about banning heading the ball completely in soccer. It’s a great part of this sport that as soccer fans we all love. However, I think the recommendation by the U.S. Youth Soccer is very valid. Only kids after age 10 should be taught heading and heading in game should be delayed until they have both the skill and physical maturity (Nitrini, 2017). If you are a parent ready to take your child to their soccer game this weekend, maybe consider this advice.


Grinberg, L. T., Anghinah, R., Nascimento, C. F., Amaro, E., Leite, R. P., Martin, M. d. G. M., . . . Nitrini, R. (2016). Chronic Traumatic Encephalopathy Presenting as Alzheimer’s Disease in a Retired Soccer Player. Journal of Alzheimer’s disease : JAD, 54(1), 169-174. doi:10.3233/JAD-160312

Kadavath, H., Hofele, R. V., Biernat, J., Kumar, S., Tepper, K., Urlaub, H., . . . Zweckstetter, M. (2015). Tau stabilizes microtubules by binding at the interface between tubulin heterodimers. 112(24), 7501-7506. doi:10.1073/pnas.1504081112 %J Proceedings of the National Academy of Sciences

Koerte, I. K., Mayinger, M., Muehlmann, M., Kaufmann, D., Lin, A. P., Steffinger, D., . . . Behavior. (2016). Cortical thinning in former professional soccer players. 10(3), 792-798. doi:10.1007/s11682-015-9442-0

McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., . . . Stern, R. A. (2009). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury. Journal of Neuropathology & Experimental Neurology, 68(7), 709-735. doi:10.1097/NEN.0b013e3181a9d503 %J Journal of Neuropathology & Experimental Neurology

Nitrini, R. (2017). Soccer (Football Association) and chronic traumatic encephalopathy: A short review and recommendation. Dementia & neuropsychologia, 11(3), 218-220. doi:10.1590/1980-57642016dn11-030002

Omalu, B. I., DeKosky, S. T., Minster, R. L., Kamboh, M. I., Hamilton, R. L., & Wecht, C. H. (2005). Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery, 57(1), 128-134. doi:10.1227/01.NEU.0000163407.92769.ED %J Neurosurgery

Penfield, W., & Rasmussen, T. (1950). The cerebral cortex of man; a clinical study of localization of function. Oxford, England: Macmillan.

Rodrigues, A. C., Lasmar, R. P., & Caramelli, P. (2016). Effects of Soccer Heading on Brain Structure and Function. 7(38). doi:10.3389/fneur.2016.00038

Zetterberg, H., Jonsson, M., Rasulzada, A., Popa, C., Styrud, E., Hietala, M. A., . . . Blennow, K. (2007). No neurochemical evidence for brain injury caused by heading in soccer. British journal of sports medicine, 41(9), 574-577. doi:10.1136/bjsm.2007.037143

Images Citation

Regan, Michael (2019). Olivier Giroud of Chelsea scores his team’s first goal.    [Photograph], Retrieved 21:08, June 4, 2019, from

File:Estátua do Bellini2.jpg. (2017, December 31). Wikimedia Commons, the free media repository. Retrieved 21:08, June 4, 2019 from