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Neuro MythBusters: The truth behind 10 common myths about your brain

Neuro MythBusters: The truth behind 10 common myths about your brain

September 13, 2023 | by Catrina Hacker, PennNeuroKnow and IAES Collaboration

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Many people find neuroscience fascinating because learning about our brains teaches us about ourselves. Unfortunately, popular interest in brain research has led to several pervasive myths that misrepresent how our brains work. Combatting these neuromyths is difficult because the truth is often much more complicated than the myth and buried in intimidating scientific literature. However, correcting misconceptions about how our brains work can have important benefits for our everyday lives. In this post I’ll break down what some of these neuromyths claim, where they came from, whether there’s any truth behind them, and why we should care about correcting them.

Myth #1: Humans only use 10% of our brains.

This is arguably the most common neuromyth1, inspiring movies like Limitless (2011) and Lucy (2014) in which characters gain superhuman abilities by tapping into the large unused portions of their brains. It’s appealing to think that we all have potential superpowers sitting in our brains waiting to be unleashed, but there’s nothing to support this claim. The reality is that neuroscientists observe activity throughout the entire brain.

While nobody is certain where it came from, some believe that this myth originates from work done by neuroscientist Wilder Penfield in the 1930s1. Penfield was a neurosurgeon who studied the effects of stimulating the brains of patients undergoing neurosurgery to learn what each part of the brain was responsible for. He found that stimulating a large portion of the brain didn’t cause any noticeable effect2, meaning he could not learn what its function might be. However, new and less invasive methods of recording brain activity show that these “silent” parts of the brain are actually active. In fact, a network of brain regions called the default mode network is even active when we are at rest3.

The bottom line: We use 100% of our brains.

Why it matters: The number of drugs and treatments that claim to enhance brain function, collectively called neuroenhancers, is on the rise. While we can always learn and grow, understanding that there is no “hidden” brain waiting to be unlocked can protect you from wasting your money.

Myth #2: Right-brained people are creative while left-brained people are analytical.

The idea that you can be either right-brained or left-brained has captured the attention of people on social media and even teachers in classrooms. It’s tempting to think that people can be categorized so easily and that differences can be attributed to our brains, but the truth isn’t that simple. While people can tend to be more creative than analytical or vice versa, those differences cannot be explained by dominance of one half of the brain over the other4.

This myth has been tricky to combat because there is some important truth behind it. There are some differences between the two halves of your brain, but creativity versus logical reasoning isn’t one of them. Your brain has two hemispheres, left and right, that communicate via a bundle of neural connections called the corpus callosum. While almost everything we do involves communication between the two halves of our brain, sometimes one half of the brain contributes a little more than the other. For example, the left hemisphere typically takes the lead in language processing5, the right hemisphere seems to play an especially important role in visual attention6, and the left and right hemispheres might do slightly different things to aid in face processing7. Things like creativity and emotional processing rely on both hemispheres and complicated networks of brain activations8,9.

The bottom line: Being right-brained or left-brained can’t explain why some people are more creative than others, but there are some differences in what your left and right hemispheres do when it comes to things like language, attention, and face recognition.

Why it matters: Categorizing people as one thing or another (left-brained or right-brained) is restrictive and ultimately harmful. Many “logical” tasks require creativity and “creative” tasks require logic. If teachers, mentors, and bosses make these assumptions about members of their teams or classrooms they risk mischaracterizing people or preventing them from working up to their true potential.

Myth #3: Listening to Mozart makes babies smarter.

This neuromyth, sometimes called the “Mozart effect”, started in 1991 when Alfred Tomatis shared his thoughts about how listening to Mozart could help children with speech and auditory disorders10. When a group of researchers showed in 1993 that listening to 10 minutes of Mozart’s K. 448 improved college students’ ability to visualize and manipulate mental images11, the media took this result and ran with it. The effects in the original study only lasted 10 to 15 minutes and only impacted mental manipulation of images, but the media wrote about general boosts to intelligence and implied that they lasted much longer. Despite the original study being done with college students, the myth was somehow generalized to include babies. Several studies published since 1993 have provided alternate explanations for the original result or have failed to replicate it while studying the same or different skills12.

Although listening to Mozart can’t make you smarter, there is some truth behind this myth. Stimulating an infant’s brain helps with their development, but activities like direct interactions with a parent, reading a book, or talking and singing with an infant are much more effective13,14. When it comes to music, passively listening might not impact development, but learning to play an instrument positively impacts a child’s cognitive abilities and their performance in school15.

The bottom line: Listening to Mozart doesn’t make babies smarter, but stimulation from things like singing to your child is an important part of their development, and children who learn to play an instrument tend to perform better in school.

Why it matters: Belief in the Mozart effect and similar claims led many people to show their children the popular Baby Einstein videos in the early 2000s. However, in 2007 a study showed that not only did viewing these baby DVDs not improve children’s intelligence, children who watched the videos tended to have a worse vocabulary than other children16.

Myth #4: Everybody has a distinct style in which they learn best.

Many people have memories like mine of being asked if they are a visual, auditory, or kinesthetic learner as a child. You may even have filled out a survey to learn what your learning style is. Even today, many teachers collect this information and personalize their teaching to each student’s supposed learning style. While this seems logical, there is no evidence that each person has a specific learning style in which they learn best17,18, and some research suggests that teaching to learning styles is more harmful than helpful19. While it’s true that people vary in ability on different kinds of tasks and that teachers should work with students as individuals to help them succeed, when “visual learners” are tasked with learning through auditory tasks, they do just as well19.

The bottom line: Everybody has different preferences, but matching teaching to a preferred learning style does not improve learning.

Why it matters: It is a waste of time and resources to focus on tailoring education to preferred learning styles when it has no impact on learning. In fact, teaching based on learning styles might actually harm students by limiting them to certain modalities and subjects that match their learning style and discouraging them from exploring20.

Myth #5: Your handwriting reveals aspects of your personality.

The use of handwriting to learn about someone’s personality is called graphology. Graphology became popular in the late 1800s, with German scientist William Preyer commenting that handwriting is “brain writing”21,22. Despite its dubious scientific validity, graphology was used to make decisions about a person’s value to society, such as in determining whether a person was trustworthy or a criminal. Fortunately, modern experiments have conclusively shown that handwriting cannot predict a person’s personality. In controlled settings, graphologists are no better at using a person’s handwriting to make judgments about them than if they were guessing23. However, many people still believe that aspects of a person’s personality can be learned from their handwriting, and some computer scientists are still trying to build computer models that can predict things like criminality and work ethic from handwriting24, repeating the mistakes of the past.

Despite the dubious link between handwriting and personality, there are some reliable links between handwriting and brain health. Our brains control the muscles that move as we write, and some neurological disorders can cause changes in the brain that impact handwriting21. For example, one early symptom of Parkinson’s Disease can be small, cramped handwriting25. For this and related disorders, handwriting can act as a window into brain health and an early warning sign that can lead to faster care and better outcomes.

The bottom line: A person’s handwriting cannot reliably predict their personality, but changes to handwriting can be early signs of neurological disorders like Parkinson’s Disease.

Why it matters: Despite there being no connection between a person’s handwriting and their personality, in 2017 then President Donald Trump tweeted about being able to tell from his handwriting that former United States Secretary of the Treasury, Jack Lew, “is secretive”22. Some scientists are still trying to build tools that can determine a person’s personality based on their handwriting to help with hiring decisions24. Without widespread acceptance that handwriting cannot predict personality, we risk repeating the mistakes of the past and using handwriting to unfairly discriminate against certain people.

Myth #6: A common sign of dyslexia is seeing letters backwards.

Dyslexia, characterized by difficulty reading, affects an estimated 20% of the population and is the most common neuro-cognitive disorder26. It is a popular misconception that a common sign of dyslexia is seeing words and letters backwards. People with dyslexia don’t see words and letters backwards, but they do have difficulty naming letters and words (think saying “was” while reading “saw”)27. When it comes to writing, there is some evidence that dyslexic children may be more likely than others to write letters and words backwards, a phenomenon called reversals. However, reversals are common in all children learning to read and write28, and not all children with dyslexia make reversals29.

There are many other reliable indicators that a person may have dyslexia. The signs of dyslexia change throughout a lifetime and range from preschool children who struggle to identify the letters in their names to high school students who struggle to read unfamiliar words30. Visit this fact page from the Yale Center for Dyslexia & Creativity for a full list of signs of dyslexia for all age groups.

The bottom line: Dyslexic children don’t see letters backwards, although they may read and write letters backwards. However, not all dyslexic readers write letters backwards and not all children who write letters backwards are dyslexic.

Why it matters: If parents and educators expect dyslexic children to describe seeing letters backwards or adults think they must see letters backwards to have dyslexia, then many people could go undiagnosed and not get the support they need to succeed.

Myth #7: Human memory works like a camera, perfectly recording what you experience.

As a child, one of my favorite book series starred Cam Jansen, a fifth grader who solves mysteries utilizing her flawless photographic memory. Any time she wanted to remember something she would say “click” and it would be perfectly captured in her memory. As an adult, I’ve watched plenty of TV shows and movies featuring similar characters who can use their perfect memory to save the day. Unfortunately, this kind of memory doesn’t exist outside books and other media.

For the rest of us here on earth, our brains forget and fill in details of our memories, even when we feel certain we remember things perfectly. A great example of this is the visual Mandela effect, wherein people consistently report strong false memories of things like whether Curious George has a tail or the Monopoly man wears a monocle (neither is true, but people consistently believe that they are)31. In general, it’s a good thing that our brains work in this imperfect way. We don’t want to get bogged down with irrelevant details of memories, so our brains act as a filter, prioritizing memory for the things that matter most and filling in the details and moments that are less important.

If our memory is so imperfect, where does the idea of photographic memory come from? This myth might have started after psychologist Ralph Haber noticed that a small percentage of children seemed to be able to hold pictures in their mind’s eye for seconds or minutes after they were removed from sight32. He called this kind of memory eidetic memory (often used interchangeably with “photographic memory” in popular media). However, these studies only looked at memory for short periods of time, and later research demonstrated that this “memory” is far from perfect33

The bottom line: Some people can remember things better or longer than others, but nobody’s memory works like a camera.

Why it matters: Our criminal justice system still relies heavily on eyewitness reports. If police officers, lawyers, and jurors don’t realize that memory is flawed, they risk inflating the value of this kind of testimony and incarcerating innocent people34.

Myth #8: People with bigger brains are smarter.

We’ve all heard or used the term “big-brained” to describe someone who does something smart, but the size of their brain has nothing to do with their intellect. If size was all that mattered, then elephants, whose brains are 3x heavier than ours, would be 3x smarter than us35. Even if we’re just looking at human brains, Albert Einstein’s brain was no bigger than average, and despite years of studying his brain, neuroscientists haven’t found any clear differences in its structure compared to other human brains36.

The myth that smarter people have bigger brains has a particularly harmful history. In the 1800s, scientists measured the skulls of people of different races and genders as an estimate of brain size to provide “scientific” evidence that Caucasian men were superior to women and other races. There are many reasons this approach was flawed, not least of which is that correcting for body size can account for many of the reported differences37. In 1898, a woman named Alice Lee challenged this idea by storming into the all-male meeting of the Anatomical Society at Trinity College Dublin, measuring the skulls of several prominent men in the audience, and demonstrating that many of these supposedly intelligent men had rather small skulls38.

Read my previous post, “The Problem of Brain Size”, for a more detailed look at this myth.

The bottom line: Brain size has nothing to do with intelligence.

Why it matters: Flawed measurements of brain size have historically been used as scientific “proof” that women and racial minorities are not as intelligent as Caucasian men. Dispelling this myth is critical to reverse the harm done by the claims made in these studies and to prevent making the same mistakes in the future.

Myth #9: Playing brain games makes you smarter.

We’ve all seen ads for games that claim to train your brain to make you smarter, or measure your IQ. However, these claims are misleading and overinflated. One study conclusively proved this by having over 11,000 people play online brain games for six weeks. At the end of the six weeks, people had gotten a little better at the specific games that they played, but they were no better at any other tests39. In other words, playing one memory game could make people better at that game, but it didn’t improve their memory overall.

In 2016, the brain game company Lumosity paid a $2 million settlement to the Federal Trade Commission (FTC) who filed false advertising charges against them40. The FTC asserted that Lumosity’s claims that playing their games could improve performance on everyday tasks, delay age-related cognitive decline, and reduce the effects of brain injuries like stroke were unfounded. Since the settlement, Lumosity has been forced to alter their claims so that they do not mislead consumers.

The bottom line: Playing brain games makes you better at those particular games, but not any smarter overall.

Why it matters: Before investing time and money into products that claim to improve brain function by playing fun brain training games, it’s important to understand that these effects are often small and improve performance on specific tasks, but don’t generalize.

Myth #10: Different regions of your tongue are specialized for different kinds of tastes.

There are five basic tastes: bitter, salty, sour, sweet, and umami41. The myth goes that there are different parts of your tongue that are specialized to sense different tastes, so sweet and salty tastes are sensed on the tip of your tongue, while bitter tastes are sensed toward the back. I remember learning this myth for the first time at a girl scout meeting where we tasted different foods by placing them on different parts of our tongue. Since then, I heard it repeated many times in school and even in some of my neuroscience classes as an undergrad. In fact, many textbooks that are still being used today include this false claim. However, the truth is that although some parts of the tongue might be more sensitive to one taste or another, all five basic tastes are sensed across the entire tongue42.

The tongue map myth started with a 1901 paper in which German scientist David Hänig measured how much taste sensitivities changed across the tongue. He noticed that some parts of the tongue were more sensitive to a particular taste than others, and he drew some graphs to show how those sensitivities changed across the tongue. In 1940, another scientist adapted these graphs for a book about the different senses. In his adaptation, he simplified things by showing a single taste that was most sensitive on each part of the tongue rather than the relative sensitivities of each taste. This gave the false impression that each region of the tongue could sense just one taste, and this oversimplified figure has been copied thousands of times into science textbooks to teach the neuroscience of taste.

The bottom line: Sensitivity to each taste varies somewhat across the tongue, but each part of the tongue senses all the basic tastes.

Why it matters: The negative consequences of this myth might not be as harmful as the others, but it’s always worth correcting our understanding of ourselves and our bodies.

Now that you’ve learned the truth behind 10 popular neuromyths, it’s worth asking how so many neuromyths have leaked into popular press and what we can do to prevent them in the future. Preventing the spread of disinformation about the brain starts at all levels. Scientists should be careful not to overgeneralize or oversimplify their findings and to always consider alternative explanations and how their work might be misinterpreted. Journalists and science communicators should carefully report the results of scientific studies and not overstate what a given experiment shows. Non-scientists should think critically about what they read, and fact check things they read from unknown sources on social media. And most importantly, now that you know the truth behind the myth, the best thing you can do is to teach it to others who still believe in these popular neuromyths.


1.         Jarrett, C. All You Need To Know About the 10 Percent Brain Myth, in 60 Seconds. Wired.

2.         Ferrier Lecture – Some observations on the cerebral cortex of man. Proc. R. Soc. Lond. Ser. B – Biol. Sci. 134, 329–347 (1947).

3.         Raichle, M. E. The Brain’s Default Mode Network. Annu. Rev. Neurosci. 38, 433–447 (2015).

4.         Nielsen, J. A., Zielinski, B. A., Ferguson, M. A., Lainhart, J. E. & Anderson, J. S. An Evaluation of the Left-Brain vs. Right-Brain Hypothesis with Resting State Functional Connectivity Magnetic Resonance Imaging. PLoS ONE 8, e71275 (2013).

5.         Bradshaw, A. R., Thompson, P. A., Wilson, A. C., Bishop, D. V. M. & Woodhead, Z. V. J. Measuring language lateralisation with different language tasks: a systematic review. PeerJ 5, e3929 (2017).

6.         Chica, A. B. et al. Attention networks and their interactions after right-hemisphere damage. Cortex 48, 654–663 (2012).

7.         Meng, M., Cherian, T., Singal, G. & Sinha, P. Lateralization of face processing in the human brain. Proc. R. Soc. B Biol. Sci. 279, 2052–2061 (2012).

8.         Amir, O. & Biederman, I. The Neural Correlates of Humor Creativity. Front. Hum. Neurosci. 10, (2016).

9.         Fossati, P. Neural correlates of emotion processing: From emotional to social brain. Eur. Neuropsychopharmacol. 22, S487–S491 (2012).

10.      Tomatis, Alfred. Pourqoi Mozart? (Diffusion, Hachette, 1991).

11.      Rauscher, F. H., Shaw, G. L. & Ky, K. N. Music and spatial task performance. Nature 365, (1993).

12.      Cong, A. FROM MOZART TO MYTHS: Dispelling the ‘Mozart Effect’. Young Sci. J. 49–53 (2014).

13.      California Childcare Health Program, UCSF School of Nursing. Building Baby’s Intelligence: Why Infant Stimulation Is So Important. (2002).

14.      Walker, S. P. et al. Cognitive, psychosocial, and behaviour gains at age 31 years from the Jamaica early childhood stimulation trial. J. Child Psychol. Psychiatry 63, 626–635 (2022).

15.      Román-Caballero, R., Vadillo, M. A., Trainor, L. J. & Lupiáñez, J. Please don’t stop the music: A meta-analysis of the cognitive and academic benefits of instrumental musical training in childhood and adolescence. Educ. Res. Rev. 35, 100436 (2022).

16.      Zimmerman, F. J., Christakis, D. A. & Meltzoff, A. N. Associations between Media Viewing and Language Development in Children Under Age 2 Years. J. Pediatr. 151, 364–368 (2007).

17.      Pashler, H., McDaniel, M., Rohrer, D. & Bjork, R. Learning Styles: Concepts and Evidence. Psychol. Sci. Public Interest 9, 105–119 (2008).

18.      Cuevas, J. Is learning styles-based instruction effective? A comprehensive analysis of recent research on learning styles. Theory Res. Educ. 13, 308–333 (2015).

19.      Riener, C. & Willingham, D. The Myth of Learning Styles. Change Mag. High. Learn. 42, 32–35 (2010).

20.      Newton, P. M. & Salvi, A. How Common Is Belief in the Learning Styles Neuromyth, and Does It Matter? A Pragmatic Systematic Review. Front. Educ. 5, 602451 (2020).

21.      The Telltale Hand. Dana Foundation

22.      Trubek, A. Sorry, Graphology Isn’t a Real Science. JSTOR Daily (2017).

23.      Dazzi, C. & Pedrabissi, L. Graphology and Personality: An Empirical Study on Validity of Handwriting Analysis. Psychol. Rep. 105, 1255–1268 (2009).

24.      Bandhu, K. C., Litoriya, R., Khatri, M., Kaul, M. & Soni, P. Integrating graphology and machine learning for accurate prediction of personality: a novel approach. Multimed. Tools Appl. (2023) doi:10.1007/s11042-023-15567-8.

25.      Small Handwriting | Parkinson’s Foundation.

26.      Dyslexia FAQ. Yale Dyslexia

27.      Shaywitz, S. E. & Shaywitz, B. A. Dyslexia (Specific Reading Disability).

28.      Cornell, J. M. Spontaneous mirror-writing in children. Can. J. Psychol. Rev. Can. Psychol. 39, 174–179 (1985).

29.      Brooks, A. D., Berninger, V. W. & Abbott, R. D. Letter Naming and Letter Writing Reversals in Children With Dyslexia: Momentary Inefficiency in the Phonological and Orthographic Loops of Working Memory. Dev. Neuropsychol. 36, 847–868 (2011).

30.      Signs of Dyslexia. Yale Dyslexia

31.      Prasad, D. & Bainbridge, W. A. The Visual Mandela Effect as Evidence for Shared and Specific False Memories Across People. Psychol. Sci.

32.      Haber, R. N. Twenty years of haunting eidetic imagery: where’s the ghost? Behav. Brain Sci. 2, 583–594 (1979).

33.      Gray, C. R. & Gummerman, K. The Enigmatic Eidetic Image: A Critical Examination of Methods, Data, and Theories.

34.      Report Urges Caution in Handling and Relying Upon Eyewitness Identifications in Criminal Cases, Recommends Best Practices for Law Enforcement and Courts | National Academies.

35.      Herculano-Houzel, S. et al. The elephant brain in numbers. Front. Neuroanat. 8, (2014).

36.      Hines, T. Neuromythology of Einstein’s brain. Brain Cogn. 88, 21–25 (2014).

37.      Gould, S. The Mismeasure of Man. (WW Northon & Company, 1996).

38.      McNeill, L. The Statistician Who Debunked Sexist Myths About Skull Size and Intelligence. Smithsonian Magazine

39.      Owen, A. M. et al. Putting brain training to the test. Nature 465, 775–778 (2010).

40.      Lumosity to Pay $2 Million to Settle FTC Deceptive Advertising Charges for Its “Brain Training” Program. Federal Trade Commission (2016).

41.      sarah. Accounting for taste. Curious (2016).

42.      Caballar, R. D. Do Different Parts of the Tongue Taste Different Things?

Cover photo made by Catrina Hacker in using image by GraphicMama-team from Pixabay.


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When Your Brain is on Fire

When Your Brain is on Fire

brain on fire

January-22-2020 | Carolyn Keating, PennNeuroKnow

Imagine you’re a bright twenty-something with a new job and a new relationship.  Everything seems to be going your way until you start becoming paranoid and acting erratically.  Then come the hallucinations and seizures.  You’re admitted to a hospital where you’re (incorrectly) diagnosed with a psychiatric disorder.  You swing from violence into a state of immobility and stupor.  And perhaps even scarier?  You don’t remember any of it.  Sound like a nightmare?  Well, it actually happened to Susannah Calahan, who details her terrifying story first-hand in her 2012 book Brain on Fire: My Month of Madness.

What caused these frightening symptoms?  The answer was a disease that had only been discovered a few years earlier (right here at Penn!): NMDAR encephalitis.  There are four main phases of the disorder.  In the prodromal phase, many but not all patients experience a flu-like illness for up to 3 weeks.  The psychotic phase is accompanied by delusions, auditory and visual hallucinations, depression, paranoia, agitation, and insomnia.  At this stage, most patients are taken to the hospital, where around 40% are misdiagnosed as having a psychiatric disorder like schizophrenia.  As this phase progresses, seizures are very common (although they can occur at any time throughout the illness), as well as involuntary muscle movements like lip-smacking or grimacing, catatonia (muscular rigidity and mental stupor), impaired attention, and memory loss.  The next phase is unresponsiveness, which includes symptoms like the inability to speak, loss of voluntary movement, and sometimes abnormal muscle contractions that cause involuntary writhing movements.  The last phase is the hyperkinetic phase and is characterized by instability of involuntary bodily functions such as breathing, blood pressure, heartbeat, and temperature.  Many patients who breathe too slowly often need to be placed on a ventilator at this stage. The decline to ventilator support can progress very rapidly after several weeks in the psychotic stage, and ultimately patients can be hospitalized for several months with the disease1–3.

What does NMDAR encephalitis actually mean?  This disease is an autoimmune disorder, meaning the body’s immune system mistakenly attacks its own healthy cells.  Normally the body identifies foreign substances by making something called an antibody that recognizes a unique part of the invader, thus targeting it for attack and destruction.  In NMDA encephalitis though, the immune system attacks the brain (that’s where to term encephalitis comes from), specifically a type of neurotransmitter receptor called an NMDA receptor (NMDAR).  These receptors bind the neurotransmitter glutamate, and play an important role in learning, memory, cognition, and behavior.  In fact, the symptoms of NMDAR encephalitis resemble those caused by drugs such as ketamine or PCP that prevent the activation of NMDARs.  For instance, at low doses ketamine and PCP cause paranoia, false perceptions, and impaired attention (like the early stages of NMDAR encephalitis), and at higher doses these drugs cause psychosis, agitation, memory and motor disturbances, and eventually unresponsiveness, catatonia, and coma2.  Several mechanisms have been proposed to explain the symptoms caused by antibodies targeting the NMDAR, but most of the evidence seems to support the idea that the receptors get removed from the cell surface and internalized.  For instance, experiments in the laboratory demonstrate that when animal neurons grown in a dish are exposed to patients’ anti-NMDAR antibodies, the number of NMDARs on the cell surface decreases as the amount of antibodies increase.  When the antibodies are removed, the number of NMDAR receptors on the cell surface returns to baseline within 4 days1.

It’s easy to remove antibodies in a dish, but how do doctors get the body to stop producing antibodies against itself?  Step one is identifying what triggers antibody production in the first case.  Interestingly, NMDAR encephalitis predominantly affects women, and ovarian teratomas (a type of tumor made up of multiple types of tissues, which can include nervous system tissue) are responsible for 50% of cases in young women2.  In patients who have some sort of tumor, removal improves symptoms in 75% of cases.  Interestingly, herpes simplex virus can also cause encephalitis (inflammation of the brain), and about 20% of these patients also develop antibodies against NMDAR2.  Treatment consists of immunotherapy: corticosteroids, IV infusion of immunoglobulins, and/or plasma exchange1, however patients with a viral trigger tend to be less responsive to treatment than those with a teratoma trigger or the 50% of patients with an unknown trigger2.  Once treatments begin improvements in symptoms start within a few weeks, though return to baseline functioning can take up to three years.  Rehabilitation is required for many patients after they leave the hospital.  Deficits in attention, memory, and executive function may linger for years, but luckily over 75% of patients with the disease recover to at or near baseline neurological functioning1.

Doctors and scientists hope to develop new treatments involving immunotherapy combined with small molecules that are able to access the brain to directly combat the effects of anti-NMDAR antibodies, ideally leading to faster control of symptoms and shorter recovery time2.  A brand new animal model of the disease was just described last week that will hopefully lead to more discoveries about how the disease is triggered and potential new therapies4.  And with increased awareness of autoimmune disorders against the brain, doctors will be able to more quickly correctly diagnose patients with this illness and get them the treatment they need.


  1. Venkatesan, A. & Adatia, K. Anti-NMDA-Receptor Encephalitis: From Bench to Clinic. ACS Chem. Neurosci. 8, 2586–2595 (2017).
  2. Dalmau, J. NMDA receptor encephalitis and other antibody-mediated disorders of the synapse: The 2016 Cotzias Lecture. Neurology 87, 2471–2482 (2016).
  3. Dalmau, J. et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 7, 1091–1098 (2008).
  4. Jones, B. E. et al. Anti-NMDA receptor encephalitis in mice induced by active immunization with conformationally-stabilized holoreceptors. bioRxiv 467902 (2018). doi:10.1101/467902

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How does Sleep Affect the Blood-brain Barrier?

How does Sleep Affect the Blood-brain Barrier?

December-11-2019 | Sarah Reitz, PennNeuroKnow

IAES PNK Partnership logo 300x251 - How does Sleep Affect the Blood-brain Barrier?Autoimmune encephalitis (AE) is the name for a group of conditions that occur when the body’s immune system mistakes its own healthy brain cells for invaders, leading to brain inflammation that ultimately triggers a number of other symptoms. Normally, the body’s immune system has only limited access to the brain, as it is protected by the blood-brain barrier (BBB). When this barrier is healthy, it can prevent an immune system attack by blocking immune cells and antibodies targeting brain cells from actually entering the brain. Like any fortress, however, the BBB isn’t completely impenetrable. Given that AE symptoms occur when immune cells or antibodies manage to cross the BBB, researchers think that the weakening of this barrier plays a critical role in AE and may even be a target for future therapies to reduce or prevent AE symptoms. But what causes the BBB to weaken, allowing cells, antibodies, and other molecules to invade the brain?


The blood-brain barrier: gatekeeper of the brain

Before discussing how the BBB becomes impaired, we need to understand how the healthy BBB functions. The BBB is often referred to as a “gateway”, made up of tightly joined endothelial cells that surround the blood vessels in the brain and spinal cord1. Outside of the brain, the endothelial cells lining blood vessels have small spaces between them, allowing for the exchange of substances between the blood and the surrounding tissue. However, the endothelial cells of the BBB are connected to each other by proteins called tight junction proteins, which squeeze the cells tightly together, blocking larger cells and molecules from freely flowing between the blood supply and the brain (Figure 1).

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Figure 1: The blood-brain barrier is made up of endothelial cells that are tightly connected to each other by tight junction proteins (purple). These tight connections prevent unwanted substances from traveling between the blood and the brain. Different types of transporter proteins (yellow & blue) shuttle only certain types of molecules between the blood and brain.

The BBB is selectively permeable, meaning it allows only certain substances to enter and leave the brain. One way that molecules can cross the BBB is by endocytosis, a process where the endothelial cells uses its cell membrane to take in a molecule on one side (say, the side facing the blood) and pass it through to the other side (facing the brain) where it is released1. The endothelial cells of the BBB also express a variety of transporter proteins, which actively move molecules between the blood and the brain (Figure 1). Additionally, small, fat-soluble molecules can cross the BBB without any help from endocytosis or transporter proteins, giving the brain access to important nutrients and energy sources1.

BBB permeability changes across the day

The permeability of the BBB is not always the same, however. Research has shown that its permeability actually changes depending on the time of day2. Like many cells in the body, BBB cells are controlled by circadian rhythms, biological processes that cycle roughly every 24 hours. These rhythms are driven by a molecular “clock” within each cell, and cells across the body are synchronized by the “master clock” located in the brain.

What do these rhythms mean for BBB permeability though? Interestingly, research in both flies and mice shows that the amount of hormones, inflammatory proteins, and other molecules that cross from the blood into the brain fluctuates across the day, with peak BBB permeability occurring at night2.

Sleep loss impairs BBB function

Circadian rhythms aren’t the only daily process that affects the integrity of the BBB. Sleep—or more appropriately, lack of sleep—is also known to affect the BBB’s protection of the brain. This relationship between sleep and the BBB is increasingly important as sleep restriction becomes more and more common in our modern society.

Sleep loss is also highly relevant to the AE community. One study found that 73% of AE patients surveyed reported sleep disturbances, including gasping/snoring and insomnia. Even further, patients with AE had decreased total sleep time and increased fragmentation of sleep compared to people without AE3. But how exactly does sleep loss affect the BBB?

Blood Brain Barrier after full sleep 300x71 - How does Sleep Affect the Blood-brain Barrier?

Figure 2: After periods of sleep loss, the blood-brain barrier is negatively affected in many ways (left). Inflammatory signaling caused by TNFα and IL-6 increases, leading to the breakdown of tight junction proteins (purple). This causes gaps between endothelial cells, allowing unwanted immune cells and antibodies to enter the brain. After sleep loss, the endothelial cells also make fewer of the transporter proteins (blue and yellow) that are required to shuttle necessary molecules between the brain and blood.

Multiple studies have now shown that sleep restriction weakens the BBB. One reason is due to the increase in inflammatory signaling that results from extended periods of wakefulness. Increases in inflammatory proteins, like TNFα and IL-6, are known to break down the tight junction proteins that keep the endothelial cells tightly joined together2 (Figure 2). Sleep-deprived mice and rats showed decreased numbers of tight junction proteins, leading to increased BBB permeability.

In addition to weakened tight junctions between endothelial cells, sleep loss also increases permeability by enhancing the rate of endocytosis across the BBB2, meaning that the endothelial cells shuttle more molecules from the blood into the brain. Relevant to AE, this increased permeability means that more immune cells and antibodies can enter the brain after sleep loss compared to after a full night’s sleep.

While these results are a bit frightening, there is good news. All of the damage to the BBB caused by sleep loss returns to normal after getting enough sleep! One study found that even an extra 1-2 hours of sleep following sleep loss restored BBB function in most brain areas4. Given even more time to sleep, the BBB throughout the brain returned to normal function5. These results suggest that treating the sleep disorders commonly associated with AE may help strengthen the BBB, increasing the brain’s protection against the immune system’s cells and antibodies and improving long-term outcomes for patients.

The BBB as a treatment target

Given that AE is caused by immune cells and antibodies infiltrating and attacking the brain, researchers are now looking at the BBB as a potential therapeutic target1. Treatments that strengthen the BBB will hopefully reduce the number of immune cells and antibodies that make it into the brain, and may also increase the effectiveness of some AE medications, such as anti-inflammatory drugs or immune-suppressants. Because these AE medications are specifically designed to cross a healthy BBB and access the brain, strengthening a weakened BBB will protect against molecules that aren’t supposed to be in the brain, while still allowing the necessary medication in.

The known circadian effects on BBB permeability can also be used in determining when to give medication that needs to cross the BBB. Medication can be given at the time of day when BBB permeability is highest to increase the amount of drug that makes it into the brain. In fact, this has already been studied with anti-seizure medication in epilepsy. For instance, in both flies and humans, when medication was given at night during peak BBB permeability, it was most effective at controlling seizures6,7.

This new strategy of “chronotherapeutic” dosing schedules has the potential to improve the efficacy of medication in many diseases. By administering drugs when it is easiest for them to enter the brain, doctors may be able to see results at lower doses of the drug, potentially reducing the risk of harmful side effects. As we continue to learn more about the BBB, scientists may identify even more ways to improve BBB health in the many disease states where it is compromised.

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  1. Platt MP, Agalliu D, Cutforth T (2017) Hello from the other side: How autoantibodies circumvent the blood-brain barrier in autoimmune encephalitis. Front. Immunol. 8:442. doi: 10.3389/fimmu.2017.00442
  2. Cuddapah VA, Zhang SL, Sehgal A (2019) Regulation of the blood-brain barrier by circadian rhythms and sleep. Trends Neurosci 42(7):500-510. doi: 10.1016/j.tins.2019.05.001
  3. Blattner MS, de Bruin GS, Bucelli RC, Day GS (2019) Sleep disturbances are common in patients with autoimmune encephalitis. J Neurol 266(4):1007-1015. doi: 10.1007/s00415-019-09230-2
  4. Gomex-Gonzalez B, et al. (2013) Rem sleep loss and recovery regulates blood-brain barrier function. Curr. Neurovasc. Res. 10, 197-207
  5. He J, Hsuchou H, He Y, Kastin AJ, Wang Y, &Pan W (2014) Sleep restriction impairs blood-brain barrier function. J Neurosci 34(44)14697-14706. doi: 10.1523/jneurosci.2111-14.2014
  6. Zhang SL, Yue Z, Arnold DM, Artiushin G, Sehgal A (2018) A circadian clock in the blood-brain barrier regulates xenobiotic efflux. Cell 173(1):130-139. doi: 10.1016/j.cell.2018.02.017
  7. Yegnanarayan R, et al. (2006) Chronotherapeutic dose schedule of phenytoin and carbamazepine in epoleptic patients. Chronobiol. Int 23, 1035-1046




The “Immune” in Autoimmune Encephalitis: The Role of T and B Cells

The “Immune” in Autoimmune Encephalitis: The Role of T and B Cells

Nov-27-2019 | Carolyn Keating, PennNeuroKnow

The Immune System: An Explainer

When we catch a cold, get an infection, or otherwise become sick, our bodies use a natural defense mechanism called the immune system to fight off what’s attacking us.  The immune system has two ways of responding1.  The first, called innate immunity, involves physical and chemical barriers like the skin and saliva, as well as many different types of cells that “eat” and destroy whatever is causing the trouble.  While this innate response happens very quickly, then the downside is that it’s not very specific, and the immune cells can damage healthy parts of the body while trying to gobble up the foreign invaders.  In order to specifically target particular offenders, the body uses its second way of responding: the adaptive immune system.  This response can take days or weeks to develop but is also able to remember what the foreign invader looked like, so if it attacks again a targeted reaction can occur faster than the first time.  To acquire this immunity against a particular foreign substance, the body uses two types of cells that act in different ways: T cells (which develop in an organ called the thymus, that’s where the “T” comes from) and B cells (which mature in the bone marrow, hence the “B”).


These two cell types are able to attack so specifically because each one recognizes a particular structure, called an antigen, on a foreign substance.  For instance, one T cell might recognize a certain part of an influenza virus, while another could recognize a specific part of a bacterium; the same situation also holds true for B cells.  The T and B cells travel around between different lymphoid tissues (organs like the spleen, tonsils, and lymph nodes, the last which are spread throughout the body) until they encounter their particular antigen.  Once activated by their antigen, the T and B cells leave the lymph tissues and work in different ways to fight off the foreign invader (Figure 1).

types of T and B cells PNK - The “Immune” in Autoimmune Encephalitis: The Role of T and B Cells

Types of T and B cells

T cells come in many varieties, but the two major types are cytotoxic and helper.  Cytotoxic T cells (sometimes referred to as CD8+ T cells due to a particular identifier on their surface) travel to the disease site to search for cells that also bear the antigen that activated them, and destroy them.  Helper T cells (sometimes referred to as CD4+ T cells), as the name might suggest, help activate other parts of the immune system.  There are many subtypes of helper T cells that activate different types of responses; for instance, some promote the cytotoxic T cell response, while others activate B cells. Another kind of CD4+ T cell called regulatory cells actually tells the immune system, not to attack2.


Unlike T cells, B cells do not destroy their target.  Instead, once they are activated by their antigen and T helper cells, they mature into plasma cells that produce antibodies, proteins that recognize the same antigen as the B cell.  These antibodies essentially enhance the innate immune system and act in several ways, including neutralizing toxins, signaling to other immune cells that a cell should be attacked and destroyed, or activating complement.  Complement is a group of proteins (not cells) that make up yet another arm of the immune system.  These complement proteins can recruit immune cells or directly kill foreign cells themselves1.


T and B Cells in Autoimmune Encephalitis

So what happens in autoimmune encephalitis (AE)?  In this and other autoimmune diseases, the body mistakenly recognizes part of itself as a foreign invader and mounts an attack. Scientists believe that AE starts when a tumor or virus causes proteins from neurons to be exposed to the immune system. The proteins get picked up by immune cells outside the brain that go on to activate T and B cells in lymphoid tissue. These activated cells then make their way into the brain where they cause AE3,4.  Which cells are responsible for causing the disease depends on what antigen sets off the immune response.

In cases where the antigen comes from inside a cell, cytotoxic T cells are the culprits.  When proteins from inside neurons like Hu, Yo, or Ma2 are the antigens, that usually indicates that the immune system first encountered the proteins in a cancerous tumor, which can express proteins from all sorts of cell types (this cancer association is why these antibodies and diseases are called “onconeural,” or “paraneoplastic”).  Cytotoxic T cells fighting the tumor can make their way into the brain and kill neurons5.  This cell death is likely part of the reason why patients with these diseases have poor recovery.  Antibodies from B cells that have matured into plasma cells can also be produced in response to the tumor, but they do not contribute to AE symptoms6.

Antibodies do have a strong role in producing AE symptoms when the antigen comes from the outside surface of a neuron, like the NMDA receptor for instance.  These antibodies can still be formed in reaction to a tumor, but this is less common.  Research on NMDAR encephalitis, in particular, has revealed the presence of B cells and antibody-secreting plasma cells in the brain7,8.  Because the antibodies have access to the surface proteins they target, they can bind to them and interfere with their function.  In the case of NMDAR encephalitis, it’s thought that the antibodies cause the receptors, which normally are exposed to the outside of the cell, to be taken back inside so that they can’t function properly.  Once the antibodies are gone the receptors can return to the cell surface, reversing many of the symptoms9.  Unlike diseases in which the antibodies target intracellular proteins, in NMDAR encephalitis there are few to no cytotoxic T cells in the brain or neuronal death5,7,8.  But while there are little to no cytotoxic T cells, there have been reports of helper T cells around blood vessels in the brain, including one type called Th17 that act to enhance the immune response10.


In other cases of encephalitis with antibodies again a cell surface protein, such as LGI1, CASPR2, or GABA receptors, the precise immune reaction is less certain and in some ways seems to be a little different from NMDAR encephalitis.  B cells and plasma cells are still found in the brain, and antibodies also play a major role in causing symptoms5,11.  For instance, antibodies against the GABAB receptor block it from functioning, while antibodies against LGI1 can disrupt interactions between proteins and lead to a decrease in AMPA receptors12.  The involvement of T cells is unclear and may vary depending on the disease-causing antibody. For example, cytotoxic and helper T cells have been found in the brain of anti-GABAB receptor patients11, while few T cells were found in anti-VGKC-complex patients5.  In addition, scientists sometimes observe signs of complement, the protein arm of the immune system that can kill cells5,6.  In line with the presence of cytotoxic T cells and complement, neuronal loss is sometimes reported5,13.


Overall, the type of immune response the body produces appears to be dependent on the specific antigen. In general, diseases with antibodies that target intracellular proteins like Hu, Yo, or Ma2 involve cytotoxic T cells that kill neurons.  In contrast, diseases with antibodies that target cell surface proteins like NMDAR, LGI1, and GABAR involve B cells in symptom production. In this second category, the role of T cells and complement may vary depending on the particular antigen.

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  1. Parkin, J. & Cohen, B. An overview of the immune system. Lancet 357, 1777–1789 (2001).
  2. Corthay, A. How do regulatory T cells work? Scand. J. Immunol. 70, 326–336 (2009).
  3. Venkatesan, A. & Adatia, K. Anti-NMDA-Receptor Encephalitis: From Bench to Clinic. ACS Chem. Neurosci. 8, 2586–2595 (2017).
  4. Dalmau, J. NMDA receptor encephalitis and other antibody-mediated disorders of the synapse: The 2016 Cotzias Lecture. Neurology 87, 2471–2482 (2016).
  5. Bien, C. G. et al. Immunopathology of autoantibody-associated encephalitides: Clues for pathogenesis. Brain 135, 1622–1638 (2012).
  6. Damato, V., Balint, B., Kienzler, A. K. & Irani, S. R. The clinical features, underlying immunology, and treatment of autoantibody-mediated movement disorders. Mov. Disord. 33, 1376–1389 (2018).
  7. Martinez-Hernandez, E. et al. Analysis of complement and plasma cells in the brain of patients with anti-NMDAR encephalitis. Neurology 77, 589–593 (2011).
  8. Tüzün, E. et al. Evidence for antibody-mediated pathogenesis in anti-NMDAR encephalitis associated with ovarian teratoma. Acta Neuropathol. 118, 737–743 (2009).
  9. Dalmau, J. et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 7, 1091–1098 (2008).
  10. Zeng, C. et al. Th17 cells were recruited and accumulated in the cerebrospinal fluid and correlated with the poor prognosis of anti-NMDAR encephalitis. Acta Biochim. Biophys. Sin. (Shanghai). 50, 1266–1273 (2018).
  11. Golombeck, K. S. et al. Evidence of a pathogenic role for CD8 + T cells in anti-GABA B receptor limbic encephalitis. Neurol. Neuroimmunol. NeuroInflammation 3, 1–8 (2016).
  12. Dalmau, J. & Graus, F. Antibody-mediated encephalitis. N. Engl. J. Med. 378, 840–851 (2018).
  13. Shin, Y.-W. et al. Treatment strategies for autoimmune encephalitis. Ther. Adv. Neurol. Disord. 11, 1–19 (2018).



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Introducing the IAES and PennNeuroKnow Partnership

Introducing the IAES and PennNeuroKnow Partnership

IAES and PNK announce partnership in autoimmune encephalitis and neuroschience education

October 16-2019 | Carolyn Keating and Sarah Reitz

Hello AE Community!


Our names are Carolyn and Sarah, and we are happy to announce the partnership between IAES and our blog, PennNeuroKnow (PNK).  We are working with IAES to learn about topics that patients and families in the AE community have trouble understanding, in order to create handouts and blog posts that explain these issues in a way that’s easy to digest.  We’re excited to begin this alliance and to introduce our team to the AE community.

PNK is a blog we founded in early 2018 to dive into the complex field of neuroscience and simplify it so that anyone can understand.  Including the two of us, we have 6 writers creating weekly articles ranging from general topics like how the brain produces curiosity, to breaking down specific journal articles on subjects like how the bacteria in your gut may be linked to depression.  All of us are PhD students in the University of Pennsylvania’s Neuroscience Graduate Group who are committed to better communicating science.  We know that scientific studies are sometimes difficult to both access and understand, so we want to use our training as scientists to share our passion for neuroscience and make our field more accessible to everyone.

We were first introduced to IAES in July 2019, when Carolyn wrote about NMDAR encephalitis in a blog post called When Your Brain is on Fire.  IAES saw the post and shared it on their Facebook page, giving the article much greater reach than we normally experience.  The amount of positive feedback we have received from the AE community has been overwhelming, and we are truly grateful to have been able to help so many people understand the science behind the disease that has affected themselves or a loved one.  Now thanks to IAES President Tabitha Orth reaching out to us about forming a partnership, we are excited to produce more easy-to-read articles on complex topics important to the AE community.

All of our writers are looking forward to learning more about AE and the issues that are difficult for patients and families to grasp.  Already we are hard at work learning and writing about how AE relates to the immune system, memory loss, and FDG-PET scans, just to name a few topics.  We hope that we can use our strengths as neuroscientists to help translate complicated subjects and journal articles into something everyone can understand, and are excited to contribute to this wonderful community. We want to make sure we are writing about topics that are most important to you and your family members, so please do not hesitate to reach out to either Tabitha or us with topics you would like to learn more about!

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E-mail Sarah and Carolyn Directly at PNK 

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Our website is not a substitute for independent professional medical advice. Nothing contained on our website is intended to be used as medical advice. No content is intended to be used to diagnose, treat, cure or prevent any disease, nor should it be used for therapeutic purposes or as a substitute for your own health professional's advice. Although THE INTERNATIONAL AUTOIMMUNE ENCEPHALITIS SOCIETY  provides a great deal of information about AUTOIMMUNE ENCEPHALITIS, all content is provided for informational purposes only. The International Autoimmune Encephalitis Society  cannot provide medical advice.

International Autoimmune Encephalitis Society is a charitable non-profit 501(c)(3) organization founded in 2016 by Tabitha Andrews Orth, Gene Desotell and Anji Hogan-Fesler. Tax ID# 81-3752344. Donations raised directly supports research, patients, families and caregivers impacted by autoimmune encephalitis and to educating healthcare communities around the world. Financial statement will be made available upon request.




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