Tag Archive for: adaptation

How today’s world is reshaping your brain

Between the COVID-19 pandemic, climate change, constant mass shootings, social injustice, political turmoil, and 24/7 exposure to social media and misinformation, one thing’s for certain: We’re all going through a lot. New terms like “climate anxiety” and “solastalgia” are entering the lexicon to address what we’re experiencing—some even call these events “collective traumas.” If you’re feeling a general sense of stress and anxiety, that makes sense. You’re not alone.

If you’re also feeling a little numb, that makes sense, too. Our brains are powerful places—we know that we can neurally adapt in certain ways, desensitizing our brains to repeated stimuli. But studies also show that these collective traumas, despite their constancy, are taking a toll on us, with long-term consequences for our mental health.

Of course, neither numbness nor anxiety and trauma are ideal. When it comes to absorbing current events, what’s going on in our brains? And how can we healthily cope in today’s world?

Neural adaptation—your brain wants to be smart and efficient

Our brains love forming heuristics—shortcuts to making decisions and predicting patterns. This happens constantly, in both minor ways (is Simone Biles going to outperform Grace McCallum? (You’ve probably heard of Simone, so she’ll likely get your vote) and major ones (would you rather apply for a job at a workplace with one job opening or a dozen? Odds are the one with fewer openings seems more competitive and desirable).

In other words, our brains are always trying to save time and energy, down to the single-cell level, sometimes at the expense of logic—or even our senses. Heuristics, selective attention, going on “autopilot,” the list of ways our brains love efficiency goes on and on.

This energy-saving phenomenon can also be seen in the form of neural adaptation: the gradual decrease over time in responsiveness to a constant stimulus. For most neurotypical individuals, this can be seen nearly every second of every day—did you feel the texture of your chair the moment before you read this sentence? What about the background noise around you that you’re just now noticing? Your brain is making a good argument: If a stimulus keeps occurring and requires no response, why should it waste its time?

But what does the brain do with a near-constant bombardment of negative media exposure? From school shootings to misinformation to climate change, does the brain deem these incessant stimuli as worth less of a response over time? Do we grow numb to the data, or do we grow anxious and stressed? The short answer: As far as we know, it’s both.

Desensitization and stress

Neural adaptation to today’s constant barrage of negative events is a huge, nebulous topic. To demonstrate how it works, Krista Lisdahl, professor of psychology at UW–Milwaukee, starts us off with a narrower, more defined example: alcohol consumption.

“Over time, as the brain gets used to alcohol, receptors and neurotransmitters get downregulated, so they’re less available,” she explains.

With your natural baseline down—in this case, the brain’s GABA (gamma-aminobutyric acid) signaling, which reduces brain activity and provides a sense of calm—you wind up drinking more alcohol to achieve that same dopamine rush. That leads to a whole slew of negative side effects; desensitization, when gone too far, comes with repercussions.

Lisdahl points to a study that’s closer to the topic at hand, where children’s brains neurally adapted in response to adverse events like divorce, abuse, substance use, and natural disasters. At first, she explains, the children demonstrated an increased cortisol response through the hypothalamic-pituitary-adrenal axis (HPA) function—aka stress. Over time, that cortisol response blunted, and the brain’s neuronal structure changed. In this scenario, adaptation resulted in poor emotional control and reduced problem-solving skills.

“In the end,” says Lisdahl, “these things are bad for the brain.”

For more abstract stressors, such as media exposure to climate change and the Covid pandemic, we don’t have as much neural evidence, says Lisdahl—it’s a difficult study to do, never mind the unethical territory of ceaselessly bombarding individuals with triggering events. But a few topical studies do exist: One climate anxiety study found that a moderate level of media exposure was actually ideal, “encouraging people to rethink actions with negative ecological impacts.” Another study found that exposure to stressful information on climate change can be overwhelming, ultimately encouraging actions with negative ecological impacts.

Those sound contradictory, but what we know about stress tells us otherwise: In short, a moderate level of stress is good—it teaches and informs us, and we can eventually desensitize appropriately. We learn new coping strategies, explains Lisdahl, who brings up her 15-year-old learning how to drive. “When he first got behind the wheel, there was a lot of fear and hesitancy,” she says, until he was driving effortlessly on the highway two months later. “That stress increased adaptation and learning, and it was good for him.”

But go too far on either end—imagine a curve shaped like an upside-down U—and the brain either doesn’t mobilize the resources needed to meet a challenge, or it can’t regulate stress and ultimately can’t recover. If too much cortisol lives in your system, says Lisdahl, you might see increased inflammation and oxidative stress, sleep disruption, emotional regulation disruption, and maladaptive neuronal changes. Like we saw in the above children’s study, vital stress counter-regulatory systems can turn off entirely. (The same principle applies for adults, too.) These chronic stressors also have the power to hinder our cognition, with negative effects on critical cognitive functions such as memory and attention.

Clearly, desensitization and stress are a dangerous game, but there’s a wrench in this system: Some studies have found that, when it comes to things like media exposure to traumatic events, we don’t desensitize at all. Instead, we sensitize, a process with similar side effects—but one we have the power to stop.

Negative media exposure and sensitization

The Orlando shooting, the Colorado River disappearing—these are serious stories. What if our brains don’t desensitize to negative media exposure? That’s what E. Alison Holman, professor of nursing science and psychological science at the University of California–Irvine, sees in her research. Instead, negative media exposure initiates a dangerous cycle: Worrying about the future draws an individual to the media, which makes them worry about the future, which draws them to the media, and so on.

“Whether it be a hurricane or mass shooting or terrorist attacks,” Holman says, “people can develop post-traumatic stress-type symptoms, both early and across time.”

In one poignant example, Holman studied the degree of acute stress following the 2013 Boston Marathon bombings in two groups: those present at the event and those exposed through the media. On average, notes Holman, the people who were at the site reported less stress than the people who watched via the media. She attributes this in part to the media’s gravitational pull to the unnecessarily violent and dramatic: In the real world, people got to see the whole picture—an act of terrorism, yes, but also an act of the community coming together.

Holman adds that negative media exposure can compound—it doesn’t have to be one event or topic. In today’s world, from Charlottesville to Canadian wildfires to Ukraine, stressful events are coming clip after clip after clip, which can be overwhelming psychologically—your brain doesn’t get a break to relax and process. “It’s what we call ‘cascading or compounding collective events’,” she describes. “It’s those moments that work together to be very psychologically distressing for many people.”

She points to a study where individuals were given MRIs and exposed to different videos, some traumatic. The ventral occipital cortex (VOC), the part of the brain associated with the development of PTSD and other mental health issues, lit up upon viewing the violent content. Specifically, the study mentioned the VOC was associated with flashbacks, or the intrusive mental re-experiencing of traumatic events. “If we know that these things that we’re looking at are triggering,” she says, “it’s a really good idea for us to stop doing it.”

How to keep your brain healthy and engaged

Both Lisdahl and Holman independently remark that the media isn’t doing society any favors—the news gravitates toward sensational headlines and traumatic imagery to get your attention. It’s part of why the self-care movement is so huge; when it comes to the media, societal self-care doesn’t exist.

“Each person really needs to be very mindful and tuned in with their own mental health and their own stress,” says Lisdahl.

We all have different barometers for stress, and it’s important to stay in that Goldilocks zone of resiliency. Not everyone can be an activist—you have to stay engaged in a way that aligns with your values and with the time or resources that you have available.

Several NAN researchers noted the importance of caring for our physical bodies in how we mediate stress and build resiliency. Some peer-reviewed resources on those subjects are here, here, here, and here.

Holman notes that you can get a lot of knowledge from your body—if you pay attention to it. Notice your breathing, the tension you feel in your core; if you’re having a physiological response, cut it off.

“I wouldn’t even wait to that point,” she adds. “If you’re starting to feel like, ‘Oh my god, this is overwhelming,’ just turn it off.”

Both researchers suggest hard and fast limits on media exposure: 30 minutes or less per day. Both even suggest picking two neutral outlets—like the Associated Press or Reuters—and making your bite-sized news consumption routine. That also limits your exposure to misinformation, which, as other studies show, sways your emotions and opinions.

Lastly, Holman notes how important it is to connect with real people in your social world—to talk about these events, to get the support you need, to create social connections in your community.

“The way things have always been fixed or changed or made for the better,” she says, “is by people coming together and supporting each other. We can do that.”

For additional resources on dealing with climate anxiety, check out this Headspace feature, this book, and, of course, NAN’s brain health brochure.

This article has been factchecked by members of NAN’s Publications Committee. For more about that process, click here.

Understanding neuroplasticity and how brains adapt

Dr. Erin Bigler has been studying the brain’s adaptability for more than 30 years. He retired in August 2018 from Brigham Young University, where he was a professor of psychology and neuroscience since 1990. His career itself spans nearly 50 years; he served as the President of the International Neuropsychological Society, and is a past president of NAN. Along with having written several neuropsychological tests, he has authored and/or edited 11 textbooks and published more than 300 peer-reviewed articles. Managing Editor Matt Villano recently caught up with Bigler over Zoom to talk about the future of brain science.

BrainWise: What interests you about neuroplasticity?

Dr. Erin Bigler: The brain is an experience dependent organ and it’s designed to adapt. And you have a hundred billion neurons, and those neurons all connect. They create these amazing brain networks that carry out a hundred trillion or more operations every second. This amazing complexity also tells you that in the face of amazing complexity, there have to be adaptive mechanisms; there have to be ways that the brain is updating and learning and modifying and pulling in different networks to function. Very early in my career, I started to study traumatic brain injury and neurodevelopmental disorders and how the brain would adapt over time to those kinds of injuries or different neurodevelopmental errors or mechanisms that altered brain structure and function.

BrainWise: You noted the brain can adapt over time. How does this compare to plasticity?

Dr. Bigler: Plasticity is probably not the correct term. It’s really adaptation. You were born with more neurons than what you are going to be utilizing as the brain emerges developmentally. In part, we believe this is related to the fact that in our hunter-gatherer and earlier heritage, the birthing process and early infant and childhood existence was an environment where there was very likely to be an acquired injury. And for the organism to live and last and thrive, it would have to be able to adapt. What happens from a brain organization standpoint is, you have these early brain cells and they connect with all kinds of other brain cells, but ultimately there’s a primary pathway that becomes established. That primary pathway is basically what we carry on with us into adolescence and adulthood. We can all sort of appreciate this to a certain extent because if you’re learning a new skill like bouncing a ball, you can almost feel your brain establishing new pathways. But once that skill level is acquired, then there’s a dominance of pathways in the brain that are conducting that. 

Now, if the brain is injured, there’s still those pathways that are in the background that were there in the beginning. They’re still there. Those pathways are activated if you have an injury and then there’s this recovery. But there’s a price to pay. There is always a price to pay. So you rob Peter to pay Paul. By that, what I mean is you never get back to precisely where you were with regards to function and capability. Of course this also depends on the nature of the injury, the pathology and all those kinds of things. There are certain areas of the brain that are hardwired. Certain visual centers, sensory centers, motor areas, and language receptive and expressive areas. Those areas often show the least amount of plasticity that occurs. It also relates to when the injury or the pathology first occurs.

There’s a series of classic studies that were done in the early part of the 20th Century by a psychology professor named Karl Lashley. And he took infant rats and lesioned different parts of the brain. And part of the amazing aspect of that was these animals would recover many functions quite well. But it had to be a very early lesion, a very early disruption so that the brain developed around it. If you did similar lesions in the adult rat, it had a different outcome. There was a greater potential for this adaptation. And he coined a term that we still use today: Equipotentiality. Some brain cells can function in multiple, multiple dimensions, and they get pulled into the learning process and then that becomes the primary function of those cells. But they had the potential to do something else and something quite different. It just depends on the environmental stimulation, the amount of stimulation, and all that goes on when the brain can be most adaptive. As you age, you lose some of that plasticity capacity.

BrainWise: We’ve talked about how the brain recovers from injury. What about how the brain recovers from genetic error?

Dr. Bigler: In studying traumatic brain injury, as we started to engage in systematic research and we started bringing together what were considered to be neurotypical control subjects, that’s when we started to discover some very substantial anomalies. With one case study a child had an in-utero stroke that was literally unknown to the mother. This child was being recruited as one of the neurotypical and we found in MRI that the child was missing an entire hemisphere and had no outward sign of that type of pathology. Another case was an infant that had what’s called an occipital encephalocele, which is part of the development of the visual cortex outside of the skull. There was literally a sac that developed outside his skull and he required neurosurgical treatment to remove it. The treatment totally obliterated the visual cortex, yet this child was able to read, and this child went on to graduate from college. Some of these very early anomalies and or acquired injuries, the brain has this capacity to shift. Remember the term I used: the equipotentiality. Areas that were not necessarily designed for language or executive functioning or these other neuropsychologic neurocognitive functions can adapt, and it’s as if there wasn’t an injury.

BrainWise: To what extent does equipotentiality something that we only see in the brain?

Dr. Bigler: The brain is unique. It’s considered the most complex biological organ and system in the universe. It’s very different than the lung or the liver or the kidney. And those have very dedicated purposes and functions. In contrast, we always talk about the brain in terms of its multi-modality capacity, that it can function in amazing integrative ways, and it controls all aspects of experience and all sensations and our response to them. You can grow back liver cells. That’s not true in terms of brain injury, although there are certain areas of the brain that do participate in what’s referred to as neurogenesis. That’s the growing of new neurons. There is some neurogenesis that occurs over the course of our lives, but the major aspect of cell development is in utero, and you’re essentially born with the full complement of what brain cells you’re going to use and develop.

Here’s another analogy. At birth, head size is about 25 to 30% of its adult size and that’s so the head can of course come through the birth canal. But by Year No. 1, that smaller head is now the bobblehead that we all love and enjoy. Little kids, as they’re starting to walk, have this big head on this smaller body because now head size is 75 to 80% of its adult size. And by the time that child is four or five years of age, you’re approaching 95%. And then the peak is somewhere around seven, eight years of age. This means the brain is developing at this remarkable rate. As the brain develops, it is laying down pathways. There’s this adaptive process that’s happening every moment of your life, but it’s especially impactful in the first few years of life. Part of that is setting the stage for whatever plasticity may come down the road.

BrainWise: How can external factors affect neuroplasticity?

Dr. Bigler: You’ve probably heard about raising rats in enriched environment and then raising them in impoverished environments. You’ve probably heard of the studies of controlling nutritional factors. Environmental complexity, the opportunity to exposure to environmental complexity, nutritional and health factors are huge, huge elements to maximizing brain development. The literature’s very clear here that socioeconomic status plays a picture, access to education and educational opportunities.

Let’s go back to that developing brain. Your brain is 25% of its adult size at birth. A major part of that growth is myelination, the growth of white matter in the brain. Gray matter gets pruned back, and all of that is going on in the context of the experience, dependent adaptation of the brain. What happens if you delay positive enriched environments until the child is five or six years of age when they start kindergarten? Well, the answer should be obvious: You’ve missed all of that equipotentiality aspect of brain development because you haven’t allowed that infant brain to be in the best optimal environment for stimulation, growth, molding, pruning, etc. This is why programs like Head Start are so important.

Nutrition is important, too. We know that if you have suboptimal nutrition, brain growth is different. If you have an impoverished environment, brain growth is different. People track “adverse childhood experiences,” often abbreviated as ACE. It’s a huge area of neurodevelopmental and neuropsychological research. If you have a stressful environment, stress alters the development of the brain. Stress limits the adaptability of the brain. And now you get into this interplay of, if you have an impoverished environment and you have a stressful environment both emotional as well as physical, it changes the brain as well.

We talked about how we have a hundred billion brain cells. There’s even more than that, because we also have glial cells, the supportive cells that are in the brain. All these cells have to get oxygenated in glucose-laden blood. So you have a microvasculature of the brain that’s just as complex as the neuronal complexity of the brain. Well, what does that mean? Cardiovascular health is equal to cerebral vascular health. And one of the very best things you can do from an aging standpoint and for helping your brain recover from injury is having good cerebral vascular flow. That tells us exercise, depending upon what the level of injury and the other problems are, is a key element.

The nutrition aspects of this are critical as well because injured brain cells may actually require different energy levels. This explains why when someone is rehabbing a brain injury, there’s typically a component that is focusing on physical health, wellbeing, nutrition, activity.

The brain is this experience, dependent organ that’s always adapting; and it has to be stimulated.

Passive stimulation, like simply watching TV, doesn’t really do anything in terms of this active adaptive process. This is where cognitive rehabilitation and the emotional support challenge kinds of therapeutic activities becomes so important—because it is assisting the patient with being active in attempting to change and alter how their brain is functioning.

BrainWise: What gets lost in adaptation?

Dr. Bigler: Think about the inside of your brain for a minute. Let’s say the primary pathway for carrying down a particular function is neuron A, and it projects to neuron B. So in order to complete this one particular function, you go from A to B. It’s a straight-line connection that’s fast. Everything in neural processing speed is happening in milliseconds. But after a Traumatic Brain Injury, the pathway gets rerouted, so neuron A now projects to neuron C, which projects to neuron D, which projects to neuron E, and then that projects to neuron B. You’re still going to be able to carry out that function because you can still get to the B neuron. But notice how many more steps you need to get there—it’s going to take longer. This one of the things that we see in traumatic brain injury—that the neural conduction time is slowed down. Remember what I said at the beginning: there’s always a price to pay. The price to pay here is in the aging process. What happens in the aging process is, you slow down. And as you slow down, that’s a neural speed issue. If you’ve already had an injury and now you’re aging and slowing down, now you’ve got a real problem.

BrainWise: Our cover feature is written by Helen Santoro, an incredible woman who is missing part of her frontal lobe. She’s an accomplished writer. She also clearly has had some serious adaptation occur in her brain. How is she able to do what she does?

Dr. Bigler: This all comes back to the equipotentiality paradigm. Sometimes, a major distinct lesion or abnormality forces the brain into making all these adaptive pathways. I like to use roadway analogies, and it’s clear her brain has rerouted. There are a few areas of the brain that are hardwired and one of those has to do with language. To use the roadway analogy again, there’s a superhighway between a part in your temporal lobe and a part in your frontal lobe that connects words and meaning and allows you to engage in expressive language. If that superhighway is damaged or dysfunctional, your brain must go through those multiple-layer connections. You’ve probably seen these beautiful images of what’s called diffusion tensor imaging tractography, where you see all the brain networks. Well, you can go from point A to any other point in the brain. It’s like the roadmap of North America. You can go start anywhere and go anywhere else in North America. The brain is the same way. Depending on where you start and where you’re headed, you might run into superhighways where the processing is going to be quite efficient, and then you may run into other areas where you must use street roads, and it’s slower and less efficient.

Her plastic brain

Helen Santoro was born with a hole in her brain. She’s still an award-winning writer. But how?

The first time I saw a picture of my brain at 22 years old, I gazed at a giant black hole where a chunk of brain tissue should have been.

I was in my boss’s office at a clinical research lab at Boston Children’s Hospital — my first job out of college. He slid a printout of a slice of my brain across the desk. The scan was taken a few weeks earlier when I hopped into the MRI machine to test a new scanning protocol. When I saw the picture, my eyes widened in astonishment.

Situated behind my left temple and eye socket was a gaping, black cavity that looked about six centimeters in length, the size of a dollar bill. The surrounding brain tissue was abnormally contorted and compressed, and the lesion — damaged or missing brain tissue — pushed up against the inside of my skull.

I had known since I was a teenager that I had a special brain. When I was born, doctors told my parents that I had a stroke in the uterus, otherwise known as a perinatal stroke. Consequently, I was missing my left temporal lobe, a region of the brain considered critical in language. My parents enrolled me in a study that tracked the developmental effects of perinatal strokes at New York University’s Langone Child Study Center from birth to 15 years old. I later wrote about it for The New York Times.

But I had never seen an image of my unusual brain. Not until my boss slid the picture across the desk.

Clearly, even with this hole in my brain, I can still write and talk — both are my personal and professional passions. The networks of neurons in my left temporal lobe have somehow reconfigured themselves. But scientists still don’t understand how this rewiring happened, or why my early-life stroke didn’t lead to the many developmental and cognitive issues about which doctors had warned my parents.

My life has been defined by the wonders of neural plasticity, but how and why my brain rewired the way it did is still a mystery. A mystery I face every single day.

The mysterious Tan

Almost everyone who has studied neuroscience or psychology knows about the French physician Pierre Paul Broca and the mysterious Patient “Tan.”

Tan wasn’t the patient’s real name. That was Monsieur Louis Victor Leborgne. Broca called his patient “Tan” because that’s the only word the adult Leborgne could say. One syllable: Tan. He usually uttered it twice in a row. Tan Tan.

It was a spring day in 1861 when Broca presented Patient Tan’s brain to his colleagues at a Société d’Anthropologie meeting in Paris. The talking point was whether or not mental functions — particularly language — are localized to certain areas of the brain. This question had been explored since ancient times, yet few had physically investigated the fast-decaying human brain.

That was until Leborgne came along. Leborgne was admitted to a hospital in Paris, and at age 51, was transferred to the surgical ward due to a gangrene infection in his leg. This is where he met Broca.

“This unfortunate man, unable to speak or to write with his paralyzed right hand was quite a difficult subject to study,” Broca jotted in his patient notes. “His general condition was furthermore so poor that it would have been cruel to torment him with over-long investigations.”

Leborgne died soon after the infection consumed his leg. Less than 24 hours later, Broca carefully cracked open Leborgne’s skull and examined his brain. Alongside a noticeable loss of tissue in parts of the left frontal and temporal lobes, Broca found a chicken-egg-shaped crater that was filled with fluid and located in the left hemisphere’s inferior frontal gyrus — a section of the brain located at the bottom of the frontal lobe that has been implicated in language comprehension and production.

The first time I heard about Leborgne, I was 17 years old and in my high school AP Psychology classroom. At the time, I had just uncovered details about my own medical history, specifically that I was missing a big section of my left hemisphere, though I still did not know where the hole was located or what it looked like.

Before this, I only knew that scientists were interested in my brain and that I was at risk of petit mal seizures — brief and sudden lapses of consciousness that cause people to stare blankly out into space for a few seconds. Consequently, I was on Topamax, an anti-seizure medication, for much of my childhood.

However, I was never convinced that I had seizures. At 12 years old, I decided to stop ingesting the little white pills and would hide them in the space between my bedframe and the wall. Nothing changed and I never had any seizures.

My mom was also skeptical about this diagnosis. I asked her if she recalls me ever having seizures. “No, never,” she responded immediately. Furthermore, she never knew that I stopped taking the Topamax.

Unusual symptoms

I never had seizures, but I have experienced other curious symptoms. Some of these come and go. Others are part of my everyday experience.

For instance, I struggle to see in the cold. Typically, I have normal vision. But when I am outside on a chilly day, it gradually worsens and eventually everything further away becomes an array of blurry colors. If I put on glasses during these periods, my vision is suddenly corrected.

One neurologist posited that my lesion, which presses up against the back of my left eye, may be constricting blood flow to the vessels that surround and fuel the optic nerve, a bundle of millions of nerve fibers that come out of the back of both eyeballs and relay messages to the brain. When it’s cold, blood vessels can constrict. Perhaps this narrowing of the vessels is exacerbated by my large lesion, thus impairing my vision. Another neurologist who I spoke to think this oddity is completely unrelated to my lesion.

Consequently, this odd symptom has been a constant companion — and puzzling mystery — throughout my entire life.

I also regularly struggle to recall words. For example, if I want to say “coral reef,” I can picture a coral reef and say words related to it, like “sea turtle” or “ocean.” I’ll also know the word starts with a c-like sound, but will only be able to recall random words like “cauliflower” or “Kraken.”

Sometimes, I can even be staring right at an object and will have no idea what it is called. This happened recently. I saw a safety pin and knew that it was an object that fastens two pieces of fabric together, but I could not conjure the words. It’s a very frustrating sensation, and one I wish I understood more.

Unraveling the research

Luckily, there has been a recent surge in research on the left hemisphere and language that may help make sense of these symptoms and how they’re connected to my unique brain development.

A study by researchers at Vanderbilt University in the journal Brain, for example, found that the location of a stroke in the left hemisphere impacts how well people recover from aphasia, or a disorder that impacts an individual’s ability to speak or understand language.

Scientists recruited 334 adults, 218 of which were experiencing aphasia who were followed for one year following their stroke. Those who had a lesion closer to the front of the brain recovered significantly better than patients who had brain damage in the region where the temporal and parietal lobes collide. This suggests that damage to some regions of the brain may have a greater impact on the language network — which encompasses the left temporal and frontal lobes, according to recent research — than others.

Aphasia impacts a third of adults following a stroke. Babies who suffer a perinatal stroke, on the other hand, are far less likely to experience aphasia, likely because the brain is remarkably plastic in newborns.

Additionally, both the left and right hemisphere appear to be equally involved in speech early in life, with language becoming more confined to the left hemisphere as people age, according to a 2020 study published in PNAS by researchers at Georgetown University and Children’s National Hospital in Washington, D.C. Additionally, in infants who had a left hemisphere perinatal stroke, the language network shifts over to the right hemisphere, based on a 2022 study published in PNAS.

Where we go from here

Before I can apply any of these findings to my own life, however, I must first answer if I had a perinatal stroke in the womb. It has been suggested by some doctors that the lesion in my brain is a large sac filled with spinal fluid, known as an arachnoid cyst. These cysts impact about 3% of all children and most are completely benign and never require any treatment. This April, I’m scheduled to see a neurologist to hopefully answer this question.

I am also participating in a study at the Massachusetts Institute of Technology to determine how damage to the brain impacts the language network. According to a preliminary analysis of my MRI scans taken last summer, I still process language using my left hemisphere. This is unlike another woman in the study who is also missing her left temporal lobe and now processes language using her right temporal and frontal lobes.

By understanding why my brain is missing so much tissue, I can better piece together how my language network adapted early in life. Maybe there was enough healthy tissue left over in my left hemisphere and the neuronal circuits that are typically in a left temporal lobe are all squished around the large hole. Maybe my language network moved to other parts of the brain like my left frontal lobe behind my forehead and parietal lobe underneath the crown of my skull, which is why I can still process language with relative ease.

There is also the question of the extent to which my condition is congenital, and whether other members of my family also are missing chunks of their brains. When I went to MIT to get my brain scanned, my mother also hopped in the MRI machine. Her brain was normal. My father has gotten his brain scanned many times and doesn’t have any noticeable irregularities. However, both of my brothers have never seen their brains, and researchers at MIT hope to scan both of them one day.

The other woman in the MIT study whose language network flipped over to her right hemisphere has a sister who is missing her right temporal lobe — and also lives a relatively normal life. Are there genetic factors that make people like me and this woman more susceptible to gaping cerebral cavities? Or is it all environmental, and something random happened during my fetal development or birth that caused my brain to develop the way it did?

Also, there factors that make some individuals’ brains more plastic than others?

I would also love to uncover why my vision is impaired in colder temperatures. I have no idea how, or if, this can be tested, and have yet to meet a researcher or neurologist who has ever heard of anyone else with this odd symptom.

My ability to understand my odd, plastic brain is entirely dependent on scientists’ ability to further decipher the complexities of neural plasticity. This will take years, as science is anything but quick. Regardless, I’m grateful that my brain can contribute to these discoveries and am excited to see what researchers uncover.

Check out our companion feature, a Q&A with Dr. Erin Bigler about neuroplasticity and adaptability of the brain.

Helen Santoro is a freelance writer.