Not too long ago, a colleague and I were lamenting the process of growing older and the inevitable increasing difficulty of remembering things we want to remember. That becomes particularly annoying when you attend a conference or a learning seminar and find yourself forgetting the entire session just days later.
But then my colleague told me about the Ebbinghaus Forgetting Curve, a 100-year-old formula developed by German psychologist Hermann Ebbinghaus, who pioneered the experimental study of memory. The psychologist’s work has resurfaced and has been making its way around college campuses as a tool to help students remember lecture material. For example, the University of Waterloo explains the curve and how to use it on the Campus Wellness website.
I teach at Indiana University and a student mentioned it to me in class as a study aid he uses. Intrigued, I tried it out too–more on that in a moment. The Forgetting Curve describes how we retain or lose information that we take in, using a one-hour lecture as the basis of the model. The curve is at its highest point (the most information retained) right after the one-hour lecture. One day after the lecture, if you’ve done nothing with the material, you’ll have lost between 50 and 80 percent of it from your memory.
By day seven, that erodes to about 10 percent retained, and by day 30, the information is virtually gone (only 2-3 percent retained). After this, without any intervention, you’ll likely need to relearn the material from scratch. Sounds about right from my experience. But here comes the amazing part–how easily you can train your brain to reverse the curve.
This is possible through the practice of what’s called spaced intervals, where you revisit and reprocess the same material, but in a very specific pattern. Doing so means it takes you less and less time to retrieve the information from your long-term memory when you need it. Here’s where the 20 minutes and very specifically spaced intervals come in.
Ebbinghaus’s formula calls for you to spend 10 minutes reviewing the material within 24 hours of having received it (that will raise the curve back up to almost 100 percent retained again). Seven days later, spend five minutes to “reactivate” the same material and raise the curve up again. By day 30, your brain needs only two to four minutes to completely “reactivate” the same material, again raising the curve back up.
Thus, a total of 20 minutes invested in review at specific intervals and, voila, a month later you have fantastic retention of that interesting seminar. After that, monthly brush-ups of just a few minutes will help you keep the material fresh.
Here’s what happened when I tried it.
I put the specific formula to the test. I keynoted at a conference and was also able to take in two other one-hour keynotes at the conference. For one of the keynotes, I took no notes, and sure enough, just shy of a month later I can barely remember any of it.
For the second keynote, I took copious notes and followed the spaced interval formula. A month later, by golly, I remember virtually all of the material. And in case if you’re wondering, both talks were equally interesting to me–the difference was the reversal of Ebbinghaus’ Forgetting Curve.
So the bottom line here is if you want to remember what you learned from an interesting seminar or session, don’t take a “cram for the exam” approach when you want to use the info. That might have worked in college (although Waterloo University specifically advises against cramming, encouraging students to follow the aforementioned approach). Instead, invest the 20 minutes (in spaced-out intervals), so that a month later it’s all still there in the old noggin. Now that approach is really using your head.
Science has proven that reading can enhance your cognitive function, develop your language skills, and increase your attention span. Plus, not only does the act of reading train your brain for success, but you’ll also learn new things! The founder of Microsoft, Bill Gates, said, “Reading is still the main way that I both learn new things and test my understanding.”
Dr. John N. Morris is the director of social and health policy research at the Harvard-affiliated Institute for Aging Research. He believes there are three main guidelines you should follow when training your mind:
Do Something Challenging: Whatever you do to train your brain, it should be challenging and take you beyond your comfort zone.
Choose Complex Activities: Good brain training exercises should require you to practice complex thought processes, such as creative thinking and problem-solving.
Practice Consistently: You know the saying: practice makes perfect! Dr. Morris says, “You can’t improve memory if you don’t work at it. The more time you devote to engaging your brain, the more it benefits.”
Practice self-awareness. Whenever you feel low, check-in with yourself and try to identify the negative thought-loop at play. Perhaps you’re thinking something like, “who cares,” “I’ll never get this right,” “this won’t work,” or “what’s the point?”
Science has shown that mindfulness meditation helps engage new neural pathways in the brain. These pathways can improve self-observational skills and mental flexibility – two attributes that are crucial for success. What’s more, another study found that “brief, daily meditation enhances attention, memory, mood, and emotional regulation in non-experienced meditators.”
Queendom has thousands of personality tests and surveys. It also has an extensive collection of “brain tools”—including logic, verbal, spatial, and math puzzles; trivia quizzes; and aptitude tests
Claiming to have the world’s largest collection of brain teasers, Braingle’s free website provides more than 15,000 puzzles, games, and other brain teasers as well as an online community of enthusiasts.
Scientists have known for years that there’s a “second brain” of autonomous neurons in your long, winding human digestive tract—but that’s about where their knowledge of the so-called abdominal brain ends.
Now, research published in 2020 shows that scientists have catalogued 12 different kinds of neurons in the enteric nervous system (ENS) of mice. This “fundamental knowledge” unlocks a huge number of paths to new experiments and findings.
The gut brain greatly affects on how you body works. Your digestive system has a daily job to do as part of your metabolism, but it’s also subject to fluctuations in functionality, and otherwise related to your emotions.
Digestive symptoms and anxiety can be comorbid, and your gut is heavily affected by stress. So scientists believe having a better understanding of what happens in your ENS could lead to better medicines and treatments for a variety of conditions, as well as improved knowledge of the connection between the ENS and central nervous system.
The research appears in Nature Neuroscience. In a related commentary, scientist Julia Ganz explains what the researchers found and why it’s so important:
“Using single-cell RNA-sequencing to profile the developing and juvenile ENS, the authors discovered a conceptually new model of neuronal diversification in the ENS and establish a new molecular taxonomy of enteric neurons based on a plethora of molecular markers.”
Neuronal diversification happens in, well, all the organisms that have neurons. Similar to stem cells, neurons develop first as more generic “blanks” and then into functional specialties. The human brain has types like sensory and motor neurons, each of which has subtypes. There are so many subtypes, in fact, that scientists aren’t sure how to even fully catalog them yet.
Neurons of the same superficial type are different in the brain versus the brain stem—let alone in the digestive tract. So researchers had to start at the very beginning and trace how these neurons develop. They tracked RNA, which determines how DNA is expressed in the cells made by your body, to follow how neurons formed both before and after birth. Some specialties emerge in utero, and some split and form afterward.
To find this new information, the scientists developed a finer way to separate and identify cells. Ganz explains:
“Using extensive co-staining with established markers, they were able to relate the twelve neuron classes to previously discovered molecular characteristics of functional enteric neuron types, thus classifying the ENCs into excitatory and inhibitory motor neurons, interneurons, and intrinsic primary afferent neurons.”
With a sharper protocol and new information, the researchers were able to confirm and expand on the existing body of ENS neuron knowledge. And now they can work on finding out what each of the 12 ENS neuron types is responsible for, they say.
By isolating different kinds and “switching” them on or off using genetic information, scientists can try to identify what’s missing from the function of the mouse ENS. And studying these genes could lead to new treatments that use stem cells or RNA to control the expression of harmful genes.
The Mind-Gut Connection is something that people have intuitively known for a long time but science has only I would say in the last few years gotten a grasp and acceptance of this concept. It essentially means that your brain has intimate connections with the gut and another entity in our gut, the second brain, which is about 100 million nerve cells that are sandwiched in between the layers of the gut.
And they can do a lot of things on their own in terms of regulating our digestive processes. But there’s a very intimate conversation between that little brain, the second brain in the gut and our main brain. They use the same neurotransmitters. They’re connected by nerve pathways. And so we have really an integrated system from our brain to the little brain in the gut and it goes in both directions.
The little brain, or the second brain, in the gut you’re not able to see it because as I said it’s spread out through the entire length of the gut from your esophagus to the end of your large intestine, several layers of nerve cells interconnected. And what they do is even if you – and you can do this in animal experiments if you completely disconnect this little brain in the gut from your main brain this little brain can completely take care of all the digestive processes, the contractions, peristaltic reflex, regulation of blood flow in the intestine.
And it has many sensors so it knows exactly what’s going on inside the gut, what goes on in the wall of the gut, any distention, any chemicals. All of this is being picked up by these sensory nerves, fed into the interior nervous system, the second brain. And then the second brain generates these stereotypic responses. So when you vomit, when you have diarrhea, when you have normal digestion, all of this is encoded in programs in your second brain.
What the second brain can’t do it cannot generate any conscious perceptions or gut feelings. That really is the only ability that allows us to do this and perceive all the stuff that goes on inside of us is really the big brain and the specific areas and circuits within the brain that process information that comes up from the gut. Still most of that information is not really consciously perceived. So 95 percent of all this massive amount of information coming from the gut is processed, integrated with other inputs that the brain gets from the outside, from smell, visual stimuli.
And only a very small portion is then actually made conscious. So when you feel good after a meal or when you ate the wrong thing and you’re nauseated those are the few occasions where actually we realize and become aware of our gut feelings. Even though a lot of other stuff is going on in this brain-gut access all the time.
When we talk about the connection between depression and the gut there’s some very intriguing observations both clinically but also now more recently scientifically that make it highly plausible that there is an integrate connection between serotonin in the gut, serotonin in our food, depression and gut function.
The enteric nervous system (ENS) or intrinsic nervous system is one of the main divisions of the autonomic nervous system (ANS) and consists of a mesh-like system of neurons that governs the function of the gastrointestinal tract. It is capable of acting independently of the sympathetic and parasympathetic nervous systems, although it may be influenced by them. The ENS is also called the second brain. It is derived from neural crest cells.
The enteric nervous system is capable of operating independently of the brain and spinal cord,but does rely on innervation from the autonomic nervous system via the vagus nerve and prevertebral ganglia in healthy subjects. However, studies have shown that the system is operable with a severed vagus nerve.
The neurons of the enteric nervous system control the motor functions of the system, in addition to the secretion of gastrointestinal enzymes. These neurons communicate through many neurotransmitters similar to the CNS, including acetylcholine, dopamine, and serotonin. The large presence of serotonin and dopamine in the gut are key areas of research for neurogastroenterologists.
Neurogastroenterology societies
American Neurogastroenterology and Motility Society
You might think that the impact of aging on the brain is something you can’t do much about. After all, isn’t it an inevitability? To an extent, as we may not be able to rewind the clock and change our levels of higher education or intelligence (both factors that delay the onset of symptoms of aging).
But adopting specific lifestyle behaviors–whether you’re in your thirties or late forties–can have a tangible effect on how well you age. Even in your fifties and beyond, activities like learning a new language or musical instrument, taking part in aerobic exercise, and developing meaningful social relationships can do wonders for your brain. There’s no question that when we compromise on looking after ourselves, our aging minds pick up the tab.
The Aging Process and Cognitive Decline
Over time, there is a build-up of toxins such as tau proteins and beta-amyloid plaques in the brain that correlate to the aging process and associated cognitive decline. Although this is a natural part of growing older, many factors can exacerbate it. Stress, neurotoxins such as alcohol and lack of (quality and quantity) sleep can speed up the process.
Neuroplasticity–the function that allows the brain to change and develop in our lifetime–has three mechanisms: synaptic connection, myelination, and neurogenesis. The key to resilient aging is improving neurogenesis, the birth of new neurons. Neurogenesis happens far more in babies and children than adults.
A 2018 study by researchers at Columbia University shows that in adults, this type of neuroplastic activity occurs in the hippocampus, the part of the brain that lays down memories. This makes sense as we respond to and store new experiences every day, and cement them during sleep. The more we can experience new things, activities, people, places, and emotions, the more likely we are to encourage neurogenesis.
With all this in mind, we can come up with a three-point plan to encourage “resilient aging” by activating neurogenesis in the brain:
1. Get your heart rate up
Aerobic exercise such as running or brisk walking has a potentially massive impact on neurogenesis. A 2016 rat study found that endurance exercise was most effective in increasing neurogenesis. It wins out over HIIT sessions and resistance training, although doing a variety of exercise also has its benefits.
Aim to do aerobic exercise for 150 minutes per week, and choose the gym, the park, or natural landscape over busy roads to avoid compromising brain-derived neurotrophic factor production (BDNF), a growth factor that encourages neurogenesis that aerobic exercise can boost. However, exercising in polluted areas decreases production.
If exercising alone isn’t your thing, consider taking up a team sport or one with a social element like table tennis. Exposure to social interaction can also increase the neurogenesis, and in many instances, doing so lets you practice your hand-eye coordination, which research has suggested leads to structural changes in the brain that may relate to a range of cognitive benefit. This combination of coordination and socializing has been shown to increase brain thickness in the parts of the cortex related to social/emotional welfare, which is crucial as we age.
2. Change your eating patterns
Evidence shows that calorie restriction, intermittent fasting, and time-restricted eating encourage neurogenesis in humans. In rodent studies, intermittent fasting has been found to improve cognitive function and brain structure, and reduce symptoms of metabolic disorders such as diabetes.
Reducing refined sugar will help reduce oxidative damage to brain cells, too, and we know that increased oxidative damage has been linked with a higher risk of developing Alzheimer’s disease. Twenty-four hour water-only fasts have also been proven to increase longevity and encourage neurogenesis.
Try any of the following, after checking with your doctor:
24-hour water-only fast once a month
Reducing your calorie intake by 50%-60% on two non-consecutive days of the week for two to three months or on an ongoing basis
Reducing calories by 20% every day for two weeks. You can do this three to four times a year
Eating only between 8 a.m. to 8 p.m., or 12 p.m. to 8 p.m. as a general rule
3. Prioritize sleep
Sleep helps promote the brain’s neural “cleaning” glymphatic system, which flushes out the build-up of age-related toxins in the brain (the tau proteins and beta amyloid plaques mentioned above). When people are sleep-deprived, we see evidence of memory deficits, and if you miss a whole night of sleep, research proves that it impacts IQ. Aim for seven to nine hours, and nap if it suits you. Our need to sleep decreases as we age.
Of course, there are individual exceptions, but having consistent sleep times and making sure you’re getting sufficient quality and length of sleep supports brain resilience over time. So how do you know if you’re getting enough? If you naturally wake up at the same time on weekends that you have to during the week, you probably are.
If you need to lie-in or take long naps, you’re probably not. Try practicing mindfulness or yoga nidra before bed at night, a guided breath-based meditation that has been shown in studies to improve sleep quality. There are plenty of recordings online if you want to experience it.
Pick any of the above that work for you and build it up until it becomes a habit, then move onto the next one and so on. You might find that by the end of the year, you’ll feel even healthier, more energized, and motivated than you do now, even as you turn another year older.
Mild cognitive impairment (MCI) is a neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual’s age and education but which are not significant enough to interfere with instrumental activities of daily living. MCI may occur as a transitional stage between normal aging and dementia, especially Alzheimer’s disease. It includes both memory and non-memory impairments.Mild cognitive impairment has been relisted as mild neurocognitive disorder in DSM-5, and in ICD-11.
The cause of the disorder remains unclear, as well as its prevention and treatment. MCI can present with a variety of symptoms, but is divided generally into two types.
Amnestic MCI (aMCI) is mild cognitive impairment with memory loss as the predominant symptom; aMCI is frequently seen as a prodromal stage of Alzheimer’s disease. Studies suggest that these individuals tend to progress to probable Alzheimer’s disease at a rate of approximately 10% to 15% per year.[needs update]It is possible that being diagnosed with cognitive decline may serve as an indicator of aMCI.
Nonamnestic MCI (naMCI) is mild cognitive impairment in which impairments in domains other than memory (for example, language, visuospatial, executive) are more prominent. It may be further divided as nonamnestic single- or multiple-domain MCI, and these individuals are believed to be more likely to convert to other dementias (for example, dementia with Lewy bodies).
In the US, a 2016 Gallup poll found that the majority of schools want to start teaching code, with 66 percent of K-12 school principals thinking that computer science learning should be incorporated into other subjects. Most countries in Europe have added coding classes and computer science to their school curricula, with France and Spain introducing theirs in 2015. This new generation of coders is expected to boost the worldwide developer population from 23.9 million in 2019 to 28.7 million in 2024.
Despite all this effort, there’s still some confusion on how to teach coding. Is it more like a language, or more like math? Some new research may have settled this question by watching the brain’s activity while subjects read Python code.
Two schools on schooling
Right now, there are two schools of thought. The prevailing one is that coding is a type of language, with its own grammar rules and syntax that must be followed. After all, they’re called coding languages for a reason, right? This idea even has its own snazzy acronym: Coding as Another Language, or CAL. Others think that it’s a bit like learning the logic found in math; formulas and algorithms to create output from input. There’s even a free online course to teach you both coding and math at the same time.
Which approach is more effective? The debate has been around since coding was first taught in schools, but it looks like the language argument is now winning. Laws in Texas, Oklahoma, and Georgia allow high school students to take computer science to fulfill their foreign language credits (the 2013 Texas law says this applies if the student has already taken a foreign language class and appears unlikely to advance).
The debate holds a special interest for neuroscientists; since computer programming has only been around for a few decades, the brain has not evolved any special region to handle it. It must be repurposing a region of the brain normally used for something else.
So late last year, neuroscientists in MIT tried to see what parts of the brain people use when dealing with computer programming. “The ability to interpret computer code is a remarkable cognitive skill that bears parallels to diverse cognitive domains, including general executive functions, math, logic, and language,” they wrote.
Since coding can be learned as an adult, they figured it must rely on some pre-existing cognitive system in our brains. Two brain systems seemed like likely candidates: either the brain’s language system, or the system that tackles complex cognitive tasks such as solving math problems or a crossword. The latter is known as the “multiple demand network.”
Coding on the brain
In their experiment, researchers asked participants already proficient at coding to lie in an fMRI machine to measure their brain activity. They were then asked to read a coding problem and asked to predict the output.The two coding languages used in the study are known for their “readability”—Python and ScratchJr. The latter was specifically developed for children and is symbol-based so that children who have not yet learned to read can still use it.
The main task involved giving participants a person’s height and weight and asking them to calculate a person’s BMI. This problem was either presented as Python-style code or as a normal sentence. The same method was done for ScratchJr, but participants were asked to track the position of a kitten as it walked and jumped.
Control tasks involved memorizing a sequence of squares on a grid (to activate participants’ multiple demand system) and reading one normal and one nonsense sentence (to activate their language system). Their results showed that the language part of the brain responded weakly when reading code (the paper’s authors think this might be because there was no speaking/listening involved). Instead, these tasks were mostly handled by the multiple demand network.
The multiple demand network is spread across the frontal and parietal (top) lobes of our brain, and it’s responsible for intense mental tasks—the parts of our lives that make us think hard. The network can be roughly split between the left part (responsible for logic) and the right (more suited to abstract thinking). The MIT researchers found that reading Python code appears to activate both the left and right sides of the multiple demand network, and ScratchJr activated the right side slightly more than the left.
“We found that the language system does not respond consistently during code comprehension in spite of numerous similarities between code and natural languages,” they write.Interestingly, code-solving activated parts of the multiple-demand network that are not activated when solving math problems. So the brain doesn’t tackle it as language or logic—it appears to be its own thing.
The distinct process involved in interpreting computer code was backed up by an experiment done by Japanese neuroscientists last year. This work showed snippets of code to novice, experienced, and expert programmers while they lay in an fMRI. The participants were asked to categorize them into one of four types of algorithms. As expected, the programmers with higher skills were better at categorizing the snippets. But the researchers also found that activity in brain regions associated with natural language processing, episodic memory retrieval, and attention control also strengthened with the skill level of the programmer.
So while coding may not be as similar to languages as we had thought, it looks like both benefit from starting young.
Fintan is a freelance science journalist based in Hamburg, Germany. He has also written for The Irish Times, Horizon Magazine, and SciDev.net and covers European science policy, biology, health and bioethics.
Researchers have succeeded in making an AI understand our subjective notions of what makes faces attractive. The device demonstrated this knowledge by its ability to create new portraits on its own that were tailored to be found personally attractive to individuals. The results can be utilised, for example, in modelling preferences and decision-making as well as potentially identifying unconscious attitudes.
Researchers at the University of Helsinki and University of Copenhagen investigated whether a computer would be able to identify the facial features we consider attractive and, based on this, create new images matching our criteria. The researchers used artificial intelligence to interpret brain signals and combined the resulting brain-computer interface with a generative model of artificial faces. This enabled the computer to create facial images that appealed to individual preferences.
“In our previous studies, we designed models that could identify and control simple portrait features, such as hair color and emotion. However, people largely agree on who is blond and who smiles. Attractiveness is a more challenging subject of study, as it is associated with cultural and psychological factors that likely play unconscious roles in our individual preferences. Indeed, we often find it very hard to explain what it is exactly that makes something, or someone, beautiful: Beauty is in the eye of the beholder,” says Senior Researcher and Docent Michiel Spapé from the Department of Psychology and Logopedics, University of Helsinki.
The study, which combines computer science and psychology, was published in February in the IEEE Transactions in Affective Computing journal.
Preferences exposed by the brain
Initially, the researchers gave a generative adversarial neural network (GAN) the task of creating hundreds of artificial portraits. The images were shown, one at a time, to 30 volunteers who were asked to pay attention to faces they found attractive while their brain responses were recorded via electroencephalography (EEG).
“It worked a bit like the dating app Tinder: the participants ‘swiped right’ when coming across an attractive face. Here, however, they did not have to do anything but look at the images. We measured their immediate brain response to the images,” Spapé explains.
The researchers analysed the EEG data with machine learning techniques, connecting individual EEG data through a brain-computer interface to a generative neural network.
“A brain-computer interface such as this is able to interpret users’ opinions on the attractiveness of a range of images. By interpreting their views, the AI model interpreting brain responses and the generative neural network modelling the face images can together produce an entirely new face image by combining what a particular person finds attractive,” says Academy Research Fellow and Associate Professor Tuukka Ruotsalo, who heads the project.
To test the validity of their modelling, the researchers generated new portraits for each participant, predicting they would find them personally attractive. Testing them in a double-blind procedure against matched controls, they found that the new images matched the preferences of the subjects with an accuracy of over 80%.
“The study demonstrates that we are capable of generating images that match personal preference by connecting an artificial neural network to brain responses. Succeeding in assessing attractiveness is especially significant, as this is such a poignant, psychological property of the stimuli.
Computer vision has thus far been very successful at categorising images based on objective patterns. By bringing in brain responses to the mix, we show it is possible to detect and generate images based on psychological properties, like personal taste,” Spapé explains.
Potential for exposing unconscious attitudes
Ultimately, the study may benefit society by advancing the capacity for computers to learn and increasingly understand subjective preferences, through interaction between AI solutions and brain-computer interfaces.
“If this is possible in something that is as personal and subjective as attractiveness, we may also be able to look into other cognitive functions such as perception and decision-making. Potentially, we might gear the device towards identifying stereotypes or implicit bias and better understand individual differences,” says Spapé.
Anjan Chatterjee uses tools from evolutionary psychology and cognitive neuroscience to study one of nature’s most captivating concepts: beauty. Learn more about the science behind why certain configurations of line, color and form excite us in this fascinating, deep look inside your brain. Check out more TED talks: http://www.ted.com The TED Talks channel features the best talks and performances from the TED Conference, where the world’s leading thinkers and doers give the talk of their lives in 18 minutes (or less). Look for talks on Technology, Entertainment and Design — plus science, business, global issues, the arts and more. Follow TED on Twitter: http://www.twitter.com/TEDTalks Like TED on Facebook: https://www.facebook.com/TED Subscribe to our channel: https://www.youtube.com/TED
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Journal Reference:
Michiel Spape, Keith Davis, Lauri Kangassalo, Niklas Ravaja, Zania Sovijarvi-Spape, Tuukka Ruotsalo. Brain-computer interface for generating personally attractive images. IEEE Transactions on Affective Computing, 2021; 1 DOI: 10.1109/TAFFC.2021.3059043
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Oct. 15, 2019 — The question may be as old as democracy itself: are physically attractive people elected more often than less attractive opponents? Scientists have found out that looking good can at least partly …
Feb. 21, 2019 — Artificial intelligence is revolutionizing the way we do business, and it can potentially allow firms to improve their decision making, given that individuals are willing to adopt algorithms in …
June 8, 2017 — School programs designed to educate children and adolescents on how to understand and manage emotions, relationships and academic goals must go beyond improving the skills of the individuals to …
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More than thirty years ago, Fred Davis developed the Technology Acceptance Model (TAM) as part of his dissertation at MIT. It’s one of the most widely cited papers in the field of technology acceptance (a.k.a. adoption). Since 1989, it’s spawned an entire field of research that extends and adds to it. What does TAM convey and how might today’s AI benefit from it?
TAM is an intuitive framework. It feels obvious yet powerful and has withstood the test of time. Davis started with a premise so simple that it’s easy to take it for granted: A person will only try, use and ultimately adopt technology if they are willing to exert some effort. And what could motivate users to expend this effort?
He outlined several variables that could motivate users, and many researchers have added to his list over the years, but these two variables are the ones that were most important: 1. Does it look easy to use? 2. Will it be useful? If the learning curve doesn’t look too steep and there’s something in it for them, a user will be inclined to adopt. Many researchers have added to this foundation over the years. For example, we’ve learned that a user’s intention can also be influenced by subjective norms.
We’re motivated to adopt new tech at work when senior leadership thinks it’s important. Perceived usefulness can also be influenced by image, as in, “Does adopting this tech make me look good?” And lastly, usefulness is high if relevance to the job is high.
TAM can be a powerful concept for an AI practitioner. It should be front-of-mind when embedding AI in an existing tool or process and when developing an AI-first product, as in, one that’s been designed with AI at the center of its functionality from the start. (Think Netflix.) Furthermore, AI can be used to drive adoption by levering TAM principles that increase user motivation.
Making AI more adoptable
With the proliferation of AI in sales organizations, AI algorithms are increasingly embedded in tools and processes leveraged by sales representatives and sales managers. Adding decision engines to assist sales representatives is becoming increasingly common. A sales organization may embed models that help determine a customer’s propensity to buy or churn, recommend next best actions or communications and more. The problem is, many of these initiatives don’t work because of a lack of adoption.
TAM can help us design these initiatives more carefully, so that we maximize the chances of acceptance. For example, if these models surface recommendations and results that fit seamlessly into reps’ tools and processes, they would perceive them as easy to use.
And if the models make recommendations that help a sales person land a new customer, prevent one from leaving and help them upsell or cross-sell when appropriate, reps would perceive them as useful. In other words, if the AI meets employees where they are and offers timely, beneficial support, adoption becomes a no-brainer.
We also see many new products and services that are AI first. For these solutions, if perceived ease of use or perceived usefulness are not high, there would be no adoption. Consider a bank implementing a tech-enabled solution like mobile check deposits. This service depends on customers having a trouble-free experience.
The Newark airport’s global entry system uses facial recognition to scan international flyers’ faces. It’s voluntary, and the experience is fantastic. The kiosk recognizes my face, and a ticket is printed for me to take to the immigration officer. Personally, I find this AI-first process a better experience than the previous system that depended on fingerprints, and now I will always opt for the new one.
Using AI to drive adoption
And perhaps counter intuitively, what if AI was used to drive elements of TAM within existing technology? Can AI impact perceived usefulness? Can AI impact perceived ease of use? Consider CRM. It has been improved and refined over the years and is in use within most sales organizations, yet the level of dissatisfaction with CRM is high and adoption remains a challenge.
How can AI help? A machine learning algorithm that uses location services can recommend that a rep visit a nearby customer, increasing the perceived usefulness of their CRM solution. Intelligent process automation can also help reps see relevant information from a contracting database as information on renewals are being entered. Bots can engage customers on behalf of the representatives to serve up more qualified leads. The possibilities are numerous. All these AI features are designed to ensure that CRM lives up to its promise as a source of value to the sales representative.
Outside of sales, consider patients. In the past few years, many new technologies have been introduced to help diabetics. Adoption of this technology is critical to self-management, and self-management is critical to treating the disease. For any new technology in this space, patients need to see that it’s useful to them.
AI can play a role in gathering information such as glucose levels, activity and food intake and make recommendations on insulin dosing or caloric intake. Such information gathering could go a long way toward reducing the fatigue that diabetics feel while they make countless health and nutrition decisions throughout the day.
AI’s algorithmic nature makes it easy to forget that it’s another technology and that it can aid technology. Its novelty can convince us that everything about it is new. TAM holds up because it’s intuitive, straightforward and proven. While we boldly innovate a path forward in the world of AI, shed convention and think like a disruptor, let’s keep an eye on our history too. There’s some useful stuff in there.
Arun provides strategy and advisory services, helping clients build their analytics capabilities and leverage their data and analytics for greater commercial effectiveness. He currently works with clients on a broad range of analytics needs that span multiple industries, including technology, telecommunications, financial services, travel and transportation and healthcare. His areas of focus are AI adoption and ethics, as well as analytics organization design, capability building, AI explainability and process optimization.
The AI Practitioners Guide for Beginners is a series that will provide you with a high-level overview of business and data strategy that a machine learning practitioner needs to know, followed by a detailed walkthrough of how to install and validate one of the popular artificial intelligence frameworks: TensorFlow on the Intel® Xeon® Scalable platform. Read the AI Practitioners Guide for Beginners article:
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You’re doing everything right—you visit your healthcare provider regularly, you take your relapsing MS medication exactly as it is prescribed—so why does it feel like that’s still not enough? It could be that you’re continuing to experience frequent relapses—a sign that your treatment may not be working well enough.
Knowing when it’s a relapse
Relapses, also known as flare-ups, are when new or existing symptoms appear or worsen, lasting for at least 24 hours and sometimes for as long as several weeks or months. While MS affects everyone differently, there are some common symptoms that people may experience during a relapse. Perhaps you’ve experienced one or more of the following symptoms.
Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.
LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.
Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.
LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.
Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.
LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.
Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.
LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.
Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.
LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.
IMPORTANT SAFETY INFORMATION
LEMTRADA can cause serious side effects including:
Serious autoimmune problems: Some people receiving LEMTRADA develop a condition where the immune cells in your body attack other cells or organs in the body (autoimmunity), which can be serious and may cause death. Serious autoimmune problems may include:
Immune thrombocytopenic purpura (ITP), a condition of reduced platelet counts in your blood that can cause severe bleeding that may cause life‑threatening problems. Call your healthcare provider right away if you have any of the following symptoms: easy bruising; bleeding from a cut that is hard to stop; coughing up blood; heavier menstrual periods than normal; bleeding from your gums or nose that is new or takes longer than usual to stop; small, scattered spots on your skin that are red, pink, or purple
Kidney problems called anti‑glomerular basement membrane disease, which, if not treated, can lead to severe kidney damage, kidney failure that needs dialysis, a kidney transplant, or death. Call your healthcare provider right away if you have any of the following symptoms: swelling of your legs or feet; blood in the urine (red or tea‑colored urine); decrease in urine; fatigue; coughing up blood
It is important for you to have blood and urine tests before you receive, while you are receiving and every month for 4 years or longer, after you receive your last LEMTRADA infusion.
Serious infusion reactions: LEMTRADA can cause serious infusion reactions that may cause death. Serious infusion reactions may happen while you receive, or up to 24 hours or longer after you receive LEMTRADA.
You will receive your infusion at a healthcare facility with equipment and staff trained to manage infusion reactions, including serious allergic reactions, and urgent heart or breathing problems. You will be watched while you receive, and for 2 hours or longer after you receive, LEMTRADA. If a serious infusion reaction happens while you are receiving LEMTRADA, your infusion may be stopped.
Tell your healthcare provider right away if you have any of the following symptoms of a serious infusion reaction during the infusion, and after you have left the healthcare facility:
swelling in your mouth or throat
trouble breathing
weakness
fast, slow, or irregular heartbeat
chest pain
rash
To lower your chances of getting a serious infusion reaction, your healthcare provider will give you a medicine called corticosteroids before your first 3 infusions of a treatment course. You may also be given other medicines before or after the infusion to try to reduce your chances of having these reactions or to treat them if they happen.
Stroke and tears in your arteries that supply blood to your brain (carotid and vertebral arteries): Some people have had serious and sometimes deadly strokes and tears in their carotid or vertebral arteries within 3 days of receiving LEMTRADA. Get help right away if you have any of the following symptoms that may be signs of a stroke or tears in your carotid or vertebral arteries:
drooping of parts of your face
weakness on one side
sudden severe headache
difficulty with speech
neck pain
Certain cancers: Receiving LEMTRADA may increase your chance of getting some kinds of cancers, including thyroid cancer, skin cancer (melanoma), and blood cancers called lymphoproliferative disorders and lymphoma. Call your healthcare provider if you have the following symptoms that may be a sign of thyroid cancer:
new lump
swelling in your neck
pain in front of neck
hoarseness or other voice changes that do not go away
trouble swallowing or breathing
cough that is not caused by a cold
Have your skin checked before you start receiving LEMTRADA and each year while you are receiving treatment to monitor for symptoms of skin cancer.
Because of risks of autoimmunity, infusion reactions, and some kinds of cancers, LEMTRADA is only available through a restricted program called the LEMTRADA Risk Evaluation and Mitigation Strategy (REMS) Program.
Do not receive LEMTRADA if you are infected with human immunodeficiency virus (HIV).
Thyroid problems: Some patients taking LEMTRADA may get an overactive thyroid (hyperthyroidism) or an underactive thyroid (hypothyroidism). Call your healthcare provider if you have any of these symptoms:
excessive sweating
unexplained weight loss
fast heartbeat
eye swelling
nervousness
unexplained weight gain
feeling cold
worsening tiredness
constipation
Low blood counts (cytopenias): LEMTRADA may cause a decrease in some types of blood cells. Some people with these low blood counts have increased infections. Call your doctor right away if you have symptoms of cytopenias such as:
weakness
chest pain
yellowing of the skin or whites of the eyes (jaundice)
dark urine
fast heartbeat
Inflammation of the liver: Call your healthcare provider right away if you have symptoms such as unexplained nausea, stomach pain, tiredness, loss of appetite, yellowing of skin or whites of eyes, or bleeding or bruising more easily than normal.
Serious infections: LEMTRADA may cause you to have a serious infection while you receive and after receiving a course of treatment. Serious infections may include:
listeria. People who receive LEMTRADA have an increased chance of getting a bacterial infection called listeria, which can lead to significant complications or death. Avoid foods that may be a source of listeria or make sure foods are heated well.
herpes viral infections. Some people taking LEMTRADA have an increased chance of getting herpes viral infections. Take medicines as prescribed by your healthcare provider to reduce your chances of getting these infections.
tuberculosis. Your healthcare provider should check you for tuberculosis before you receive LEMTRADA.
hepatitis. People who are at high risk of, or are carriers of, hepatitis B (HBV) or hepatitis C (HCV) may be at risk of irreversible liver damage.
These are not all the possible infections that could happen while on LEMTRADA. Call your healthcare provider right away if you have symptoms of a serious infection such as fever or swollen glands. Talk to your healthcare provider before you get vaccinations after receiving LEMTRADA. Certain vaccinations may increase your chances of getting infections.
Progressive multifocal leukoencephalopathy (PML): A rare brain infection that usually leads to death or severe disability has been reported with LEMTRADA. Symptoms of PML get worse over days to weeks. It is important that you call your doctor right away if you have any new or worsening medical problems that have lasted several days, including problems with:
thinking
eyesight
strength
balance
weakness on 1 side of your body
using your arms or legs
Inflammation of the gallbladder without gallstones (acalculous cholecystitis): LEMTRADA may increase your chance of getting inflammation of the gallbladder without gallstones, a serious medical condition that can be life-threatening. Call your healthcare provider right away if you have any of the following symptoms:
stomach pain or discomfort
fever
nausea or vomiting
Swelling of lung tissue (pneumonitis): Some people have had swelling of the lung tissue while receiving LEMTRADA. Call your healthcare provider right away if you have the following symptoms:
shortness of breath
cough
wheezing
chest pain or tightness
coughing up blood
Before receiving LEMTRADA, tell your healthcare provider if you:
have bleeding, thyroid, or kidney problems
have a recent history of infection
are taking a medicine called Campath® (alemtuzumab)
have received a live vaccine in the past 6 weeks before receiving LEMTRADA or plan to receive any live vaccines. Ask your healthcare provider if you are not sure if your vaccine is a live vaccine
are pregnant or plan to become pregnant. LEMTRADA may harm your unborn baby. You should use birth control while receiving LEMTRADA and for 4 months after your course of treatment
are breastfeeding or plan to breastfeed. You and your healthcare provider should decide if you should receive LEMTRADA or breastfeed.
Tell your healthcare provider about all the medicines you take, including prescription and over‑the‑counter medicines, vitamins, and herbal supplements. LEMTRADA and other medicines may affect each other, causing side effects. Especially tell your healthcare provider if you take medicines that increase your chance of getting infections, including medicines used to treat cancer or to control your immune system.
The most common side effects of LEMTRADA include:
rash
headache
thyroid problems
fever
swelling of your nose and throat
nausea
urinary tract infection
feeling tired
trouble sleeping
upper respiratory infection
herpes viral infection
hives
itching
fungal infection
joint pain
pain in your arms or legs
back pain
diarrhea
sinus infection
mouth pain or sore throat
tingling sensation
dizziness
stomach pain
sudden redness in face, neck, or chest
vomiting
Tell your healthcare provider if you have any side effect that bothers you or that does not go away. These are not all the possible side effects of LEMTRADA.
You may report side effects to the FDA at 1-800-FDA-1088.
Listen as Dr. Daniel Ontaneda, Cleveland Clinic Mellen Center for Multiple Sclerosis Treatment and Research, reviews relapses in the MS disease course, what a relapse is, and why it is important to better understand them with one of his patients. For more information about MS relapse or other related MS questions, visit http://my.clevelandclinic.org/service….
The brain of a sleep-deprived person is imbued with excess of two proteins that are substantially associated with Alzheimer’s disease.
According to the study published in the journal Science, a protein called tau is found in excess in the fluid that fills the brain and spinal cord of individuals with chronic sleep deprivation. The protein also drives neuron degeneration, and during Alzheimer’s, it scatters throughout the brain.
Similarly, sleep deprivation also induces accumulation of protein called amyloid-beta – a chunk of which dots the brains of Alzheimer’s patients.
In the study, researchers went over the samples of cerebrospinal fluid of eight adult participants who were sleep-deprived for nearly 36 hours. They found 51.5 percent increase in their tau levels. Similarly, mice that were rob of sleep were found to have twice the level of tau compared to well-rested ones.
Another study also reported that the lack of sleep to be the legitimate cause of increased level of A-beta in the cerebrospinal fluid, and if preceded by a week of poor sleep, the levels of tau also increased.
Since lack of sleep increases the levels of tau and A-beta in the brain, it appears that the only way to curtail the risk of developing Alzheimer’s symptom is to treat sleep disorders during mid-life and get good amount of sleep as much as possible. Proper sleep helps our brain get rid of excess proteins and other unnecessary stuffs, so getting less sleep means that wash cycle is disturbed.
References:
Lack of sleep is tied to increases in two Alzheimer’s proteins (Science News)
The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans (Science)
Association of Excessive Daytime Sleepiness With Longitudinal β-Amyloid Accumulation in Elderly Persons Without Dementia (Jama Neurology)
This 4-minute video shows how Alzheimer’s disease changes the brain and looks at promising ideas to treat and prevent the disease. Alzheimer’s disease is the most basic form of dementia, and scientists are trying to understand how the affects the nervous system. This video illustrates how neurons communicate in a healthy brain compared to that of a person with Alzheimer’s disease. In a healthy brain, cells such as astrocytes and microglia help keep neurons healthy by clearing away debris that builds up over time. In a person with Alzheimer’s disease, toxic changes in the brain destroy the ability of these cells to maintain a healthy environment for the neurons in the brain, ultimately causing a loss of neurons. Researchers believe that the Alzheimer’s disease process involves two proteins: beta amyloid protein and tau protein. Within the brain of a person with Alzheimer’s disease, these proteins become compromised. Over time, abnormal tau accumulates and eventually forms tangles inside the neurons, and the beta amyloid clumps into plaques, which build up between the neurons. As the level of amyloid increases, tau rapidly spreads throughout the brain. Other changes that affect the brain may play a role in the disease, such as the inability of the vascular system to deliver enough blood and nutrients to the brain. These factors cause the brain to shrink in size, starting with the hippocampus. A person with Alzheimer’s gradually loses the ability to think, remember, make decisions, and function independently. Researchers are working on the key to understanding Alzheimer’s disease so that Alzheimer’s disease research can lead to the development of more effective therapies with the hope that we can delay or even prevent the devastation of dementia. This video was developed by the National Institute on Aging (https://www.nia.nih.gov/), part of the National Institutes of Health (https://www.nih.gov/). Want to learn more? Subscribe to the National Institute on Aging’s YouTube channel: https://www.youtube.com/user/NatlInst…. Find more information about Alzheimer’s disease from the National Institute on Aging: https://www.nia.nih.gov/health/alzhei…. Find more health information from the National
Lea Grinberg, a neuropathologist and associate professor at the UCSF Memory and Aging Center in San Francisco’s Mission Bay, holds slides of brain tissue used for research on August 15, 2019. (Lindsey Moore/KQED)
People who donate their bodies to science might never have dreamed what information lies deep within their brains.
Even when that information has to do with sleep.
Scientists used to believe that people who napped a lot were at risk for developing Alzheimer’s disease. But Lea Grinberg with the UCSF Memory and Aging Center started to wonder if “risk” was too light a term — what if, instead, napping indicated an early stage of Alzheimer’s?
About a decade ago, Grinberg — a neuropathologist and associate professor — was working with her team to map a protein called tau in donated brains. Some of their data, published last week, revealed drastic differences between healthy brains and those from Alzheimer’s patients in the parts of the brain responsible for wakefulness.
Lea Grinberg uses a program that takes a microscope’s magnification of brain tissue on a slide and projects it on a computer screen on August 15, 2019. The different colors represent different biological features in the brain tissue sample, including neurons and tau protein. (Lindsey Moore/KQED)
Wakefulness centers in the brain showed the buildup of tau — a protein that clogs neurons, Grinberg says, and lets debris accumulate. Gradually, these clogged neurons die. Some areas of the diseased brains had lost as much as 75% of their neurons. That may have led to the excessive napping scientists had observed before. Although the team only studied brains from 13 Alzheimer’s patients and 7 healthy individuals, Grinberg says that the degeneration caused by Alzheimer’s was so profound they were sure of its significance.
“We are kind of changing our understanding of what Alzheimer’s disease is,” she says. “It’s not only a memory problem, but it’s a problem in the brain that causes many other symptoms.”
Although these symptoms aren’t as severe as complete loss of memory or motor functions, Grinberg says they can still hold real consequences for a person’s quality of life. “Because if you don’t sleep well every day and if you… are not in the mood to do things like you were before, it’s very disappointing, right? My grandparents were like this.”
Grinberg says it’s important to know whether napping could be an early sign of Alzheimer’s, for treating symptoms and developing drugs that could slow the progression of the disease. Although there are no prescription drugs available to treat tau buildup, she says, a few are in clinical trials.
Lea Grinberg holds boxes filled with samples of brain tissue for study on August 15, 2019. (Lindsey Moore/KQED)
A public health professor and neuroscientist at UC Berkeley says the new information offers hope to researchers. William Jagust, who has studied Alzheimer’s for over 30 years, says the results could help select patients for clinical trials of new drugs that require early treatment. “It’s also just very important for understanding the evolution of Alzheimer’s disease with the hope that we eventually will have a drug,” he adds.
It’ll be awhile before doctors can diagnose anyone with Alzheimer’s based on how often they doze off. “There’s no practical application of this to clinical medicine as of today,” Jagust says, “but I think it’s on the cutting edge of the very, very important questions.”
What is Alzheimer’s disease? Alzeimer’s (Alzheimer) disease is a neurodegenerative disease that leads to symptoms of dementia. Progression of Alzheimer’s disease is thought to involve an accumulation of beta-amyloid plaque and neurofibrillary tangles in the brain. Find more videos at http://osms.it/more. Study better with Osmosis Prime. Retain more of what you’re learning, gain a deeper understanding of key concepts, and feel more prepared for your courses and exams. Sign up for a free trial at http://osms.it/more. Subscribe to our Youtube channel at http://osms.it/subscribe. Get early access to our upcoming video releases, practice questions, giveaways and more when you follow us on social: Facebook: http://osms.it/facebook Twitter: http://osms.it/twitter Instagram: http://osms.it/instagram Osmosis’s Vision: Empowering the world’s caregivers with the best learning experience possible.
For one patient, a decade of recovery took determination, persistence and the courage to weather repeated setbacks.
Strange as it may seem, the stroke Ted Baxter suffered in 2005 at age 41, leaving him speechless and paralyzed on his right side, was a blessing in more ways than one. Had the clot, which started in his leg, lodged in his lungs instead of his brain, the doctors told him he would have died from a pulmonary embolism.
And as difficult as it was for him to leave his high-powered professional life behind and replace it with a decade of painstaking recovery, the stroke gave his life a whole new and, in many ways, more rewarding purpose.
Before the stroke, Mr. Baxter’s intense work-focused life as a globe-trotting executive in international finance had eroded his marriage and deprived him of fulfilling relationships with family and friends. Unable to relax even on vacation, he rarely took time to smell the roses. Now, he told me, he leads a richer, calmer, happier life as a volunteer educator for stroke victims and their caregivers and for the therapists who treat them.
The stroke began with a cramping pain in his leg after a long international flight during which he wore compression hose to support his varicose veins. He didn’t take the pain seriously until suddenly he couldn’t talk or move the right side of his body. The clot that caused his leg pain had broken loose and cut off blood flow to the left side of his brain.
He nearly died. But once stabilized, the doctors discovered that he was born with a hole in his heart that had allowed the clot to bypass his lungs and go directly to his brain. Two of his siblings turned out to have the same defect, called patent foramen ovale, which they subsequently had repaired.
Mr. Baxter readily admits that his Type A personality, which was the driving force behind his professional success, was also a major factor that helped him reverse the extensive losses he suffered when the clot severely damaged his brain. And it inspired him to recount his 14 years of recovery and renewal in a fascinating book, “Relentless: How a Massive Stroke Changed My Life for the Better,” an apt title for what it took for him to regain full physical function, comprehension and intelligible speech.
His mantra, which could help many others facing a devastating health setback, is that recovery takes determination, focus, resiliency, persistence and courage — the courage to weather repeated setbacks and frustrations. He admits, however, that it can also take the financial resources and personal support he had to get the kind of help that can make a difference.
At first, his goal was to get right back in the saddle, working nonstop in finance. But after months of intense rehab, he still could neither use nor understand language, spoken or otherwise.
“It took seven or eight months for me to realize I wasn’t going back to my job,” he said. “I didn’t even understand that the words coming from my mouth weren’t making any sense.”
The learning curve was steep: “I couldn’t read; I couldn’t write. I could see the hospital signs, the elevator signs, the therapists’ cards, but I couldn’t understand them,” he wrote. The aphasia — the inability to understand or express speech — “had beaten and battered” his pride.
But he refused to give up. With age and prestroke physical conditioning on his side, he had convinced himself that “100 percent recovery was possible as long as I pushed hard enough.”
Mr. Baxter figured if he could get his body functioning again, his language facility might also return. The brain, he learned, was plastic and capable of renewal. So he devoted countless hours to physical therapy, worked out in the gym long and hard, and had his left arm tied behind his back, forcing himself to use the right. He found that as his physical abilities improved, so did his comprehension and communication skills.
When what he tried to say came out garbled, many people assumed he was either mentally slow or a foreigner with limited English. As one of his speech therapists said of people with aphasia, “It’s hard to understand that they have their intellectual faculties and know what they want to say, but they don’t have the ability to communicate it.”
Mr. Baxter researched and enrolled in several different aphasia programs throughout the country. For many hours a day, he did language practice, starting with books and flash cards for preschoolers and doing endless repetitions to relearn speech until eventually — after years of hard work — he was finally able to read books and have real conversations.
His original therapists at the Rehabilitation Institute of Chicago, admittedly amazed at the progress he made, asked what benefited him the most and solicited his help developing a new, intensive aphasia program. He was also invited to participate in Archeworks, a design program in Chicago for students working to solve urban problems.
“I faced the challenge of using my right hand, making new friends, and communicating effectively with a team,” he wrote. He was building things with his hands and tools and suddenly he realized he was problem-solving, a skill he had used often in finance.
Sports also aided his recovery. As he slowly regained use of his right side, he took lessons in golf and boxing, aided by watching others do things correctly.
“If I could see somebody do something, then I could follow it and mimic what they did,” he wrote. “I had to focus on visualization — picturing the task, the actions needed to perform that task, and the intended result.”
Art therapy was another helpful pursuit, which he said reduced his stress, countered depression and improved his self-esteem and emotional health. With art as a new source of fulfillment came an invitation to join a museum board that gave him additional conversational practice and “withered away my aphasia every day.”
Gradually, Mr. Baxter said he “started to realize that by doing more for others, I’d be happier with myself.”
Living now in Newport Beach, Calif., with his second wife, the 55-year-old stroke survivor devotes his life to inspiring other survivors and their caregivers. “I go to universities and hospitals to present my story — what I had experienced, how I rehabbed myself, how it changed my life for the better, and what it took to get my life back,” he wrote.
“Sometimes, I can’t believe how far I’ve come,” he said. He credited family members and friends who “never gave up on my recovery, nor did they ever treat me as if I were lost, and because of that, I never felt lost. None of it would have worked without a positive attitude.”
Intellipaat
