How Creative Thinking Gets Done

I like to think that each of us have some measure of creativity within our grasp.  But new research points to the likelihood that some of us have more flexible neurons than others and that the ability to come up with creative ideas might be a result of such flexibility rendering higher connectivity between brain networks. Here’s the gist of the story from The Guardian:

Creative thinking is one of the primary drivers of cultural and technological change, but the brain activity that underpins original thought has been hard to pin down. In an effort to shed light on the creative process, Harvard psychologist Roger Beaty teamed up with colleagues in Austria and China to scan people’s brains as they came up with original ideas.

The scientists asked the volunteers to perform a creative thinking task as they lay inside a brain scanner. While the machine recorded their white matter at work, the participants had 12 seconds to come up with the most imaginative use for an object that flashed up on a screen. Three independent scorers then rated their answers.

One of the barriers to creative thinking is the ease with which common, unoriginal thoughts swamp the mind. Some people in the study could not get past these. For example, when asked for creative uses for a sock, soap and chewing gum wrapper, less creative people gave answers such as “covering the feet”, “making bubbles” and “containing gum” respectively. For the same items, more original thinkers suggested a water filtration system, a seal for envelopes, and an antenna wire.

Reported in the Proceedings of the National Academy of Sciences, the study found distinct patterns of brain activity in the most and least creative people. In the highly original thinkers, the scientists saw strong connectivity between three networks of the brain. One, known as the default mode network, is linked to spontaneous thinking and mind wandering, while a second, the executive control network, is engaged when people focus in on their thoughts. The third, called the salience network, helps to work out what best deserves our attention.

The first two of these three brain networks tend to work against one another, each dampening the other down. But the scans suggest that more creative people can better engage both networks at once. 

Initial scans on men and women from the University of North Carolina were backed up by further scans in Austrian and Chinese volunteers. To make sure enough creative people took part in the study, the researchers recruited plenty of artists, musicians and scientists. Now, Beaty wants to look at brain activity in different creative pursuits, such as the arts and sciences, and investigate whether training helps boost creative powers.

In 2016, David Melcher, who studies creativity at the University of Trento, identified brain networks used in visual art. “A critical open question, for future research, is whether this ability to put the brain in creative mode transfers across tasks,” he said. “Do we learn to network our brain regions for creativity in new domains once we learn to do it, for example, in painting or freestyle rap?”

“There has been an educational policy, in many countries including the US, of reducing teaching hours in the arts and focusing instead on rote learning for yearly testing of basic knowledge,” he added. “We need to understand whether creativity is a transferable skill, a way of using the brain that students learn to use across fields.”

For the full story, click here:

Think You’re Losing It? Maybe You Don’t Need to Worry

I have a family member who told me this Christmas that she is “really losing her memory” and this notion has her extremely distressed.  

And each of us, I expect, has experienced some fear or at least embarrassment when we’re caught forgetting something that we should have remembered.  (Insert “senior moment” joke here.)

But a new study suggests that if you are aware of memory loss, then you’re much less likely to actually develop Alzheimer’s Disease.  The bigger concern is losing memory without such awareness.  According to a large-scale study published in last October’s Journal of Clinical Psychiatry, those who are aware of memory problems pose much less risk of developing dementia.

The study, believed to be the largest of its kind on illness awareness, had data on 1,062 people aged 55 to 90 from the Alzheimer's Disease Neuroimaging Initiative (ADNI). This included 191 people with Alzheimer's disease, 499 with mild cognitive impairment and 372 as part of the healthy comparison group.

The researchers also wanted to identify which parts of the brain were affected in impaired illness awareness. They examined the brain's uptake of glucose, a type of sugar. Brain cells need glucose to function, but glucose uptake is impaired in Alzheimer's disease.

Using PET brain scans, they showed that those with impaired illness awareness also had reduced glucose uptake in specific brain regions, even when accounting for other factors linked to reduced glucose uptake, such as age and degree of memory loss.

Lead study author Dr. Philip Gerretsen, Clinician Scientist in CAMH's Geriatric Division and Campbell Family Mental Health Research Institute has heartening news for those of us fretting over memory slips. "If patients complain of memory problems, but their partner or caregiver isn't overly concerned, it's likely that the memory loss is due to other factors, possibly depression or anxiety.”  

"They can be reassured that they are unlikely to develop dementia, and the other causes of memory loss should be addressed."

The bigger concern is when the partner or caregiver is more likely to be distressed while patient doesn’t feel that they have any memory problems.   Lack of awareness of memory loss is called “anosognosia”.

To read the full story (and breathe a collective sigh of relief,) click here:

To a happy and brain health 2018!

Nouns vs Names: Common “Tip of the Tongue” Memory Slips

We’ve all been there.  Staring desperately into the face of someone whose name you should know.  After all, she seems to know you and once upon a time you had frequent interactions with this person.  Perhaps you recall the first letter of their name and how many syllables.  But for Heaven’s sake, the name just won’t come to mind.

You just experienced what researchers call a “tip-of-the-tongue” state, that agonizing moment when you know precisely what you want to say but you fail to produce the word or phrase.

Far from being telltale signs of dementia or Alzheimer’s disease, these moments are simply part of the way we communicate, and they’re more or less universal.

Researchers have even found occurrences among sign language users. (Those, they call tip-of-the-finger states.)

We’re more likely to draw blanks on words we use less frequently — like abacus or palindrome — but there are also categories of words that lead to tip-of-the-tongue states more often.

Proper names are one of those categories. There’s no definitive theory, but one reason might be that proper names are arbitrary links to the people they represent, so people with the same name don’t possess the same semantic information the way that common nouns do.

Here’s an experiment: Think of the first and last name of the foul-mouthed chef who has a cooking show on Fox. Now think of the hand-held device with numbered buttons you use to add, subtract, multiply or divide.

Which was easier to recall?

In all likelihood it was “calculator,” since every calculator you’ve ever seen shares those exact same attributes, giving you more context you can draw from when trying to produce the word. (That chef, by the way, is Gordon Ramsay.)

The bad news is there’s not a whole lot we can do in the moment to jog our memory when this happens. However, using certain words or names more often can make you less likely to draw a blank when you’re trying to produce that word, name or phrase.

Another suggestion:  try to come up with a visual association for the name of the person you are trying to remember.  Bald Bob.  Loud Laura.  The trick is to assign the association when you are first acquainted so the visual cue triggers the name. 

Sometimes if I have an inkling that the name begins with a certain letter, I’ll go through the alphabet in my head to try to link the next letter and land on the name.  Sally? Sarah?  Susan? Of course, you have to process these configurations pretty quickly while politely stalling.

Other tricks?  If I recognize the person, I’ll say my name first hoping that they will respond in kind. Or perhaps I’ll pretend to have a sudden need to consult my phone while quickly scrolling through my contacts.

The default solution, of course is to admit my shortcomings and go from there.  So I’ll say (as apologetically as possible) “Please remind me of your name again.”  And usually this is not a big deal.  After all, they can’t remember my name either.

Nametags anyone?

Excerpts used from this link:

In Order to Remember, We Need to Forget

It sounds completely counter-intuitive.  But forgetting is actually helpful for memory and for general cognitive processing.  In fact, once we forget something and then have to retackle the subject again, our understanding becomes better than ever.  

A full report of this phenomenon was covered in a recent story by Ulrich Boser in the New York Times. I thought it was fascinating and am now experimenting with revisiting some things I’d studied once and forgotten (like re-reading an old textbook or sight-reading a piano piece I knew in high school). 

Here’s an excerpt of the Times story:

Forgetting is supposed to be the antithesis of learning, and whether we’re a kid or an adult, most of us are plainly embarrassed if we can’t recall a name or fact. But it turns out that forgetting can help us gain expertise, and when we relearn something we couldn’t recall, we often develop a richer form of understanding.

The notion that forgetting is a hidden educational virtue goes back a century or more. In a series of studies, the German psychologist Hermann Ebbinghaus found that when people relearn information, they’re more likely to recall that information in the future.

Research explains why forgetting delivers this memory boost. Memories don’t fly out of our brains like sparrows from a barn. Instead, our brain will make memories more or less accessible. Some recollections, like the name of a close friend, are easily recalled. Other details, like the color of your childhood bedroom, have been tucked into deep storage and are much harder — if not impossible — to retrieve.

In this sense, a forgotten memory is a lot like an old file on your computer. While the document still exists, you don’t have a good way of getting to it, and today many memory researchers don’t even use the word “forgetting.” The term implies that a recollection is gone forever. Instead, forgetting is a matter of “retrieval failure.”

Besides the occasional memory gaffe, the brain’s approach to forgetting serves us well, and our retrieval failures help prune away memories that we don’t really need. Or consider living with an unending library of easily recalled memories. It would be overwhelming: Dates, names, phone numbers — they would all be constantly top of mind.

In this model of forgetting, when we extract a detail from the brain’s long-term storage, that detail becomes easier to recall in the future. 

So if you want to recall where you parked the car today, then practice remembering that specific location. If you want to easily summon the names of state capitals, then make sure to draw regularly on the names of state capitals.

Our brain is built to foster this sort of forgetting and remembering, according to a paper released in June in the journal Neuron. In the article, the researchers argue that many of the brain cells associated withmemory actively foster memory loss. “The growth of new neurons seems to promote forgetting,” the researcher Blake Richards said. “If you add new neurons, it effectively overwrites memories and erases them.”

The benefits of forgetting go far beyond facts or even brain cells, and when we relearn something that we’ve forgotten, we often gain deeper forms of insight. 

Studies show that forgetting can even promote better reasoning. In a study released in 2011, a group of psychologists gave some subjects a problem-solving exam. Known as the Remote Associates Test, it requires a subject to read three words (like “playing,” “credit” and “report”) and then come up with a word that would link all three ideas (“card”).

The researchers added a wrinkle to the test, and they provided the subjects with some “misleading” training, giving the subjects the wrong cues before they took the exam. The results showed that people had to push the misleading association out of their minds to solve the problem. “Creative cognition,” the authors wrote, “may rely not only on one’s ability to remember but also on one’s ability to forget.”

Benjamin Storm, a psychologist at the University of California, Santa Cruz, led the 2011 study, and he now takes the idea of forgetting pretty seriously. If Professor Storm writes a paper, he’ll start it early so that he has time to revisit his writing. Similarly, he will read important articles twice with a long break in between so that he gains more from the text.

A lack of remembering comes with plenty of downsides. Forgetting can have uncomfortable consequences. After Justin Bieber blanked out on the words to his Latin pop hit “Despacito” in May, the backlash was fierce, and TMZ ran the headline “Justin Bieber, No Hablo Espanol.”

What’s more, people can’t leave too much time in between recalling something or they’ll have a hard time pulling that detail from memory. This explains why parents and teachers are right to worry about summer learning loss after all. If a student has not recalled a math fact for months, it will be hard to recall that fact come September.

Still, forgetting can be a crucial driver of learning. Expertise is what fills our memory gaps. A learning loss can be a learning gain. In his song “Sorry,” Mr. Bieber crooned that he wanted “one more shot at second chances.” At least when it comes to learning and forgetting, he’s right.

You can read the full story here:

The Brain, the Lymphatic System and Glowing Heads of Mice

The brain and the lymphatic system have always been known as exclusive to each other.  In other words, the lymphatic system, critical to carrying immune cells and removing wastes from the body, stopped at the brain.  

But recent research from Finland involving glowing mouse heads (yes, you read that correctly) has altered this long-held notion.

Read on:

Three years ago, Kari Alitalo, a scientist at the University of Helsinki, wanted to develop a more precise map of the lymphatic system. To do this, he used genetically modified mice whose lymphatic vessels glowed when illuminated by a particular wavelength of light. (The mice had been given a gene from a species of glowing jellyfish.)

When viewing the modified mice under the light, Aleksanteri Aspelund, a medical student in Alitalo’s laboratory, saw something unexpected: The heads of the mice glowed. At first, he suspected that there was something wrong — with the animals, the lighting or the measuring equipment. But when Alitalo and Aspelund repeated the experiment, they got the same result. It seemed that the lymphatic vessels extended to the brain after all.

The discovery is much more than a historical footnote. It has major implications for a wide variety of brain diseases, including Alzheimer’s, multiple sclerosis, stroke and traumatic brain injury.

Researchers have identified two networks: the vessels that lead into and surround the brain, and those within the brain itself. The first is known as the lymphatic system for the brain, while the latter is called the glymphatic system. The “g” added to “lymphatic” refers to glia, the kind of neuron that makes up the lymphatic vessels in the brain. The glymphatic vessels carry cerebrospinal fluid and immune cells into the brain and remove cellular trash from it.  One scientist described the glymphatic system as “a dishwasher for the brain.”

Could a Malfunctioning Lymphatic System Promote Alzheimer’s?

Alitalo and others have found evidence that when the systems malfunction, the brain can become clogged with toxins and suffused with inflammatory immune cells. Over decades, this process may play a key role in Alzheimer’s disease, Huntington’s disease, Parkinson’s disease and other neurodegenerative illnesses.

 Scientists at Yale University, have found evidence linking problems in the lymphatic and glymphatic systems to Alzheimer’s. In a study on mice, they showed that glymphatic dysfunction contributes to the buildup in the brain of amyloid beta, a protein that plays a key role in the disease.

Last year, Jeff Iliff, a neuroscientist at Oregon Health & Science University, and several colleagues examined postmortem tissue from 79 human brains. They focused on aquaporin-4, a key protein inglymphatic vessels. In the brains of people with Alzheimer’s, this protein was jumbled; in those without the disease, the protein was well organized. This suggests that glymphatic breakdowns may play a role in the disease, Iliff says.

Recent research has also found evidence that the glymphatic system may extend into the eye. For decades, scientists have noted that many people with Alzheimer’s disease also have glaucoma, in which damage to the optic nerve causes vision loss. But they struggled to find a common mechanism; the glymphatic system may be the link.

In January, Belgian and Swiss researchers identified a rich network of glymphatic vessels within the optic nerve. The scientists also found that when these vessels malfunction, they seem to leave behind deposits of amyloid beta as well as other neurotoxins that damage the optic nerve.

How Sleep and Sleep Position Clear the Brain

One key to glymphatic performance seems to be sleep.  In mice, the system processes twice as much fluid during sleep as it does during wakefulness.  In studies, the lymphatic system removed much more of the protein when the animals were asleep than when they were awake.  The lead scientist suggests that over time, sleep dysfunction may contribute to Alzheimer’s and perhaps other brain illnesses. “You only clean your brain when you’re sleeping,” she says. “This is probably an important reason that we sleep. You need time off from consciousness to do the housekeeping.”

The same researchers have also found that sleep position is crucial.  In an upright position — someone who is sitting or standing — waste is removed much less efficiently. Sleeping on your stomach is also not very effective; sleeping on your back is somewhat better, while lying on your side appears to produce the best results. 

Sleep is probably not the only way to improve glymphatic flow. For instance, a paper published in January by Chinese researchers reported that in mice, omega-3 fatty acids improved glymphatic functioning. And in a small human study, other scientists have found that deep breathing significantly increases the glymphatic transport of cerebrospinal fluid into the brain.

Alitalo is experimenting with growth factors, compounds that can foster regrowth of the vessels in and around the brain. He has used this method to repair lymphatic vessels in pigs and is now testing the approach in the brains of mice that have a version of Alzheimer’s.

“Right now there are no clinical therapies in this area,” he says. “But give it a little time. This has only just been discovered.”

To read more and reference the studies, go here:

How Our Brains Make Two Copies of the Same Memory

One thing I love about studying neuroscience is that it is constantly changing, upending long-held views with more sophisticated research.  This particular discovery, published earlier this month, overturned a neuroscience tenet of some 50 years – here’s the story as reported by the PBS Nova site:

For decades, we’ve thought that memories were formed in two distinct stages—short-term first, then long-term later.

We might be wrong.

New research suggests that our brains make two copies of each memory in the moment they are formed. One is filed away in the hippocampus, the center of short-term memories, while the other is stored in cortex, where our long-term memories reside.

These findings were published April 6 in the journal Science.

The historically well-known patient Henry Molaison, also known as H.M., helped solidify the prevailing theory of memory formation and storage during the mid-1950’s. After a brain surgery to treat his epilepsy damaged his hippocampus, he could no longer form new memories. But those memories he made before his surgery still existed, leading neuroscientists to believe that the hippocampus was key to forming new memories.

And in the new theory, it still is. Though the research suggests that the link between the hippocampus and the cortex is as linear as once thought. When the link is blocked, the mice in the experiment didn’t develop long-term memories, just like H.M.

But when the connection is present, memories form in both the cortex and the hippocampussimultaneously. For the first few days, though, the neurons in the hippocampus are the only ones that fire during memory retrieval. Eventually, the memories in the cortex mature, and the neurons involved light up when the memory is recalled.

The researchers, based at the Riken-MIT Center for Neural Circuit Genetics in Japan, used a relatively new technique known as optogenetics to both trace memory formation and test the roles of the hippocampus and cortex. Optogenetics involves genetically engineering animals—in this case mice—to express a light-sensitive protein in certain neurons. By implanting fine fiber-optic cables into their brains, researchers are effectively able to turn specific neurons on and off, which allows them to probe their function.

Here’s a link to the full story:

To Keep Your Brain I Hope You Dance

Take heart two-steppers.

Over the past few years I’ve noticed a number of research studies popping up in neuroscience literature related to dancing and the effect on cognition. Yes, dancing – be it in a Zumba gym class or on a ballroom floor – has been suggested as a protective practice for cognition in later years.  After all, it combines the benefits of a mentally and physically challenging activity with socialization.

Now a new study compares the neurological effects of country dancing with those of walking and other activities and results were reported last week in the following story from the New York Times. Read on.

Neuroscientists and those in middle age or beyond know that brains alter and slow as we grow older. Processing speed, which is a measure of how rapidly our brains can absorb, assess and respond to new information, seems to be particularly hard hit. Most people who are older than about 40 perform worse on tests of processing speed than those who are younger, with the effects accelerating as the decades pass.

Scientists suspect that this decline is due in large part to fraying of our brain’s white matter, which is its wiring. White matter consists of specialized cells and their offshoots that pass messages between neurons and from one part of the brain to another. In young brains, these messages whip from neuron to neuron with boggling speed. But in older people, brain scans show, the white matter can be skimpier and less efficient. Messages stutter and slow.

Whether this age-related decline in white matter is inexorable, however, or might instead be changeable has been unclear.

So for the new study, which was published this month in Frontiers in Aging Neuroscience, researchers from the University of Illinois in Urbana and other schools decided to look at the effects of several different types of exercise on the wiring and the function of older people’s brain.

They began by recruiting 174 healthy people in their 60s and 70s with no signs of cognitive impairment. Most were sedentary, although some occasionally exercised.

Then they invited the men and women to a university lab for tests of their aerobic fitness and mental capacities, including processing speed and a brain scan with a sophisticated M.R.I. machine.

Finally, the researchers randomly divided the volunteers into several groups. One began a supervised program of brisk walking for an hour three times a week. Another started a regimen of supervised gentle stretching and balance training three times a week.

The last group was assigned to learn to dance. These men and women showed up to a studio three times a week for an hour and practiced increasingly intricate country-dance choreography, with the group shaping itself into fluid lines and squares and each person moving from partner to partner.

After six months, the volunteers returned to the lab to repeat the tests and the brain scans from the study’s start.

The differences proved to be both promising and worrisome.

By and large, everyone’s brain showed some signs of what the scientists termed “degeneration” of the white matter. The changes were subtle, involving slight thinning of the size and number of connections between neurons.

But the effects were surprisingly widespread throughout people’s brains, given that only six months had elapsed since the first scans. The degeneration was especially noticeable in the oldest volunteers and those who had been the most sedentary before joining the study.

However, one group showed an actual improvement in the health of some of the white matter in their brains, compared to six months before. The dancers now had denser white matter in their fornix, a part of the brain involved with processing speed and memory.

It seems likely that the cognitive demands of the dancing, which required people to learn and master new choreography throughout the six months of the study, affected the biochemistry of the brain tissue in the fornix, making it thicker and denser.

Interestingly, none of the changes in the volunteers’ white matter were obviously reflected in their cognitive performance. Almost everyone performed better now on thinking tests than at the study’s start, including tests of their processing speed, even if their white matter was skimpier.

These results indicate that there could be a time lag between when the brain changes structurally and when we start having trouble thinking and remember.  But the researchers also suggest that engaging in “any activities involving moving and socializing,” as each of these group programs did, might perk up mental abilities in aging brains.

Find the full story here:

Warning: Sleeping too long may be a harbinger for Dementia

Without dispute, sleep is essential for physical and mental health.  But sleeping excessively (more than 9 hours a nightmay actually set you up for dementia and even make your brain smaller.

Those are among the findings in a new study, “Prolonged sleep duration as a marker of early neurodegeneration predicting incident dementia,” that appeared recently in the journal Neurology. The study is significant as it is long-term (10 years) with nearly 2500 participants.

Past studies have suggested associations between both long and short sleep duration and an increased risk of dementia. However, the question remains whether sleep duration is a risk factor or a marker for dementia. Sleep may provide a restorative function, removing metabolic waste from the brain and preventing accumulation of the amyloid protein, a hallmark of Alzheimer disease (AD). On the other hand, sleep disorders may also emerge as a result of atrophy of brain regions involved in sleep and wakefulness, or as a consequence of mood disturbances, which are common in dementia.

To evaluate the association between sleep duration and the risk of incident dementia and brain aging, researchers at Boston University School of Medicine evaluated sleep duration in 2,457 adults taking part in the Framingham Heart Study.

Participants told researchers how long they typically slept each night. The researchers then observed them for 10 years to see who developed Alzheimer’s disease and other forms of dementia. Over the 10-year period, 234 patients developed all-cause dementia. Researchers then linked prolonged sleep duration with a higher risk of incident dementia.

They also discovered links between longer sleep periods and both smaller cerebral brain volume and poorer cognitive function, and suggested that screening for sleeping problems may help detect such cognitive impairment and dementia.

Those who developed dementia also had a correlation with lower levels of education (lacking a high school degree). 

 “Participants without a high-school degree who sleep for more than nine hours each night had six times the risk of developing dementia in 10 years compared to participants who slept for less,” said the lead researcher in a press release.  “These results suggest that being highly educated may protect against dementia in the presence of long sleep duration.”

But is excessive sleep a symptom or a cause of dementia?  The researchers suggest the former and that interventions to restrict sleep are unlikely to reduce the risk of dementia.

To read the full article, go here:

Another Clinical Trial Drug Bites the Dust

Another hopeful drug for treating Alzheimer’s in Phase III trials was shut down last week by pharma giant Merck, adding one more to the  impressive list of clinical failures.

And also leaving researchers scratching their heads over what really causes Alzheimer’s if the amyloid hypothesis (the idea that beta amyloid is the root cause of symptoms) is without validation.

Levels of the Beta-secretase  enzyme have been shown to be elevated in the far more common late-onset sporadic Alzheimer's . Drugs to block this enzyme (BACE inhibitors) in theory would prevent the buildup of beta-amyloid and may help slow or stop Alzheimer’s disease.

Merck is shuttering its trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues.

BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab— which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down.

Merck’s effort was the most advanced in the pipeline, but other drug companies are still in hot pursuit with their own persistent BACE efforts. 

Lilly recently decided to go ahead and stop its own prodromal Phase III for solanezumab after concluding that there was no logical reason to believe it could succeed after the study in patients with a mild form of the memory-wasting disease ended in disaster.

No significant new drug for Alzheimer’s has been approved in the past 14 years, despite massively expensive trials aimed at tackling the disease. 

To read the full story, click here:

Does “Brain Speed” Cause Falling?

For many seniors, taking a bad fall can result in horrendous consequences – scrapes, fractures, pain, broken teeth, maybe even a trip to the emergency room.   This research study caught my attention because it is a new take on an old problem, measuring “brain speed” with respect to fall risk. Read on:

Why does a 30-year-old hit their foot against the curb in the parking lot and take a half step and recover, whereas a 71-year-old falls and an 82-year-old falls awkwardly and fractures their hip?" asks James Richardson, M.D., professor of physical medicine and rehabilitation at the University of Michigan Comprehensive Musculoskeletal Center.

For the last several years, Richardson and his team set out to answer these questions, attempting to find which specific factors determine whether, and why, an older person successfully recovers from a trip or stumble. All this in an effort to help prevent the serious injuries, disability, and even death, that too often follow accidental falls.

Richardson's latest research finds that it's not only risk factors like lower limb strength and precise perception of the limb's position that determine if a geriatric patient will recover from a perturbation, but also complex and simple reaction times, or as he prefers to refer to it, a person's "brain speed." The work is published in the January 2017 edition of American Journal of Physical Medicine and Rehabilitation.

Measuring simple and complex reaction time

Using a device developed with U-M co-inventors James T. Eckner, Hogene Kim and James A. Ashton-Miller, simple reaction time is measured much like a drop-ruler test used in many school science classes, but is a bit more standardized.

The clinical reaction time assessment device consists of a long, lightweight stick attached to a rectangular box at one end. The box serves as a finger spacer to standardize initial hand position and finger closure distance, as well as housing for the electronic components of the device.

To measure simple reaction time, the patient or subject sits with the forearm resting on a desk with the hand off the edge of the surface. The examiner stands and suspends the device with the box hanging between the subject's thumb and other fingers and lets the device drop at varying intervals. The subject catches it as quickly as possible and the device provides a display of the elapsed time between drop and catch, which serves as a measurement of simple reaction time.

Although measuring simple reaction time is useful, the complex reaction time accuracy is more revealing. The initial set up of the device and subject is the same. However, in this instance, the subject's task is to catch the falling device only during the random 50 percent of trials where lights attached to the box illuminate at the moment the device is dropped, and to resist catching it when the lights do not illuminate.