After Einstein’s death, his brain was preserved for future study. Scientists were naturally curious to see how the brain of this genius compared with the brain of a person of ordinary intelligence. Would there be an abundance of neurons (grey matter) or some unusual wiring of the neurons that distinguished his brain? When the brain was dissected, however, the only difference was that the numbers of cells that were not neurons (white matter) was dramatically increased. It is also true that, from evolutionary point of view, as brains became larger and “smarter”, what increased was not the percentage of neurons but of white matter. What does this mean?

When most of us–scientists and lay people alike—imagine the brain, we think of neurons, those cells carrying information in the form of electrical impulses. Neurons are ‘brains of the brain’, so to speak, and the rest of the cells were thought to be there only for support. But neurons account for only 15 percent of the brain, while these so-called ‘support’ cells occupy 85 percent.

The group name for white matter cells, glia—derived from the world ‘glue’—reflects their lowly status. First seen clearly by anatomists in the late 1800’s, Glia were initially thought to be little more than structural support for neurons, because, like scaffolding, glial cells literally hold neurons in place.

It was later found that glia can speed transmission of electrical signals and also deliver energy to neurons and remove neuronal waste products. While appearing to be a little more interesting than originally thought, glia still seemed about as sexy as wire insulation, food delivery and waste management devices.

Unlike neurons, there is no electrical activity within glia to send messages and information. It was therefore assumed that glia were deaf and dumb, incapable of communicating with either neurons or other glia, and therefore not particularly compelling as a focus of research. A good analogue would be the under-appreciated dark matter in astronomy. Dark matter is undetectable because it emits no electromagnetic radiation as the matter in the “visible” universe does. The existence of dark matter was eventually inferred from its gravitational effects on visible matter. While we had believed that the visible universe is the universe, the ordinary matter of our visible universe accounts for less than five percent of the total; dark matter accounts for more than 20 percent.

Today, the pace of knowledge about glia has begun to accelerate, as outlined in an exciting new book, The Other Brain, by Dr. R. Douglas Fields[i] (the title refers to the 85 percent of the brain that is glial). Fields is a neuroscientist specializing in glial cell research, and the information in his book is so new that it isn’t found in standard medical textbooks. Two review articles in the May, 2010 issue of the research journal Nature Neuroscience attest to how much still needs to be learned, and how potentially revolutionary are the implications.

So, are glial cells really dumb as a doorknob? First, we are just now learning that glial cells do communicate, not through synapses but through “gap junctions”. These gap junctions are protein channels connecting one cell to another, like a spaceship docking at the mother station. Glia can pass messages among themselves by using calcium as a chemical messenger instead of sending an electric signal as neurons do. In his research, Fields showed that after a 15-second delay, changes in response to a neuronal firing were seen in the surrounding glial cells. As Fields puts it, glial cells are “listening in” on what neurons are doing, something virtually no one in neuroscience thought possible.

Contrary to all established dogma, it is now known that glia not only communicate directly from one cell to an adjacent one, but also with cells very far away. Glia are even able to “jump” over barriers like a ping pong ball going over a net. And whereas neurons transmit their signals in linear lines, like telephone wires, glia communicate, as Fields puts it, by “broadcasting signals widely, like cell phones.”

Glia are also critical to the growth of neurons. Neuron cells grown in the lab without accompanying glial cells were found to have many fewer synapses than neurons grown with glial cells. Glia seem to play a central role in the number of synapses a neuron develops.

Contrary to what scientists thought, glia also have neurotransmitters; in fact, the same ones that neurons do. And there are receptors for these neurotransmitters both inside and on the outer surface of glial cells. Glial cells have receptors for glutamate, the principal stimulating neurotransmitter in the cortex, and GABA, which acts as a “brake” to calm down neurons. In other words, glia can excite or depress neurons and stimulate or calm the brain, just like medications.

And, unlike neurons, glia can move. They have enormous cellular “fingers” like the elastic Mr. Fantastic of comic book fame, and can move between and on neurons. This constantly changes the circuitry of the brain. These glial fingers also form around synapses. They secrete substances that remodel tissue or stimulate neuron growth during development and repair of the brain making it likely that they function in a similar role during learning in the healthy brain.

Glia repair injury, defend against disease, nurse neurons back to health and act as guide dogs for the re-growth of injured nerve fibers. Glia detect and react to bacteria and viruses, “gobble up” pathogens and release toxic chemicals to kill bacteria. And new research suggests that immature glial cells can act like stem cells and mature glia can stimulate stem cells dormant in the adult brain to form replacement neurons and glia. This could have implications for repair of the nervous system, including new possibilities for treating spinal cord injuries.

This is about as far removed from mere insulation, food delivery and waste management services as can be imagined. Glia are a lot smarter than we thought they were. A 2005 study shows a correlation between organization of fibers made of glial cells and IQ. Finding a greater proportion of glial cells in Einstein’s brain is not so surprising after all.

We still know very little about glia—even the basics such as how many kinds of glial cells there are and what they look like in detail. Their discovery, however, broadens our appreciation of the complexity of the brain. The brain, with its 100 billion neurons and an average of 10,000 synapses per neuron, has more potential connections than the atoms of our galaxy!

We don’t know yet if diet, exercise, supplements and other factors affect glial cells. However, the implications for health and illness—seizures, infections, cancer, addictions, mental illness and diseases such as Parkinson’s and multiple sclerosis may be far-reaching and profound.

As Fields says near the end of his book, “Here are cells that can build the brain of a fetus, direct the connection of its growing axons to wire up the nervous system, repair it after it is injured, sense impulses crackling through axons and hear synapses speaking, control the signals neurons use to communicate with one another at synapses, provide the energy source and substrates for neurotransmitters to neurons, couple large areas of synapses and neurons into functional groups, integrate and propagate the information they receive from neurons through their own private network, release neurotoxic or neuroprotective factors, plug and unplug synapses, move themselves in and out of the synaptic cleft, give birth to new neurons, communicate with the vascular and immune systems, insulate the neuronal lines of communication, and control the speed of impulse traffic through them. And some people ask, ‘Could these cells have anything to do with higher brain function?’ How could they possibly not?”

People with obsessive-compulsive disorder, or OCD, have recurrent thoughts and behaviors that can be crippling.  What follows is a discussion of the biology of the disorder and several aspects of treatment.

Obsessive compulsive disorder is not a single disorder; rather, it’s of a cluster of conditions. In OCD, sufferers might obsess and be anxious and compulsive about hoarding, cleaning, ordering and checking. Patients can also exhibit body dysmorphic disorder (BDD), where they imagine possessing a defect in physical appearance.  Other diseases that overlap with OCD include Tourette’s syndrome and hypochondria. OCD also has a genetic component and runs in families; relatives of someone with OCD are 8 times more likely to present symptoms.

The areas of the brain that appears involved with OCD are the orbito-frontal cortex (OFC), a center for decision-making, and the thalamus, which filters and relays information. In these brain regions, the neurotransmitter glutamate is responsible for neuronal signaling. It’s thought that the deficit of glutamate production and function might contribute to the condition of OCD and other counter-productive behavior, including making decisions based on inappropriately perceived danger.

Obsessive Compulsive Disorder Treatment

The neurotransmitter serotonin may play an important role in whether someone gets obsessive compulsive disorder. Researchers have found a defect in the gene that makes a protein that “mops up” serotonin from between neurons. When there’s too much of this protein there is not enough serotonin, and that’s what is found in some with OCD. This is why Serotonin Re-uptake Inhibitors (SRIs) such as Prozac, which makes serotonin more available to the brain, are perhaps the most popular OCD treatment.

Another commonly used OCD treatment is exposure and response prevention (ERP), where the patient is exposed to stimuli that trigger the repetitive behavior but do not allow the patient to actually perform the compulsive behavior. Eventually the patient can learn that nothing bad happens when they don’t act out their compulsion.

Unfortunately, ERP is a stressful treatment for patients to endure. And significant numbers of patients drop out of treatment. Various drugs, such as the SRIs, are now being used in conjunction with ERP.

Anxiety usually is significant part of obsessive compulsive disorder. While anxiety does not appear to be the actual cause of OCD, anxiety can drive persistent thoughts and behaviors. A reduction in anxiety can be important in the treatment of OCD.  Various modalities for treating anxiety include medication, neurofeedback (both traditional and LENS Neurofeedback), and/or behavioral approaches.

When anxiety is successfully brought under control, there are not only fewer obsessive thoughts, but those obsessive thoughts that do persist become less prominent.  Instead being the dominant focus, compulsive become background music as opposed to a loud concert. These thoughts demand less attention and this makes it easier to control compulsive behavior.

There are many approaches to the treatment of the anxiety, fear, depression and other symptoms of PTSD that do not involve medication. The most common non-pharmacological treatment is trauma-focused cognitive-behavioral therapy (CBT).  Cognitive restructuring helps people make sense of the bad memories. Sometimes people remember the event differently than how it happened. They may feel guilt or shame about what is not their fault. The therapist helps people with PTSD look at what happened in a more realistic way. Other than in the initial stages, psychodynamic talk therapy alone has a limited role in treating PTSD.

“Exposure Therapy” involves gradually “exposing” a client to thoughts, feelings, and situations that bring back the memory of the trauma in order to wear out or “extinguish” their impact. This helps people with PTSD cope with their extreme anxiety and fear. A major drawback of exposure therapy is a greater than 50% dropout rate. Because the client has to revisit the traumatic events, however gradually, many find this too painful to continue.

Another modality that is increasingly being for PTSD is Eye Movement Desensitization and Reprocessing, more commonly known as EMDR.  The premise of EMDR is that when a traumatic experience occurs, it overwhelms our usual cognitive and neurological coping mechanisms. The memory and associated stimuli of the event aren’t properly processed, and are dysfunctionally stored in an isolated memory network. EMDR therapy supposedly helps the client process these traumatic memories, reducing their influence and allowing him to develop more adaptive coping mechanisms.

In EMDR treatment, the patient recalls a trauma while at the same time receiving “bilateral stimulation” such as rapidly moving his eyes from side to side. Tapping movements on different sides of the body or other modalities such as light and sound are used. Despite it’s name, eye movement is not essential in EMDR.

There are a number of other approaches associated with “complementary medicine”, that show promise for treating PTSD. One study demonstrated that acupuncture was as successful as CBT for treating PTSD. The improvements persisted at 3-month follow-up.

Other studies have found yoga to be helpful, particularly with veterans, where it reduced hyper-arousal and helped them sleep.

One of the most promising techniques for PTSD is mindfulness meditation, inspired by Buddhist teaching, which focuses awareness on the present moment. Mindfulness-based training for PTSD has been looked at in a number small studies, most showing about 80 percent of subjects showed clinically significant decrease in PTSD symptoms.

Mindfulness meditation medicine groups have a dropout rate of virtually zero. Members can talk about their past trauma if they wish, but there is no pressure to do so. Instead, the groups are centered on the present, helping members to cultivate present moment awareness and other practical skills they can employ immediately. Another advantage of mindfulness meditation is that it is “broad-spectrum”, showing success not only with PTSD but depression, anxiety, panic attacks, pain, insomnia, and substance abuse.

Along the lines of meditation, there is even a group in the Puget Sound V.A. Hospital in Seattle that treats PTSD - including among Navy Seals – using the Buddhist practice of “loving kindness meditation.” (They had a bit of debate about changing the name but decided to keep it. According to the director of the study, it worked out just fine.)

Two additional therapies with clinical evidence are traditional neurofeedback and LENS neurofeedback. The traditional neurofeedback method, commonly call Alpha-Theta (A-T) Neurofeedback, employs low frequency signals that bring the brain to a “twilight” state half-way between awake and asleep. This state that appears conducive to processing emotions.

An example of this treatment is to have the client relax in a darkened room. He or she is connected to EEG sensors and wears earphones. The client receives soothing sounds (like a river or ocean), which subtly change based on changes in brainwaves. These sounds both relax a client and at the same time help prevent the client from falling asleep.

An A-T session typically lasts about 30 minutes. Various guided visualizations can be used, but the basic instruction is to let the mind wander. Because the client is in an altered and profoundly relaxed state, her usual defenses are not as vigilant, and when something traumatic arises, instead of being re-traumatized, the brain can process these intense emotions. Initial changes with A-T can often be seen after one to three sessions. Typically, 10 – 20 sessions are required. Alpha theta is often in conjunction with talk therapy.

Lens Neurofeedback PTSD Treatment

Another form of neurofeedback, LENS (Low Energy Neurofeedback System) has shown in clinical reports to be an effective modality for the treatment of PTSD. Clinical reports indicate that it reduces the flight or fight response and clients feel more relaxed and emotionally “lighter” and more resilient.

In a LENS treatment, the client receives a series of unobtrusive, brief (1/100th sec), extremely weak brain signals, hundreds of times less than a cell phone. These minute feedback signals constantly change, responding to the client’s brain function. The introduction of these signals is thought to cause a slight fluctuation in brain waves that “shifts” the brain out of frozen, stuck patterns, such as the traumatic memories that give rise to PTSD. This is analogous to rebooting a frozen computer and allowing it to return to its previously functional state.

Read Part 1—PTSD & Painful Memories

An article entitled Erasing Painful Memories in the May 2012 issue of Scientific American reviews some of the current research on the treatment of post-traumatic stress disorder (PTSD).

Memory is no longer seen as a passive process of recording impressions. Rather, it is ongoing activity at the cellular and neurochemical level. It is this ongoing activity that allows some new openings for medical intervention.

We tend to think of a memory as a kind of object or a file that can be recalled when needed. But that’s not the case. We are finding out that memory is stored in at different sites in the brain. For example, the auditory part of a particular memory is stored in the auditory cortex in the temporal lobe, and the visual part of the same memory is stored in the visual cortex.  When that memory occurs, those various memories are “reassembled” into a single, unified experience. That’s why we now think that memory is not so much “recalled” as it is “recreated”. If so, it is might be possible to “un-create” memories too. That could be hugely helpful in treating PTSD.

The basic animal used in research of memory is the lab rat. When a caged rat is given a single mild shock to its foot, the rat turns around and heads in the opposite direction. It never returns to the spot where it received the shock. A rat will play out this avoidance over and over. Without an intervention, the rat will never learn that the shock will not be repeated. In other words, the rat is stuck with the original traumatic memory.

In 2006 a scientist injected a compound directly into the memory center of a rat’s brain that had been exposed to a foot shock. The compound interfered with new memory formation. Afterward the rat exhibited no fear behavior—the fear was no longer there. The original fear memory had been blocked from “re-creating” itself. The only problem with this approach is that it’s not specific for traumatic memories; it affects non-traumatic memories as well. It’s too non-specific to be practical.

Another neurochemical approach involves not removing particular memories but in removing the “charge” associated with a traumatic memory. The emotional “charge” provokes physical symptoms of fear such as increased heart rate and faster breathing.

A drug that reduces the body’s fear reaction is propanolol. It slows down the pulse and heart rate, thereby limiting the “fight or flight” response. While it was hoped that injecting propanolol within a few hours of exposure to trauma might prevent PTSD from becoming established, current studies have been mixed.

› Part II of this blog will cover some of the newer non-drug approaches to treating PTSD.

There has always been dissatisfaction among doctors and patients with anti-depressants. They often take 4-6 weeks to work, have significant side effects, and when they are helpful, relief it is often partial. A significant percentage of depressed patients find that anti-depressants provide no relief at all. Recent research suggests that anti-depressants work not so much by changing the balance of neurotransmitters but by increasing the number of synapses, the connections between nerve cells. In fact, there is reduced size in brain regions that regulate cognition and mood. These are the prefrontal cortex and the hippocampus.

As reported in this month’s Journal Science, ketamine can produce a stunningly rapid response, within hours, in patients resistant to standard antidepressants. Ketamine rapidly increases synaptic connections. This reverses the synaptic deficits caused by chronic stress/anxiety. Ketamine has been used in medicine primarily as a general anesthetic.

While initial research was done with rat brains, there is a recent clinical study of 30 depressed patients who received ketamine. The researchers found changes in brainwave activity that suggested strengthened connections between neurons. This potentially opens what may be a whole new direction for ketamine related antidepressant medication.

The LENS Neurofeedback Ketamine Connection

There is an additional reason these findings are particularly interesting to me as a LENS neurofeedback practitioner. When treating depression it is common for us to see (temporary) reversal of depression within minutes. LENS neurofeedback is unlikely to increase synaptic growth in such a short period of time. We think that LENS works by getting the brain out of frozen, stuck patterns. This allows the brain to use pre-existing healthy patterns that were no longer functionally available. In this theory, LENS would not be causing the growth of new synapses as much as removing the “blockage” of already existing neural connections. The two mechanisms might be functionally very similar—they both promote increased neuro-connectivity. Naturally this is highly speculative, but it suggests an area that researchers studying LENS might look at in the future. Regardless, ketamine might finally provide relief for so many who have not been able to find it elsewhere.

The importance of coping with stress is not just a quality of life issue. It’s also a quantity of life issue.

We all know chronic stress isn’t good for our health. But an important new study shows how devastating it can be and why you need to be vigilant and know your options.  This recently published research in the journal BMJ (British Medical Journal) reveals that even normal levels of stress will increase the likelihood of dying by 20% over a 10-year period.

This long-term study, the results of 68,000 people filling out questionnaires in England’s National Health Surveys, reveals more disturbing results: It concluded that people with only mild stress are about 29% more likely to die of heart disease or stroke than people who reported none.  Those with moderate stress levels are 43% more likely to die of any cause. And people with high stress levels were 94% more likely to die during the 10-year study.

Stress Relief Options

So what can you do to deal with your stress and anxiety? The usual recommendations include meditation, medication, biofeedback, more exercise, regular sleep times and reduction of risk factors for heart disease.  But there are challenges with these modalities.

First off, other than sleeping regularly, all these techniques require time and effort, both of which are often in scarce supply. Paradoxically, trying to follow these regimens might actually increase your stress. And even if someone does achieve relaxation using these techniques, it’s often difficult to integrate that relaxation into daily life.

But there is another way…and a quick one at that. It might not be a panacea for stress, but it’s certainly a good start. And a simple one. Just smile.

It doesn’t even have to be a genuine smile. Even a forced one is effectively contributes to a lower heart rate and blood pressure, leads to easier breathing, feeling more relaxed and emotional resilience. It’s another example of the intimate mind/body connection. Your body just naturally reacts to the stimulation of your facial muscles. It’s not so different from feeling less depressed and more dignified when we stand up straight.

While the momentary stress relief of a smile is a start a more enduring choice for stress relief is LENS Neurofeedback.  All you have to do is sit down and close your eyes for a few seconds at a time. A sensor tracks your brainwaves and sends back an extremely brief (1/100^th of a second) and tiny (hundreds of times less than a cell phone) radiofrequency. This signal is a mirror image of your own brainwave pattern plus an offset. This causes is a slight fluctuation in your own brainwaves and the brain gets out of its frozen, stuck patterns and relaxes. After a number of sessions this more relaxed brain becomes this state of mind we naturally come back to, even under trying circumstances. This is the only treatment I know that’s even easier than smiling.

The symptoms of sleep deprivation in children resemble those of Attention Deficit Hyperactivity Disorder (ADHD). These include being wired, moody and uncooperative, unable to pay attention or sit still, and to have poor social skills.

The truth is that many children are given a diagnosis of ADHD when in fact the real problem may lie in a sleep disorder such as sleep apnea. This misdiagnosis may account for a significant 22% increase from 2003-2007 in the number of children adjudged to have ADHD.

The latest study to propose a link between inadequate sleep and ADHD symptoms appeared last month in the journal Pediatrics.  Researchers followed 11,000 British children for six years, starting when they were 6 months old.  The findings were eye-opening: children whose sleep was affected by breathing problems were 40 percent to 100 percent more likely to develop behavioral problems resembling A.D.H.D. than normal breathers.

Karen Bonuck, the study’s lead author and a professor of family and social medicine at Albert Einstein College of Medicine in New York says, “Lack of sleep is an insult to a child’s developing body and mind that can have a huge impact.”

Other studies now under way indicate that removal of a child’s adenoids (tonsils) improves behavioral issues and resulted in less likelihood of an ADHD diagnosis.  But perhaps most significant is the finding that most children already found to have ADHD before tonsillectomy surgery subsequently behaved so much better that they no longer fit the ADHD profile.

Dr. Ronald Chervin, a neurologist and director of University of Michigan Sleep Disorders Center in Ann Arbor feels that behavioral problems linked to nighttime breathing difficulties are more attributable to  inadequate sleep than oxygen deprivation.  Other sleep experts point out that children who lose as little as half an hour of needed sleep per night can exhibit behaviors typical of ADHD.  To compound this misdiagnosis, drugs like Ritalin prescribed to treat ADHD in children may only exacerbate the problem because they can cause insomnia.

Sleep deprivation is difficult to spot in children.  Of the 10,000 members of the American Academy of Sleep Medicine, only 500 have specialty training in pediatric sleep issues.  Professor Bonuck says, “It’s incredible that we don’t screen for sleep problems the way we screen for vision and hearing problems.”

For questions or further information please contact Susan at The Dubin Clinic of LENS Neurofeedback:
Phone: 310-694-1056 | susanpitts21@gmail.com

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We look forward to seeing you at the presentations.

It’s thought that the sooner a child who has ASD is identified the sooner treatment and training and other resources can be applied. (There is an array of interventions, none of them entirely effective, which can help. A very promising new intervention showing noticeable improvements is neurofeedback.) Early identification and treatment can result in improved development, and this leads to a happier and healthier child. However, it is often difficult to identify if a child is at risk. The best early indicators of ASD are developmental delays. An article in Science Daily News lists the ten most common ones:

1. Rarely smiles when approached by caregivers
2. Rarely tries to imitate sounds and movements made by others such as smiling and laughing
3. Delayed or infrequent babbling
4. Does not exhibit increasing consistency in response to his or her name being spoken as the child develops from months 6 to 12.
5. Does not make gestures to communicate with the parent or caregiver by ten months.
6. Poor eye contact. The infant makes no particular effort to visually interact, a central component of healthy development.
7. There is little to no effort to attract caregiver attention if hungry or any other particular urge.
8. There is a range of atypical body movements that can be seen. These include stiffening of the arms, hands, or legs. Also unusual body movements such as rotating the hands on the wrists, unusual postures or any other repetitive movement or behavior.
9. When the caregiver reaches to pick up the child she does not respond and reach back.
10. There are a variety of delays in motor development. These include delayed rolling over, pushing up or crawling.

While certainly not all delays lead to autism, the authors of the article encourage parents to become good observers. That way they will be better able to identify these types of developmental delays. While it’s generally agreed that delays or other problems are often seen before 14 months, diagnosis may be possible as early as three months.

When the potential of ASD presents itself, parents shouldn’t adopt a “wait and see” attitude. It’s best to begin intervention early while the brain is most malleable and its circuitry is still evolving. The younger the age ASD is treated, the better the chances for healthy development.

Parents who suspect their child suffers from ASD are advised to consult with their pediatrician without delay.

What is the problem with having too many connections? An effective brain must be flexible. It must be able synchronize and then later desynchronize neuronal patterns to effectively regulate mood, solve problems and respond to others. From a superficial point of view, we might correlate increased connectivity and synchronization with enhanced performance, not clinical symptoms. But that isn’t the case: too much of a good thing (connectivity) can prove to be very detrimental. The brain is literally overwhelmed and no longer reliably able to turn off certain connections. This is particularly true when those connections become linked with depression.

It’s as if the brain is trying to hold itself together as even more and more problems pile on. It’s too much for the brain to handle, and in response more and more brain connections become rigid. The upshot of an overwhelmed over-connected brain is the persistence of debilitating symptoms.  A clinically depressed person is not just unhappy. He or she is often suffering from a whole range of problems. Anxiety, poor concentration, memory loss, insomnia, and isolating from others are often part of depression syndrome. That there is such a multitude of symptoms suggests that depression isn’t simply a particular part of the brain that’s involved, but multiple areas of the brain along with the networks and connections linking them together.

Hyper-connectivity is an issue with other diseases besides depression. For example, many people on the ASD (autistic spectrum disorder) evidence brain hyper-connectivity with similar rigid patterns and lack of flexibility.  We will likely find hyper-connectivity plays a role in other diseases as well.

The good news is that these insights into brain interconnectivity support the use of LENS Neurofeedback in the treatment of depression and other diseases. By untangling the brain where it is stuck, LENS Neurofeedback helps the brain become more pliant. In fact, we see the whole range of symptoms associated with depression all improve with LENS Neurofeedback. We don’t just see enhancement of mood, but also reduced anxiety, improved attention, better memory, increased concentration, more motivation and capacity for enjoyment, less isolation and improved sleep. And we usually begin to see these changes within the first four sessions. Additional sessions (typically about fifteen) are needed so these changes become enduring. The brain wants to stay in this more effective state. After all, it’s a lot more work for the brain to compensate for rigid patterns than it is to maintain healthy, flexible ones.