“The brain is so complicated it staggers its own imagination.”
“Neurons that fire together, wire together”, “neurons that fire out of sync, fail to link”.
We can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses. The power to direct our attention, focus, has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.
The causal arrows between brain and mind point in both directions. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.
Daniel J. Siegel, MD, is a clinical professor of psychiatry at the UCLA School of Medicine, co-director of the UCLA Mindful Awareness Research Center, and executive director of the Mindsight Institute.
The ability of the brain to form and reorganize synaptic connections, especially in response to learning or experience or following injury. “neuroplasticity offers real hope to everyone from stroke victims to dyslexics”
It’s easy to get overwhelmed thinking about the brain. With more than one hundred billion interconnected neurons stuffed into a small, skull-enclosed space, the brain is both dense and intricate. And as if that weren’t complicated enough, each of your average neurons has ten thousand connections, or synapses, linking it to other neurons. In the skull portion of the nervous system alone, there are hundreds of trillions of connections linking the various neural groupings into a vast spiderweb-like network. Even if we wanted to, we couldn’t live long enough to count each of those synaptic linkages.
Given this number of synaptic connections, the brain’s possible on-off firing patterns, its potential for various states of activation, has been calculated to be ten to the millionth power, or ten times ten one million times. This number is thought to be larger than the number of atoms in the known universe. It also far exceeds our ability to experience in one lifetime even a small percentage of these firing possibilities. As a neuroscientist once said, “The brain is so complicated it staggers its own imagination.” The brain’s complexity gives us virtually infinite choices for how our mind will use those firing patterns to create itself. ‘If we get stuck in one pattern or the other, we’re limiting our potential.
Patterns of neural firing are what we are looking for when we watch a brain scanner “light up” as a certain task is being performed. What scans often measure is blood flow. Since neural activity increases oxygen use, an increased flow of blood to a given area of the brain implies that neurons are firing there. Research studies correlate this inferred neural firing with specific mental functions, such as focusing attention, recalling a past event, or feeling pain.
We can only imagine how a scan of my brain might have looked when I went down the low road in a tense encounter with my son one day: an abundance of limbic firing with increased blood flow to my irritated amygdala and a diminished flow to my prefrontal areas as they began to shut down. Sometimes the out-of-control firing of our brain drives what we feel, how we perceive what is happening, and how we respond. Once my prefrontal region was off-Iine, the firing patterns from throughout my subcortical regions could dominate my internal experience and my interactions with my kids. But it is also true that when we’re not traveling down the low road we can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses.
One of the key practical lessons of modern neuroscience is that the power to direct our attention has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.
As you become more familiar with the various parts of the brain, you can more easily grasp how the mind uses the firing patterns in these various parts to create itself. It bears repeating that while the physical property of neurons firing is correlated with the subjective experience we call mental activity, no one knows exactly how this actually occurs. But keep this in the front of your mind:
Mental activity stimulates brain firing as much as brain firing creates mental activity.
When you voluntarily choose to focus your attention, say, on remembering how the Golden Gate Bridge looked one foggy day last fall, your mind has just activated the visual areas in the posterior part of your cortex. On the other hand, if you were undergoing brain surgery, the physician might place an electrical probe to stimulate neural firing in that posterior area, and you’d also experience a mental image of some sort.
The causal arrows between brain and mind point in both directions.
Keeping the brain in mind in this way is like knowing how to exercise properly. As we work out, we need to coordinate and balance the different muscle groups in order to keep ourselves fit. Similarly, we can focus our minds to build the specific “muscle groups” of the brain, reinforcing their connections, establishing new circuitry, and linking them together in new and helpful ways. There are no muscles in the brain, of course, but rather differentiated clusters of neurons that form various groupings called nuclei, parts, areas, zones, regions, circuits, or hemispheres.
And just as we can intentionally activate our muscles by flexing them, we can “flex” our circuits by focusing our attention to stimulate the firing in those neuronal groups. Using mindsight to focus our attention in ways that integrate these neural circuits can be seen as a form of “brain hygiene.”
WHAT FIRES TOGETHER, WIRES TOGETHER
You may have heard this before: As neurons fire together, they wire together. But let’s unpack this statement piece by piece. When we have an experience, our neurons become activated; What this means is that the long length of the neuron, the axon, has a flow of ions in and out of its encasing membrane that functions like an electrical current. At the far end of the axon, the electrical flow leads to the release of a chemical neurotransmitter into the small synaptic space that joins the firing neuron to the next, postsynaptic neuron. This chemical release activates or deactivates the downstream neuron. Under the right conditions, neural firing can lead to the strengthening of synaptic connections. These conditions include repetition, emotional arousal, novelty, and the careful focus of attention! Strengthening synaptic linkages between neurons is how we learn from experience.
One reason that we are so open to learning from experience is that, from the earliest days in the womb and continuing into our childhood and adolescence, the basic architecture of the brain is very much a work in progress.
During gestation, the brain takes shape from the bottom up, with the brainstem maturing first. By the time we are born, the limbic areas are partially developed but the neurons of the cortex lack extensive connections to one another.
This immaturity, the lack of connections within and among the different regions of the brain, is what gives us that openness to experience that is so critical to learning.
A massive proliferation of synapses occurs during the first years of life. These connections are shaped by genes and chance as well as experience, with some aspects of ourselves being less amenable to the influence of experience than others. Our temperament, for example, has a nonexperiential basis; it is determined in large part by genes and by chance. For instance, we may have a robust approach to novelty and love to explore new things, or we may tend to hang back in response to new situations, needing to “warm up” before we can overcome our initial shyness. Such neural propensities are set up before birth and then directly shape how we respond to the worId-and how others respond to us.
From our first days of life, our immature brain is also directly shaped by our interactions with the world, and especially by our relationships. Our experiences stimulate neural firing and sculpt our emerging synaptic connections. This is how experience changes the structure of the brain itself, and could even end up having an influence on our innate temperament.
As we grow, then, an intricate weaving together of the genetic, chance, and experiential input into the brain shapes what we call our “personality,” with all its habits, likes, dislikes, and patterns of response. If you’ve always had positive experiences with dogs and have enjoyed having them in your life, you may feel pleasure and excitement when a neighbor’s new dog comes bounding toward you. But if you’ve ever been severely bitten, your neural firing patterns may instead help create a sense of dread and panic, causing your entire body to shrink away from the pooch. If on top of having had a prior bad experience with a dog you also have a shy temperament, such an encounter may be even more fraught with fear. But whatever your experience and underlying temperament, transformation is possible. Learning to focus your attention in specific therapeutic ways can help you override that old coupling of fear with dogs.
The intentional focus of attention is actually a form of self-directed experience: It stimulates new patterns of neural firing to create new synaptic linkages.
You may be wondering, “How can experience, even a mental activity such as directing attention, actually shape the structure of the brain?” As we’ve seen, experience means neural firing. When neurons fire together, the genes in their nuclei, their master control centers, become activated and “express” themselves. Gene expression means that certain proteins are produced. These proteins then enable the synaptic linkages to be constructed anew or to be strengthened.
Experience also stimulates the production of myelin, the fatty sheath around axons, resulting in as much as a hundredfold increase in the speed of conduction down the neuron’s length. And as we now know, experience can also stimulate neural stem cells to differentiate into wholly new neurons in the brain.
This neurogenesis, along with synapse formation and myelin growth, can take place in response to experience throughout our lives. As discussed before, the capacity of the brain to change is called neuroplasticity. We are now discovering how the careful focus of attention amplifies neuroplasticity by stimulating the release of neurochemicals that enhance the structural growth of synaptic linkages among the activated neurons.
An additional piece of the puzzle is now emerging. Researchers have discovered that early experiences can change the long-term regulation of the genetic machinery within the nuclei of neurons through a process called epigenesis.
If early experiences are positive, for example, chemical controls over how genes are expressed in specific areas of the brain can alter the regulation of our nervous system in such a way as to reinforce the quality of emotional resilience. If early experiences are negative, however, it has been shown that alterations in the control of genes influencing the stress response may diminish resilience in children and compromise their ability to adjust to stressful events in the future.
The changes wrought through epigenesis will continue to be in the science news as part of our exploration of how experience shapes who we are.
In sum, experience creates the repeated neural firing that can lead to gene expression, protein production, and changes in both the genetic regulation of neurons and the structural connections in the brain. By harnessing the power of awareness to strategically stimulate the brain’s firing, mindsight enables us to voluntarily change a firing pattern that was laid down involuntarily. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.
THE BRAIN IN THE BODY
It’s important to remember that the activity of what we’re calling the “brain” is not just in our heads. For example, the heart has an extensive network of nerves that process complex information and relay data upward to the brain in the skull. So, too, do the intestines, and all the other major organ systems of the body. The dispersion of nerve cells throughout the body begins during our earliest development in the womb, when the cells that form the outer layer of the embryo fold inward to become the origin of our spinal cord. Clusters of these wandering cells then start to gather at one end of the spinal cord, ultimately to become the skull-encased brain. But other neural tissue becomes intricately woven with our musculature, our skin, our heart, our lungs, and our intestines. Some of these neural extensions form part of the autonomic nervous system, which keeps the body working in balance whether we are awake or asleep; other circuitry forms the voluntary portion of the nervous system, which allows us to intentionally move our limbs and control our respiration. The simple connection of sensory nerves from the periphery to our spinal cord and then upward through the various layers of the skull-encased brain allows signals from the outer world to reach the cortex, where we can become aware of them. This input comes to us via the five senses that permit us to perceive the outer physical world.
The neural networks throughout the interior of the body, including those surrounding the hollow organs, such as the intestines and the heart, send complex sensory input to the skull-based brain. This data forms the foundation for visceral maps that help us have a “gut feeling” or a “heartfelt” sense. Such input from the body forms a vital source of intuition and powerfully influences our reasoning and the way we create meaning in our lives.
Other bodily input comes from the impact of molecules known as hormones. The body’s hormones, together with chemicals from the foods and drugs we ingest, flow into our bloodstream and directly affect the signals sent along neurai routes. And, as we now know, even our immune system interacts with our nervous system. Many of these effects influence the neurotransmitters that operate at the synapses. These chemical messengers come in hundreds of varieties, some of which, such as dopamine and serotonin, have become household names thanks in part to drug company advertising. These substances have specific and complex effects on different regions of our nervous system. For example, dopamine is involved in the reward systems of the brain; behaviors and substances can become addictive because they stimulate dopamine release. Serotonin helps smooth out anxiety, depression, and mood fluctuations. Another chemical messenger is oxytocin, which is released when we feel close and attached to someone.
Throughout this book, I use the general term brain to encompass all of this wonderful complexity of the body proper as it intimately intertwines with its chemical environment and with the portion of neural tissue in the head. This is the brain that both shapes and is shaped by our mind. This is also the brain that forms one point of the triangle of well-being that is so central to mindsight.
By looking at the brain as an embodied system beyond its skull case, we can actually make sense of the intimate dance of the brain, the mind, and our relationships with one another. We can also recruit the power of neuroplasticity to repair damaged connections and create new, more satisfying patterns in our everyday lives.
Mindsight, change your brain and your life
by Daniel J. Siegel MD
get it at Amazon.com
Neuroplasticity – Wikipedia
Neuroplasticity, also known as brain plasticity and neural plasticity, is the ability of the brain to change throughout an individual’s life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time.
Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are “plastic”) even through adulthood.“ However, the developing brain exhibits a higher degree of plasticity than the adult brain.
Neuroplasticity can be observed at multiple scales, from microscopic changes in individual neurons to larger-scale changes such as cortical remapping in response to injury. Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.
At the single cell level, synaptic plasticity refers to changes in the connections between neurons, whereas non-synaptic plasticity refers to changes in their intrinsic excitability.
One of the fundamental principles underlying neuroplasticity is based on the idea that individual synaptic connections are constantly being removed or recreated, largely dependent upon the activity of the neurons that bear them. The activity-dependence of synaptic plasticity is captured in the aphorism which is often used to summarize Hebbian theory: “neurons that fire together, wire together”/”neurons that fire out of sync, fail to link”. If two nearby neurons often produce an impulse in close temporal proximity, their functional properties may converge. Conversely, neurons that are not regularly activated simultaneously may be less likely to functionally converge.
Cortical organization, especially in sensory systems, is often described in terms of maps. For example, sensory information from the foot projects to one cortical site and the projections from the hand target another site. As a result, the cortical representation of sensory inputs from the body resembles a somatotopic map, often described as the sensory homunculus.
In the late 1970s and early 1980s, several groups began exploring the impact of interfering with sensory inputs on cortical map reorganization. Michael Merzenich, Jon Kaas and Doug Rasmusson were some of those researchers. They found that if the cortical map is deprived of its input, it activates at a later time in response to other, usually adjacent inputs. Their findings have been since corroborated and extended by many research groups. Merzenich’s (1984) study involved the mapping of owl monkey hands before and after amputation of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third digit, the area in the cortical map formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation. This study demonstrates that only those regions that border a certain area invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Reorganization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.“
Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also part of the somatosensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. The work of Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations causing a substantial impact on the cortical plasticity in that system.
Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1-2 days when a new sensory motor behavior is first acquired, and changes are largely finalised within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, they are strongest for the stimuli that are associated with reward, and they occur with equal ease in operant and classical conditioning behaviors.
An interesting phenomenon involving plasticity of cortical maps is the phenomenon of phantom limb sensation. Phantom limb sensation is experienced by people who have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limb sensation is still not entirely understood it is believed that cortical reorganization plays an important role.
Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of “positive plasticity”. Changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or excessive neurotransmitter release in response to injury that could result in nerve cell death, are considered as an example of “negative” plasticity. In addition, drug addiction and obsessive-compulsive disorder are both deemed examples of “negative plasticity” by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.
A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students’ brains were imaged during the period of studying for their exams. In a matter of months, the students’ gray matter increased significantly in the posterior and lateral parietal cortex.
Applications and example
The adult brain is not entirely “hard-wired” with fixed neuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that neurogenesis (birth of brain cells) occurs in the adult mammalian brain, and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well. However, the degree of rewiring induced by the integration of new neurons in the established circuits is not known, and such rewiring may well be functionally redundant.
There is now ample evidence for the active, experience-dependent reorganization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The way experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind and Neural Darwinism. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia.
Treatment of brain damage
A surprising consequence of neuroplasticity is that the brain activity associated with a given function can be transferred to a different location; this can result from normal experience and also occurs in the process of recovery from brain injury. Neuroplasticity is the fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.
Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in functional outcomes with physical therapy post-stroke. Rehabilitation techniques that are supported by evidence which suggest cortical reorganization as the mechanism of change include constraint-induced movement therapy, functional electrical stimulation, treadmill training with body-weight support, and virtual reality therapy. Robot assisted therapy is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.
One group has developed a treatment that includes increased levels of progesterone injections in brain-injured patients. “Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory motor recovery.” In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections?” However, a study published in the New England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.”
For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.
Several companies have offered so-called cognitive training software programs for various purposes that claim to work via neuroplasticity; one example is Fast ForWord which is marketed to help children with learning disabilities. A systematic metaanalytic review found that “There is no evidence from the analysis carried out that Fast ForWord is effective as a treatment for children‘s oral language or reading difficulties”. A 2016 review found very little evidence supporting any of the claims of Fast ForWord and other commercial products, as their task-speciflc effects fail to generalise to other tasks.
Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system. Due to a sensitive period for plasticity, there is also a sensitive period for such intervention within the first 2-4 years of life. Consequently, in prelingually deaf children, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.
Phantom limb sensation
In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60-80% of amputees. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb.
The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Hertz Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.” Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization. This phenomenon is sometimes referred to as maladaptive plasticity.
In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body. The authors stated that: “In fact, this finding extends our understanding of the brain’s plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms, the brain truly does change itself.”
Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.“ For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.
Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus. However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.
A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, and the ability of the body to heal itself. These functional changes may be caused by changes in the physical structure of the brain.
Fitness and exercise
Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1), and vascular endothelial growth factor (VEGF). Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory. Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus; moderate improvements are seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens. Higher physical fitness scores (measured by V02 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.
Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 and 2011 using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.
Reviews of MRI studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudatenucleus of the basal ganglia.
Neuroplasticity is most active in childhood as a part of normal human development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency. Trauma is considered a great risk as it negatively affects many areas of the brain and puts strain on the sympathetic nervous system from constant activation. Trauma thus alters the brain’s connections such that children who have experienced trauma may be hyper vigilant or overly aroused. However a child’s brain can cope with these adverse effects through the actions of neuroplasticity.
In a single lifespan, individuals of an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages. Some changes occur seasonally in species to enhance or generate response behaviors.
Seasonal brain changes
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals. These changes can improve the chances of mating during breeding season. Examples of seasonal brain morphology change can be found within many classes and species.
Within the class Aves, black-capped chickadees experience an increase in the volume of their hippocampus and strength of neural connections to the hippocampus during fall months. These morphological changes within the hippocampus which are related to spatial memory are not limited to birds, as they can also be observed in rodents and amphibians?“ In songbirds, many song control nuclei in the brain increase in size during mating season. Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common. Gonadotropin-releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.
The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain. Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals. In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.
Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year.
Humans experience a change in the size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it during the fall, when these parts are larger. In the spring, both reduce in size.
Traumatic brain injury research
Randy Nudo’s group found that if a small stroke (an infarction) is induced by obstruction of blood flow to a portion of a monkey’s motor cortex, the part of the body that responds by movement moves when areas adjacent to the damaged brain area are stimulated. In one study, intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys. Some underwent ischemic-infarction procedures and the others, ICMS procedures. The monkeys with ischemic infarctions retained more finger flexion during food retrieval and after several months this deficit returned to preoperative levels.
With respect to the distal forelimb representation, “postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex.” Understanding of interaction between the damaged and undamaged areas provides a basis for better treatment plans in stroke patients. Current research includes the tracking of changes that occur in the motor areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization process of the brain can be ascertained. Nudo is also involved in studying the treatment plans that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.
Jon Kaas, a professor at Vanderbilt University, has been able to show “how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys.” Adult brains have the ability to change as a result of injury but the extent of the reorganization depends on the extent of the injury. His recent research focuses on the somatosensory system, which involves a sense of the body and its movements using many senses. Usually, damage of the somatosensory cortex results in impairment of the body perception. Kaas’ research project is focused on how these systems (somatosensory, cognitive, motor systems) respond with plastic changes resulting from injury.
One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer. Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in the estrus cycle, females recovered even better. This difference may be attributed to different levels of progesterone, with higher levels of progesterone leading to the faster recovery from brain injury in mice. However, clinical trials showed progesterone offers no significant benefit for traumatic brain injury human patients.
The term “plasticity” was first applied to behavior in 1890 by William James in The Principles of Psychology. The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.
In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But these findings were eventually forgotten.
The idea that the brain and its function are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected. Until around the 1970s, neuroscientists believed that the brain’s structure and function was essentially fixed throughout adulthood.
The term has since been broadly applied:
“Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that it was well defined and that a basic and universal framework served to direct current and future hypotheses and experimentation. Sadly, however, this is not the case. While many neuroscientists use the word neuroplasticity as an umbrella term it means different things to different researchers in different subflelds. In brief, a mutually agreed upon framework does not appear to exist.”
Research and discovery
In 1923, Karl Lashley conducted experiments on rhesus monkeys that demonstrated changes in neuronal pathways, which he concluded were evidence of plasticity. Despite this, and other research that suggested plasticity took place, neuroscientists did not widely accept the idea of neuroplasticity.
In 1945, Justo Gonzalo concluded from his research of brain dynamics, that, contrary to the activity of the projection areas, the “central” cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a “maneuvering mass”, rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties. He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment, and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder. He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.
Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.
Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.
In the 1960s, Paul Bach-y-Rita invented a device that was tested on a small number of people, and involved a person sitting in a chair, in which were embedded nubs that were made to vibrate in ways that translated images received in a camera, allowing a form of vision via sensory substitution.
Studies in people recovering from stroke also provided support for neuroplasticity, as regions of the brain that remained healthy could sometimes take over, at least in part, functions that had been destroyed; Shepherd Ivory Franz did work in this area.
Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London’s layout in local taxi drivers. A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media worldwide.
Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for over three decades. He has made some of “the most ambitious claims for the field that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia, that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning, how we learn, think, perceive, and remember are possible even in the elderly.
Merzenich’s work was affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was “…as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself.”
This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, “If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic.” Merzenich received the 2016 Kavli Prize in Neuroscience “for the discovery of mechanisms that allow experience and neural activity to remodel brain function.”