If you gathered some of the most prominent neuroscientists from a few decades ago and got them to engage in a round-table discussion on whether the human brain can change and modify its structure and function based on experience and/or injury in adulthood, the consensus would have been a resounding “no.” Until at least the 1960s, the prevailing wisdom among the scientific community was that human brains changed, grew, and developed at a rapid rate during childhood, and then all of a sudden, just stopped doing so.
Hardwired or capable of change?
In fact, scientists were so fond of thinking about the human brain as a machine that they extended several computer-related metaphors to the brain as well. “Hardwiring” was a term commonly used to describe the brain. Much like a machine, it was assumed that the brain was a rigid structure, incapable of dramatic change.
It was presumed, for instance, that brain cells that were injured or failed to develop properly had no way of being replaced. Also, if part of the human brain were damaged, it could not find new pathways to perform those same functions.
This had all sorts of implications — people born with brain damage or those who sustained it in adulthood due to some sort of injury were doomed to live with their failings. Scientists of the time were also deeply resistant to the now mainstream idea that adults can grow and improve their brain function (and even preserve brain function in old age) through lifestyle habits and mental exercise.
In his book 'The Brain that Changes Itself', psychiatrist Norman Doidge dubs the culture that had taken hold within the scientific community “neurological nihilism.” He goes as far as to claim that this limited view of the human brain had implications for the way human nature was perceived as well. Since brains were rigid and incapable of change, perhaps human nature was so as well.
There were several reasons why the belief that brains were hardwired got so ingrained into medical and scientific wisdom, not least of which was that the tools to study the microscopic structure and activities of the living brain did not exist back then.
The concept of neuroplasticity
Over the years, however, the scientific community made a series of discoveries that gradually but surely changed the view of the brain as being hardwired and rigid. As we shall see, our brains are changing every minute — each activity that our brains perform cause our brains to modify their very structure, and perfect the connections between brain cells or neurons to be more efficient at the task at hand. We also know now that if certain brain structures “fail,” then other parts can compensate to a certain degree. All this has led to a shift in the mainstream wisdom about the brain. Yes, the brain can indeed change, modify connections between various neurons and adapt based on experience, and this ability has been dubbed “neuroplasticity.”
In stark contrast to the machine metaphor then, neuroplasticity deems the human brain to be malleable and dynamic. While a lot is yet unknown about the mechanisms by which plasticity occurs, there is probably no feature of the human brain that is as remarkable, and which offers as much sheer hope. Plasticity is not merely about adapting to change, it is about the brain literally reorganising itself to compensate for lost function or in response to a new stimulus.
Examples abound
Pick up any modern neuroscience textbook, and examples of brain plasticity abound. We have all heard of people recovering at least some of their brain function after a stroke, and one of the main drivers of this recovery is neural reorganisation.
Within hours of someone having a stroke, their brain begins to show signs of plasticity — neurons grow new dendrites, which are the regions that receive input from other neurons; there is also an increase in the number of connections between healthy neurons, and one area of the brain might take over the function of another area. This spontaneous recovery of function plateaus after three months, especially with respect to some functions like movement.
Beyond the time window of six months post-stroke, recovery of brain function is rare enough to qualify the remaining deficits as chronic, although with intensive training and therapy, some more cognitive functions like language can be recovered.
This, of course, begs the question — if our brains were so great at reorganising themselves, why doesn’t everyone recover completely following a stroke? Of course, the matter is complicated, and several factors come into play — individual and genetic differences aside, how old was the person when they had the stroke? How large was the area of the brain that was damaged? And of course, how thorough was the rehabilitation effort?
Digging a little deeper
Read the textbook chapter on neural plasticity a little further, and some of it begins to sound like science fiction. There are several studies to show that people who lose their eyesight early in their life perform non-visual tasks better than sighted people. This seems to be especially true for hearing.
It is no coincidence that there are several incredibly gifted musicians, like Stevie Wonder, who lost their sight at a very young age. But how does this enhancement of other senses happen? At least with respect to hearing, scientists might have found a part of the answer — brain imaging studies have shown that when blind people engage in a task that requires them to use their hearing, the areas of the brain that usually respond to sight are activated. Much about this process is yet unknown, including how the visual areas are used to sense hearing, and why some blind people are better than others at sensing hearing.
To dig a little deeper into the molecular mechanisms underlying such plasticity between two different senses, scientists studied a roundworm. Yes, you read right. Neuroscientists are fond of studying molecular mechanisms of basic neural processes using a simple worm called Caenorhabditis elegans, or C. elegans in short, given that it has a remarkably simple nervous system, and that the organism lends itself very well to being bred in a laboratory for study. A study on C. elegans found that worms that have a genetic mutation that causes an inability to sense touch, show an enhanced sense of smell. Given that C. elegans has a simple nervous system that can be studied in detail, the scientists who authored this study were able to pinpoint exactly how this enhancement occurred.
In normal C.elegans worms, the neurons that responded to touch secreted a chemical that caused a decrease in the activity of a neuronal connection important for the sense of smell. In the mutant worms on the other hand, there was no touch input being sensed by the touch neurons, and thus no chemical secreted to inhibit the sense of smell. Relieved of this inhibition, the mutant worms were able to transform themselves into super-sensors of smell. While this example is just one way in which neural plasticity occurs at a molecular level, it provides an insight into some of the ways by which neural reorganization and thus functional gain can occur.
Critical periods of plasticity
While the previous few paragraphs might have given the impression of the brain being a super-organ, plasticity has its limitations. Learning during childhood, for instance, is not as innate as it sometimes seems. There needs to be appropriate environmental input for the brain to develop various aspects of its function in the right manner.
Nobel laureates David Hubel and Torsten Wiesel performed a rather grotesque experiment in the 1960s that showed that for many of our faculties to develop correctly, there needs to be appropriate input during a specific time period in our childhood. Each of our faculties, for example, hearing, or vision, has a critical time window (called the critical period) during which, in the absence of the required input from the environment, the development of the faculty will not occur.
Hubel and Wiesel sutured shut one eye of a kitten during the entire critical period for visual development in cats (which lasts from three weeks to a few months of age), and what they found was astonishing. The sutured eye of the kitten, on reopening, remained functionally blind for the rest of its life, despite the fact that its retina and all the other parts of its eye were all working perfectly fine.
During critical periods, learning happens extremely quickly, assuming that there is appropriate environmental input. This is why, for instance, children learn languages so much quicker than adults do. It is not impossible for adults to learn a new language; it is just much harder because the critical period for language has long passed.
Critical periods have also been studied in detail with respect to cochlear implants for children with deafness. These devices, which use a sound processor to capture sounds and deliver them to the hearing (auditory) nerve, must be implanted during a specific time window in childhood for maximum benefit.
When children are implanted with cochlear implants early in childhood, they can achieve remarkable success with the acquisition of language, especially if they have a committed support system and access to an environment of enriched language input. However, children who are implanted at elementary school age or later usually find it hard to discriminate between complex sounds used in the language despite being able to hear sounds, even after many years of wearing the device.
Not all is good news
This ability — and willingness — of our brain to reorganise following an injury does not always come with welcome effects. People who have their limbs amputated sometimes experience excruciating “phantom pain” — pain in a limb that does not even exist. Why this happens is a classic illustration of plasticity in the cortex.
There are a few hypotheses about why phantom limbs occur, but the prevailing scientific explanation is that of neuronal reorganisation within a part of the brain called the cortex, one of the functions of which is recognising and responding to sensation.
According to this theory, neurons that used to respond to sensations from the now missing limb start responding to input from other nearby neurons in the cortex. This creates a kind of cross-wiring if you will — sensations from other parts of the body, say the face, end up activating neurons that used to respond to the missing limb, giving the brain the illusion that the missing limb still exists. Recent research also suggests that not just the sensation of the limb, but also phantom limb pain can be explained by cortical reorganisation, given that the greater the reorganisation of the cortex, the more intense the pain from the missing limb.
It is not just phantom limb pain that is an unfortunate outcome of our brain’s plasticity. Any environmental influence — such as drug addiction — that acts on our brain and changes our behaviour does so by exploiting the ability of our brain to change drastically in response to stimuli. Norman Doidge refers to this ability of plasticity to sometimes give rise to more rigid and repetitive behaviours as the “plastic paradox.” Once a plastic change is entrenched in the brain, he says, it can sometimes act to prevent other modifications from occurring.
The author is a neuroscience PhD turned science writer who is fascinated by the workings of the brain and how we can ‘rewire’ it to our advantage.
The Mind’s Eye is a column that explores neuroscience in everyday life.
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