The Brain's Ability to Rewire: Plasticity and Adaptation

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The Brain's Ability to Rewire: Plasticity and Adaptation

Abnormal Psychology · Chapter 3: Biological Underpinnings of Psychological DisordersSection 3.3 · lesson 11 of 9719 min · free with a free account

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In this lesson

One mechanism, pointed in two directions - and why that is grounds for optimism.

  • Define neuroplasticity and describe its principal mechanisms
  • Separate adaptive from maladaptive plasticity, and say why the mechanism is neutral
  • Explain how plasticity underwrites both a condition and recovery from it
  • Apply the transfer problem to claims about cognitive training

Transcript

Everything said in the video, section by section (2,520 words). Read along, or search it.

Biological Underpinnings of Psychological Disorders

The Brain's Ability to Rewire

The brain changes. That fact is true, important, and constantly overstated. This section takes it seriously and keeps it honest. What neuroplasticity actually is, and the mechanisms that carry it. Then the point the whole section turns on. The mechanism is neutral. It does not know what it is strengthening. The same process that makes a skill automatic makes an avoidance automatic. So plasticity explains how a condition develops, and how treatment works. Those are the same story, pointed in two directions. We finish with two composite cases, side by side. One is called rehabilitation. One is called a problem. The mechanism is identical.

Before You Begin

The Most Overclaimed Idea in the Chapter

Two notes before we begin. This material is educational, and not a basis for any treatment decision. Now the second note, and it is the important one here. Plasticity is the most overclaimed idea in this chapter. And the overclaiming does harm in a specific direction. That the brain can change does not mean a person can reverse a serious condition through effort. And it does not mean that someone who has not recovered failed to try hard enough. Recovery depends on the condition, and on the treatment available. On the circumstances, and on a great deal of chance. Nothing here places responsibility for an outcome on the person living with it.

The Concept

What Plasticity Is, and What Supports It

Neuroplasticity is the capacity of the nervous system to change its structure and function. In response to experience, activity, injury, and environment. The word covers changes at several scales. From the strength of a single synapse, to the reorganization of whole regions. For much of the twentieth century, the working assumption was the opposite. That the brain was substantially fixed after early development. That assumption has been overturned, and two corrections keep the shift accurate. Plasticity is not unlimited. The adult brain changes less readily than the developing brain in several respects. And some capacities genuinely do not recover. Second, plasticity is not inherently good. It is a capacity for change in whichever direction experience pushes it. Several factors are associated with better maintenance of plasticity across life. Physical activity has the most consistent evidence, though the effect size stays debated. Sleep is directly implicated in the consolidation of learning. Cognitive and social engagement is associated with better later-life outcomes. Though the direction of effect there is hard to establish. And sustained stress is associated with dendritic changes, particularly in the hippocampus. Now hear what that list is not. It is not a program that reverses conditions. And it is not a set of instructions whose neglect explains why someone is unwell. Someone with a serious condition may be unable to do several of these because of it.

Mechanisms

Four Processes, Differing in How Well Established They Are

Four mechanisms account for most of what is meant by plasticity. Synaptic strengthening and weakening is the best established. When one neuron repeatedly participates in firing another, the connection becomes more effective. More transmitter released, more receptors on the receiving side, a larger contact area. When a connection goes unused, the reverse happens. The principle is summarized as cells that fire together wire together. Accurate as far as it goes, provided you do not read it as saying co-occurrence is enough. Dendritic and synaptic change operates at the level of structure rather than strength. Dendrites grow new branches and new receiving spines with enriched experience. And lose them with disuse, or with prolonged stress. So the number of connections available changes, not only their efficiency. Myelination is the wrapping of axons in a fatty insulating sheath. It greatly increases the speed of signal conduction. It continues into early adulthood, notably in the prefrontal regions. And it is modified by activity. Heavily used pathways become better insulated, and faster. The fourth requires the most caution. Adult neurogenesis. The generation of new neurons in the adult brain. It is well established in some other mammals. In adult humans the evidence is genuinely contested. Studies using different methods have reached opposing conclusions. The honest position is that it may occur to a limited degree, in limited regions. Its functional significance is unresolved. And popular accounts calling it a route to self-improvement have gone beyond the evidence.

Two Uses Of Experience

Expected Input, and Individual Input

The nervous system uses experience in two different ways. Distinguishing them prevents a common confusion about what deprivation does. Experience-expectant plasticity depends on input the developing system assumes it will receive. Input every member of the species gets. Patterned light, sounds, touch, movement, social contact. The system is built to await this input, and to organize itself around it. Because the input is reliably available, the system need not encode the detail genetically. It needs only to be ready to use it. But if the input is absent at the expected time, the organization does not occur normally. And the resulting deficit can be severe and lasting. Experience-dependent plasticity is driven by experience particular to the individual. A language, a skill, a route through a city, a trade. Nothing about it is expected by the system. It has no fixed timetable, and it continues throughout life. So the practical distinction is this. The first kind is about whether a system develops at all, and is tied to a window. The second is about what a developed system comes to contain, and is open-ended. A person deprived of patterned visual input in infancy faces a different situation. A different situation from a person who never learned to read.

Windows

Most of Them Narrow Rather Than Close

A critical period is a window during which particular input is required. Required for normal development, and after which the opportunity is largely lost. A sensitive period is a window of unusually high responsiveness. But one that narrows rather than closes. Change remains possible afterward. More slowly, and with more effort. Most windows in human development are sensitive rather than strictly critical. Genuine critical periods are best documented for basic sensory systems. Now the evidence on deprivation, and state it carefully because both halves matter. Studies of children raised in severely deprived institutional environments found substantial difficulties. Cognitive, social, and emotional development were all affected. Considerable recovery followed placement into responsive care. Recovery was greater the earlier that placement occurred. And some difficulties persisted for those deprived longest. Deprivation causes real harm, and the system retains substantial capacity to recover. So why do some windows close while others narrow? The current account is that closure is not the exhaustion of a capacity. It is the accumulation of brakes. The maturing system develops structures that stabilize what has been built. Protecting established organization from being overwritten. On that account, closure is a feature rather than a failure. And because those brakes are physical, researchers ask whether windows might be reopened. That is an active research question, and not a current treatment.

After Injury

Reorganization, and What It Cannot Promise

When part of the brain is damaged, some function is often recovered. The mechanisms are worth distinguishing from the hopeful vagueness that surrounds them. Functional reorganization is the takeover of a lost function by tissue that did not perform it. Most often adjacent to the damaged area, or in the matching region of the other hemisphere. Recruitment of adjacent tissue describes neighboring representations expanding into vacated territory. Much early recovery is the resolution of swelling and inflammation. Not reorganization at all. Which is why the first weeks after an injury are misleading about the eventual outcome. The limits are real, and should be stated plainly. Recovery is usually partial. It depends on the size and location of the damage, on age, and on rehabilitation intensity. Some functions recover much better than others. And reorganization can carry costs, since recruited tissue may do its original job less well. One historical case is conventionally cited here. A nineteenth-century railway worker survived a severe injury to the front of the brain. His personality and conduct were reported to change substantially afterward. The record is incomplete, and contemporaneous documentation is thin. The most colorful descriptions were written long after the events, by people who never met him. The case establishes that frontal damage can change personality and conduct. It is not sound evidence for anything more specific than that.

Neutral Mechanism

The Same Strengthening, Entrenching a Problem

Now the turn this whole section depends on. Maladaptive plasticity is change of exactly the kind just described. Change that produces a worse outcome. The same mechanisms, entrenching a pattern rather than building a useful one. The mechanism does not know what it is strengthening. Each time a feared situation is avoided, the relief reinforces the avoidance. The pathways supporting it strengthen, while those supporting approach weaken. The avoidance becomes easier, and the approach becomes harder. That is a plasticity account of why anxiety conditions tend to expand rather than settle. Rumination works the same way. Repeatedly running the same sequence of thought strengthens that sequence. So it is entered more readily, and left less easily. That describes at the neural level what is otherwise called a habit of thought. Chronic pain is a third case. With prolonged pain signaling, the pathways carrying it become more sensitive. So pain can persist, or spread beyond what the original tissue damage would account for. And substance-related change is a fourth, described at the mechanism level only. Repeated exposure produces lasting change in motivational and reward-related circuitry. Cues acquire strong power to drive behavior, while the regulatory systems become less effective. The neutrality of the mechanism is the point. There is no separate bad-plasticity system. And this is grounds for optimism rather than the reverse. If a pattern was built by repeated experience, different repeated experience can build a competing one.

Side By Side

The Same Mechanism, Two Outcomes

Put the pairs side by side and the neutrality becomes concrete. Learning a skill, and entrenching a compulsion. The shared mechanism is that repeated activation strengthens the pathway. The response becomes automatic. An automatic skill is useful. An automatic compulsion is not. But both were built by repetition, so both can be reshaped by different repetition. Recovering from injury, and losing an unused ability. The shared mechanism is that used pathways strengthen and unused ones weaken. Practicing the affected function restores it. Compensating away from it does not. Which is why rehabilitation deliberately prevents compensation. Exposure treatment, and avoidance. Whichever response is repeated becomes the more available one. Repeated approach builds a competing pathway. Repeated avoidance strengthens the existing one. The treatment and the problem use the same mechanism in opposite directions. And an adaptive pain response, against chronic pain sensitization. Repeated signaling increases the sensitivity of the pathway carrying it. Useful when it protects an injury. Harmful when it outlasts the injury. Read that shared mechanism column down and notice it does not change. The rows differ only in what was repeated. Which is why the clinical question is never whether plasticity is occurring. The question is what it is being pointed at.

Treatment

Why Talking Is a Physical Intervention

Psychological treatment is often contrasted with biological treatment. As though one worked on the mind and the other on the brain. Plasticity dissolves that contrast. If experience changes neural structure, then structured repeated experience is a physical intervention. And the convergence is not merely rhetorical. It makes testable predictions. Exposure-based treatment works by repeated approach to a feared situation. Approach without the expected outcome occurring. That builds a competing pathway, which must be strengthened through repetition. So it predicts that repeated, sustained, and varied practice beats brief or narrow practice. And it does. It also predicts measurable brain change following psychological treatment. That has in fact been reported, in some cases resembling changes following medication. Now one caution, and it is important. That psychological treatment produces brain change is not evidence that it works. A treatment that made things worse would also produce brain change. Whether a treatment works is settled by controlled designs, not by imaging. The plasticity account explains the mechanism of a treatment already shown to be effective. This also explains something people find puzzling. Why a therapist sets practice between sessions, rather than doing the work in the room. An hour a week is not repetition. If the competing pathway is practiced weekly while the avoidance is practiced daily. Then the arithmetic of strengthening runs the wrong way.

Transfer

Practice Improves the Practiced Thing

The transfer problem is a repeated finding, and it constrains a lot of claims. Practice on a task improves performance on that task. And on tasks closely resembling it. It improves performance on distant tasks very little, or not at all. Near transfer, to similar tasks, is commonly observed. Far transfer, to different tasks or to everyday functioning, is much harder to demonstrate. And it follows directly from the mechanism. Strengthening applies to the pathways that were active. Practicing one task activates the circuits that task recruits. There is no general-purpose faculty being exercised. So there is no obvious route by which improvement should generalize. This is the standard against which commercial cognitive-training products should be assessed. Participants reliably improve at the trained tasks. That is not in dispute. Evidence for far transfer is weak and inconsistent. And the better-controlled a study is, the smaller the transfer it tends to find. Many early positive studies compared training against no activity at all. Which leaves expectancy uncontrolled, exactly the failure described earlier. The fair conclusion is neither that the products are fraudulent. Nor that they deliver what is advertised. Practice produces real, specific improvement. The claim that this generalizes to broad cognitive enhancement is not currently supported. And notice where the same standard leads with treatment. Exposure therapy also produces specific rather than general change. Which is why it is practiced in the situations the person actually needs to manage.

Two Composites

One Called Rehabilitation, One Called a Problem

Two composites, constructed for instruction, describing no real people. Elena is fifty-two, with weakness and reduced coordination in her right hand and arm. Following a stroke four months ago. Recovery over the first three weeks was rapid, and then it slowed. She cannot yet write legibly or fasten buttons. And she has been using her left hand for nearly all tasks. Her rapid early recovery was substantially resolving swelling, not reorganization. Which is why it slowed. That is expected, not a sign that recovery has stopped. And her use of the left hand for everything is entirely sensible in the short term. It also weakens the affected pathways through disuse. So the rehabilitation program constrains the compensation. And requires many repetitions with the affected hand, on the specific tasks she needs. Now Tom, who is thirty-one. He avoids driving on highways, following a collision two years ago. Nobody was seriously hurt in it. He avoided highways for a few weeks afterward, which felt reasonable. The avoidance then extended to major roads, then to unfamiliar routes. And more recently to driving at all when tired. His journey to work has tripled in length, and he has declined a promotion. Each avoidance produced immediate relief, which strengthened the avoidance pathway. While the pathways supporting driving weakened through disuse. Now compare the two cases directly, because this is the point of the section. Elena's repeated practice is called rehabilitation. Tom's repeated practice is called a problem. The neural process is the same in both. Tom did not do anything wrong. Avoidance after a collision is a normal response. The mechanism did the rest, and the expansion was predicted rather than surprising.

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About The Brain's Ability to Rewire: Plasticity and Adaptation

What is neuroplasticity?
Neuroplasticity is the nervous system's capacity to change its structure and function in response to experience, activity, injury, and environment. It ranges from changes in the strength of single synapses to the reorganization of whole regions. Main mechanisms include synaptic strengthening and weakening, growth and loss of dendritic connections, and myelination. Plasticity is real but not unlimited, and the adult brain changes less readily than the developing brain in several respects.
What is maladaptive plasticity?
Maladaptive plasticity is brain change through the ordinary mechanisms of plasticity that produces a worse outcome. Because the mechanism is neutral, repetition strengthens whatever is practiced. Each time a feared situation is avoided, the relief reinforces avoidance and makes approach harder, which helps explain why anxiety can expand. Rumination and chronic pain sensitization follow the same pattern, and different repeated experience can build a competing pathway.
What is the difference between a critical period and a sensitive period in brain development?
A critical period is a window when particular input is required for normal development, after which the opportunity is largely lost, while a sensitive period is a window of heightened responsiveness that narrows rather than closes. Most windows in human development are sensitive, with strict critical periods best documented for basic sensory systems. Studies of children leaving deprived institutions showed considerable recovery after placement in responsive care, greater with earlier placement.
Do brain training games improve general intelligence?
The evidence does not currently support claims that brain training produces broad cognitive enhancement. Practice reliably improves performance on the trained task and on closely similar tasks, called near transfer, but far transfer to different tasks or everyday functioning is weak and inconsistent. Better-controlled studies tend to find smaller transfer, and many early positive studies lacked an active comparison, leaving expectancy effects uncontrolled.

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Abnormal Psychology (Psychology 180) carries a NCCRS credit recommendation for 3 semester credits. ACE and NCCRS have over 2,100 cooperating colleges that will consider accepting credits; the final decision is with the universities.
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