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Neural plasticity

Neural plasticity is “the ability of the central nervous system (CNS) to adapt in response to changes in the environment or lesions”. It has been recognised since 1912. Publications about rehabilitation have increasingly referred to neural plasticity as central to rehabilitation’s success; for example, Zuha Warraich and Jeffrey Kleim said, “an understanding of neural plasticity might guide the development of more effective rehabilitation interventions.”. This page reviews aspects of neural plasticity. My goal is to question some of the almost magical features that some authors and speakers attribute to neural plasticity; it is no more than saying that the brain adapts and learns. We must understand how the brain learns and adapts to optimise our approach to our patients. If we can safely improve its ability to adapt and learn, all human educational and training activities will benefit, including rehabilitation. We should avoid giving this phenomenon a memorable phrase, placing it on a pedestal, or considering it a magic bullet. We all learn and adapt; this process primarily occurs in the brain; people with an illness learn and adapt just as people who lose a job, have a child to look after, or come into additional money do.

Table of Contents

Introduction

The General Theory of Rehabilitation has normalised rehabilitation, showing that it is one of many named services that help people adapt to change. Its unique feature is its focus on people adapting to illness, just as most education focuses on people (children) who are growing and developing towards adulthood, and most financial advisors focus on giving financial advice to people who want it.

A search of PubMed for Rehabilitation and “Neural Plasticity” gives 1037 hits, growing from 0-1 annually before 2000 to 90 or more annually since 2016. As mentioned above, it lends authority and scientific credibility to an article. Anyone casually reading texts might consider it to be unique to rehabilitation.

For example, “This brain plasticity can lead to an extreme degree of spontaneous recovery and rehabilitative training may modify and boost the neuronal plasticity processes.”, “VR-induced changes in neural plasticity for survivors of stroke. Positive correlations between the neural plasticity changes and functional recovery elucidates the mechanisms of VR-based therapeutic effects in stroke rehabilitation.”, [VR = Virtual Reality] and “This special issue focused on the efficacy and mechanism by which neurorehabilitation can induce neural plasticity and functional recovery.”

These phrases imply that rehabilitation should enhance neural plasticity, and even though most research is in the context of practising activities, the general impression is that the goal is to increase plasticity rather than to learn the activity. For example, a piece on the Stroke Association website for patients and family referred to “… presentation examined how lessons from studying the neuroscience of brain injury, particularly the idea of brain plasticity, can bring hope to stroke survivors.”

Neural plasticity, rehabilitation, and recovery.

Stroke is the topic in 382 of the 1037 papers identified above, brain injury in 82, multiple sclerosis in 21, and eight concerning amputations, most of which concerned phantom limb phenomena. Recovery was associated with 407, and (recovery and “neural plasticity”) gave 865 hits.

These data support the impression that neural plasticity in rehabilitation is associated with acute conditions where spontaneous recovery is expected.

Rehabilitation is effective in many situations where recovery cannot or does not occur, such as after complete spinal cord injury, amputation of a limb, or slowly progressive disorders such as secondary progressive multiple sclerosis. Indeed, most rehabilitation given is probably to people where recovery, as usually conceived, does not occur.

My first point, therefore, is that a link between rehabilitation and neural plasticity has been generalised from articles concerned with a sub-population of people benefitting from rehabilitation.

Recovery has two components. First, in many neurological conditions, the damaged brain will contain some irretrievably damaged brain, which will die and some brain that is still alive but no longer functioning. In some people, the latter may return to a functioning state, for example, as cerebral oedema lessens or circulation improves. The return of function is related to many physiological or biochemical changes.

The second component is adaptation to the lost function, which occurs naturally and starts immediately. For example, if a dominant arm is injured severely so that it cannot be used, the person will use their non-dominant arm, or if putting weight on an injured foot gives pain, the person limps to reduce the pain and, as the pain lessens, the limp improves.

Adaptation is a process that depends on neural plasticity, the ability of the brain to learn and alter how it works. It is not restricted to adaptation to disease or injury, nor is it limited to people with neurological damage. It is universal. Most adaptation is likely due to synaptic changes, including loss of synapses and formation of new synapses, with accompanying changes in axonal contacts to other neurones.

Thomas Carmichael and colleagues reviewed the molecular, cellular and functional events in axonal sprouting after stroke brain injury. It is mainly local to the injured area. Evidence exists for local, peri-infract reactive axonal sprouting and some contralateral cortical axonal sprouting. These reactive processes may contribute to recovery. They also discuss reparative and unbounded axonal sprouting, with axons growing outside their once-occupied locality. The evidence for this is limited, and reparative axonal sprouting is unlikely to contribute to recovery.

New neurons form in the adult brain, but this is restricted to the hippocampus, which does not contribute to recovery, although, in principle, it might contribute to cognitive improvement.

Adverse neural plasticity.

Most neural plasticity changes occur in the undamaged brain as a person learns and adapts. Neural plasticity is not always advantageous.

Changes in bodily representation in the cerebral cortex have been known for years; for example, Peter Halligan et al. demonstrated that, after arm amputation, the face became connected to the sensory cortex previously responsive to the hand; a follow-up study found that the adaptation changed over time.

Cortical reorganisation after limb loss explains, in part at least, the phenomenon of “phantom pain”, better referred to as pain in the phantom limb. Flor et al. found a “… very strong direct relationship between the amount of cortical reorganisation and the magnitude of phantom limb pain …”. More recently, Sandra Preißler and colleagues studied ten people with an amputated arm. They used a myoelectric prosthesis with somatosensory feedback. After two weeks of training, they found patients had decreased pain and increased function. There were associated changes in cerebral cortical thickness in visual and pain areas.

These findings demonstrate neural plasticity occurring in the absence of brain injury that is not necessarily beneficial but can be influenced.

A second example of adverse neural plasticity is learned non-use. This phenomenon, observed in monkeys with deafferentation of one arm, is the lack of use of a limb despite motor control being present. The presumption is that the person finds it more accessible to achieve the goal in other ways, suppressing potential function in the affected limb. It was first described in 1966, though Jean-Marie André and colleagues suggest the phenomenon was first recognised in 1904, called “functional motor amnesia”.

This theory led to constraint-induced movement therapy, which is now widely used. In most patients, the success achieved probably arises from intense practice rather than reversing maladaptive neural plasticity.

Conclusions.

This overview of neural plasticity and its importance in rehabilitation shows that it occurs in the brain in everyone and all the time; it is the physiological mechanism underpinning adaptation and learning. It happens in the brain after damage, as the person adapts to their neurological loss. In the damaged brain, there may be additional local reactive axonal sprouting, which could account for some observed recovery from acute brain injury. Neural plasticity also causes some adverse effects, such as the development of pain in a phantom limb and learned non-use.

All adaptation depends upon neural plasticity, and as rehabilitation facilitates and encourages adaptation to changes associated with an illness, it will be associated with altered brain structure and function. However, other than by practice and learning, there is no way to increase the extent of neural plasticity or influence beneficially reactive axonal sprouting. Neural plasticity is not a phenomenon that is unique to people receiving rehabilitation. It is the mechanism underlying all change; it is not the target of rehabilitation.

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