Date:

Feb 01, 1997

The brain is constantly reorganizing structurally and functionally as it responds to stimuli and to injury. This ability to reorganize is referred to as “neuroplasticity”. In very general terms, all areas of the brain adapt to a change in any one area of the brain because of the wealth of neurological connections to and from each area. Most of these changes are very subtle and do not usually result in dramatic changes in brain structure or function; however, significant alterations in behavior and/or performance can occur if the reorganization is either in a very specialized area of the brain or in a large volume of the brain.

The period of most dramatic plasticity is during the first 2 years of life as the infant’s brain becomes organized in response to its environment. At birth, most of the nerve circuits are in place anatomically but functional connections are awaiting stimuli. Plasticity is also challenged dramatically at any age when the brain responds to an injury (e.g.: a developmental injury; head trauma; stroke; a convulsion). The scientific issues are: what are the several mechanisms underlying neuroplasticity and what are the results on brain function of each of these several mechanisms, individually and collectively?

On December 3-4, 1996, the National Institute of Neurological Disorders and Stroke of the National Institutes of Health conducted a research workshop exploring these issues. Basic and clinical research scientists from around the world met together and shared their research findings. Our Foundation participated in these discussions. The topic addressed was: what brain mechanisms underlie changes in performance following brain injury? Four mechanisms were discussed:

Compensatory Masquerade: This mechanism involves “learning,” the result of which permits one body part to compensate for loss of function in another body part. It is the basis of many clinical approaches used in rehabilitation and in orthopedic surgery. The brain and spinal cord “reorganize” as they learn to provide for the substitution; the changes in neurological organization are driven by the changes in demand. This mechanism is most successful for very specific tasks involving only one of a few areas of the brain. However, it can be unsatisfactory if coordination of several areas of the brain are required to provide for the substituted demand. Thus, the nervous system can accommodate to a tendon transplant and result in movement of a joint; however, compensatory masquerade is of little use in the control of a substituted process for swallowing which involves a number of coordinated neurological activities.

Functional Map Expansion: This mechanism of neuroplasticity provides for an area of the “healthy” brain to “grow into” an adjacent area of the “damaged” brain that has lost its function. The area of growth is usually in the border zone bounding both areas. Thus, if a person were to lose his arm, the brain area which recognizes the sensation of touch in the arm would no longer be functional. The adjacent area of brain recognizing touch on the face can send fibers into the arm area. When the face is touched, the person perceives touch in both the face and the arm, even though the arm has been amputated. When this occurs in the brain’s motor control system (as in cerebral palsy), it can result in contractions of inappropriate muscles in conjunction with a purposeful muscle contraction; this double response is not desirable. On the plus side, if the healthy area’s function is minor or related, functional map expansion provides for the adjacent healthy area of brain to take over the function of a damaged area of brain. Under these conditions, lost function is partially restored.

Homologous Region Adoption: This mechanism of neuroplasticity provides for one area of the brain to take over the function of a distant area that has been injured. The new functional area can be in the same half or in the other half of the brain. (The human brain has two halves connected by a bridge. Each half controls somewhat different functions, but can share in control of a single function). The mechanism involved is thought to be possible because of the existence of a minor, but existing neural pathway in the distant area which has been non-functional as long as the major pathway was in operation. This “uncovering” of existing pathways can return some function, but it can be at the cost of a decrease in the function of the uninjured part of the brain; the uncovered pathway is usually less efficient than the original, no longer functional pathway. Also uncovering the substitute pathway can interfere with the principle function of that section of the brain.

Cross Model Reassignment: This aspect of neuroplasticity provides for one sensory input to replace another. For example: in braille, the sense of touch replaces the sense of vision in the “reading areas” of the brain. This mechanism resembles compensatory masquerade (point 1 above) but generally involves the sensory systems (vision, hearing, touch, pain).

Comments: What does this all mean, particularly to a person with a disability due to cerebral palsy? It tells us that there are mechanisms by which the injured brain can and does rearrange itself. Thus, the possibility exists for restoring lost function. However, the restoration of a brain function is often at the price of impinging upon the quality of another brain function. The evidence at this time indicates that in order to restore a detailed function, compensatory mechanisms (points 1 and 4 above) are more likely to be successful. Points 2 and 3 above can also be useful, but generally interfere with other brain functions.

For the restoration of a broad function involving the coordinated interaction of several areas of brain (e.g.: speech and language; swallowing), learning how to influence neuroplasticity will provide the ultimate answer. Understanding the basic mechanisms of neuroplasticity provides the building blocks for achieving this goal. In the interim, we are learning: why the methods we use successfully, appear to work; how we might improve the success of the methods that do work; and why the methods that don’t work, aren’t working.

© UCP Research & Educational Foundation, February 1997