Recovery Of Function and Age Research Paper

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When the brain is injured in adulthood there is a loss of function followed by a prolonged period during which there is partial recovery of some types of cognitive and motor functions. The extent of functional recovery varies with age and although injury to the infant brain can have less severe consequences than similar injury in adulthood, there are times when injury is especially devastating. These differences are related to the details of anatomical changes at different stages of brain development. The difference in functional outcome after injury at different ages is related to the injury-induced changes in neuronal structure, changes that are referred to as plastic changes. These plastic changes are similar to the neural and glial changes that are associated with learning in the normal brain. Various factors, such as experience, hormones, and drugs, modulate these plastic changes. Even these factors cannot completely restore lost functions because there are limits to brain plasticity.

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1. The Nature Of ‘Recovery’ After Brain Injury

There are many ways to damage the brain (e.g., stroke, disease, trauma) and it is rare indeed for a family not to contain a member who is affected by one of them. For example, it is estimated that about 400,000 people with new head injuries are admitted to hospitals each year in the United States. Similarly, it is estimated that there are about 400,000 new cases of stroke every year in the United States and most surviving stroke victims experience significant cognitive loss. These figures do not include neurological disorders such as Parkinson’s and Alzheimer’s diseases, which together affect more than 1 percent of the population. The estimate in the United States is that about 48 million people have some sort of neurological disorder, excluding mental diseases such as schizophrenia, which are clearly a result of neural dysfunction.

The high incidence of brain injury and disease thus poses perhaps the most perplexing clinical neurological problem, which is the issue of how to repair the damaged brain. It is tempting to assume that if behavior improves after injury, then there is recovery of the original behavior. However, just because a behavior appears to recover does not mean that the lost behavior itself has returned. The problem is to determine when recovery has actually occurred. In fact, true recovery is a rare occurrence after brain injury.

We can identify at least three outcomes that could occur after brain injury. First, there may be compensation resulting from an adaptation to the lost function. Compensation could reflect a change in strategy or it may represent a substitution of a new behavior for the lost one. For example, a person who has a deficit in moving the eyes can be expected to have difficulty in reading. This difficulty can be solved, however, by moving the head, which allows restitution of function (reading) by substitution of one behavior for another. Similarly, if, following a stroke, a person can walk only with the aid of a cane, the ability to walk has returned but the original walking ability has not returned, just an adaptation to the behavioral difficulty.

A second outcome might be partial restitution of the original behavior. This could reflect recovery from some sort of nonspecific effect of the injury, such as swelling, or it may reflect a genuine return of function. Behaviors that return over a period of months are likely to reflect a partial restitution of function. This is most clearly seen in people with significant language disturbances (i.e., aphasias) in which the severe deficits in making the movements of the tongue and mouth necessary to speak may diminish leaving the person with more subtle language disturbances, such as in finding words (anomia).

Third, there is the possibility that there could be a complete restitution of the original behavior. Although it is at least theoretically possible for lost functions to return completely in a plastic brain, careful behavioral analysis shows that this is rarely, if ever, the case in either adult laboratory animals or human patients. In principle, however, it ought to be possible to reorganize the brain to allow at least some functions to completely recover. This process is most likely in the developing brain and it has been documented for over 100 years that children with damage to language areas can show an almost complete recovery of lost language functions.

2. Age-Dependent Recovery

Broca first noticed in the late 1800s that damage to the speech zones of the left hemisphere during infancy did not interfere with the later development of language (for a review, see Finger and Almli 1988). Rasmussen and Milner (1977) later showed that the sparing of language functions was due to the shifting of the speech zones either to the opposite hemisphere or, in some circumstances, within the left hemisphere. In these later studies the critical factor was age: lesions of the left hemisphere language zones prior to 5 years of age changed the speech representation so that the affected language zone moved to the right hemisphere.

Similar lesions from the ages of about 6 to 12 still allowed recovery of language functions but this was accomplished by intrahemispheric reorganization (see also Krashen 1973). The studies of the recovery of language functions after infant brain injury led to the idea that damage to the infant brain led to better functional outcomes than damage after similar injury in adulthood. This conclusion was supported by the studies of Margaret Kennard in the late 1930s in which she showed that unilateral motor cortex impairments are less severe after motor cortex injury if the lesion occurs in infancy rather than adulthood (e.g., Kennard 1940). One difficulty with the studies of both Kennard and the language reorganization in children is that there are also many examples in which early brain damage results in rather severe functional loss, such as in cerebral palsy or hemiplegia resulting from unilateral cerebral injury at birth. In fact, Hebb (1949) noted that children with frontal lobe injuries in infancy showed little functional recovery in adulthood and for some behavior, such as social behavior, these children might actually have more severe deficits than adults with similar injuries.

The apparent contradiction between the recovery of language and some motor functions on the one hand, and the poor recovery of some executive, social, and other motor functions on the other hand, has been resolved by laboratory studies in which precise age at injury and the nature of the behavioral deficits have been systematically examined. A key element of these studies is that the age of the brain is measured not in relation to the birth day, but rather it is measured by its stage of anatomical development. For example, compared to humans, newborn rats are approximately equivalent to about 6-month old fetuses when they are born. Thus, if the newborn rat brain is damaged, we would anticipate functional symptoms similar to those of human infants whose brain is injured at the beginning of the third trimester. In order to compare across species we can separate the periods of brain development into five broad stages: neurogenesis, cell migration, cell differentiation, synaptogenesis, and gliogenesis.

Studies on both laboratory rats and cats have shown that if the cortex is injured bilaterally during neurogenesis, when neurons are formed, there is substantial recovery and, if the injury is not too extensive, there can be virtually complete functional recovery. In contrast, however, if the cortex is injured in the first few days after birth in the rat, which is a time of neural migration and cell differentiation, the effect is functionally devastating as animals show far more severe effects of injury than would be expected even in aging animals. This poor outcome is not a function of extent of injury, nor is it localized to particular cortical areas (see Kolb 1995).

Rather, there is something about the rat cortex shortly after birth that makes it especially vulnerable. For example, damage during this time may disturb the subsequent process of synapse formation or may even alter stem cell activity in some way. Once this phase of development is over, however, and brain development moves to the production of connections and glia, the brain shows a remarkable ability to compensate for injury. Rats or cats with cortical injuries during this phase show far better behavioral capacities in adulthood than animals with similar lesions at any other time. In fact, on some behavioral tests these animals show recovery that is virtually complete.

Importantly, this recovery is far more extensive in cognitive tasks, such as the learning of various spatial navigation problems, than it is on tests of speciestypical or motor behavior (e.g., Bachevalier and Malkova 2000, Kolb and Whishaw 1989). In humans, spatial behavior appears to show less recovery than verbal behavior (Stiles 2000). This behavior-specific recovery likely reflects the relative ease of reorganizing cortical circuitry in supporting different types of behavior. The neural substrates for less plastic behavior are presumably more highly specified and constrained during development than the neural substrates for more plastic behavior. It also reflects a difference in the way the brain produces cognitive processes versus basic sensory and motor processing. Thus, the most extensive recovery is associated with lesions of the frontal areas and the least extensive recovery is associated with damage to the primary sensory areas.

3. Mechanisms Underlying Recovery Of Function

The fundamental assumption here is that recovery of function can occur only if there is some type of modification of the structure of the remaining brain. This structural change is necessary if the remaining brain cells are to be recruited in some manner to control behaviors that preinjury were controlled by the lost neurons. In principle, there are three ways that the brain could make changes that might support recovery. First, there could be changes in the organization of the remaining, intact, circuits in the brain. The general idea is that the brain could reorganize in some way to do ‘more with less.’ It is unlikely that a complexly integrated structure like the cerebral cortex could undergo a wholesale reorganization of cortical connectivity, but rather, recovery from cortical injury would be most likely to result from a change in the intrinsic organization of local cortical circuits in regions directly or indirectly disrupted by the cortical injury. Although it might be possible to produce significant reorganization of cortical connections in the young brain, the overwhelming evidence in experimental animals is that this is rare and it is just as likely to be associated with abnormal functioning as with recovery.

Second, there could be a generation of new circuitry. Cerebral reorganization can be stimulated either by some sort of behavioral therapy or the application of some sort of pharmacological treatment. In either event, the stimulus could influence reparative processes in the remaining brain or could enhance the production of new circuitry. Once again, it seems most likely that the induced neuronal changes would be in the intrinsic organization of the cortex. One might predict that induced neuronal changes might be more extensive than in the case of endogenous change, in part because the treatment can act upon the whole brain rather than just on affected regions.

Third, there could be a generation of new neurons and glia to replace at least some lost cells. Stem cells that give rise to the neurons and glia of the brain remain active in the brain throughout life. It is thus possible that neurogenesis could be stimulated after injury, especially during development, and that these new neurons could replace those lost to injury or disease (e.g., Weiss et al. 1996). All three of these possibilities for cerebral plasticity do occur, but the likelihood of each type of change varies with age at injury.

4. Structural Correlates Of Functional Recovery

When the brain is damaged, there is a loss of neurons in the injured area but, in addition, many neurons that are not directly injured lose their normal synaptic inputs. The immediate effect of this synaptic loss is (a) neuronal death, (b) atrophy of the dendritic and/or axonal fields that have lost their connections, and/or subsequent reorganization of the connections. This reorganization can be inferred by using a Golgi stain to visualize the dendritic fields of the remaining neurons. Because the dendritic branches of a neuron provide the substrate for most of a cell’s synapses, a decrease (or increase) in the amount of dendritic space available is correlated with a decrease (or increase) in the number of synapses.

The hippocampal formation of adult rats has provided a good model to study synaptic replacement. When input to the hippocampus is reduced by damage to the major input pathway via the entorhinal cortex, there is a massive denervation of the hippocampal formation, which can be seen in the atrophy of the dendritic fields of the hippocampal cells in the week after injury. Beginning at about 7–10 days after the injury, there is then a slow regrowth of the dendritic fields, although the pattern of regrowth is different from the original pattern. This regrowth reflects a reorganization of the circuitry and it is correlated with a partial recovery of function. The restructuring of the synaptic organization of the hippocampus occurs primarily because the remaining inputs to the hippocampus expand to occupy the regions of lost inputs.

A similar process appears to occur after restricted neocortical injury in adulthood as well, although the changes are less dramatic than in the hippocampus and there is much less functional recovery (for a review, see Kolb 1995). In contrast, however, there is extensive reorganization after cortical injury during development, and this reorganization is correlated with functional outcome. Golgi analyses of cortical neurons of rats with perinatal lesions consistently show a general atrophy of dendritic fields and a drop in spine density across the cortical mantle. In contrast, rats with cortical lesions around 10 days of age show an increase in dendritic fields and an increase in spine density relative to normal control littermates. Thus, animals with the best functional outcome show the greatest synaptic increase whereas animals with the worst functional outcome have a decrease in synapses relative to control animals.

But infant animals not only show changes in local cortical circuits but also in more distant cortical connectivity. Perhaps the most extensive studies of changes in cortical connectivity are those showing that after unilateral motor cortex lesions in infant rats or cats there is a major expansion of the ipsilateral corticospinal pathway from the undamaged hemisphere, which is correlated with partial recovery of skilled forelimb use (e.g., Castro 1990). These expanded connections do not reflect the growth of new pathways, however, but rather reflect the failure of superfluous pathways to die off during development. That is, in development there is normally a period during which many pathways are eliminated but after some types of brain injury these pathways are maintained (for a review, see O’Leary 1992). The presence of these abnormal pathways may support some types of functional recovery but it may also interfere with the normal functioning of remaining cortical functions. This possibility has been termed ‘crowding’ to reflect the idea that the normal functions of a cortical region can be crowded out by the development of abnormal connections (e.g., Teuber 1975). Thus, there may be recovery of some types of behavior, such as motor functions, at the expense of other functions (e.g., Kolb et al. 2000). This appears to be especially likely if the injury occurs during the period of neuronal migration and unlikely if it occurs during the period of maximal synaptogenesis.

As noted earlier, synaptic change may also occur after injury because the brain generates new neurons. Although this is likely to be rare in the adult, it does occur during development, but the generation of these neurons varies with precise embryonic age and location of injury. If it is damaged during the time of neuronal generation, the brain can compensate by generating rather large numbers of new cells that appear to support at least partial restitution of function (e.g., Hicks et al. 1984). It is not known if this regenerative process occurs after injury to specific regions of the brain but it is likely a general phenomenon. Thus, if the brain is injured while it is still producing neurons, it appears capable of generating replacements (e.g., Kolb et al. 1998a). In contrast, if the brain is injured during neuronal migration there appears to be little generation of new neurons. If the same injury occurs during maximal glial formation, there is neuronal generation. This generation is selective, however, and occurs only if the midline telencephalon is damaged, namely the olfactory bulb or midline cortex (e.g., Kolb et al. 1998b). The newly generated tissue is functional and animals regain at least partial function.


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