In the late 1930s, Margaret Kennard was among the first to propose that recovery from brain damage is more effective following early lesions than after lesions occurring later in life.1 She also recognized, however, that the sparing effect on functions such as locomotion and grasping observed in infant monkeys, was not shared by vision, which failed to be restored after early damage to the occipital cortex.1 Does this mean, then, that the visual system is equally plastic at all stages of brain development? If we exclude the blindsight phenomenon, i.e. the (predominantly) unconscious visual perception in the blind field, there is still little evidence to show that an actual lesion of the geniculostriate pathway is compatible with sparing of vision. In a large series of children with congenital hemiplegia almost 10 years ago, we found that some children, despite showing clear damage to the optic radiations or the occipital cortex on magnetic resonance imaging (MRI), had perfectly normal visual fields.2 Our findings suggested a higher level of plasticity in the young visual brain, but the underlying mechanisms and the factors that could justify the variability between participants were a mystery to us.
In their study, Jacobson et al.3 start putting some of the pieces of the puzzle in place. In their series of children with congenital hemiplegia, they found that damage to the central visual pathway was compatible with normal vision, but only when the lesion had occurred early in the third trimester of gestation or earlier, thus showing that not only the timing of the insult is important, but even a few weeks can matter. What happens, then, in such a short time to change so dramatically brain response to damage?
Around the early part of the third trimester of gestation, white matter can be particularly vulnerable to insult, exposing the developing optic radiations to injury. However, plasticity of thalamocortical fibres is remarkable at this time. The afferents from the subplate zone are still migrating into the cortical plate, and there is a significant amount of growth-promoting molecules and axonal guidance cues.4 This particular environment gives the brain additional opportunities for plastic reorganization. Somatosensory function, for example, was shown to be particularly resilient to brain damage occurring early in the third trimester.5 A recent study combining magneto-encephalography and diffusion tractography, provided convincing evidence that in these infants, somatosensory projections might still develop after the lesion has occurred, and bypass it to reach their cortical destination in the postcentral gyrus.6 This mechanism is also likely to be active for other thalamocortical pathways, including optic radiations, but it is certainly not the only one. In children with malformations of cortical development, for example, a different mechanism was shown, consisting of the development of a functioning cortex within the dysplastic tissue.7 Normal cortical organization of early visual areas on functional MRI was found in children with diffuse occipital polymicrogyria and normal vision, suggesting that dysplastic tissue can be actively involved in the processing of visual information, as a result of plastic reorganization within the abnormal cortex.
The work by Jacobson et al. makes a significant contribution to the growing evidence that plasticity of the visual brain is heavily influenced by the timing of the insult; however, research in this field is still in its first stages. Many questions remain to be answered and among them the most important one: how can we take advantage of the unique environment of the young visual brain to improve the efficacy of early intervention? Enriching our knowledge and understanding on the mechanisms that regulate early plasticity is, however, a good and necessary start.