Early brain lesions and face‐processing development

Abstract

Studies of functional plasticity after pre- or perinatal brain damage can tell us whether the neural substrate normally involved in the development of a given ability is specific and, if so, when it becomes functionally specified and unique. Development of face processing was investigated in 5- to 17-year-old children who had a unilateral brain injury in the pre-, peri-, or postnatal period. In Studies 1 and 2, patients with a posterior injury involving the temporal regions exhibited a face-processing deficit that was independent of their age at test time. Even though differences were observed between the two hemispheres in face processing during infancy as well as in adults in cases of normal development, no clear differences between right and left injury were observed here in face-processing deficit. Poor postlesional face-processing plasticity seems to contrast with results of several studies on speech development after early unilateral injury. If the difference in the time window for postlesional plasticity between these two areas of competency is confirmed, it would suggest that the two kinds of abilities rely on neural cells which are sensitive to different plasticity factors.

What is so critical?: A commentary on the reexamination of critical periods

“…These findings suggest that the time period of post-lesional plasticity for the neural areas involved in the development of face perception is very short. Based on evidence that some face processing skills mature late in childhood, this finding is not one that would be readily predicted (de Schonen et al, 2005). Differences in the apparent time course of plasticity for face processing skills after early damage or during normal development provide further support for the usefulness of Lewis and Maurer's (2005) distinction between plasticity in visually-driven normal development, in sensitive periods for damage, and in sensitive periods for recovery.…”

“…Recalling the above example, grating acuity becomes adultlike by age 4-6 years, and children who suffer from a period of visual deprivation due to cataracts within this period show permanent deficits in grating acuity. Similarly, face processing is a skill that takes many years to develop, and brain lesions that occur as late as 12 years of age lead to permanent deficits (de Schonen, Mancini, Camps, Maes, & Laurent, 2005). However, global motion becomes adultlike at 6-11 years of age, and yet, visual deprivation only leads to permanent deficits in global motion if it happens in the first year of life (Lewis & Maurer, 2005).…”

“…Furthermore, there does not appear to be a simple correlation between the timing of milestones in cortical maturation and the time at which damage leads to permanent deficits. Although face processing is a relatively lateralized skill in adulthood, damage to either hemisphere both before and after the development of effective hemispheric communications can result in permanent deficits (de Schonen et al, 2005).…”

The computational modeling of sensitive periods

“…A focus on resources prompts the following conclusion: one cannot interpret a developmental failure to recover from brain damage as a lower level of plasticity unless it is established that the domain(s) in question can definitely be acquired with the reduced level of resources, were this reduced level to be present at the start of development. Thus, when de Schonen, Mancini, Camps, Maes, and Laurent (2005) observe in children with pre-, peri-, or postnatal brain damage a failure to later acquire face recognition expertise, the authors interpret this in terms of ''poor postlesional face-processing plasticity'' (p. 184); yet it may be that the remaining processing resources available to the child were simply insufficient to acquire the normal level of expertise whatever the level of plasticity.…”

Complementary neural representations for faces and words: A computational exploration

“…Relatedly, there are no apparent differences in the face recognition deficits of individuals with unilateral lesions in infancy that impacted either the LH or the RH (de Schonen et al, 2005).…”