Language Development in Children with Neurological Lesions
Heidi M Feldman, MD PhD

Background:
Many lines of evidence support the concept that the left hemisphere (LH) has an essential and specialized role for language processing in adults. Studies of adults with focal brain injury find that approximately 95% of cases of aphasia are associated with LH damage. In the traditional view, damage to the Broca’s area in the frontal lobe is associated with problems in language production whereas damage to Wernicke’s area in the temporal is associated with problems in language comprehension. Though recent research is suggesting that the picture is more complex than this traditional view, nonetheless, the LH contribution to adult language functioning seems to be necessary.

How, when and why the LH becomes specialized for language functions? In rare circumstances, children who have not yet learned to speak or are still developing language skills sustain brain injury to areas of the LH that typically serve language function in adults. If children with LH damage prior to language learning subsequently demonstrate serious delays in language development, the implication is that the mechanisms for language development reside within the damaged regions of the LH, a position called early specialization. Such findings would suggest that the neural architecture for language is determined by innate and probably genetic mechanisms. If, by contrast, children with LH damage successfully master language skills, then the implication is that, at least under extreme circumstances, alternative organizations can be established. Such findings would suggest that the neural architecture of language is an outcome of language learning. If children with LH damage show only minor delays, the implication is that alternative neural organizations are less favorable to language development or processing than are classical language areas, an intermediate position called constrained plasticity or ontogenetic specialization. This last position would suggest that some aspects of brain structure may be determined by early and possibly genetic factors but that the full development of LH specialization emerges through development.

Previous studies:
We have studied children with LH damage to classical speech areas during the developmental period. These children are typically not aphasic. Compared to the chronic sensory and motor deficits that follow injury in these children, and the severe disruption of language that follow similar injuries in adults, it is remarkable that their conversational language is normal or near normal. However, despite the favorable prognosis, children with focal injury to either hemisphere may experience developmental delays in vocabulary development and use of word combinations in parent-child conversations [1-3]. They are also slower at learning new vocabulary items.[4] Once these children begin to acquire functional skills, their rate of developmental progress is comparable to each other and to children developing typically [5]. These findings suggest to us that a wide neural network involving both cerebral hemispheres is necessary to launch language development such that damaged neural substrate in either hemisphere may delay language development. Once language skills begin to develop, and presumably an initial neural network is beginning to become established, neural organization progresses at similar rates as it does in an intact system.

We have also studied children with periventricular lesions. These children, with damage to white matter connections within and between the hemispheres also have delays in language development. We found that their skills in language correlated with their general cognitive abilities[6].

At school age, the children with LH damage have greater language difficulties on formal tests than peers with other lesions.[7] They also showed developmental delays in the development of grammar, though the differences between children with LH and RH injury was very minor.

We have also studied children with focal injury in a novel way, using on-line reaction time methodology to determine if particular information processing abilities are selectively compromised in children with LH damage.[7] Children with both LH and RH had slower reaction times than did age-matched normal peers on all of the auditory and visual reaction time tasks studied. The two tasks that best distinguished children with LH damage from children with other lesions and normal children were verbally repeating numbers presented in the auditory mode and naming numbers presented in the visual mode, both tasks requiring rapid verbal output.

Current project: Reorganization after early injury
The current research direction is to use modern structural and functional imaging to describe how language skills are reorganized in the damaged brain. These new methods offer exciting opportunities to study actual brain structure as well as activity during cognitive tasks in awake and functioning subjects. In adults, functional magnetic resonance imaging (fMRI) has shown that a wide network of areas is involved in sentence interpretation; activation was more likely to include RH locations as the sentence difficulty increased. In a previous study [8], we used the fMRI paradigm to compare 6 children with perinatal injuries, 5 with damage to LH areas, to normal adults and normal children during sentence comprehension. In adults and normal children, the task produced more activation in the LH than in the RH; adults showed RH recruitment for difficult sentences but children, who on average made more mistakes than did adults, did not. The children with LH damage were even less accurate than were normal children on the task. These children activated primarily a RH network and did not show an increase in activation as a function of sentence difficulty. The children with LH damage also had very poor performance on a mental rotation task that typical activates RH areas. This finding suggests that reorganization of language to the RH may compromise skills typically served by the RH.

Our future plans involve more sophisticated structural imaging and more systematic use of fMRI to describe patterns of activation in simple and complex language tasks. We will compare children with cortical damage and children with subcortical white matter damage to children developing typically. In this way we can evaluate the role of specialized neural tissue and of connections within and across hemispheres in completing the tasks. We will systematically vary task difficulty to see how children developing typically and children with brain injuries respond behaviorally and neurologically to the challenge.

1. Feldman, H.M., et al., Early language and communicative abilities of children with periventricular leukomalacia. American Journal of Mental Retardation., 1992. 97(2): p. 222-34.

2. Feldman, H.M., et al., Language abilities following prematurity, periventricular brain injury, and cerebral palsy. Journal of Communication Disorders., 1994. 27(2): p. 71-90.

3. Feldman, H.M., A.L. Holland, and R.E. Brown, A fluent language disorder following antepartum left-hemisphere brain injury. Journal of Communication Disorders., 1992. 25(2-3): p. 125-42.

4. Keefe, K.A., H.M. Feldman, and A.L. Holland, Lexical learning and language abilities in preschoolers with perinatal brain damage. Journal of Speech & Hearing Disorders., 1989. 54(3): p. 395-402.

5. Feldman, H.M., et al., Language development after unilateral brain injury. Brain & Language, 1992. 42(1): p. 89-102.

6. Feldman, H.M., M.S. Scher, and S.S. Kemp, Neurodevelopmental outcome of children with evidence of periventricular leukomalacia on late MRI. Pediatric Neurology., 1990. 6(5): p. 296-302.

7. MacWhinney, B., et al., Online measures of basic language skills in children with early focal brain lesions. Brain & Language., 2000. 71(3): p. 400-31.

8. Booth, J.R., et al., Functional organization of activation patterns in children: whole brain fMRI imaging during three different cognitive tasks. Progress in Neuro-Psychopharmacology & Biological Psychiatry., 1999. 23(4): p. 669-82.