Brain, Vol. 124, No. 5, 995-1002,
May 2001
© 2001 Oxford University Press
Behavioural profiles of children and adolescents after pre- or perinatal unilateral brain damage
1 Department of Neurosciences, UCSD School of Medicine, La Jolla, California and 2 Department of Neurology, NYU Medical Center, New York, USA
Correspondence to:
Doris A. Trauner, MD, Department of Neurosciences, UCSD, School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0935, USA E-mail: dtrauner@ucsd.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Recent case reports of individuals with early-onset damage to the prefrontal cortex have suggested that such early insults could result in severely impaired social behaviour in later childhood and adolescence. The investigators speculated that the acquisition of complex social conventions and moral rules had been impaired. In a large cohort of children, we sought to determine whether early focal brain insults might result in clinically significant behavioural or emotional problems. This study reports on 39 children with pre- or perinatal-onset unilateral brain damage (focal lesion) from cerebral infarction or intraparenchymal haemorrhage, using the Achenbach Child Behavior Checklist to assess the presence or absence of behavioural and emotional difficulties. Two-thirds of the subjects had left hemisphere (LH) lesions and one-third had right hemisphere (RH) lesions. Age range was 4.0–15.4 years at the time of questionnaire completion. Their results were compared with those of 54 control children. Analyses were conducted on focal lesion versus controls, RH versus LH lesion, frontal versus non-frontal lesion, and seizure versus non-seizure groups. When the effect of IQ was partialled out, there were no significant differences on the nine Behavior Problem scales, the Internalizing–Externalizing dichotomy or the Total Problem score for any of the group comparisons. Our subjects showed no evidence of clinically significant behavioural or emotional problems, even when the frontal lobe was involved. Individuals with more extensive and bilateral damage may be at higher risk of significant behavioural and emotional dysfunction than were those in our study population. In future studies of brain–behaviour relationships in developing children, all potential causes for any observed behavioural abnormalities, such as genetic and environmental factors and toxin exposure, must be considered before concluding that specific anatomical lesions are causally related to specific behavioural outcomes.
focal lesions; behaviour; perinatal stroke; social-emotional function; Child Behavior Checklist
CBCL = Achenbach Child Behavior Checklist; LH = left hemisphere; RH = right hemisphere; WISC-R = Wechsler Intelligence Scale for Children—Revised; WPPSI-R = Wechsler Preschool and Primary Scale of Intelligence—Revised
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Numerous studies have demonstrated that normal adults may develop personality changes, social impairments or problems in decision-making and other executive functions following focal brain damage, in particular to the frontal lobe, e.g. from a stroke, intracerebral haemorrhage or closed head injury (e.g. Stuss and Benson, 1984; Mesulam, 1986; Heilman et al., 1993). The well-known case of Phineas Gage, a railway worker who developed major personality changes following trauma to his frontal lobes, is a prime example of such an effect of focal brain damage (discussed in Gainotti, 1972). The type of behavioural change observed frequently correlates with the side and site of the lesion (e.g. Sackeim et al., 1982; Damasio and Van Hoesen, 1983; Borod, 1992, 1993; Anderson et al., 1999). Adults who suffer right hemisphere (RH) strokes may develop difficulty with comprehension or expression of affective cues, both vocally and in facial expression and gesture (Borod, 1992
; Heilman et al., 1993; Ross, 1993). Some individuals with RH lesions may have a flattened or be indifferent to, their disabilities (Gainotti, 1972; Heilman et al., 1978; Ross and Mesulam, 1979; Benowitz et al., 1983); others are hypomanic or even manic (Gainotti, 1972; Robinson and Starkstein, 1990; Borod, 1992). Adults with left hemisphere (LH) lesions are often depressed (Ross and Rush, 1981; Robinson et al., 1984; Robinson et al., 1986; Nelson et al., 1993). Adults with right or left frontal lobe damage may display disinhibition, inappropriate affective responses and impaired judgement (Damasio and Van Hoesen, 1983).
In contrast to lesion effects in adults, less is known about the effects of focal brain damage sustained early in life on behavioural and emotional changes during development than about the effects of such damage in adults. Infants with early RH lesions have been found to have more negative temperaments than normal infants and those with LH lesions (Nass and Koch, 1987; Reilly et al., 1995). It is more difficult to elicit positive responses from infants with right posterior lesions than from infants with posterior LH or no lesions (Reilly et al., 1995). Older children with pre- or perinatal RH strokes also have a more negative temperament (Nass and Koch, 1991) and have more difficulty comprehending and expressing emotion vocally than do those with LH lesions and controls (Trauner et al., 1996a). In several studies, children with neurological findings suggestive of RH dysfunction (such as the presence of left hemiparesis), although not necessarily shown to have definable lesions by neuroimaging techniques, have been found to have more social difficulties than normal children (Denckla, 1983; Weintraub and Mesulam, 1983; Voeller, 1986; Tranel et al., 1987; Goodman and Yude, 1997).
Children with hemiplegic cerebral palsy have been reported to have an increased incidence of psychiatric problems. Approximately 50% of hemiplegic children identified through the London Hemiplegia Register were found during psychiatric interviews to have behavioural or psychiatric problems, including hyperactivity, conduct disorders, aggression and oppositional behaviours (Goodman and Graham, 1996; Goodman and Yude, 1997). Longitudinal testing indicated that the psychiatric problems were present early in life (often in the preschool period) and persisted when tests were repeated in the school-age years (Goodman, 1998). Furthermore, the London hemiplegia study found a good correlation between questionnaire results and individual psychiatric assessments of the children, suggesting that a questionnaire would be likely to identify such problems if they existed. Unfortunately, the ascertainment process for this hemiplegia study precluded definite documentation of the lesion site or sites through neuroimaging studies. Rather, the children were identified by the clinical finding of hemiplegia, making it difficult to interpret the findings with respect to the presence of unilateral versus bilateral brain damage or the site of the lesion within the hemisphere (e.g. frontal lobe).
In a study of behavioural profiles in children with early focal brain damage (focal lesion) documented by neuroimaging studies, using the Personality Inventory for Children, Trauner and colleagues found that the focal lesion group, regardless of the side of the lesion, tended to have more abnormal scores on scales assessing cognitive function, adjustment and social skills (Trauner et al., 1996b). When the presence or absence of frontal lobe involvement was taken into consideration, the children with frontal involvement had more abnormal scores on scales evaluating cognitive function, whereas subjects without frontal involvement scored more poorly on scales assessing social skills. These results suggested that there was evidence of social skills problems in children and adolescents after early unilateral brain damage, but the location of the lesion did not map on to behavioural profiles described in adults after late-onset stroke.
Recent case reports of individuals with early-onset damage to prefrontal cortex brain regions suggest that such early insults may result in severely impaired social behaviour during childhood, with worsening of behaviours in adolescence (Anderson et al., 1999). One of the individuals studied had sustained a closed head injury at 15 months of age, with resulting bilateral frontal lobe damage on MRI. Her behaviour was severely abnormal from the age of 3 years. Another subject had undergone resection of a large tumour in the right frontal lobe at 3 months of age. Social and behavioural problems were noted by the age of 9 years, although they were present to a milder extent even earlier. The authors suggested that the acquisition of complex social conventions and moral rules had been impaired by these early-onset, localized brain insults. If this is the case more generally, this observation could have profound implications for the management of children who have suffered early focal brain damage.
The present study was undertaken to determine whether children with very early unilateral brain injury from pre- or perinatal stroke are at high risk of developing social, emotional or behavioural disorders. We used the Achenbach Child Behavior Checklist (CBCL) (Achenbach, 1985, 1991), which is a widely used, standardized, empirically based parental report instrument designed to assess behavioural problems and competencies of children ages 4–18 years. We used the parent report form because parents are usually the most knowledgeable about their child's behaviour across time and situations (Achenbach, 1991). A large longitudinal study of children with at least one `sign of disturbance' on the CBCL parent report form found high predictive value for later social, academic, emotional and behaviour problems (Stanger et al., 1993), suggesting that the CBCL is a valid and reliable indicator of clinically significant behavioural dysfunction.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Subjects
Thirty-nine children with pre- or perinatal-onset unilateral focal brain lesions from cerebral infarction or intraparenchymal haemorrhage and 54 control subjects participated in the study. Thirty of the focal lesion children were identified from clinical referrals from a wide geographic region, including all of San Diego County and parts of Imperial and Orange Counties in Southern California. Nine were similarly identified in the New York metropolitan area. The presence of unilateral brain damage was typically recognized either in the newborn period, as a consequence of a neuroimaging procedure performed because of seizures, poor feeding, hypotonia or similar neonatal problems, or later in the first year of life, when the parents noted that the infant was only using one hand to reach for toys, or a similar asymmetry of arm or leg use. Every child had the lesion documented by either CT or MRI of the brain. Each child was identified as either having a history of clinical seizures beyond the neonatal period or not having seizures, on the basis of a medical history questionnaire completed by a parent and by personal interview of the parent when possible. Children were excluded from the study if they had bilateral or multifocal lesions, if the lesion was the result of closed head injury, bacterial meningitis or another condition believed to cause more widespread brain damage, or if there was a history of intrauterine drug exposure. Twenty-five subjects had LH lesions and 14 had RH lesions. Eighteen had lesions that involved the frontal lobe (12 LH and six RH). Age range was 4.0–15.4 years at the time of questionnaire completion. There were 23 males and 16 females in the focal lesion group.
Control subjects (age range 4.0–18.1 years) were identified from a large number of sources, including general paediatric clinics, advertisements in parent magazines and at local fairs, radio advertisements, and through contacts with preschools and elementary and high schools. All control children had normal neurodevelopmental histories and were at an appropriate grade level for their chronological age. Potential controls were excluded if there was a history of developmental delay or a condition that might have caused brain damage, such as severe closed head injury, hypoxic–ischaemic encephalopathy or meningitis. There were 23 males and 31 females in the control group. Focal lesion and control children were group-matched for age and socioeconomic status.
Informed consent was obtained prior to conducting the studies in accordance with UCSD Institutional Review Board procedures and guidelines.
Lesion specification
Lesions were classified according to the side of the lesion and the lobe(s) involved. In addition, the size of the lesion was rated on a five-point scale adapted from Vargha-Khadem and colleagues (Vargha-Khadem et al., 1985), in which 1 = minimal ventricular dilatation or atrophy; 2 = moderate ventricular dilatation or atrophy; 3 = small focal porencephaly (involving only one lobe); 4 = focal porencephaly involving one lobe but seen in more than three cuts on CT or MRI; 5 = large porencephaly involving multiple lobes.
Measures
The CBCL (Achenbach, 1991) was administered to the parents of the focal lesion and control children participating in the study, to assess the presence or absence of behavioural and emotional difficulties. The CBCL is a 113-item checklist completed by parents of children ages 4–18 years. From these items, nine Behavior Problem scales, an Internalizing–Externalizing dichotomy and one Total Problem score are derived. Results are expressed as T-scores, scores above 70 indicating clinically significant problems and scores of 67–70 representing a `borderline clinical' range. Each item is scored on a response scale of 0–2, where 0 = not true, 1 = somewhat or sometimes true and 2 = very true or often true. The responses are based on current observations or behaviours observed within 2 months prior to the completion of the questionnaire.
Each child also received a test to assess global cognitive functioning. The Wechsler Preschool and Primary Scale of Intelligence—Revised (WPPSI-R) (Wechsler, 1989) was administered to children ages 4–5 years and the Wechsler Intelligence Scale for Children–Revised (WISC-R) (Wechsler, 1974) was used for children between the ages of 6 and 16 years. Because this study was part of a larger, longitudinal study of language and learning in infants and children, the WISC-R rather than the WISC-III was used throughout for continuity.
Differences between focal lesion and control groups, left and right hemisphere groups, frontal and non-frontal lesion groups, and seizure and non-seizure groups were analysed using an analysis of variance framework. The nine Behavior Problem scales and the Internalizing–Externalizing dichotomy were analysed separately using MANOVA (multivariate analysis of variance) or MANCOVA (multivariate analysis of covariance), and the Total Problem score was analysed using ANOVA (analysis of variance) or ANCOVA (analysis of covariance). For all analyses, age and IQ were evaluated as covariates and, if significant, were included in the model.
Because the statistical analyses do not fully account for the score distributions, qualitative descriptions of the data were also included.
Nine controls (eight females, one male) and 12 focal lesion children (five females, seven males) had at least two CBCL questionnaires completed; the interval between the first and second questionnaires was 4.2 years for the controls and 3.5 years for the focal lesion group. This enabled longitudinal analyses, using dependent t tests, to be conducted. Only the Social Problem scale and the Total Problems score were analysed in the longitudinal group, as these were deemed a priori to be of most interest in determining whether there would be problems as the children grew older.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Lesion characteristics are outlined in Table 1
. For all analyses, age and IQ were assessed as covariates. Age was consistently not a legitimate covariate, whereas IQ was consistently a legitimate covariate. The mean Full-Scale IQ (FSIQ) was 93.4 ± 22 for the focal lesion group and 116.2 ± 13 for the control group (P < 0.0001). There were no significant differences in mean socioeconomic status between the focal lesion and control groups.
|
When IQ was used as a covariate, there was no difference between the focal lesion and control groups on the Syndrome scales, on the Internalizing–Externalizing scales or on the Total Problem score. Moreover, all mean T-scores were within the normal range (Fig. 1
). When IQ was not used as a covariate, significant differences were found between the two groups on the Behavior Problem scales of Social Problems, Thought Problems and Attention Problems; on the Internalizing scale; and on the Total Problem score. Again, all mean T-scores were still well within the normal range for both the focal lesion and control groups.
|
When the focal lesion group was analysed by side of the lesion, whether or not IQ was used as a covariate (mean LH FSIQ = 90.1 ± 22, mean RH FSIQ = 97.4 ± 22), there were no significant differences between the LH and RH groups on the Syndrome scales, the Internalizing–Externalizing dichotomy or the Total Problem score, and all mean T-scores were in the normal range (Fig. 1
). The focal lesion group was divided, on the basis of CT or MRI scan analyses, into those with frontal lobe involvement (regardless of the side of the lesion) (n = 18) and those without frontal lobe involvement (n = 21). Whether or not IQ was used as a covariate, there were no significant differences in mean T-scores on the Syndrome scales, on the Internalizing–Externalizing dichotomy or on the Total Problem score, and all mean T-scores were in the normal range for both groups.
Within the focal lesion group, subjects were divided into those with a history of seizures (after the neonatal period) (n = 17) and those without a history of seizures (n = 17). Seizure history was unknown for five subjects. There were no significant differences between the seizure and non-seizure groups in mean T-scores on the Syndrome scales, the Internalizing–Externalizing dichotomy or the Total Problem score, whether or not IQ was used as a covariate.
Within the control group, one of 54 subjects (2%) had a Total Problem score within the clinically significant range (T = 74). Four children in the control group (7%) had scores of 
70 on one or more of the Behavior Problem scales. In the focal lesion group, three of 39 children (8%) had a Total Problem score of 70. All three had left hemisphere lesions and in each case the lesion did not involve the frontal lobe (one was temporal, one parietal and one temporo-occipital). Twelve of 39 focal lesion children (31%) had a score of 70 or higher on one or more of the Behavior Problem scales. Nine of the 12 had left hemisphere lesions. Of these, four involved the frontal lobe. There were no consistent patterns of elevated T-scores (i.e. 70) in the control group. In the focal lesion group, scores on the Social Problems scale were elevated in seven children (three children with RH lesions and four with LH lesions; two of the children had frontal lobe lesions). Scores on the Attention Problems scale were elevated in five children (one with an RH lesion and four with LH lesions; four of the five had frontal lobe involvement). Other elevated scores were fairly equally distributed among the remaining Problem scales.
Longitudinal analyses
For the control group, there were no significant differences in mean scores for either the Total Problem score (46.0 ± 10.1 and 38.9 ± 13.4 for the first and second administrations, respectively) or the Social Problems scale (53.4 ± 5.9 and 50.7 ± 2.0) between the first and second questionnaires. For the focal lesion group, there were no significant differences in mean scores for the Total Problem score between the first and second administrations (47.5 ± 11.4 versus 51.4 ± 12.7). However, there was a significantly higher mean score on the Social Problems scale on the second administration of the CBCL for the focal lesion children (54.6 ± 4.3 and 59.2 ± 9.0 for the first and second administrations, respectively; P = 0.041). Two children in the focal lesion group (5%) had T-scores of 70. These scores were elevated on the second administration only, when the children were 11 and 10 years old. Both had LH lesions, one in the parietal lobe and one involving both temporal and parietal lobes. Neither of these subjects had a history of seizures.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
We found no evidence of consistent, clinically significant behavioural or emotional problems using the CBCL parent report form to evaluate behaviour in a large group of children and adolescents who had suffered pre- or perinatal focal brain damage. There were no significant group differences in behaviour related to the side of the lesion (LH or RH), to the involvement of the frontal lobe in the lesion or to the presence or absence of seizures. Furthermore, there was no systematic effect of age on T-scores; e.g. we found no evidence of increasing behavioural problems with increasing age. Because the mean IQs were different in the control and focal lesion groups, we covaried for IQ and subsequently found no differences in mean T-scores between focal lesion and control groups. Because covariance analysis may be seen as somewhat artificial (i.e. the child is a unitary whole who does not function apart from his or her IQ), we also believed it to be of theoretical importance to perform the statistical analyses without covarying for IQ. When IQ was not taken into account, there were significant CBCL differences between the focal lesion and control groups. Our analyses indicate that the T-score differences between the focal lesion and control groups were due largely to IQ differences rather than to true social and behavioural differences. Moreover, the T-scores were all within the non-clinical range for both control and focal lesion groups.
Although there were no significant differences in mean T-scores between the focal lesion and control groups in covariance analyses, qualitatively there were more children in the focal lesion group than in the control group who had T-scores within the clinically significant (abnormal) range on both the Total Problem score and one or more of the Behavior Problem scales. Most of the abnormal scores were on the Social Problems and Attention Problems scales. There was no consistent pattern of site of the lesion within the hemisphere and the presence of elevated T-scores, although there appeared to be over-representation of LH lesions with scores in the clinical range. It is apparent that there may be individuals within the focal lesion group who may develop behavioural or emotional problems, but this does not appear to be a consistent feature in our subjects. In an earlier study from this laboratory (Trauner et al., 1996b) using the Personality Inventory for Children (Wirt et al., 1984) in a different group of children with early focal brain damage, we found a higher incidence of social problems in children with posterior lesions than in controls, whereas children with anterior lesions had a higher incidence of academic difficulties. IQ was not taken into account in the analyses in the earlier study, and certainly could account for the reported academic and social differences. Despite the disparity between the two studies, the earlier report also found no evidence of social or behavioural difficulties in association with frontal lobe lesions.
In the past decade, there has been an increasing body of literature linking frontal lobe damage in early childhood with later social, emotional and personality disorders. Price and colleagues described two adults who had severely aberrant behaviour and had suffered bilateral prefrontal damage early in life (Price et al., 1990). Neuropsychological testing in these patients suggested that social and moral development was arrested at an immature stage. Deficits were found in the areas of insight, social judgement, empathy and complex reasoning. A case study of a woman who had acquired frontal lobe damage at age 7 years reported deficits in social development and behaviour, with limited empathy, impaired moral reasoning and defects in self-regulation of emotion and affect (Eslinger et al., 1992; Grattan and Eslinger, 1992). Anderson and colleagues presented case studies of two individuals who had sustained early, localized brain damage involving the frontal lobes (Anderson et al., 1999). Both exhibited early evidence of severe social, emotional and behavioural problems, even before adolescence. The behavioural disorders became even more severe as they reached adolescence. Davidson and colleagues reviewed data from two individuals who had suffered early damage to the frontal area (Davidson et al., 2000). Both of the subjects had histories of verbal and physical abusiveness and intermittent, explosive episodes of anger. The subjects in these reports had involvement of the orbital or mesial prefrontal cortex, and the authors suggested that the involvement of these particular regions within the frontal cortex, particularly in the RH, were more likely to be associated with significant social and emotional sequelae than lesions involving other areas of the brain. The lesion locations in our subjects were varied, and because the lesion location was determined from a clinical neuroradiological reading of the scans, it was not possible to determine in every case whether these specific areas of the frontal lobe were involved. One of the reasons for the possible discrepancy between our findings and those of the earlier reports cited above may be the difference in the site of the lesion within the frontal lobe in our subjects as opposed to the lesion locations identified in the previous studies. The causes of brain damage differed between the subjects in the previous reports and our subjects. Most had a closed head injury with bilateral frontal lobe damage, whereas all of our subjects had suffered only unilateral damage from strokes or haemorrhages. It is evident from our study that one must be careful to evaluate the cause of the lesion, as well as the definition of `focal', when examining the potential cognitive and behavioural consequences of early brain damage. The presence of bilateral brain damage, for example, may have very different implications for cognitive and behavioural outcome from that of unilateral damage. The timing of the insult may be a crucial factor in determining outcome as well. In most of the case reports cited above, the subjects had postnatal onset of their brain injury, whereas our subjects all had pre- or perinatal onset. We postulate that the brain is more likely to achieve significant reorganization, resulting in a lower likelihood of significant clinical dysfunction, when the injury takes place very early in brain development.
The reports from the London hemiplegia study of early psychiatric disorders in children with hemiplegic cerebral palsy (Goodman and Graham, 1996; Goodman and Yude, 1997; Goodman, 1998) would appear to be at odds with the findings of the present study as well. The difference in ascertainment of the study populations may be a major factor. The hemiplegia studies used children clinically identified as having a hemiplegia, without verification of the side or sites of lesions in the brain that might have led to the motor deficits. It is possible that some of these children may have had more diffuse or bilateral lesions, with the primary motor manifestation of hemiplegia. The subjects who participated in the current study were identified on the basis of the medical history and a neuroimaging procedure that documented a single, unilateral brain lesion acquired in the pre- or perinatal period. Children with bilateral lesions, slowly evolving lesions such as tumours or arteriovenous malformations, and lesions acquired through closed head trauma were specifically excluded because these lesions may have produced more widespread brain damage. When the early lesion was confined to one hemisphere, we could find no evidence of widespread, clinically significant behavioural or emotional disturbances. Another potential explanation for the discrepancy between our findings and those of Goodman (Goodman, 1998) is the choice of measures. In the hemiplegia studies, the investigators used both questionnaire data and direct psychiatric interviews, whereas we used questionnaire data only. The hemiplegia studies found a good correlation between questionnaire results and the findings of direct patient interviews, however, suggesting that questionnaires are valid indicators of behavioural dysfunction. Other investigators (e.g. Stanger et al., 1993) have also found good correlations between questionnaire results and those of clinical interviews. We therefore believe that the CBCL data obtained on our focal lesion subjects represent a valid indicator of behavioural function.
In our smaller longitudinal sample, there was a small but significant increase on the Social Problems scale for the focal lesion group, but not for controls, over time, suggesting the possibility that some of the children in the focal lesion group may be at risk of social problems as they get older. All of the mean T-scores were well within the normal range, however, and did not reflect any indication of clinically significant problems. Because our focal lesion group was relatively young (mean age 8.7 years), it is still possible that behavioural, social or psychiatric problems may become evident as more of the subjects reach adolescence. In the British hemiplegia studies, children in the study population demonstrated evidence of behaviour problems even during childhood, again in contrast to our findings with the unilateral pre- and perinatal stroke group.
The major advantages of the present study were the ability to localize the lesion in every case using a neuroimaging study, the large number of children studied (for such a rare population) and the fact that the lesions were all acute and confined to the pre- or perinatal period. By excluding children with brain lesions of diverse causes, such as closed head trauma and tumours, and differing ages of lesion acquisition, we were able to study a relatively pure sample of individuals with early, acute, unilateral brain damage. In this way, confounding issues such as more diffuse damage, timing of the lesion or the effects of a chronic evolving lesion were avoided. Potential limitations of the present study include the lack of ability to identify the presence or absence of orbital or mesial prefrontal cortical involvement in every case and the fact that the CBCL is a parent report form and might thus be somewhat subjective, particularly when parents might be more lenient in their judgement of a child with a neurological disability. A third potential limitation is that, despite the large sample size for such a rare population, the number of children with specific mesial or orbital prefrontal involvement might be small, and thus the results might be biased in a more favourable direction by the large number of children with lesions in other areas of the brain.
It is particularly important to define whether children with early evidence of focal brain damage are at risk for potential behavioural and emotional dysfunction for several reasons. Parents of these children are very concerned about all aspects of their child's development, and would like information about potential areas of problems. If behaviour problems are likely, early interventions could be instituted to modify or improve the long-term prognosis. Finally, studies of behaviour after early-acquired unilateral brain lesions, in comparison with the behaviour of individuals after later-acquired or bilateral lesions, can inform about the developing brain's potential for reorganization and provide inferences about the degree of plasticity, and limitations thereof, in the developing human nervous system.
Given the disparity in findings between our studies and those of others using different methods of ascertainment and different definitions of focal lesions, it will be very important in future studies of the brain–behaviour relationships in the developing human nervous system to consider all potential causes for any observed behavioural abnormalities, such as genetic and environmental factors, toxin exposure, the cause and extent of the lesion and the method of lesion localization, before concluding that specific anatomical lesions are causally related to specific behavioural outcomes.
|
Acknowledgments |
|---|
This research was funded by grants NINDS P50 NS 22343 and by NIDCD P50 DC01289 from the National Institutes of Health.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Achenbach TM. Assessment and taxonomy of child and adolescent psychopathology. Newbury Park (CA): Sage Publications; 1985.
Achenbach TM. Manual for the child behavior checklist 4–18 years and 1991 profile. Burlington (VT): Department of Psychiatry, University of Vermont; 1991.
Anderson SW, Bechara A, Damasio H, Tranel D, Damasio AR. Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nat Neurosci 1999; 2: 1032–7.[Web of Science][Medline]
Benowitz LI, Bear DM, Rosenthal R, Mesulam MM, Zaidel E, Sperry RW. Hemispheric specialization in nonverbal communication. Cortex 1983; 19: 5–11.[Web of Science][Medline]
Borod J. Interhemispheric and intrahemispheric control of emotion: A focus on unilateral brain damage. J Consult Clin Psychol 1992; 60: 339–48.[Web of Science][Medline]
Borod JC. Cerebral mechanisms underlying facial, prosodic, and lexical emotional expression: a review of neuropsychological studies and methodological issues. Neuropsychology 1993; 7: 445–63.
Damasio A, Van Hoesen G. Emotional disturbances associated with focal lesions of the frontal lobe. In: Heilman K, Satz P, editors. The neuropsychology of human emotion. New York: Guilford Press; 1983. p. 85–110.
Davidson RJ, Putnam KM, Larson CL. Dysfunction in the neural circuitry of emotion regulation—a possible prelude to violence. [Review]. Science 2000; 289: 591–4.
Denckla MB. The neuropsychology of social–emotional learning disabilities [editorial]. Arch Neurol 1983; 40: 461–2.
Eslinger PJ, Grattan LM, Damasio H, Damasio AR. Developmental consequences of childhood frontal lobe damage. Arch Neurol 1992; 49: 764–9.
Gainotti G. Emotional behavior and hemispheric side of the lesion. Cortex 1972; 8: 41–55.[Medline]
Goodman R. The longitudinal stability of psychiatric problems in children with hemiplegia. J Child Psychol Psychiatry 1998; 39: 347–54.[Web of Science][Medline]
Goodman R, Graham P. Psychiatric problems in children with hemiplegia: cross-sectional epidemiological survey. BMJ 1996; 312: 1065–9.
Goodman R, Yude C. Do unilateral lesions of the developing brain have side-specific psychiatric consequences in childhood? Laterality 1997; 2: 103–15.
Grattan LM, Eslinger PJ. Long-term psychological consequences of childhood frontal lobe lesion in patient DT. Brain Cogn 1992; 20: 185–95.[Web of Science][Medline]
Heilman KM, Schwartz HD, Watson RT. Hypoarousal in patients with the neglect syndrome and emotional indifference. Neurology 1978; 28: 229–32.
Heilman KM, Bowers D, Valenstein E. Emotional disorders associated with neurological diseases. In: Heilman KM, Valenstein E, editors. Clinical neuropsychology. 3rd ed. New York: Oxford University Press; 1993. p. 461–97.
Mesulam MM. Frontal cortex and behavior. Ann Neurol 1986; 19: 320–5.[Web of Science][Medline]
Nass R, Koch D. Temperamental differences in toddlers with early unilateral right- and left-brain damage. Dev Neuropsychol 1987; 3: 93–9.
Nass R, Koch D. Specialization for emotion: temperament after congenital unilateral injury. In: Amir N, Rapin I, editors. Pediatric neurology: behavior and cognition of the child with brain dysfunction. Basel: Karger; 1991. p. 1–17.
Nelson LD, Cicchetti D, Satz P, Stern S, Sowa M, Cohen S, et al. Emotional sequelae of stroke. Neuropsychology 1993; 7: 553–60.
Price BH, Daffner KR, Stowe RM, Mesulam MM. The comportmental learning disabilities of early frontal lobe damage. Brain 1990; 113: 1383–93.
Reilly JS, Stiles J, Larsen J, Trauner D. Affective facial expression in infants with focal brain damage. Neuropsychologia 1995; 33: 83–99.[Web of Science][Medline]
Robinson RG, Starkstein SE. Current research in affective disorders following stroke. [Review]. J Neuropsychiat Clin Neurosci 1990; 2: 1–14.
Robinson RG, Lipsey JR, Rao K, Price TR. Two-year longitudinal study of poststroke mood disorders: comparison of acute-onset with delayed-onset depression. Am J Psychiatry 1986; 146: 1238–44.[Web of Science][Medline]
Robinson RG, Kubos KL, Starr LB, Rao K, Price TR. Mood disorders in stroke patients. Brain 1984; 107: 81–93.
Ross ED. Nonverbal aspects of language. [Review]. Neurol Clin 1993; 11: 9–23.[Web of Science][Medline]
Ross ED, Mesulam MM. Dominant language functions of the right hemisphere? Prosody and emotional gesturing. Arch Neurol 1979; 36: 144–8.
Ross ED, Rush AJ. Diagnosis and neuroanatomical correlates of depression in brain-damaged patients. Arch Gen Psychiatry 1981; 38: 1344–54.
Sackeim HA, Greenberg MS, Weiman AL, Gur RC, Hungerbuhler JP, Geschwind N. Hemispheric asymmetry in the expression of positive and negative emotions. [Review]. Arch Neurol 1982; 39: 210–8.
Stanger C, Achenbach TM, McConaughy SH. Three-year course of behavioral/emotional problems in a national sample of 4- to 16-year-olds. 3. Predictors of signs of disturbance. J Consult Clin Psychol 1993; 61: 839–48.[Web of Science][Medline]
Stuss DT, Benson DF. Neuropsychological studies of the frontal lobes. Psychol Bull 1984; 95: 3–28.[Web of Science][Medline]
Tranel D, Hall LE, Olson S, Tranel NN. Evidence for a right-hemisphere developmental learning disability. Dev Neuropsychol 1987; 3: 114–27.
Trauner DA, Ballantyne A, Friedland S, Chase C. Disorders of affective and linguistic prosody in children after early unilateral brain damage. Ann Neurol 1996a; 39: 361–7.[Web of Science][Medline]
Trauner DA, Panyard-Davis JL, Ballantyne AO. Behavioral differences in school age children after perinatal stroke. Assessment 1996b; 3: 265–76.[Abstract]
Vargha-Khadem F, O'Gorman AM, Watters GV. Aphasia and handedness in relation to hemispheric side, age at injury and severity of cerebral lesion during childhood. Brain 1985; 108: 677–96.
Voeller KK. Right-hemisphere deficit syndrome in children. Am J Psychiatry 1986; 143: 1004–9.
Wechsler D. Manual for the Wechsler Intelligence Scale for Children—Revised (WISC-R). San Antonio (TX): Psychological Corporation; 1974.
Wechsler D. Manual for the Wechsler Preschool and Primary Scale of Intelligence—Revised (WPPSI-R). Cleveland (OH): Psychological Corporation; 1989.
Weintraub S, Mesulam MM. Developmental learning disabilities of the right hemisphere: emotional, interpersonal, and cognitive components. Arch Neurol 1983; 40: 463–8.
Wirt R, Lachar D, Klinedinst J, Seat P. Multidimensional description of child personality: A manual for the Personality Inventory for Children (1984 revision). Los Angeles: Western Psychological Services; 1984.
Received September 6, 2000. Revised December 7, 2000. Accepted January 5, 2001.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J Parkes, M White-Koning, N McCullough, and A Colver Psychological problems in children with hemiplegia: a European multicentre survey Arch. Dis. Child., June 1, 2009; 94(6): 429 - 433. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Juhasz, E.M. Haacke, J. Hu, Y. Xuan, M. Makki, M.E. Behen, M. Maqbool, O. Muzik, D.C. Chugani, and H.T. Chugani Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome AJNR Am. J. Neuroradiol., May 1, 2007; 28(5): 900 - 906. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. R. Golomb, K. S. Carvalho, and B. P. Garg A 9-Year-Old Boy with a History of Large Perinatal Stroke, Infantile Spasms, and High Academic Achievement J Child Neurol, May 1, 2005; 20(5): 444 - 446. [Abstract] [PDF]
|
|
|
|
 |
|
 E. Mercuri, A. Barnett, M. Rutherford, A. Guzzetta, L. Haataja, G. Cioni, F. Cowan, and L. Dubowitz Neonatal Cerebral Infarction and Neuromotor Outcome at School Age Pediatrics, January 1, 2004; 113(1): 95 - 100. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||