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The objective was to clarify occurrence, phenomenology, and risk factors for novel psychiatric disorder (NPD) in the first 3 months after mild traumatic brain injury (mTBI) and orthopedic injury (OI). Children aged 8-15 years with mTBI (n = 220) and with OI but no TBI (n = 110) from consecutive admissions to an emergency department were followed prospectively at baseline and 3 months post-injury with semi-structured psychiatric interviews to document the number of NPDs that developed in each participant. Pre-injury child variables (adaptive, cognitive, and academic function, and psychiatric disorder), pre-injury family variables (socioeconomic status, family psychiatric history, and family function), and injury severity were assessed and analyzed as potential confounders and predictors of NPD. NPD occurred at a significantly higher frequency in children with mTBI versus OI in analyses unadjusted (mean ratio [MR] 3.647, 95% confidence interval [CI(95)] (1.264, 15.405), p = 0.014) and adjusted (MR = 3.724, CI(95) (1.264, 15.945), p = 0.015) for potential confounders. In multi-predictor analyses, the factors besides mTBI that were significantly associated with higher NPD frequency after adjustment for each other were pre-injury lifetime psychiatric disorder [MR = 2.284, CI(95) (1.026, 5.305), p = 0.043]; high versus low family psychiatric history [MR = 2.748, CI(95) (1.201, 6.839), p = 0.016], and worse socio-economic status [MR = 0.618 per additional unit, CI(95) (0.383, 0.973), p = 0.037]. These findings demonstrate that mild injury to the brain compared with an OI had a significantly greater deleterious effect on psychiatric outcome in the first 3 months post-injury. This effect was present even after accounting for specific child and family variables, which were themselves independently related to the adverse psychiatric outcome.

The objective of the study was to compare psychiatric outcomes in adults with and without history of pediatric traumatic brain injury (TBI). Youth ages 6 to 14 years hospitalized for TBI from 1992 to 1994 were assessed at baseline and at 3, 6, 12, and 24 months post-injury. In the current study, psychiatric assessments were repeated at 24 years post-injury with the same cohort, now adults ages 29 to 39 years. A control group of healthy adults also was recruited for one-time cross-sectional assessments. Outcome measures included: 1) presence of a psychiatric disorder since the 24-month assessment not present before the TBI ("novel psychiatric disorder," NPD), or in the control group, the presence of a psychiatric disorder that developed after the mean age of injury of the TBI group plus 2 years; and 2) Time-to-Event for onset of an NPD during the same time periods. In the TBI group, NPDs were significantly more common, and presence of a current NPD was significantly predicted by presence of a pre-injury lifetime psychiatric disorder and by abnormal day-of-injury computed tomography (CT) scan. Compared with controls, the TBI group also had significantly shorter Time-to-Event for onset of any NPD. These findings demonstrate that long-term psychiatric outcomes in adults previously hospitalized for pediatric TBI are significantly worse when compared with adult controls without history of pediatric TBI, both in terms of prevalence and earlier onset of NPD. Further, in the TBI group, long-term NPD outcome is predicted independently by presence of pre-injury psychiatric disorder and abnormal day-of-injury CT scan.

Mild traumatic brain injury (mTBI) accounts for the vast majority of all pediatric TBI. An important minority of children who have suffered an mTBI have enduring cognitive and emotional symptoms. However, the mechanisms of chronic symptoms in children with pediatric mTBI are not fully understood. This is in part due to the limited sensitivity of conventional neuroimaging technologies. The present study examined resting-state magnetoencephalography (rs-MEG) source images in 12 children who had mTBI and 12 age-matched control children. The rs-MEG exams were performed in children with mTBI 6 months after injury when they reported no clinically significant post-injury psychiatric changes and few if any somatic sensorimotor symptoms but did report cognitive symptoms. MEG source magnitude images were obtained for different frequency bands in alpha (8-12 Hz), beta (15-30 Hz), gamma (30-90 Hz), and low-frequency (1-7 Hz) bands. In contrast to the control participants, rs-MEG source imaging in the children with mTBI showed: 1) hyperactivity from the bilateral insular cortices in alpha, beta, and low-frequency bands, from the left amygdala in alpha band, and from the left precuneus in beta band; 2) hypoactivity from the bilateral dorsolateral prefrontal cortices (dlPFC) in alpha and beta bands, from the ventromedial prefrontal cortex (vmPFC) in beta band, from the ventrolateral prefrontal cortex (vlPFC) in gamma band, from the anterior cingulate cortex (ACC) in alpha band, and from the right precuneus in alpha band. The present study showed that MEG source imaging technique revealed abnormalities in the resting-state electromagnetic signals from the children with mTBI.

This investigation explored whether differences in cortical thickness could be detected in children who sustained a mild traumatic brain injury (mTBI) compared to those with orthopedic injury (OI) and whether cortical thickness related parental reporting of symptoms. To achieve this objective, FreeSurfer®-based cortical thickness measures were obtained in 330 children, 8 to 15 years of age, with either a history of mTBI or OI. Imaging was performed in all participants with the same 3 Tesla MRI scanner at six-months post-injury, where a parent-rated Post-Concussion Symptom Inventory (PCSI) was also obtained. Robust age-mediated reductions in cortical thickness were observed, but no consistent group-based differences between the mTBI and OI groups were observed. Also, the relation between mechanism of injury (i.e., sports-related, recreational, fall, motor vehicle accident or other) and cortical thickness was examined. Injuries associated with any type of abuse were excluded and children with OI could not have experienced a MVA. Mechanism of injury did not differentially relate to cortical thickness, although in the fall group, parental rating using the PCSI showed increased symptom reporting to be associated with reduced cortical thickness in the left interior frontal, temporal pole and lateral temporal lobe as well as in the right temporal pole. Results from these preliminary findings are discussed in terms of injury variables and developmental factors associated with mTBI in childhood.

Personality change due to traumatic brain injury (PC) in children is an important psychiatric complication of injury and is a form of severe affective dysregulation. This study aimed to examine neurocognitive correlates of PC. The sample included 177 children 5-14 years old with traumatic brain injury who were enrolled from consecutive admissions to five trauma centers. Patients were followed up prospectively at baseline and at 6 months, and they were assessed with semistructured psychiatric interviews. Injury severity, socioeconomic status, and neurocognitive function (measures of attention, processing speed, verbal memory, IQ, verbal working memory, executive function, naming/reading, expressive language, motor speed, and motor inhibition) were assessed with standardized instruments. Unremitted PC was present in 26 (18%) of 141 participants assessed at 6 months postinjury. Attention, processing speed, verbal memory, IQ, and executive function were significantly associated with PC even after socioeconomic status, injury severity, and preinjury attention deficit hyperactivity disorder were controlled. These findings are a first step in characterizing concomitant cognitive impairments associated with PC. The results have implications beyond brain injury to potentially elucidate the neurocognitive symptom complex associated with mood instability regardless of etiology.

The present study compared executive dysfunction among children with attention-deficit/hyperactivity disorder (ADHD) after traumatic brain injury (TBI), also called secondary ADHD (S-ADHD), pre-injury ADHD and children with TBI only (i.e., no ADHD). Youth aged 6–16 years admitted for TBI to five trauma centers were enrolled (n=177) and evaluated with a semi-structured psychiatric interview scheduled on three occasions (within 2 weeks of TBI, i.e., baseline assessment for pre-injury status; 6-months and 12-months post-TBI). This permitted the determination of 6- and 12-month post-injury classifications of membership in three mutually exclusive groups (S-ADHD; pre-injury ADHD; TBI-only). Several executive control measures were administered. Unremitted S-ADHD was present in 17/141 (12%) children at the 6-month assessment, and in 14/125 (11%) children at 12-months post-injury. The study found that children with S-ADHD exhibited deficient working memory, attention, and psychomotor speed as compared to children with pre-injury ADHD. Furthermore, the children with S-ADHD and the children with TBI-only were impaired compared to the children with pre-injury ADHD with regard to planning. No group differences related to response inhibition emerged. Age, but not injury severity, gender, or adaptive functioning was related to executive function outcome. Neuropsychological sequelae distinguish among children who develop S-ADHD following TBI and those with TBI only. Moreover, there appears to be a different pattern of executive control performance in those who develop S-ADHD than in children with pre-injury ADHD suggesting that differences exist in the underlying neural mechanisms that define each disorder, underscoring the need to identify targeted treatment interventions. (JINS, 2014,20, 971–981)

The objective was to assess the nature, rate, predictive factors, and neurocognitive correlates of novel psychiatric disorders (NPD) after mild traumatic brain injury (MTBI). Children age 5-14 years with MTBI (N=87) from consecutive admissions to five trauma centers were enrolled and studied with semistructured psychiatric interviews soon after injury (baseline), and 70 of these children were assessed again 6 months post-injury. Injury severity; lesion characteristics; pre-injury variables, including psychiatric disorder, family psychiatric history, family functioning, socioeconomic status, psychosocial adversity, and adaptive functioning; and post-injury neurocognitive and adaptive functioning measures were assessed with standardized instruments. NPD occurred in 25 of 70 participants (36%) in the first 6 months after injury. NPD at 6 months was predicted by the presence of frontal white-matter lesions on MRI at 3 months post-injury, and was associated with concurrent decrements on neurocognitive indices of processing speed, expressive language, and intellectual functioning. NPD was not predicted by other indices of severity, pre-injury psychosocial variables, estimated pre-injury academic functioning, or adaptive and executive function decrements 6 months post-injury. These findings suggest that short-term psychiatric morbidity associated with MTBI in children and adolescents may be more common than previously thought and may have readily identifiable neuroimaging and neurocognitive correlates.

Ineffective emotion regulation and abnormal amygdala activation have each been found in adolescent-onset major depressive disorder. However, amygdala activation during emotion regulation has not been studied in adolescent-onset major depressive disorder.Fourteen unmedicated adolescents diagnosed with current depression without comorbid psychiatric disorders and fourteen well-matched controls ages 13 to 17 years underwent an emotional regulation task during functional magnetic resonance imaging. During this task, participants viewed negatively-valence images and were asked to notice how they were feeling without trying to change it and maintain their emotional reaction ("Maintain") or to interpret the image in such a way as minimize their emotional response ("Reduce").Imaging analyses demonstrated that adolescents with depression showed: (1) greater right amygdala activation during the maintain condition relative to controls, (2) less connectivity during the maintain condition between the amygdala and both the insula and medial prefrontal cortex than controls, and (3) a significant positive correlation between amygdala-seeded connectivities during maintenance of emotion and psychosocial functioning.The current study is a cross-sectional comparison and longitudinal investigations with larger sample sizes are needed to examine the association between amygdala reactivity and emotion regulation over time in adolescent MDD.During the maintain condition, adolescents with depression showed a heightened amygdala response and less reciprocal activation in brain regions that may modulate the amygdala. A poorly modulated, overreactive amygdala may contribute to poor emotion regulation.

The objective was to examine the effects of traumatic brain injury (TBI), as compared with orthopedic injury (OI), relative to the risk for psychiatric disorder. There has only been one previous prospective study of this nature. Participants were age 7-17 years at the time of hospitalization for either TBI (complicated mild-to-severe) or OI. The study used a prospective, longitudinal, controlled design, with standardized psychiatric assessments conducted at baseline (reflecting pre-injury functioning) and 3 months post-injury. Assessments of pre-injury psychiatric, adaptive functioning, family adversity, and family psychiatric history status were conducted. Severity of injury was assessed by standard clinical scales. The outcome measure was the presence of a psychiatric disorder not present before the injury ("novel"), during the first 3 months after TBI. Enrolled participants (N=141) included children with TBI (N=75) and with OI (N=66). The analyses focused on 118 children (84%) (TBI: N=65; OI: N=53) who returned for follow-up assessment at 3 months. Novel psychiatric disorder (NPD) occurred significantly more frequently in the TBI (32/65; 49%) than the OI (7/53; 13%) group. This difference was not accounted for by pre-injury lifetime psychiatric status; pre-injury adaptive functioning; pre-injury family adversity, family psychiatric history, socioeconomic status, injury severity, or age at injury. Furthermore, none of these variables significantly discriminated between children with TBI who developed, versus those who did not develop, NPD. These findings suggest that children with complicated mild-to-severe TBI are at significantly higher risk than OI-controls for the development of NPD in the first 3 months after injury.

Object The aim of this study was to determine whether the presence of intracranial pathophysiology on computed tomography (CT) scans obtained within 24 hours of mild traumatic brain injury (MTBI) in children adversely affects neuropsychological outcome during the 1st year postinjury. Methods A prospective longitudinal design was used to examine the neuropsychological outcomes in children (ages 5–15 years) who had been treated for MTBI, which was defined as a loss of consciousness for up to 30 minutes and a lowest Glasgow Coma Scale (GCS) score of 13–15. Exclusion criteria included any preinjury neurological disorder. Outcome assessments were performed within 2 weeks and at 3, 6, and 12 months postinjury. Outcomes were compared between patients with MTBI whose postinjury CT scans revealed complications of brain pathophysiology (32 patients, CMTBI group) and those with MTBI but without complications (48 patients, MTBI group). Results Significant interactions confirmed that the pattern of recovery over 12 months after injury differed depending on the intracranial pathology, presence and severity of injuries to body regions other than the head, preinjury attention-deficit hyperactivity disorder (ADHD), and socioeconomic status. Children in the CMTBI group had significantly poorer episodic memory, slower cognitive processing, diminished recovery in managing cognitive interference, and poorer performance in calculating and reading than patients in the MTBI group. Among the patients with mild or no extracranial injury, visuomotor speed was slower in those in the CMTBI group; and among patients without preinjury ADHD, working memory was worse in those in the CMTBI group. Conclusions Neuropsychological recovery during the 1st year following MTBI is related to the presence of radiographically detectable intracranial pathology. Children with intracranial pathology on acute CT performed more poorly in several cognitive domains when compared with patients whose CT findings were normal or limited to a linear skull fracture. Depending on the presence of preinjury ADHD and concomitant extracranial injury, working memory and visuomotor speed were also diminished in patients whose CT findings revealed complications following MTBI. Computed tomography within 24 hours postinjury appears to be useful for identifying children with an elevated risk for residual neuropsychological changes.

We investigated changes in inattentive and hyperactive symptoms over 2 years following traumatic brain injury (TBI) in relation to preinjury attention-deficit/hyperactivity disorder (ADHD), injury, and socioeconomic status (SES) variables. Postinjury stimulant medication treatment was also documented. Of 175 consecutive patients of ages 5 to 15 years with acute TBI, 148 consented, including 114 without preinjury ADHD (mean age, 10.0 years, SD = 2.76) and 34 with preinjury ADHD (mean age 10.36 years, SD = 2.75). The Schedule for Affective Disorders and Schizophrenia for School-Age Children, Present and Lifetime Version, was administered at baseline and at 6, 12, and 24 months post-injury to assess the presence of nine core inattentive and nine hyperactive symptoms and associated impairment. The baseline assessment was performed within 1 month post-injury to establish preinjury diagnosis.Nonlinear change in inattentive symptoms in patients without preinjury ADHD contrasted with higher and more stable symptom levels in children with preinjury diagnosis, including the cubic trend (chi2(1) = 6.23, p = .0126). There was also a significant interaction of group x gender effect (chi2(1) = 4.08, p = .0435) as males had higher numbers of inattentive symptoms than females in the preinjury ADHD group. Change in hyperactive symptoms over time also differed by group, including both linear (chi2(1) = 5.42, p = .0199) and cubic trends (chi2(1) = 8.91, p = .0029), reflecting greater and more frequent fluctuations in children without preinjury ADHD. Socioeconomic level also contributed to change in hyperactive symptoms as reflected by the interaction of SES and linear time (chi2(1) = 6.91, p = .009), as well as quadratic time (chi2(1) = 4.90, p = .027). Occurrence of ADHD diagnosed post-injury ranged from 14.5% (12 months) to 18.3% (24 months) in the group without preinjury ADHD compared with a range from 86.4% (12 months) to 96.2% (6 months) in children with preinjury ADHD. In children without preinjury ADHD, SES was the only patient variable that predicted onset of ADHD, t(110) = -2.85, p = .0052. Treatment with stimulant medication post-injury was more frequently associated with preinjury ADHD (39% vs 7% of children without preinjury ADHD), p.0001 (Fisher exact test). Children with preinjury ADHD who were treated pre-injury with stimulant medication had fewer total symptoms at 24 months post-injury relative to untreated patients with preinjury ADHD (F[1,14] = 3.93, p = 0.069, Cohen's d = 1.28).Change in ADHD symptoms after TBI varies with preinjury diagnosis, reflects injury severity in children without preinjury ADHD, and is treated with stimulant medication mainly in those patients with preinjury ADHD.

BackgroundFunctional magnetic resonance imaging research suggests that major depressive disorder (MDD) in both adults and adolescents is marked by aberrant connectivity of the default mode network (DMN) during resting state. However, emotional dysregulation is also a key feature of MDD. No studies to date have examined emotion-related DMN pathology in adolescent depression. Comprehensively understanding the dynamics of DMN connectivity across brain states in individuals with depression with short disease histories could provide insight into the etiology of MDD.MethodsWe collected functional magnetic resonance imaging data during an emotion identification task and during resting state from 26 medication-free adolescents (13-17 years old) with MDD and 37 well-matched healthy control subjects. We examined between-group differences in blood oxygenation level-dependent task responses and emotion-dependent and resting-state functional connectivity of the two primary nodes of the DMN: medial prefrontal cortex and posterior cingulate cortex (PCC). Additionally, we examined between-group differences in DMN functional connectivity and its relationship to depression severity and onset.ResultsRelative to healthy control subjects, unmedicated adolescents with MDD demonstrated reduced medial prefrontal cortex and PCC emotion-related deactivation and greater medial prefrontal cortex and PCC emotion-dependent functional connectivity with precuneus, cingulate gyrus, and striatum/subcallosal cingulate gyrus. The PCC-subcallosal cingulate connectivity remained inflexibly elevated in the subjects with MDD versus healthy control subjects during resting state. Stronger PCC emotion-dependent functional connectivity was associated with greater depression severity and an earlier age of depression onset.ConclusionsAdolescent depression is associated with inflexibly elevated DMN connections. Given more recent evidence of DMN maturation throughout adolescence, our findings suggest that early-onset depression adversely affects normal development of functional brain networks.

This study aimed to better understand the occurrence of novel psychiatric disorders (NPDs) in children with mild traumatic brain injury (mTBI) in relation to preinjury variables, injury-related variables, and concurrent neurocognitive outcome. Eighty-seven children aged 5-14 years who had experienced mTBI were studied from consecutive hospital admissions with semistructured psychiatric interviews soon after injury (baseline). Fifty-four children were reassessed 24 months postinjury. Standardized instruments were used to evaluate injury severity, lesion characteristics, preinjury variables (lifetime psychiatric disorder, family psychiatric history, family function, socioeconomic status, psychosocial adversity, adaptive function, and academic function), and finally, postinjury neurocognitive and adaptive function. At 24 months postinjury, NPDs had occurred in 17 of 54 (31%) participants. NPD at 24 months was related to frontal white matter lesions and was associated with estimated preinjury reading, preinjury adaptive function, and concurrent deficits in reading, processing speed, and adaptive function. These findings extend earlier reports that the psychiatric morbidity after mTBI in children is more common than previously thought, and moreover, it is linked to preinjury individual variables and injury characteristics and is associated with postinjury adaptive and neurocognitive functioning.

Objective To investigate the association between focal stroke lesions of Posner's executive attention network and a specific region of interest in the frontal lobes (orbital frontal and mesial frontal) and either attention-deficit/hyperactivity disorder (ADHD) or traits of the disorder (ADHD symptomatology). Method Twenty-nine children with focal stroke lesions were studied with standardized psychiatric assessments and anatomical brain magnetic resonance imaging. The pattern of lesion overlap in subjects with ADHD symptomatology was determined. Results Fifteen of 28 subjects with no prestroke ADHD were diagnosed with ADHD symptomatology at the time of assessment. The extent of lesions within the executive attention network was marginally related to ADHD symptomatology (p = .088; effect size = 0.66), whereas the extent of lesions in the specific frontal region of interest was significantly related to ADHD symptomatology (p = .040; effect size = 0.82). Conclusions Lesions within Posner's executive attention network and its orbital frontal connections may be linked to important mechanisms in the expression of ADHD symptomatology after childhood stroke. These findings are consistent with functional and structural imaging findings in studies of idiopathic ADHD.

We investigated attentional outcome after childhood stroke and orthopedic diagnosis in medical controls. Twenty-nine children with focal stroke lesions and individually matched children with clubfoot or scoliosis were studied with standardized attention and neuroimaging assessments. Stroke lesions were quite varied in location and commonly involved regions implicated in Posner's model of attention networks. Children with stroke lesions performed significantly more poorly regarding attention function compared with controls. Performance on the Starry Night, a test demanding alerting and sensory-orienting but not executive attention function, was significantly associated with lesion size in the alerting and sensory-orienting networks but not the executive attention network. Furthermore, earlier age at lesion acquisition was significantly associated with poorer attention function even when lesion size was controlled. These findings support the theory of dissociable networks of attention and add to evidence from studies of children with diffuse and focal brain damage that early insults are associated with worse long-term outcomes in many domains of neuropsychological function. In addition, these results may provide clues towards the understanding of mechanisms underlying attention in children. (JINS, 2004,10, 976–986.)

Verbal learning and memory (VLM) following pediatric stroke was characterized in a cross-sectional neuropsychological and neuroimaging study of 26 subjects, aged 5 to 17, with a history of pediatric stroke and 26 age, SES, and gender matched orthopedic controls. Further comparisons were made between the VLM profiles of stroke subjects with rightversusleft hemisphere lesions and early (≤12 months)versuslate (>12 months) strokes. Overall, stroke subjects scored significantly lower than control subjects on several VLM indices (California Verbal Learning Test–Children; CVLT–C), as well as on measures of intellectual functioning (IQ) and auditory attention/working memory (Digit Span). Subgroup analyses of the stroke population foundnosignificant differences in VLM, Digit Span, Verbal IQ or Performance IQ when left-hemisphere lesion subjects were compared to right-hemisphere lesion subjects. In contrast, early strokes were associated with significantly fewer words recalled after delay, reduced discriminability (fewer correct hits relative to false positive errors on recognition testing), and relatively worse auditory attention/working memory scores (Digit Span). These findings indicate that pediatric stroke subjects demonstrated more VLM impairment than control subjects, and early strokes were associated with greater recall and recognition deficits. In stark contrast with adult-onset stroke, both left- and right-hemisphere lesions during childhood resulted in similar VLM performance. (JINS, 2004,10, 742–752.)

The purpose of the current study was to examine the effect of side of lesion on neuropsychological performance in childhood stroke. While laterality effects have been shown fairly consistently in adults who have experienced stroke, results from studies on children who have experienced childhood stroke are not as clear. Numerous methodological differences between previous studies on laterality effects in childhood stroke make it difficult to draw overall conclusions regarding laterality findings. The current study aimed to study a single group of children who experienced stroke in childhood across a number of cognitive domains. The participants were 13 children/adolescents with left hemisphere lesions and 16 children/adolescents with right hemisphere lesions, with a range of onset from prenatal to 13 years. All participants were administered a broad battery of neuropsychological tests including tests of intelligence, achievement, language skills, visuospatial skills, memory, and executive functioning. No significant differences were found between the groups on any of the measures and the calculated effect sizes were small for all but one of the measures examined. These results have implications for a greater understanding of the ability of the young brain to reorganize after childhood stroke. (JINS, 2004,10, 698–708.)

To examine the relationship of child and family psychosocial variables and traumatic brain injury (TBI) severity as it relates to sustained attention (the Paediatric Assessment of Cognitive Efficiency, PACE).Forty-two children and adolescents were recruited and participated in a 2 year longitudinal study to evaluate sustained attention using the computerized testing metric, PACE. More specifically, errors of omission (inattention) and commission (impulsiveness) were measured.Significant improvement on inattention and impulsiveness were observed over time. High pre-injury psychosocial adversity and low pre-injury adaptive functioning significantly predicted a greater number of inattention errors. Severity of injury predicted the reduction of impulsiveness. Moreover, omission errors immediately after TBI predicted later secondary attention-deficit/hyperactivity disorder (SADHD, ADHD that emerges after TBI).Based on these findings, it is important to consider pre-injury child and family psychosocial characteristics in addition to severity of injury when predicting outcome of TBI in children.

[corrected] To evaluate the convergence between the Kiddie Schedule for Affective Disorders and Schizophrenia (K-SADS) for the diagnosis of psychiatric disorders and the Child Behavior Checklist (CBCL).Cross-sectional psychiatric study of 72 children with traumatic brain injuries or orthopaedic injuries aged 5-14.Sensitivity, specificity, total predictive value and odds ratio were calculated to evaluate the association between CBCL summary scores and K-SADS diagnosis of at least one psychiatric disorder (K-SADS-1), and of CBCL subscales and K-SADS diagnosis of Attention-Deficit/Hyperactivity Disorder (ADHD). Lowered cut-off scores of tor = 60 were used.Convergence between the CBCL total problem scale and K-SADS-1 was poor. Convergence between 'at least one elevated CBCL subscale' and K-SADS-1, and between CBCL attention problems and social problems scales and K-SADS diagnosis of ADHD was excellent.Caution is needed when using the total problem scale of CBCL in predicting global psychological impairment because underestimation of problems is likely. The attention and social problems scales of CBCL can be used to estimate ADHD.

We examined the effect of closed head injury (CHI) on the development of symptoms of secondary attention deficit hyperactivity disorder (SADHD), emotional disturbance, and impaired response inhibition. We also investigated the relation of developmental and recovery variables to SADHD symptoms and inhibition. Participants were 200 children aged 5-17 years, 137 children who had CHI, and 63 children with no history of CHI served as controls. We assessed preinjury behavior problems, head injury variables (severity, age at time of injury, time since injury), postinjury SADHD, and anxiety symptoms at least 2 years following the head injury. Response inhibition was measured with the stop-signal task. CHI predicted the development of SADHD symptoms and anxiety with more severe injury predicting more severe outcomes. Only the combination of severe CHI and a high level of SADHD symptoms predicted poor response inhibition. Postinjury anxiety was not associated with poor inhibition. The consequences of CHI did not vary with age at injury or time since injury, but poorer outcome was predicted by preinjury behavior problems. CHI in children leads to SADHD symptoms and anxiety even after taking preinjury disturbance into account. Poor response inhibition is a consequence of CHI but only when the CHI is severe and the child manifests high levels of SADHD symptoms.

To better characterize pediatric psychopathology after neurological insult, secondary attention deficit hyperactivity disorder (SADHD)-or ADHD that develops after traumatic brain injury (TBI)-and its clinical and neuroimaging correlates were investigated. Outcome data were available for 118 children, ages 5 through 14 at the time of hospitalization following TBI (severe TBI n = 37; mild-moderate TBI n = 57) and orthopedic injury (n = 24). Standardized psychiatric, adaptive functioning, cognitive functioning, family functioning, and family psychiatric history assessments were conducted on all participants. Severity of injury and neuroimaging lesion assessments were conducted on TBI participants only. The diagnosis of SADHD was mutually exclusive with preinjury ADHD, which occurred in 13 of 94 TBI participants and 4 of 24 orthopedic injury participants. SADHD occurred in 13 of 34 eligible participants with severe TBI but resolved in 4 of 13 of these participants. SADHD also occurred in 1 of 8 eligible moderate TBI participants, only in the presence of preinjury ADHD traits and 3 of 39 of eligible mild TBI cases. SADHD occurred in 1 of 20 of eligible participants with orthopedic injury without any brain injury. SADHD was significantly associated with TBI severity recorded by categorical and dimensional measures, intellectual and adaptive functioning deficits, and personality change due to TBI, but not with lesion area or location. These results suggest that SADHD is a clinically important syndrome after severe TBI in children and adolescents.

The impact of traumatic brain injury (TBI) on working memory (WM) was studied in 144 children (79 with mild, 23 with moderate, and 42 with severe injuries) who underwent magnetic resonance imaging (MRI) at 3 months and were tested at baseline and at 3, 6, 12, and 24 months postinjury. An n-back WM task for letter identity was administered with memory load ranging from 1- to 3-back and a 0-back condition. A TBI Severity x Quadratic Tune interaction showed that net percentage correct (correct detections of targets minus false alarms) was significantly lower in severe than in mild TBI groups. The Left Frontal Lesions x Age interaction approached significance. Mechanisms mediating late decline in WM and the effects of left frontal lesions are discussed.

Objectives: To determine the rate, types, and correlates of psychiatric disorder (PD) following stroke and orthopedic disorders in children and adolescents. Method: Children aged 5 to 19 were assessed. The study used a cross-sectional design that compared 29 stroke subjects with 29 congenital clubfoot or scoliosis subjects. Assessments of psychiatric status; cognitive, adaptive, academic, and family functioning; family psychiatric history; neuroimaging; and neurological status were conducted. The main outcome measure was a current PD not present before the stroke or orthopedic disorder. Results: Poststroke PD occurred significantly more often than postorthopedic diagnosis PD (17/29 [59%] versus 4/29 [14%], p ≤ .001). Subjects with ongoing poststroke PD had significantly more impaired intellectual and adaptive functioning, higher intensity family psychiatric history scores, and tended toward higher neurological severity index scores, but they were not different regarding lesion volume or family functioning compared with stroke subjects without PD. Regression analyses showed that neurological severity and family psychiatric history independently contributed significantly to predicting PD. Conclusions: The data suggest that there are significant biopsychosocial correlates of PD in children with focal neurological lesions. These include a relatively abnormal neurological exam, lower IQ, and increased family psychopathol

Pediatric traumatic brain injury (TBI) is a major public health problem. Psychiatric disorders with onset before the injury appear to be more common than population base rates. Novel (postinjury onset) psychiatric disorders (NPD) are also common and complicate child function after injury. Novel disorders include personality change due to TBI, secondary attention-deficit/hyperactivity disorder (SADHD), as well as other disruptive behavior disorders, and internalizing disorders. This article reviews preinjury psychiatric disorders as well as biopsychosocial risk factors and treatments for NPD.

The authors aimed to contribute a clinically rich description of personality change due to traumatic brain injury (PC) in children. The sample consisted of consecutively injured children. Ninety-four subjects ages 5 to 14 years were assessed at the time of hospitalization after a traumatic brain injury (TBI). A standardized psychiatric interview, the Neuropsychiatric Rating Schedule, was used to elicit symptoms of PC. PC occurred in 59% of severe (22/37) and 5% of mild/moderate (3/57) TBI subjects. Among the 37 severe TBI subjects, the labile subtype of PC was the most common (49%), followed by the aggressive and disinhibited subtypes (38% each), apathy (14%), and paranoia (5%). Also frequent in severe TBI was perseveration (35%). A detailed case example, numerous clinical vignettes of PC symptoms, and a tabulation of their frequencies provide clinicians a broader frame of reference for eliciting symptoms of PC.

The occurrence of personality change due to traumatic brain injury (PC), and its clinical and neuroimaging correlates were investigated. Ninety-four children, ages 5 through 14 at the time of hospitalization following traumatic brain injury (TBI; severe TBI N = 37; mild–moderate TBI N = 57), were assessed. Standardized psychiatric, adaptive functioning, cognitive functioning, family functioning, family psychiatric history, severity of injury, and neuroimaging assessments were conducted. The Neuropsychiatric Rating Schedule (NPRS) was used to establish a diagnosis of PC. Approximately 40% of consecutively hospitalized severe TBI participants had ongoing persistent PC an average of 2 years postinjury. An additional approximately 20% had a history of a remitted and more transient PC. PC occurred in 5% of mild–moderate TBI but was always transient. Interrater reliability for the diagnosis of PC was good (Kappa = .70). In severe TBI participants, persistent PC was significantly associated with severity of injury, particularly impaired consciousness over 100 hr, adaptive and intellectual functioning decrements, and concurrent diagnosis of secondary attention deficit hyperactivity disorder, but was not significantly related to any psychosocial adversity variables. These findings suggest that PC is a frequent diagnosis following severe TBI in children and adolescents, but is much less common following mild–moderate TBI. (JINS, 2000, 6, 279–289.)

The purpose of this study was to quantify and to identify predictors of posttraumatic stress disorder (PTSD) symptomatology after traumatic brain injury (TBI). Fifty children aged 6 to 14 years, hospitalized after TBI, were assessed soon after TBI regarding injury severity and preinjury psychiatric, socioeconomic, family functioning, and family psychiatric history status; neuroimaging was also analyzed. Psychiatric assessments were repeated 3, 6, 12, and 24 months after TBI. Only 2 of 46 (4%) subjects with at least one follow-up assessment developed PTSD. However, the frequency with which subjects experienced at least one PTSD symptom ranged from 68% in the first 3 months to 12% at 2 years in assessed children. The presence of an internalizing disorder at time of injury followed by greater injury severity were the most consistent predictors of PTSD symptomatology. It is apparent, therefore, that PTSD and subsyndromal posttraumatic stress disturbances occur despite neurogenic amnesia. These problems should be treated, particularly if symptoms persist beyond 3 months.

Objective To study prospectively the course of attention-deficit hyperactivity (ADH) symptomatology in children and adolescents after traumatic brain injury (TBI). It was hypothesized that ADH symptomatology would be significantly related to severity of injury. Method Subjects were children (n = 50) aged 6 to 14 years at the time they were hospitalized after TBI. The study used a prospective follow-up design. Assessments of preinjury psychiatric, behavioral, socioeconomic, family functioning, and family psychiatric history status were conducted. Severity of injury was assessed by standard clinical scales, and neuroimaging was analyzed. Results The main finding of this study was that change in ADH symptomatology in the first 2 years after TBI in children and adolescents was significantly related to severity of injury. Overall ADH symptomatology during the study was significantly related to a measure of family dysfunction when family psychiatric history, socioeconomic status, and severity of injury were controlled. Conclusion The presence of a positive “dose-response” relationship between severity of injury and change in ADH symptoms, present from the 3-month assessment, was consistent with an effect directly related to brain damage.

Objective To study psychiatric and behavioral morbidity associated with severe traumatic brain injury (TBI). Method A consecutive series (n = 24) of children aged 5 through 14 years who suffered a severe TBI were matched to subjects who sustained a mild TBI and to a second matched group who sustained an orthopedic injury with no evidence of TBI. Standardized psychiatric, behavioral, and neuroimaging assessments were conducted on average 2 years after injury. Results Severe TBI was associated with a significantly higher rate of current “novel” psychiatric disorders (15/24; 63%) compared with children with mild TBI (5/24; 21%) and orthopedic injury (1/24; 4%). Higher effect sizes were evident for child and adolescent self-report of internalizing symptoms rather than externalizing symptoms, for parents' report of overall behavior and internalizing symptoms rather than externalizing symptoms, and for teachers' reports of overall behavior and externalizing symptoms rather than internalizing symptoms. Conclusions Severe TBI is a profound risk factor for the development of a psychiatric disorder. Survivors should be assessed for organic personality syndrome, which is the most common psychiatric disorder after this type of injury.

Objective To extend our findings from child psychiatry outpatients to child psychiatry inpatients regarding the similarity of children with a history of traumatic brain injury (TBI), particularly mild TBI, to matched children without such a history. Method This is a chart review of patients consecutively admitted to a child psychiatry inpatient unit over a 5-year period. Children with TBI were matched by age, sex, race, and social class to children with no history of TBI. Axis I and II diagnoses and diagnostic clusters and use of special education services and IQ scores were compared. Results Fifty-six (8.1%) of 694 consecutive patients admitted had a definite TBI. Not one of more than 50 variables compared between TBI and control subjects was significantly different. Conclusion In a child psychiatry inpatient unit, patients with a history of TBI were virtually indistinguishable from matched children without TBI. Caution should be exercised before attributing the child's problems, especially long-term problems, to the TBI unless the injury was severe or the child is exhibiting related phobic or posttraumatic stress symptomatology.

Objective To extend findings regarding predictive factors of psychiatric outcome from the first to the second year after traumatic brain injury (TBI) in children and adolescents. Method Subjects were children aged 6 to 14 years at the time they were hospitalized after TBI. The study used a prospective follow-up design. Assessments of preinjury psychiatric, behavioral, adaptive functioning, family functioning and family psychiatric history status were conducted. Severity of injury was assessed by standard clinical scales and neuroimaging was analyzed. The outcome measure was the presence of a psychiatric disorder, not present before the injury (“novel”), during the second year after TBI. Results Fifty subjects enrolled, and the analyses focused on 42 subjects followed at 24 months. Severity of injury, preinjury family function, and preinjury lifetime psychiatric history predicted the development of a “novel” psychiatric disorder present in the second year. Conclusions These data suggest that there are children, identifiable through clinical assessment, at increased risk for “novel” psychiatric disorders in the second year after TBI.

A record review focused on children and adolescents, with a history of traumatic brain injury, who were consecutively admitted to a brain injury clinic in which all new patients are psychiatrically evaluated. The development of a 'novel' psychiatric disorder (not present before injury) occurred in 76% (38/50) of the cohort and was correlated significantly with family psychiatric history and family function, but not with severity of injury, preinjury psychiatric status, intellectual/educational functioning, or socioeconomic status. Psychiatric consultation is often necessary in this paediatric population even though much of the psychopathology, particularly following mild injury, may not be directly related to brain trauma.

Background The subgenual anterior cingulate cortex (sgACC) and its connected circuitry have been heavily implicated in emotional functioning in adolescent-onset major depressive disorder (MDD). While several recent studies have examined sgACC functional connectivity (FC) in depressed youth at rest, no studies to date have investigated sgACC FC in adolescent depression during negative emotional processing. Methods Nineteen medication-naïve adolescents with MDD and 19 matched healthy controls (HCL) performed an implicit fear facial affect recognition task during functional magnetic resonance imaging (fMRI). We defined seeds in bilateral sgACC and assessed FC using the psychophysiological interaction method. We also applied cognitive behavioral modeling to estimate group differences in perceptual sensitivity in this task. Finally, we correlated connectivity strength with clinical data and perceptual sensitivity. Results Depressed adolescents showed increased sgACC-amygdala FC and decreased sgACC-fusiform gyrus, sgACC-precuneus, sgACC-insula, and sgACC-middle frontal gyrus FC compared to HCL (p

Objective Although substantial literature has reported regional cerebral blood flow (rCBF) abnormalities in adults with depression, these studies commonly necessitated the injection of radioisotopes into subjects. The recent development of arterial spin labeling (ASL), however, allows noninvasive measurements of rCBF. Currently, no published ASL studies have examined cerebral perfusion in adolescents with depression. Thus, the aim of the present study was to examine baseline cerebral perfusion in adolescent depression using a newly developed ASL technique: pseudocontinuous arterial spin labeling (PCASL). Method A total of 25 medication-naive adolescents (13-17 years of age) diagnosed with major depressive disorder (MDD) and 26 well-matched control subjects underwent functional magnetic resonance imaging. Baseline rCBF was measured via a novel PCASL method that optimizes tagging efficiency. Results Voxel-based whole brain analyses revealed significant frontal, limbic, paralimbic, and cingulate hypoperfusion in the group with depression (p

Children with attention-deficit hyperactivity disorder (ADHD) and traumatic brain injury (TBI) show deficient response inhibition. ADHD itself is a common consequence of TBI, known as secondary ADHD (S-ADHD). Similarity in inhibitory control in children with TBI, S-ADHD, and ADHD would implicate impaired frontal-striatal systems; however, it is first necessary to delineate similarities and differences in inhibitory control in these conditions. We compared performance of children with ADHD and those with TBI without pre-injury ADHD on a stop signal, response inhibition task. Participants were 274 children aged 6-14 years. There were 92 children with ADHD, 103 children with TBI, and 79 typically developing children who served as controls. Among the TBI participants, injury severity ranged from mild to severe. Children with ADHD and TBI showed deficient inhibition. The deficit in children with ADHD was as great as or greater than that in children with TBI, regardless of degree of TBI severity or the presence of S-ADHD. The finding indicates that TBI results in deficient inhibition regardless of the development of S-ADHD.

The objective of this study was to understand how novel psychiatric disorders (NPD) in children with mild traumatic brain injury (MTBI) are related to pre-injury variables, injury-related variables, and concurrent neurocognitive outcome. A group of 79 children, ages 5 to 14 years, who had experienced MTBI, were studied from consecutive hospital admissions with semistructured psychiatric interviews soon after injury (baseline); 60 children were reassessed 12 months post-injury. Standardized instruments were used to assess injury severity; lesion characteristics; pre-injury variables, including psychiatric disorder, family psychiatric history, family functioning, socioeconomic status, psychosocial adversity, adaptive functioning, and post-injury neurocognitive and adaptive functioning. NPD occurred in 17 of 60 participants (28%) in the 6-12-month interval after injury, with disorders that were significantly associated with socioeconomic status, psychosocial adversity, estimated pre-injury academic functioning, and concurrent deficits in adaptive functioning, academic performance, processing speed, memory, and expressive language. NPD was not significantly associated with pre-injury adaptive functioning, injury severity, family psychiatric history, pre-injury psychiatric disorder, lesion location, gender, or age at injury. These findings suggest that the short-term psychiatric morbidity associated with MTBI in children occurs more commonly than previously reported and is related to both pre-injury social factors and concurrent neurocognitive functioning.

A relatively enduring and counterintuitive antimanic response to dextroamphetamine in a brain-injured adolescent who had failed trials involving divalproex, lithium, haloperidol, and carbamazepine is described. This finding combined with data from previous reports of antimanic effects of test doses of stimulants imply that such a pharmacological probe may prove relevant for the prediction of treatment response of mania to dextroamphetamine and perhaps for subclassification of bipolar disorder.

Background Very few studies have been performed to understand the underlying neural substrates of adolescent major depressive disorder (MDD). Studies in depressed adults have demonstrated that the subgenual anterior cingulate cortex (sgACC) plays a pivotal role in depression and have revealed aberrant patterns of resting-state functional connectivity (RSFC). Here, we examine the RSFC of the sgACC in medication-naive first-episode adolescents with MDD. Methods Twenty-three adolescents with MDD and 36 well-matched control subjects underwent functional magnetic resonance imaging to assess the RSFC of the sgACC. Results We observed elevated connectivity between the sgACC and the insula and between the sgACC and the amygdala in the MDD group compared with the control subjects. Decreased connectivity between the sgACC and the precuneus was also found in the MDD group relative to the control subjects. Within the MDD group, higher levels of depression significantly correlated with decreased connectivity between the sgACC and left precuneus. Increased rumination was significantly associated with reduced connectivity between sgACC and the middle and inferior frontal gyri in the MDD group. Conclusions Our study is the first to examine sgACC connectivity in medication-naive first-episode adolescents with MDD compared with well-matched control participants. Our results suggest aberrant functional connectivity among the brain networks responsible for salience attribution, executive control, and the resting-state in the MDD group compared with the control participants. Our findings raise the possibility that therapeutic interventions that can restore the functional connectivity among these networks to that typical of healthy adolescents might be a fruitful avenue for future research.

ObjectiveTo study magnetic resonance imaging (MRI) correlates of novel (new-onset) psychiatric disorders (NPD) after traumatic brain injury (TBI) and orthopedic injury (OI).MethodParticipants were 7 to 17 years of age at the time of hospitalization for either TBI or OI. The study used a prospective, longitudinal, controlled design with standardized psychiatric assessments conducted at baseline (reflecting pre-injury function) and 3 months post-injury. MRI assessments including diffusion tensor imaging (DTI)-derived fractional anisotropy (FA), volumetric measures of gray and white matter regions, volumetric measures of lesions, and cortical thickness were conducted. Injury severity was assessed by standard clinical scales. The outcome measure was the presence of an NPD identified during the first 3 months after injury.ResultsThere were 88 participants (TBI, 44; OI, 44). NPD occurred more frequently in the TBI (21/44; 48%) versus the OI (6/44; 14%) group (Fisher's exact test, p = .001). NPD in TBI participants was not related to injury severity. Multivariate analysis of covariance of the relationship between FA in hypothesized regions of interest (bilateral frontal and temporal lobes, bilateral centrum semiovale, bilateral uncinate fasciculi) and NPD and group (TBI versus OI) was significant, and both variables (NPD, p < .05; group, p < .001) were jointly significantly related to FA. NPD was not significantly related to volumetric measures of white or gray matter structures, volumetric measures of lesions, or cortical thickness measures.ConclusionsLowered white matter integrity may be more important in the pathophysiology of NPD than indices of gray matter or white matter atrophic changes, macroscopic lesions, and injury severity.

The study's objective was to assess the nature, rate, predictive factors, and neuroimaging correlates of novel (new-onset) definite anxiety disorders and novel definite/subclinical anxiety disorders (in a broader group of children with at least subclinical anxiety disorders) after traumatic brain injury (TBI). Children with TBI from consecutive admissions to five trauma centers were enrolled and studied with psychiatric interviews soon after injury (baseline) and again 6 months post-injury. Novel definite anxiety disorder and novel definite/subclinical anxiety disorders were heterogeneous and occurred in 8.5% (N=12) and 17% (N=24) of participants, respectively, in the first 6 months after injury. Novel definite anxiety disorder was significantly associated with younger age at injury and tended to be associated with novel depressive disorder, as well as lesions of the superior frontal gyrus. Novel definite/subclinical anxiety disorder was significantly associated with concurrent psychiatric problems of personality change due to TBI and novel definite/subclinical depressive disorder, as well as with lesions of the superior frontal gyrus and a trend-association with frontal lobe white-matter lesions. These findings suggest that anxiety after childhood TBI may be part of a broader problem of affective dysregulation related to damaged dorsal frontal lobe and frontal white-matter systems, with younger children being at greatest risk for developing novel anxiety disorder after TBI.

The authors aim to investigate brain plasticity and vulnerability through the study of the relationship of age at the time of brain injury and neurocognitive and psychiatric outcome. Children with early stroke performed more poorly compared with children with late stroke in a wide variety of domains including intellectual function, language, memory, visuospatial function, academic function, and psychiatric problems. The exception to this pattern was that children with late stroke performed more poorly in two of three executive function tests. These findings suggest that in children with focal brain injury, as in those with more diffuse brain insults, younger age at injury predicts worse neurocognitive outcomes, although this may not apply to selected executive function outcomes. Adverse psychiatric outcome after early stroke is less direct but is evident in terms of severity in affected cases.

Phenomenology and predictive factors of personality change due to traumatic brain injury (TBI) 6 to 24 months after injury was investigated in children, ages 5 to 14 years, enrolled from consecutive admissions and followed prospectively for 2 years. Injury and preinjury psychosocial variables were assessed. Personality change occurred in 13% of participants between 6 and 12 months after injury and 12% in the second year after injury. Severity of injury consistently predicted personality change, and preinjury adaptive function predicted personality change only in the second year postinjury. Lesions of the superior frontal gyrus were associated with personality change between 6 and 12 months following injury, after controlling for severity of injury and the presence of other brain lesions. Only lesions in the frontal lobe white matter were significantly related to personality change in the second year after injury. After childhood TBI, neural correlates of personality change evolve between 6 and 12 months and 12 to 24 months after injury. The data implicate the dorsal prefrontal cortex and frontal lobe white matter in the emergence of personality change involving the effortful or conscious regulation of affective states.

Children who experience traumatic brain injury (TBI) often show cognitive impairments postinjury, some of which recover over time. We examined the recovery of motor response inhibition immediately following TBI and over 2 years. We assessed the role of injury severity, age at injury, and lesion characteristics on initial impairment and recovery while considering the role of pre-injury psychiatric disorder. Participants were 136 children with TBI aged 5-16 years. Latency of motor response inhibition was measured with the stop-signal task within 1 month of the injury and again at 3, 6, 12, and 24 months. The performance of the TBI participants at each measurement occasion was standardized with 117 children of similar age, but without injury. Residualized latency scores were calculated. Growth curve analyses showed an initial impairment in response inhibition and improvement over the 2 years following injury. Younger TBI patients were initially more impaired although they exhibited greater recovery of response inhibition than did older TBI patients. Longer duration of coma, but not reactivity of pupils or Glasgow Coma Scale score, predicted initial deficit. Lesion characteristics or pre-injury attention deficit hyperactivity disorder did not predict initial impairment or recovery. Replication with longitudinal testing of a comparison group of children sustaining extracranial injury is necessary to confirm our findings.

Two modalities of family assessment based on the McMaster Model of Family Functioning (MMFF), including a self-report questionairre (Family Assessment Device-FAD) and a clinical interview (McMaster Structured Interview For Families-McSIFF) as scored on the McMaster Clinical Rating Scale (MCRS) were compared in an attempt to explore the inter-changeability of the two. Significant correlations were hypothesized between the FAD and MCRS in both prospective and retrospective groups and that correlations would increase over three data points in the prospective study. The sample included 50 children and adolescents (ages 6-4) with traumatic brain injury (TBI) from a prospective study. In addition, 72 children and adolescents (ages 5-14), consisting of 24 patients with severe TBI, individually matched to a comparison group of 24 mild TBI patients and a control group of 24 orthopaedic patients were included from a retrospective study. Significant correlations between the FAD and MCRS were found across both studies, with increasing correlations at each successive data point in the prospective study. Agreement between the two measures regarding classification of families as clinical vs healthy was also statistically significant at the majority of assessment occasions; however, most specific indices of agreement were only modest. The clinical and research implications of these findings are discussed.

Objective To assess the phenomenology and predictive factors of attention-deficit/hyperactivity disorder (ADHD) after traumatic brain injury (TBI), also called secondary ADHD (SADHD). Method Children without preinjury ADHD 5-14 years old with TBI from consecutive admissions ( n = 143) to five trauma centers were observed prospectively for 6 months (baseline and 6 months), with semistructured psychiatric interviews. Injury severity, lesion characteristics, and preinjury variables including psychiatric disorder, family psychiatric history, family psychiatric history of ADHD, family function, socioeconomic status, psychosocial adversity, and adaptive function were assessed with standardized instruments. Results SADHD in the first 6 months after injury occurred in 18 of 115 (16%) of returning participants. All subtypes of ADHD occurred. Socioeconomic status ( p = .041) and orbitofrontal gyrus lesions ( p = .005) independently significantly predicted SADHD. Conclusions These findings are consistent with research on developmental ADHD that implicate psychosocial factors and prefrontal structural and functional differences between those with and without the disorder.

Objective: To assess the phenomenology and predictive factors of attention-deficit/hyperactivity disorder (ADHD) after traumatic brain injury (TBI), also called secondary ADHD (SADHD). Method: Children without preinjury ADHD 5–14 years old with TBI from consecutive admissions (n = 143) to five trauma centers were observed prospectively from 6 to 12 months (12-month assessment) and from 12 to 24 months (24-month assessment) postinjury with semistructured psychiatric interviews. Injury and preinjury psychosocial variables were assessed. Results: SADHD occurred in 15 of 103 (15%) of participants between 6 and 12 months after injury and 17 of 82 (21%) in the second year after injury. SADHD was significantly (p < .05) comorbid with personality change due to TBI and new-onset disruptive behavior disorders. Preinjury adaptive function was a consistent predictor of SADHD. Regression analyses revealed that preinjury psychosocial adversity was an independent predictor of SADHD in the second year after injury. Neither severity of injury nor lesion location predicted SADHD from 6 to 24 months postinjury. Conclusions: Determination of preinjury psychosocial adversity and the child’s preinjury functioning during the index hospitalization would improve identification of children at highest risk of development of SADHD. J. Am. Acad. Child Adolesc. Psychiatry, 2005;44(10):1041–1049. Key Words: traumatic brain injury, children and adolescents, secondary attention-deficit/hyperactivity disorder, adaptive function.

The literature on neuroplasticity lacks a direct comparison of chronic neuropsychological and social outcomes following brain damage acquired in childhood versus adulthood, when lesions are matched across adults and children for size and location.We paired adults and children with similar unilateral stroke lesions and then compared chronic neuropsychological and social outcomes. Quantitative comparisons were conducted, as well as qualitative analyses of each subject pair, focusing on specific domains of cognitive impairment and changes in social functioning.We found that learning and memory impairments were most common in both children and adults. Left hemisphere-lesioned children were normal on speech/language ratings, whereas their adult counterparts were borderline impaired. Impairments in social functioning were highly associated with hemispheric side of damage in adults, but not in children: Specifically, adults with right hemisphere lesions developed social defects much more frequently than adults with left hemisphere lesions, whereas this asymmetry was not evident in the children. Most importantly, though, was the overarching finding of a high degree of similarity between chronic neuropsychological and social function outcomes in adults and children with similarly located brain lesions due to unilateral stroke.On balance, the findings suggest that lesion location and size are prepotent factors determining neuropsychological and social recovery from stroke.

To evaluate effects of unilateral frontal lesions on psychosocial and global outcome of traumatic brain injury (TBI) in children, Study 1 compared matched groups of 22 school aged children who had sustained TBI either with or without unilateral frontal lesions. Study 2 evaluated effects of unilateral extrafrontal lesions in 18 TBI patients as compared with 18 nonlesional TBI patients. Communication, Daily Living, and Socialization domains and the Maladaptive Behavior Scale of the Vineland Adaptive Behavior Scales (VABS) were used to assess psychosocial outcome, and the Glasgow Outcome Scale (GOS) measured global outcome. All patients underwent magnetic resonance imaging at least 3 months post injury. Children with frontal lesions had worse scores on the Daily Living and Socialization domains and a higher frequency of maladaptive behavior than those without frontal lesions, but there was no difference in cognitive function. Disability was twice as common in the frontal lesion group relative to children without frontal lesions. Volume of frontal lesion was related to the Socialization domain. Side of lesion had no effect, nor did presence of an extrafrontal lesion (Study 2). Unilateral frontal lesions adversely affect late psychosocial outcome of TBI in children. (JINS, 2004, 10, 305‐316.)

We investigated the frequency and neurocognitive correlates of attention deficit hyperactivity disorder and traits of this disorder (ADHD/Traits) after childhood stroke and orthopedic diagnosis in medical controls. Twenty-nine children with focal stroke lesions and individually matched children with clubfoot or scoliosis were studied with standardized psychiatric, intellectual, academic, adaptive, executive, and motivation function assessments. Lifetime ADHD/Traits were significantly more common in stroke participants with no prestroke ADHD than in orthopedic controls (16/28 vs. 7/29; Fisher's Exact p < .02). Lifetime ADHD/Traits in the orthopedic controls occurred exclusively in males with clubfoot (7/13; 54%). Participants with current ADHD/Traits functioned significantly worse (p < .005) than participants without current ADHD/Traits on all outcome measures. Within the stroke group, current ADHD/Traits was associated with significantly lower verbal IQ and arithmetic achievement (p < .04), more nonperseverative errors (p < .005), and lower motivation (p < .004). A principal components analysis of selected outcome variables significantly associated with current ADHD/Traits revealed “impaired neurocognition” and “inattention-apathy” factors. The latter factor was a more consistent predictor of current ADHD/Traits in regression analyses. These findings suggest that inattention and apathy are core features of ADHD/Traits after childhood stroke. This association may provide clues towards the understanding of mechanisms underlying the syndrome. (JINS, 2003, 9, 815–829.)

To investigate the effects of traumatic brain injury on working memory in children, we administered semantic (letter identity) and phonological (letter rhyme) N-back tasks to children who were on average 5 years post-mild (n = 54) or -severe (n = 26) traumatic brain injury and 44 typically developing children who were comparable in age. The correct detection of targets and false alarms were measured for each task. Memory load (which varied from 0 to 3 letters back) and age significantly affected the detection of targets and false alarms in both tasks. The severity of traumatic brain injury affected the correct detection of letters on the identity task and false alarms on the rhyme task. Traumatic brain injury severity also interacted with memory load in its effect on false alarms on the rhyme task. Traumatic brain injury results in impaired working memory and diminished inhibition in children. The N-back working memory task is feasible for administration to brain-injured children and potentially could be useful for studying brain activation associated with working memory and effects of drug therapy in this group of patients.