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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: J Neuropsychiatry Clin Neurosci. 2015 Jul 17;27(4):272–279. doi: 10.1176/appi.neuropsych.15030073

Personality Change due to Traumatic Brain Injury in Children and Adolescents: Neurocognitive Correlates

Elisabeth A Wilde 1, Erin D Bigler 1, Gerri Hanten 1, Maureen Dennis 1, Russell J Schachar 1, Ann E Saunders 1, Linda Ewing-Cobbs 1, Sandra B Chapman 1, Wesley K Thompson 1, Tony T Yang 1, Harvey S Levin 1
PMCID: PMC4618043  NIHMSID: NIHMS688311  PMID: 26185905

Abstract

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. The aim of the study was to examine neurocognitive correlates of PC. The sample included children (n=177) aged 5-14 years with traumatic brain injury from consecutive admissions to 5 trauma centers were followed prospectively at baseline and 6 months with semi-structured 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 26/141 (18%) participants assessed at 6 months post-injury. Attention, processing speed, verbal memory, IQ, and executive function, were significantly associated (p < .05) with PC even after socioeconomic status, injury severity, and pre-injury 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.

Keywords: Traumatic brain injury, children and adolescents, cognition, personality change

Introduction

Personality change due to traumatic brain injury (PC) is the most common and important acquired psychiatric disorder following brain trauma in children and adolescents 1-5. We have previously described the phenomenology of PC in detail, however the neurocognitive correlates of PC have not been studied 5. The rationale for investigating the neurocognitive profile of PC is that this may shed light on the neurobiological systems or networks that are perturbed, and provide a link between neurobiology and observed behaviors 6,7.

PC has five specific subtypes including affectively labile, aggressive, disinhibited, apathetic, and paranoid. The first three subtypes are common and often co-occur while the latter two subtypes are uncommon 5. Studies show that most, if not all, cases of PC are accounted for by having at least the affectively labile subtype with impairing irritability 3. The irritability has numerous potential antecedents including a frustrated need for constant attention, sensitivity to criticism, concrete thinking, delay in gratification, unpredictability or change in routine, intellectual or concentration deficits increasing the effort in task completion, communication difficulties resulting in misunderstanding humor and instructions, and sensitivity to pain or accidental mild injury 5. The course of PC is continuous rather than episodic. The temper tantrums or rages that are associated with PC may be interspersed with euthymia or with persistent irritability varying case by case. PC manifests as a disorder of mood regulation with associated behavioral disruption. Consequently, PC rarely occurs alone as a new-onset psychiatric disorder after TBI. The comorbid new-onset disorders include anxiety disorders 8, depressive disorders 9, mania/hypomania 10, ADHD 2, and oppositional defiant disorder 2. There are a number of misperceptions regarding the diagnosis of PC. Most importantly, PC is not a personality disorder. Rather PC is a collection of clinically significant symptoms described by its phenomenologically evocative named subtypes. Children, adolescents, and adults who develop PC are so impaired and radically altered as to be considered to have had a change in their personality.

PC occurs in up to 40% of cases of consecutively hospitalized children with severe traumatic brain injury (TBI) 2. The disorder is significantly associated with measures of severity of injury rather than psychosocial variables 2-4. PC is associated with lesions within the superior frontal gyrus within the first year post-injury 3,4 consistent with proposed models of affective dysregulation 11-13. In the second year after injury, PC is associated with frontal white matter lesions and pre-injury adaptive function suggesting that function is limited by network (rather than gray matter) damage as well as pre-injury brain-behavioral reserve within each individual 4.

In the absence of studies of the neurocognitive correlates of PC, our approach was to examine the relationship of PC with neurocognitive domains that are each known to be sensitive to the effects of TBI. These domains include attention, processing speed, verbal memory, intellectual function, working memory, executive function, naming, expressive language, and motor speed 14. Pediatric TBI studies generally have found that motor inhibition measured by the Stop Signal Task is not significantly related to brain injury and only even inconsistently related to the diagnosis of post-injury new-onset (secondary) ADHD 15. We therefore did not expect PC to be related to motor inhibition even though emotional and/or behavioral inhibition is present in PC.

Methods

The methodology of this study has been reported in detail previously 3.

Participants

Children and adolescents (n=177) aged 5-14 years were enrolled from consecutively hospitalized patients after a single TBI at five academic medical centers including three in Texas, one in San Diego, and one in Toronto. Enrollment ranged from severe to mild TBI at every center except San Diego, where recruitment was limited to severe to complicated mild TBI. Youth with pre-injury schizophrenia, autistic disorder, mental deficiency, and injury from child abuse or penetrating bullet injury were excluded. Children and adolescents with pre-injury ADHD were excluded in San Diego. Parents or guardians of all children and adolescents signed informed consent, and all children and adolescents signed an assent to participate in accordance with each site's Institutional Review Board. Demographic and injury indices are shown for participants in Table 1.

Table 1.

Demographic and Psychosocial data of traumatic brain injury cohort (n=177)

Demographic Variables N
    Age at injury mean (SD) 10.13 (2.77) 177
    Gender: males (%) 125 (71%) 177
    Socioeconomic Status mean (SD) 37.01 (12.90) 173
Race
    Caucasian 100 (56.5%)
    Hispanic 32 (18.1%)
    African American 31 (17.5%)
    Asian 5 (2.8%)
    Other 9 (5.1%)
Psychosocial Variables
    Preinjury lifetime psychiatric disorder number (%) 56 (31.6%) 177
Injury Variables
    Lowest post-resuscitation GCS Score mean (SD) 10.85 (4.20) 177
    Severe Traumatic Brain Injury (GCS 3-8) 64 (36%)
    Moderate Traumatic Brain Injury (GCS 9-12) 26 (15%)
    Mild Traumatic Brain Injury (GCS 13-15) 87 (49%)
    Depressed skull fracture (N; %) 17 (9.6) 177
    Mechanism of Injury N (%) 177
Hit by motor vehicle 49 (27.7)
Fall 41 (23.2)
Auto, truck, bus passenger 40 (22.6)
Sports or play 15 (8.5)
Recreational vehicle/Off-road vehicle 10 (5.6)
Bicycle 9 (5.1)
Motorcycle-moped 5 (2.8)
Hit by a falling object 5 (2.8)
Other 3 (1.7)
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Psychiatric measures

The Neuropsychiatric Rating Schedule (NPRS) 1 is a semi-structured interview to identify symptoms and subtypes of PC. Parents and children served as informants in the interview that took place at baseline (within a month post-injury), and at 6 months post-injury. At baseline, the lifetime pre-injury psychiatric history was the focus of inquiry, and at the 6-month assessment the focus was the period from injury to the 6 months post-injury. The NPRS interview generated ratings defining the five major subtypes of PC. We waived the one-year duration of symptomatology criterion to allow us to monitor the course of the disorder for the first six months after injury and to assess the neurocognitive correlates of PC. The NPRS has been shown to provide reliable and valid diagnoses of the common subtypes of PC 1. Good convergent validity and good discriminant validity has been demonstrated for PC subtypes by using subscales from validated parent and teacher-completed questionnaires that measure lability, aggression, impaired social judgment/disinhibition, apathy, and psychotic symptoms. Inter-rater agreement for NPRS items is fair to excellent, test-retest reliability is fair to good, and sensitivity to change has been demonstrated 1.

Other DSM-IV psychiatric diagnoses 16 were derived by using the Schedule for Affective Disorders and Schizophrenia for School-Aged Children, Present and Lifetime version (K-SADS-PL) 17. The K-SADS-PL is a parent-child interview that generates diagnoses based on a clinician synthesizing data collected from parent and child separately, reviewing present and lifetime symptoms (at baseline) and symptoms present or past from injury to 6 months (at 6 month assessment).

Best-estimate psychiatric diagnoses 18 were generated by the interviewer after integrating the accounts of the parent and the subject from the NPRS and the K-SADS interviews and, when available, from the Survey Diagnostic Instrument 19 completed by the teacher.

TBI Classification

The classification of severity of TBI was based on the lowest post-resuscitation score on the Glasgow Coma Scale (GCS) 20 which was recorded from clinical notes. The GCS is the standard measure of severity of acute brain injury associated with TBI. The scale measures eye opening, motor, and verbal responsiveness. Scores range from 3 (unresponsive) to 15 (normal).

Socioeconomic Status (SES)

SES assessment was derived from the Four Factor Index 21. Classification depends on scores generated from a formula involving both the maternal and paternal occupational and educational levels. Scores range from 8-66 with lower scores indicating lower educational and occupational levels and lower SES.

Neurocognitive Measures

Attention

Attentional processes in single and dual task performance were measured with the Divided Attention Task (DAT) 22. The DAT assesses the ability to allocate attentional resources when simultaneously engaged in performing two independent tasks. Timed comparisons were evaluated for performing the single task of finger tapping versus simultaneously performing the dual tasks of right finger tapping and reciting a nursery rhyme. The outcome variable is number of words correct.

Processing Speed

Symbol Search and Coding subtests of the Wechsler Intelligence Scale for Children –III (WISC-III) 23 measure visual scanning, tracking ability, and psychomotor processing speed. These tasks require interpreting whether a target symbol appears in a row of symbols, and digit-symbol codes. Correct responses less the number of errors completed within the allotted 120 seconds for each subtest was noted. Together, these measures provide a Processing Speed Index.

Verbal Memory

The California Verbal Learning Test-Children's Version 24 (CVLT-C) was administered and assesses verbal learning and memory abilities. Children were instructed to learn 15 words in 3 categories across 5 learning trials and 1 distraction trial. Verbal memory for long delay free recall was assessed and expressed as a z-score.

Intellectual Function

The Wechsler Abbreviated Scale of Intelligence (WASI) 25 was administered to all children at 6 months post-injury. The WASI is a test of intelligence that consists of the following four subtests: Vocabulary, Similarities, Block Design, and Matrix reasoning. These four components evaluate a person's verbal and non-verbal knowledge and reasoning, and general cognitive functioning, and together, produce a full-scale intelligence quotient (FSIQ) which was the variable reported here as a standard score.

Verbal Working Memory

Working memory was evaluated with a computerized N-back experimental task 26. The Letter Identity task has 3 levels of memory load:1-back, 2-back, and 3-back. As well, there is a 0-back condition that imposes minimal memory load while controlling for attention to the task. Children were instructed to match the same alphabetic letters printed in different cases. For each level, there were 40 trials in which a string of 40 letters appeared 1 at a time for 2 seconds on the screen. The child responded by pressing a button with the preferred hand when a match occurred or, in the 0-load condition, when a designated target appeared. Training and practice occurred before experimental trials. The percentage of hits (i.e., detection of targets) was recorded.

Executive Function

A modified version of the Tower of London (TOL) 27 was used to assess planning skills that involve the ability to look ahead, follow rules, conceive of alternative solutions to the problem, and to weigh and make choices. The test required that children arrive at the most direct, fewest move solution by determining the order of moves necessary within set rules (e.g., “pick up one bead at a time”) to rearrange three colored beads on pegs of three disks of differing heights. We report data of total solution time, i.e., the time, measured in seconds, taken to come to the final solution for that trial.

Naming

The Rapid Automatized Naming task 28 was administered by asking the participant to rapidly name line drawings of five common objects which are reproduced ten times each and interspersed on a board. This task is related to processing speed and reading. The time required to complete the task was measured and expressed as a z-score.

Expressive Language

Expressive language was assessed with the Clinical Evaluation of Language Fundamentals – Third Edition (CELF-3) 29 Formulated Sentence Subtest consisting of 22 items. Children were shown an image with a target word/phrase and they were instructed to construct a sentence in response. Standard scores were recorded and analyzed.

Motor Speed

The Grooved Pegboard Test (GPT) assesses fine motor coordination and manual dexterity 30. Participants are instructed to insert 25 grooved pegs into a pegboard using one hand at a time as quickly as possible. Time to completion expressed as a z-score for the dominant hand was recorded and used in the analysis.

Motor Inhibition

The Stop Signal Task (SST) assesses ability to inhibit ongoing response in a choice reaction time task 31. The stop signal reaction time will be used in the analyses. A prolonged stop signal reaction time has been identified as one of the signature executive deficits associated with ADHD.

Data Analysis

Effect sizes were used to compare neurocognitive scores between the groups with PC versus without PC. However, because these scores could be influenced by severity of injury 14, socioeconomic status 32, and pre-injury ADHD 6, linear regressions were conducted for each neurocognitive measure of interest controlling for these variables. Alpha was kept at .05 because each of the regressions tested an independent hypothesized relationship between the neurocognitive measure and PC guided by previous findings that each neurocognitive domain is sensitive to the effects of TBI 14.

Results

Of the original 177 children and adolescents, 141 (80%) returned for the 6-month psychiatric assessment. The returning participants were not significantly different from those who did not return with regard to age, race, gender, GCS score, or SES. PC occurred in 31/141 (22%) at some point from injury to the 6-month assessment. However, in 5 cases the symptoms of PC remitted before the 6-month assessment, yielding 26/141 (18%) of unremitted cases of PC. The affectively labile subtype occurred in 23 of the 26 cases. Of the 3 cases of PC that did not meet criteria for the affectively labile subtype, 2 were diagnosed with the aggressive subtype of PC, and 1 was diagnosed with the disinhibited subtype. A detailed list including each child diagnosed with PC along with their PC subtypes and specific brain lesions was previously published 3. As in previous reports, comordity is common 2. Unremitted PC was significantly associated with the following unremitted new onset disorders: 1) new-onset ADHD was present in 6/19 children with PC versus 11/96 children with no PC; Fisher's Exact = .035; and 2) new-onset oppositional defiant disorder/conduct disorder/disruptive behavior disorder, not otherwise specified (ODD/CD/DBD) was present in 7/24 children with PC versus 4/110 children with no PC; Fisher's Exact = .001. PC was not significantly associated with new-onset unremitted depressive disorder (major depression/dysthymic disorder/depressive disorder, not otherwise specified) which was present in only 6 children including 3/25 children with PC versus 3/113 with no PC; Fisher's Exact = .073. The denominators differ for the above disorders depending on pre-injury diagnoses, e.g., children with pre-injury ADHD would not be eligible to develop new-onset ADHD.

Relationship of Neurocognitive Measures to PC

Tables 2 and 3 provide details of the relation of each neurocognitive domain and PC. Table 2 demonstrates large effect sizes for processing speed (d=.89) and for full-scale IQ (d=1.14), moderate effect sizes for verbal memory (d=.66), verbal working memory (d=.73), expressive language (d=.73), executive function (d=.68), attention (d=.54), small effect size for naming (d=.36), and trivial effect sizes for motor speed (d=.13) and motor inhibition (d=17).

Table 2.

Attention, Processing, Verbal Memory, Intellectual Function, Working Memory, Executive Function, Naming, Expressive Language, and Motor Speed correlates of PC 6 months post-iniury

PC (n=26) No PC (n=115) t df sig Cohen's d
Attention
    Divided Attention rhyme/right tapping 72.0 (26.0) n=25 85.4 (23.3) n=105 2.53 128 .013 .54
Processing Speed
    WISC-3 Processing Speed Index scale score 93.1 (19.6) n=24 109.9 (18.0) n=110 4.06 132 .000 .89
Verbal Memory
    CVLT-C long delay free recall (z-score) −.31 (1.43) .52 (1.07) n=114 2.77 31.7 .009 .78
Intellectual Function
    WASI Full Scale IQ standard score 87.4 (8.8) n=21 101.8 (15.6) n=105 5.88 49.1 .000 1.14
Working Memory N-Back task
    Letter Identity target detection .55 (.22) n=24 .70 (.19) n=106 3.22 128 .002 .73
Executive Function
    Tower of London Total solution time (sec) 260.7 (71.8) 341.7 (152.7) n=114 4.04 83.6 .000 .68
Naming
    Rapid Automatized Naming (z-score) −.28 (2.07) .34 (1.27) 1.47 29.4 ns .36
Expressive Language
    CELF-3 Formulated Sentences standard score 7.9 (2.3) n=24 9.9 (3.1) n=111 3.60 43.9 .001 .73
Motor Speed
    Grooved Pegboard dominant hand time (z-score) .18 (1.18) .30 (.64) n=112 .70 136 ns .13
Motor Inhibition
    Stop Signal Reaction time (milliseconds) 460.8 (244.8) n=16 420.2 (226.0) n=83 −.47 97 ns .17
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Legend: CVLT-C = California Verbal Learning Test – Children's Version; CELF = Clinical Evaluation of Language Fundamentals; PC = Personality change due to traumatic brain injury; WASI = Wechsler Abbreviated Scale of Intelligence; WISC = Wechsler Intelligence Scale for Children

Table 3.

Linear Regression Analyses for PC and Neurocognitive Outcomes

Dependent Variables Independent Variables R2 df F Sig of F (p) B Beta t statistic p
Attention .09 4, 124 3.18 .016
PC −13.25 −.26 −2.36 .020
GCS −.17 −.03 −.30 .762
SES .33 .17 1.93 .056
ADHD 9.46 .15 1.67 .097
Processing Speed .22 4, 128 8.87 .000
PC −10.62 −.21 −2.51 .013
GCS 1.22 .26 3.05 .003
SES .18 .12 1.45 .150
ADHD −9.47 −.19 −2.35 .020
Verbal Memory .16 4, 133 7.63 .000
PC −.64 −.21 −2.53 .013
GCS .04 .16 1.82 .072
SES .02 .22 2.66 .009
ADHD .11 .04 .43 .669
Intellectual Function .42 4, 119 21.52 .000
PC −6.56 −.16 −2.08 .040
GCS 1.24 .34 4.33 .000
SES .50 .41 5.70 .000
ADHD −2.67 −.06 −.89 .378
Working Memory .16 4, 124 5.91 .000
PC .51 −.22 −2.43 .017
GCS 0.00 .01 .15 .881
SES 0.00 .29 3.40 .001
ADHD −.02 −.04 −.42 .673
Executive Function .10 4, 134 3.61 .008
PC −81.59 −.22 −2.55 .012
GCS −1.16 −.03 −.38 .705
SES −1.02 −.09 −1.05 .295
ADHD −74.56 −.20 −2.37 .019
Naming .09 4, 134 3.11 .017
PC −.40 −.11 −1.23 .220
GCS .03 .08 .94 .350
SES .02 .21 2.43 .017
ADHD −.25 −.07 −.79 .434
Expressive Language .23 4, 128 9.50 .000
PC −1.07 −.13 −1.60 .113
GCS .16 .21 2.47 .015
SES .08 .32 4.02 .000
ADHD −.56 −.07 −.88 .382
Motor Speed .08 4, 131 2.91 .024
PC .06 .03 .37 .710
GCS .05 .29 3.21 .002
SES .00 .03 .33 .742
ADHD −.11 −.06 −.66 .510
Motor Inhibition .00 4, 93 .97 .430
PC 15.97 .03 .24 .812
GCS −4.96 −.09 −.77 .445
SES 1.35 .07 .66 .508
ADHD 97.73 .18 1.73 .088
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Legend: The specific tests for each domain of neurocognitive function correspond to those listed in Table 2. Bold face type indicates where PC is independently significantly related to the neurocognitive domain.

Table 3 illustrates in detail the linear regression analyses of the 10 neurocognitive domains and their respective relationships with PC, controlling for injury severity as measured by the GCS score, SES, and pre-injury ADHD (present versus absent). PC was independently related to full-scale IQ (p=.04), divided attention (p=.02), processing speed (p=.013), verbal memory (p=.013), verbal working memory (p=.017), and executive function (p=.012) and not significantly related to naming, expressive language, motor speed, or motor inhibition. Consistent with extensive literature, naming/reading was significantly related to SES 33. Expressive language was significantly related to injury severity and SES. Motor speed was significantly related to injury severity. Motor inhibition was related to ADHD at a trend level.

All statistical analyses reported in Tables 2 and 3 were repeated comparing only the participants with the affective lability subtype of PC (n=23) versus all other participants. Results were essentially unchanged.

Discussion

The most important finding from this investigation is that PC was significantly associated with deficits in important neuropsychological domains including intellectual function, processing speed, divided attention, verbal memory, working memory, expressive language, and executive function. Furthermore, these associations (except for expressive language) remained significant even when severity of brain injury, SES, and pre-injury ADHD were taken into account.

The relationship between PC and neurocognitive function is clearly not uniform as evidenced by effect sizes ranging from large to small. This is not surprising given previous brain lesion-behavior correlates implicating the dorsal frontal area especially the superior frontal gyrus in PC. The weak relationship between PC and reading and expressive language may be because these neurocognitive domains are relatively crystallized and more closely related to SES than to a specific pattern of brain damage 33. Neurocognitive processes including executive function, verbal memory, working memory, and attention, which are mediated by frontal networks 14 might be expected to be deficient in children with disrupted affective regulation caused by damage to similar or overlapping neuronal networks. Our negative Stop Signal Task findings suggest, as anticipated, that motor inhibition is distinct from the disinhibition or overreactivity of emotional response characteristic of PC.

Individuals with TBI are known to have difficulty understanding negative emotions such as anger, sadness, and fearfulness compared to positive emotions such as happiness 34,35, and this may be associated with marked increased reactivity to negative emotional stimuli manifested verbally or behaviorally in children with PC. Further, children with TBI exhibit impairments in understanding a form of affect regulation involving social suppression of emotional expressions 34,36. Ecologically, better understanding of affect regulation predicts less rejection-victimization in the classroom 37.

The relationship between PC and the neuropsychological domains studied is strikingly similar to the corresponding relationship previously reported for another condition characterized by significant affective dysregulation, namely bipolar disorder 6. For example, the respective effect sizes for bipolar disorder and PC and the specific neuropsychological domain are verbal memory (d=0.77 versus d=.66), attention (d=0.62 versus d=.54), executive function (d=0.60 versus d=.68), working memory (d=.60 versus d=.73), naming/reading (d=0.40 versus d=.36), motor speed (d=0.33 versus d=.13). The corresponding relationship bipolar disorder and PC with full-scale IQ (d=0.32 versus d=1.14) was notably different, a finding driven most likely due to the association of IQ and PC with greater severity of injury 2. Another less striking difference from a recent study suggested a significant relationship with a small effect size between bipolar disorder and motor inhibition on the Stop Signal Task in contrast to the trivial relationship in the current study 38.

It is difficult to outline a clear mechanism whereby affective dysregulation, which is the core feature of PC (and an important feature of bipolar disorder), is related to the neurocognitive findings. One possibility is that the pattern of brain network damage leads independently to both PC and neurocognitive dysfunction. Clinically, this seems likely because affective dysregulation and neurocognitive problems are evident within the first few days of brain injury in children. Another possibility is that regulation of affect is modified by multiple neurocognitive processes. For example, an individual with slow processing, problematic divided attention, and poor memory may become overwhelmed and frustrated by environmental and interpersonal stimuli. Deficits in their working memory, planning and problem solving ability may lead to selection of more angry or aggressive responses because of difficulties working adaptively with new challenges. A third possibility, although much less likely, is that the affective dysregulation leads to the array of neurocognitive problems. This is unlikely because the child's explosive irritability, while frequent, is not constant and generally not present during the formal neurocognitive testing.

Our findings must be appreciated within the context of limitations of this study. First, the neurocognitive measures administered in the study included a broad array of domains known to be sensitive to brain injury. However, more specific neurocognitive measures, and psychophysiological and functional brain imaging modalities targeting recognition and understanding of negative emotion, suppression of emotional expression, and executive function with emotional distractors were not used. This limited the potential for a more in-depth understanding of mechanisms underlying the expression of PC. Second, a continuous measure of affective lability might shed more light on the relationship with neurocognitive domains. Third, attrition was approximately 20%. However, participants were not significantly different to non-participants with respect to age, race, gender, injury severity, and SES. Fourth, this study examined only short term (6 month) outcome of PC and its relationship with neurocognitive measures. We intend to examine whether the relationships reported here are sustained with regard to PC persisting to 12 and 24 months post-injury in the same pediatric TBI cohort.

Strengths of the study should also be appreciated. The cohort studied is a large sample of non-referred consecutively hospitalized children and adolescents with semi-structured psychiatric interviews and standardized neuropsychological tests encompassing multiple domains of function. Data reported in this study extend previously published findings that focused on psychosocial and lesion correlates of PC in the same cohort. The investigation of the neuropsychology of PC is a unique aspect of this study.

Conclusions and Implications

Ultimately the purpose of understanding the neural and psychological mechanisms inherent in children and adolescents with PC is to develop treatment strategies. In theory, stimulation of brain networks whose function is to regulate the expression of affect (e.g., dorsal frontal areas) or partial inhibition of networks responsible for generating affect (e.g., ventral frontal area, amygdala) could be helpful. Clinical trials of mood stabilizers are very difficult to accomplish, especially for children with PC, but should be done. Cognitive rehabilitation targeting processing speed, attention, problem solving, and memory may enhance cognitive control (a form of executive function) over emotional expression and should be tested 39. It is conceivable that more specific emotional probes such as utilized in social cognition and affect recognition studies will further clarify important mechanisms in children with PC and possibly other disorders of affective dysregulation 34,36,40-42.

Acknowledgements

This study was supported by National institute of Mental health (NIMH) Grant K-08 MH01800 (Dr. Max) and National Institute of Neurological Disorders and Stroke (NINDS) Grant NS-21889 (Dr. Levin).

Footnotes

This work was completed at the Department of Psychiatry, University of California, San Diego, and Rady Children's Hospital, San Diego.

Disclosures: Drs. Max and Bigler independently provide expert testimony in cases of traumatic brain injury on an ad hoc basis for plaintiffs and defendants on a more or less equal ratio. This activity constitutes approximately 5% of their respective professional activities. Dr. Schachar is a consultant for Eli Lily Corporation and Purdue Pharma (Canada). None of the other authors has financial disclosures to make relative to for-profit enterprises.

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