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Tics peak in late childhood and decline during adolescence. Yet, for some with Tourette's disorder, tics persist into adulthood. We evaluated childhood predictors of adult tic severity and tic impairment, and change over time. Eighty adolescents/adults were evaluated 11 years following a randomized-controlled trial of behavior therapy. An independent evaluator rated tic severity and tic impairment at baseline, posttreatment, and long-term follow-up. At baseline, parents completed demographics/medical history, and youth tic, internalizing, and externalizing symptom ratings. Youth rated premonitory urge severity and family functioning. After controlling for prior tic treatment effects, female sex and higher tic severity predicted higher tic severity in adulthood; and female sex, no stimulant medication use, higher tic severity, and poorer family functioning predicted higher tic impairment. Higher tic severity and premonitory urge severity predicted smaller reductions in tic severity, whereas higher externalizing symptoms predicted greater reduction in tic severity. Female sex predicted smaller reduction in tic impairment, and externalizing symptoms predicted greater reduction in tic impairment. Female sex and childhood tic severity are important predictors of tic severity and tic impairment in adulthood. Family functioning, premonitory urge severity, and tic severity are important modifiable targets for early or targeted intervention to improve long-term outcomes.

OBJECTIVE: Treatment guidelines for Tourette’s Disorder (TD) are based on patients’ degree of tic severity and impairment. However, clear benchmarks for determining tic severity and impairment have not been established. This study examined benchmarks of tic severity and tic impairment using the Yale Global Tic Severity Scale (YGTSS) and the Clinical Global Impression of Severity (CGI-S). METHOD: Individuals with TD or another Tic Disorder (N = 519) recruited across nine sites were administered a diagnostic interview, the YGTSS, and the CGI-S. Correlations and trend analyses contrasted YGTSS scores across CGI-S ratings. A logistic regression model examined predictive benchmarks for tic severity, tic impairment, and global severity. Model classifications were compared against CGI-S ratings, and agreement was examined using kappa. RESULTS: Spearman correlations between the CGI-S and YGTSS scores ranged from 0.54 to 0.63 (p < 0.001). Greater CGI-S ratings were associated with a linear stepwise increase in YGTSS Total Tic scores, Impairment scores, and Global Severity scores. Despite moderate-to-strong associations (ρ = 0.45–0.56, p < 0.001) between the CGI-S and predictive logistical regression models, only fair agreement was achieved when applying classification benchmarks (κ = 0.21–0.32, p < 0.001). CONCLUSIONS: CGI-S ratings are useful to characterize benchmarks for tic severity, tic impairment, and global severity on the YGTSS. Logistic regression model benchmarks had only fair agreement with the CGI-S and underscore the heterogeneity of TD symptoms. Collectively, findings offer guidance on the delineation of tic severity categorizations to apply evidence-based treatment recommendations.

The Comprehensive Behavioral Intervention for Tic Disorders (CBIT) has demonstrated efficacy in large randomized controlled trials for children (≥9 yrs), adolescents and adults with Tourette Syndrome and Chronic Tic Disorders. Given the early age of onset for tic disorders, a large portion of affected individuals with chronic tic disorders are less than 9 years of age and appropriate developmental adaptations of behavioral treatment have not yet been tested. The goal of this study was to adapt and evaluate the acceptability and utility of a family-based adaptation of CBIT for children under 9 years of age. Children 5–8 years of age (N = 15) with chronic tics were recruited from three study sites. CBIT was adapted for use with young children and included habit reversal strategies introduced in a developmentally appropriate game format and function-based interventions to reduce family accommodation of and attention to tic symptoms. Children and parents described high level of treatment satisfaction and study retention rate was 100%. Treatment response rate was 54% (CGI-I = 1 or 2) with a significant decrease in the YGTSS total score (Cohen’s d = 0.73) that was largely maintained at 3-month and 1-year follow-up assessments. Treatment was associated with reduction of some symptoms of tic-related comorbid syndromes and with changes in parental accommodation and attention to tics. Future research should determine if parental attention to tics and symptom accommodation are important mediators of treatment outcome, or if participating in this intervention at a younger age may prevent the chronic course of tic symptoms.

This paper examined neurocognitive functioning and its relationship to behavior treatment response among youth with Tourette’s Disorder (TD) in a large randomized controlled trial. Participants diagnosed with TD completed a brief neurocognitive battery assessing inhibitory functions, working memory, and habit learning pre- and post-treatment with behavior therapy (CBIT, Comprehensive Behavioral Intervention for Tics) or psychoeducation plus supportive therapy (PST). At baseline, youth with tics and Attention Deficit Hyperactivity Disorder (ADHD) exhibited some evidence of impaired working memory and simple motor inhibition relative to youth with tics without ADHD. Additionally, a small negative association was found between antipsychotic medications and youth’s performance speed. Across treatment groups, greater baseline working memory and aspects of inhibitory functioning were associated with a positive treatment response; no between-group differences in neurocognitive functioning at post-treatment were identified. Within the behavior therapy group, pre-treatment neurocognitive status did not predict outcome, nor was behavior therapy associated significant change in neurocognitive functioning post-treatment. Findings suggest that co-occurring ADHD is associated with some impairments in neurocognitive functioning in youth with Tourette’s Disorder. While neurocognitive predictors of behavior therapy were not found, participants who received behavior therapy exhibited significantly reduced tic severity without diminished cognitive functioning.

Evidence of associations between obsessive compulsive disorder (OCD) and alterations in neural indices of performance monitoring, i.e., elevated neural activity following errors, have accelerated interest in the error-related negativity (ERN) as a biomarker for pediatric OCD. The study investigates the degree to which attention bias training is linked to changes in neural measures of performance monitoring (ERN, correct response negativity or CRN) and whether pre-to-post training changes in these neural indices are associated with symptom changes in youth with OCD. The sample included 36 youth (8-17 years) diagnosed with OCD who completed a 12-session attention training program and pre- and post-training EEG assessment of performance monitoring using cognitive and emotional flanker tasks. The emotional flanker task was individualized to each participant's negative ratings of stimuli at pre-treatment to enhance salience of threat-related stimuli across youth. Results indicated that unlike participants who received attentional control protocol (CON), those who received attentional bias modification protocol (ABM) showed significant attenuations in neural activity following erroneous and correct responses in the emotional flanker task. The ERN amplitude during the cognitive flanker task was unchanged in both ABM and CON groups. Attenuations in the ERN were also linked to decreases in social anxiety and depressive symptoms. Findings highlight the relevance of including emotionally-salient tasks when investigating potential neural mechanisms of treatments and suggest that alterations in neural processes underlying performance monitoring can be targeted via attention training programs in pediatric OCD.

Objective To date, few studies of childhood obsessive compulsive disorder (OCD) have been adequately powered to examine patterns and predictors of comorbidity, despite the frequency with which it occurs. We address this gap, drawing on a large sample of youth with OCD who were systematically assessed through research and clinical programs in a university-based specialty program for children and adolescents with OCD. We examine patterns of comorbidity across different epochs of development and predict specific classes of OCD (comorbidity internalizing/externalizing/both) from key demographic and clinical variables that may be useful in guiding individualized treatment. Method A total of 322 youths (mean age = 12.28, 53% male) were assessed using the Anxiety Disorders Interview Schedule (ADIS; Silverman and Albano, 1996), the Children's Yale Brown Obsessive Compulsive Scale (CYBOCS; Scahill et al., 1997) and other standardized measures. Results Consistent with prior research, 50% of youth met criteria for a co-occurring anxiety or depressive disorder. Rates of externalizing disorders were lower (16%). Developmental differences emerged such that older youth met criteria for a higher number of co-occurring disorders. As expected, adolescents in particular were more likely to have a co-occurring internalizing disorder compared to early or pre-adolescent peers. Surprisingly, they were also more likely to have a comorbid externalizing disorder. Developmental trends were particularly striking with respect to depression, with adolescents with OCD demonstrating a six-fold greater likelihood of co-occurring depressive disorder compared to younger counterparts. Discussion Clinical implications are discussed with eye toward tailoring interventions, particularly during the transition to adolescence when youth are at heightened risk for depression.

Background Little is known about the neural underpinnings of pediatric trichotillomania (TTM). We examined error-related negativity (ERN)-amplitude and theta-EEG power differences among youth with TTM, OCD, and healthy controls (HC). Methods Forty channel EEG was recorded from 63 pediatric participants (22 with TTM, 22 with OCD, and 19 HC) during the Eriksen Flanker Task. EEG data from inhibitory control were used to derive estimates of ERN amplitude and event-related spectral power associated with motor inhibition. Results TTM and HC were similar in brain activity patterns in frontal and central regions and TTM and OCD were similar in the parietal region. Frontal ERN-amplitude was significantly larger in OCD relative to TTM and HC, who did not differ from each other. The TTM group had higher theta power compared to OCD in frontal and central regions, and higher theta than both comparison groups in right motor cortex and superior parietal regions. Within TTM, flanker task performance was correlated with EEG activity in frontal, central, and motor cortices whereas global functioning and impairment were associated with EEG power in bilateral motor and parietal cortices. Conclusions Findings are discussed in terms of shared and unique neural mechanisms in TTM and OCD and treatment implications.

The neurophysiological bases of cognitive-behavioral therapy (CBT) for obsessive–compulsive disorder (OCD) are incompletely understood. Previous studies, though sparse, implicate metabolic changes in pregenual anterior cingulate cortex (pACC) and anterior middle cingulate cortex (aMCC) as neural correlates of response to CBT. The goal of this pilot study was to determine the relationship between levels of the neurochemically interlinked metabolites glutamate + glutamine (Glx) and N -acetyl-aspartate + N -acetyl-aspartyl-glutamate (tNAA) in pACC and aMCC to pretreatment OCD diagnostic status and OCD response to CBT. Proton magnetic resonance spectroscopic imaging ( 1 H MRSI) was acquired from pACC and aMCC in 10 OCD patients at baseline, 8 of whom had a repeat scan after 4 weeks of intensive CBT. pACC was also scanned (baseline only) in 8 age-matched healthy controls. OCD symptoms improved markedly in 8/8 patients after CBT. In right pACC, tNAA was significantly lower in OCD patients than controls at baseline and then increased significantly after CBT. Baseline tNAA also correlated with post-CBT change in OCD symptom severity. In left aMCC, Glx decreased significantly after intensive CBT. These findings add to evidence implicating the pACC and aMCC as loci of the metabolic effects of CBT in OCD, particularly effects on glutamatergic and N -acetyl compounds. Moreover, these metabolic responses occurred after just 4 weeks of intensive CBT, compared to 3 months for standard weekly CBT. Baseline levels of tNAA in the pACC may be associated with response to CBT for OCD. Lateralization of metabolite effects of CBT, previously observed in subcortical nuclei and white matter, may also occur in cingulate cortex. Tentative mechanisms for these effects are discussed. Comorbid depressive symptoms in OCD patients may have contributed to metabolite effects, although baseline and post-CBT change in depression ratings varied with choline-compounds and myo -inositol rather than Glx or tNAA.

Background The brain mechanisms of cognitive–behavioral therapy (CBT), a highly effective treatment for pediatric obsessive–compulsive disorder (OCD), are unknown. Neuroimaging in adult OCD indicates that CBT is associated with metabolic changes in striatum, thalamus, and anterior cingulate cortex. We therefore probed putative metabolic effects of CBT on these brain structures in pediatric OCD using proton magnetic resonance spectroscopic imaging ( 1 H MRSI). Method Five unmedicated OCD patients (4 ♀, 13.5 ± 2.8) and 9 healthy controls (7 ♀, 13.0 ± 2.5) underwent MRSI (1.5 T, repetition-time/echo-time = 1500/30 ms) of bilateral putamen, thalamus and pregenual anterior cingulate cortex (pACC). Patients were rescanned after 12 weeks of exposure-based CBT. The Children's Yale–Brown Obsessive–Compulsive Scale (CY-BOCS) of OCD symptoms was administered before and after CBT. Results Four of 5 patients responded to CBT (mean 32.8% CY-BOCS reduction). Multiple metabolite effects emerged. Pre-CBT, N -acetyl-aspartate + N -acetyl-aspartyl-glutamate (tNAA) in left pregenual anterior cingulate cortex (pACC) was 55.5% higher in patients than controls. Post-CBT, tNAA (15.0%) and Cr (23.9%) in left pACC decreased and choline compounds (Cho) in right thalamus increased (10.6%) in all 5 patients. In left thalamus, lower pre-CBT tNAA, glutamate + glutamine (Glx), and myo -inositol (mI) predicted greater post-CBT drop in CY-BOCS ( r = 0.98) and CY-BOCS decrease correlated with increased Cho. Conclusions Interpretations are offered in terms of the Glutamatergic Hypothesis of Pediatric OCD. Similar to 18 FDG-PET in adults, objectively measurable regional MRSI metabolites may indicate pediatric OCD and predict its response to CBT.

Objective To examine the efficacy of exposure-based cognitive-behavioral therapy (CBT) plus a structured family intervention (FCBT) versus psychoeducation plus relaxation training (PRT) for reducing symptom severity, functional impairment, and family accommodation in youths with obsessive-compulsive disorder (OCD). Method A total of 71 youngsters 8 to 17 years of age (mean 12.2 years; range, 8–17 years, 37% male, 78% Caucasian) with primary OCD were randomized (70:30) to 12 sessions over 14 weeks of FCBT or PRT. Blind raters assessed outcomes with responders followed for 6 months to assess treatment durability. Results FCBT led to significantly higher response rates than PRT in ITT (57.1% vs 27.3%) and completer analyses (68.3% vs. 35.3%). Using HLM, FCBT was associated with significantly greater change in OCD severity and child-reported functional impairment than PRT and marginally greater change in parent-reported accommodation of symptoms. These findings were confirmed in some, but not all, secondary analyses. Clinical remission rates were 42.5% for FCBT versus 17.6% for PRT. Reduction in family accommodation temporally preceded improvement in OCD for both groups and child functional status for FCBT only. Treatment gains were maintained at 6 months. Conclusions FCBT is effective for reducing OCD severity and impairment. Importantly, treatment also reduced parent-reported involvement in symptoms with reduced accommodation preceding reduced symptom severity and functional impairment. Clinical Trials Registry Information Behavior Therapy for Children and Adolescents with Obsessive-Compulsive Disorder (OCD); http://www.clinicaltrials.gov; NCT00000386.

The comorbidity of tic disorders (TD) and obsessive-compulsive disorder (OCD) has long been recognized in the clinical literature and appears to be bidirectional, affecting 20-60% of individuals with each disorder. Coffey et al. (1998) found that adults with TD+OCD had a more severe comorbidity profile than adults with OCD or TD alone. This exploratory study in children attempts to evaluate whether heightened diagnostic severity, increased comorbidity load, and lower functioning is more commonplace in youth with TD+OCD in comparison to either syndrome alone. Participants were 306 children (seeking clinical evaluation) with TD, OCD, or TD+OCD. Assessment consisted of a diagnostic battery (including structured diagnostic interviews and standardized parent-report inventories) to evaluate diagnostic severity, comorbid psychopathology, behavioral and emotional correlates, and general psychosocial functioning. Data from this study sample were not supportive of the premise that youth with both a tic disorder and OCD present with elevated diagnostic severity, higher risk-for or intensity-of comorbidity, increased likelihood of externalizing/internalizing symptomatology, or lower broad-based adaptive functioning. The OCD group had elevated rates of comorbid anxiety disorders and attention-deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) were more prevalent among youth in the TD group. The three groups also differed on key demographic variables. Our findings suggest that, in contrast to adults, TD+OCD in children and adolescents does not represent a more severe condition than either disorder alone on the basis of diagnostic comorbidity, symptom severity, or functional impairment.