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Objective: Pediatric social anxiety disorder (SAD) is associated with an increased risk of comorbid mental disorders, with implications for prognosis and treatment strategy. The aim of this study is to explore predictors of treatment response, and the role of comorbidity in affecting refractoriness., Methods: One hundred and forty consecutive youths (81 males, 57.9%), ages 7-18 years (mean age 13.7 ± 2.5 years, mean age at onset of SAD 10.6 ± 2.7 years) met American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) criteria for SAD as primary diagnosis, according to a structured clinical interview (Kiddie Schedule for Affective Disorders and Schizophrenia for School-Aged Children-Present and Lifetime Version [K-SADS-PL]). All received a pharmacological treatment with serotonin reuptake inhibitors (SSRIs) targeted to SAD, associated with additional medications for comorbidities (mood stabilizers in 27.1%, antipsychotics in 12.8%) and 57.9% received an additional psychotherapy., Results: Eighty-nine patients (63.6%) responded to treatments after 3 months, namely 72.8% with psychotherapy plus medication and 50.8% with medication only. Nonresponders had more severe symptoms at baseline in terms of both clinical severity and functional impairment, and had more comorbid disruptive behavior disorders. The backward logistic regression indicated that clinical severity and functional impairment at baseline, comorbid disruptive behavior disorders, and bipolar disorders were predictors of nonresponse., Conclusion: Our data suggest that SSRIs can be effective in pediatric SAD, but that the more severe forms of the disorder and those with heavier comorbidity are associated with poorer prognosis.

This paper reports on implications of bipolar disorder (BD) co-morbidity in 120 children and adolescents with obsessive-compulsive disorder (OCD) (84 males, 36 females, age 13.7 +/- 2.8 years), diagnosed using a clinical interview according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria, and naturalistically followed-up for 12 +/- 6 months. The aim of this naturalistic, retrospective study was to explore the effect of BD co-morbidity, disentangling it from other co-occurring variables, namely the co-morbidity with disruptive behavior disorders. Forty three patients (35.8%) had a bipolar co-morbidity. Compared with OCD patients without BD, they had an earlier onset of OCD, a greater severity and functional impairment, more frequent hoarding obsessions and compulsions, and a poorer response to treatments. They had a higher co-morbidity with attention-deficit/hyperactivity disorder (ADHD) and oppositional-defiant disorder (ODD), and a lower co-morbidity with generalized anxiety disorder (GAD). Finally, they received more mood stabilizers, and 30.2% of them did not receive serotonin-selective reuptake inhibitors (SSRIs) because of pharmacological (hypo)mania. When all the OCD responders and nonresponders were compared, nonresponders (n = 42, 35%) were more severe at baseline and at end of the follow-up, had more frequently hoarding obsessions and compulsions, and had more frequent BD, ODD, and conduct disorder (CD) and less GAD and panic disorder. In the final regression model, hoarding obsessions and compulsions, co-morbidity with ODD, and CD were negative predictors of treatment outcome. This study suggests that even though bipolar co-morbidity is frequent and affects phenomenology and co-morbidity in pediatric OCD, its effect on treatment response seems prevalently accounted for by co-morbidity with disruptive behavior disorders. The significance of the hoarding subtype deserves further research on larger samples of pediatric patients.

Background: This study on a large sample of unselected, consecutive children and adolescents referred to a third-level hospital who received a diagnosis of bipolar disorder (BD) was aimed at exploring whether childhood-onset BD, as compared with adolescent-onset BD, presents specific clinical features in terms of severity, functional impairment, course, prevalent mood, pattern of co-morbidity, and treatment outcome., Methods: A total of 136 patients, 81 males (59.6%) and 55 females (40.4%), mean age 13.5 +/- 2.9 years, meeting the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) diagnosis of BD according to a structured clinical interview Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (KSADS-PL), were included in the study., Results: Eighty patients (58.8%) had a childhood-onset BD (before 12 years of age) and 56 (41.2%) had an adolescents-onset BD. Compared with the adolescent-onset BD, patients with childhood-onset were more frequently males and had a more frequent co-morbidity with attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD). An episodic course was found in only 42.5% of bipolar children, but 76.8% of youngsters with adolescent-onset BD. Severity, 6-month treatment outcome, prevalent mood (elated versus irritable), and co-morbid anxiety did not differentiate the two groups., Conclusions: Our findings suggest that a very early age at onset may identify a form of BD with a more frequent subcontinuous course and a heavy co-morbidity with ADHD.

Even though juvenile bipolar disorder (BD) is reported to be more treatment-resistant than adult BD, predictors of nonresponse are not well studied. The aim of this study was to address this issue in a naturalistic sample of bipolar children and adolescents with manic or mixed episodes treated under the condition of routine clinical practice. This study was comprised of 40 patients (19 females and 21 males; mean age, 14.2 years; SD = 3.3; range, 7-18) with a Diagnostic and Statistical Manual of Mental Disorders-fourth edition (DSM-IV) diagnosis of manic (n = 23) or mixed episodes (n = 17). The clinical characteristics of 20 patients considered to be treatment responders, according to the Clinical Global Impression-Improvement (CGI-I) scores, were compared to those of the 20 nonresponders. The effect of predictors on the probability of treatment nonresponse was analyzed using the multiple stepwise logistic regression, backward procedure. Demographic variables (mean age, gender ratio, socioeconomic status), as well as the inpatients-outpatients ratio (75% versus 65%), duration of the follow-up (10.5 +/- 2.5 months versus 9.6 +/- 3.2 months), index episode (manic versus mixed), and rates of pharmacologic hypomania did not differentiate the 2 groups. According to stepwise logistic regression, predictors of nonresponse were the presence of comorbidity with conduct disorder (odd ratio, 3.36; 95% CI, 2.20-4.52), attention deficit hyperactivity disorder (ADHD) (odd ratio, 2.30; CI, 1.24-3.26), and the baseline CGI Severity score (odd ratio, 2.31; CI, 1.33-3.29). It is relevant to point out that patient age at the onset of BD, and at the first visit, and comorbid anxiety disorders did not influence treatment response. Follow-up studies with a larger sample size with BD and/or externalizing disorders appropriately managed with different treatment options and/or combinations are warranted.

Some bipolar patients with acute manic episodes can be refractory to conventional treatment with mood stabilizers. Clozapine, an atypical antipsychotic, has been reported to be effective in adults with treatment-resistant bipolar disorder. We describe the therapeutic effect of clozapine in 10 adolescent inpatients (12- to 17-year-olds) with severe acute manic or mixed episodes who did not improve after treatment with conventional drugs (mood stabilizers, antipsychotics). At hospital discharge, 15 to 28 days after clozapine treatment, all patients had responded positively according to the Clinical Global Impression-Improvement Scale scores. The mean changes in Mania Rating Scale, Brief Psychiatric Rating Scale, Children's Global Assessment Scale, and Clinical Global Impression-Severity Scale were significant (p < 0.001). Clozapine dosage was 142.5 +/- 73.6 mg/day (range 75-300 mg/day). Side effects (increased appetite, sedation, enuresis, sialorrhea) were frequent but not severe enough to require reduction of dosage. Mean weight gain after 6 months was 6.96 +/- 3.08 kg (10.7%). Neither decrease of white cells nor epileptic seizures were reported during follow-up (12-24 months). These preliminary findings suggest that clozapine may improve the clinical picture in adolescents with treatment-refractory manic or mixed episodes. Controlled studies on larger samples are warranted.

Although hyperprolactinemia is a common side effect during risperidone treatment in adult patients, no information is available on young children. The aim of this study is to report on serum prolactin levels in 25 young autistic children (22 males and 3 females, age range 3.9-7 years, mean age 4.10 years) during treatment with risperidone (dosage range 0.25-0.90 mg/day, mean dosage 0.52 mg/day). Prolactin levels were measured at baseline and after 10 weeks of treatment. The clinical outcome measure used was the Clinical Global Impression-Improvement. Serum prolactin was 9.77 +/- 3.94 ng/mL at baseline and 25.92 +/- 13.9 ng/mL during the 10th week of treatment (p < 0.001). Six children (24%) showed prolactin levels lower than 15 ng/mL, which is the upper normal level; eight children (28%) had prolactin levels higher than two times the upper limit (30 ng/mL). Hyperprolactinemia did not show significant correlations with age, weight, or risperidone dosage. There was no relation with clinical outcome. Dose reduction of risperidone resulted in a decrease of prolactin levels. None of the children showed clinical signs of hyperprolactinemia. Given the paucity of available data on potential effects of long-term hyperprolactinemia, a monitoring of prolactin during treatment with risperidone and other typical and atypical antipsychotics may be warranted.

Paroxetine has repeatedly been shown to be effective in the treatment of panic disorder (PD) in adults, and, according to previous case observations, it may be useful in treating children and adolescents with PD as well. This preliminary naturalistic study examines effectiveness and safety of paroxetine in the treatment of children and adolescents with PD. A chart review was conducted on 18 patients with Diagnostic and Statistical Manual of Mental Disorders PD admitted to the Division of Child Neurology and Psychiatry and to the Department of Psychiatry at the University of Pisa. Paroxetine was given at an initial mean dosage of 8.9 +/- 2.1 mg/day and was gradually increased up to 40 mg/day, depending on clinical response and side effects. Clinical status was assessed with the Clinical Global Impression (CGI) and adverse effects were assessed retrospectively at each visit. Patients with final CGI-Improvement scores of 1 or 2 were considered responders. Mean paroxetine treatment duration was 11.7 +/- 8.3 months, with a mean final dosage of 23.9 +/- 9.8 mg/day (range, 10-40 mg/day). No patient had to interrupt the treatment because of side effects. Fifteen patients (83.3%) were considered responders. The mean change on the CGI-Severity scale was statistically significant (p < 0.0001). Paroxetine was well tolerated and effective in the treatment of PD in these children and adolescents.