Am J Psychiatry current issue

[In This Issue] In This Issue

2008-05-01

[Editorials] Cost-Effectiveness of Depression Treatment for Adolescents

Norquist, G., McGuire, T. G., Essock, S. M. — 2008-05-01

[Editorials] Does Childhood Treatment of ADHD With Stimulant Medication Affect Substance Abuse in Adulthood?

Volkow, N. D., Swanson, J. M. — 2008-05-01

[Editorials] Psychotherapies and Lasting Change

Levy, K. N. — 2008-05-01

[Editorials] Recognizing Each Other and the Effects of Racial Differences

Bell, C. C. — 2008-05-01

[Images in Neuroscience] Controlling Neuronal Activity

Schneider, M. B., Gradinaru, V., Zhang, F., Deisseroth, K. — 2008-05-01

[Introspections] Doubt

Ablon, S. — 2008-05-01

[Treatment in Psychiatry] Cross-Cultural Evaluation of Maternal Competence in a Culturally Diverse Society

Seeman, M. V. — 2008-05-01

[Clinical Case Conference] Remission From Depression Comorbid With Chronic Illness and Physical Impairment

Turvey, C. L., Klein, D. M. — 2008-05-01

[Images in Psychiatry] Karl Bonhoeffer (1868-1948)

Strohle, A., Wrase, J., Malach, H., Gestrich, C., Heinz, A. — 2008-05-01

[Images in Psychiatry] Dietrich Bonhoeffer (1906-1945)

Strohle, A., Wrase, J., Malach, H., Gestrich, C., Heinz, A. — 2008-05-01

[Reviews and Overviews] Premorbid IQ in Schizophrenia: A Meta-Analytic Review

Woodberry, K. A., Giuliano, A. J., Seidman, L. J. — 2008-05-01

OBJECTIVE: Over the past three decades, there have been significant changes in the diagnostic criteria for schizophrenia as well as changes in measurement of IQ. The last quantitative review of the literature on premorbid IQ in schizophrenia was published more than two decades ago. Since that time, there have been many published studies of data sets pertaining to this issue. The purpose of the present review was to provide an updated meta-analysis of premorbid IQ in individuals who later develop schizophrenia. METHOD: The authors performed a systematic literature search, which yielded 18 studies that met criteria for the meta-analysis. Inclusion criteria were 1) premorbid psychometric measures of IQ in subjects who were later diagnosed with schizophrenia, schizoaffective disorder, or schizophreniform disorder, 2) similar comparison data, and 3) sufficient data for calculation of an effect size. The analogue to the analysis of variance method was used to model between-study variance due to key study-design features. RESULTS: Overall, schizophrenia samples demonstrated a reliable, medium-sized impairment in premorbid IQ. The heterogeneity of effect sizes was minimal and almost exclusively the result of one study. Methodological differences, such as diagnostic criteria, type of IQ measure, sample ascertainment, and age at premorbid testing, contributed minimally to the effect size variance. A cross-sectional analysis of all studies by age and a descriptive review of studies that used repeated measures of IQ in a single sample did not support the presence of a relative decline in IQ during the premorbid period in individuals with schizophrenia. However, all studies with pre- and post-onset testing within the same sample suggested that a significant decline in the IQ of individuals with schizophrenia, relative to comparison subjects, was associated with the onset of frank psychosis. CONCLUSIONS: Years before the onset of psychotic symptoms, individuals with schizophrenia, as a group, demonstrate mean IQ scores approximately one-half of a standard deviation below that of healthy comparison subjects.

[Articles] Cost-Effectiveness of Treatments for Adolescent Depression: Results From TADS

2008-05-01

OBJECTIVE: While the evidence base for treatments for adolescent depression is building, little is known about the relative efficiency of such treatments. Treatment costs are a relevant concern given the competing demands on family and health care budgets. The authors evaluated the cost-effectiveness of three active treatments among adolescents with major depressive disorder. METHOD: Volunteers (N=439) ages 12 to 18 with a primary diagnosis of major depressive disorder participated in a randomized, controlled trial conducted at 13 U.S. academic and community clinics from 2000 to 2004. Subjects included those participants who did not drop out and had evaluable outcome and cost data at 12 weeks (N=369). Subjects were randomly assigned to 12 weeks of either fluoxetine alone (10–40 mg/day), CBT alone, CBT combined with fluoxetine (10–40 mg/day), or placebo (equivalent to 10–40 mg/day). Both placebo and fluoxetine were administered double-blind; CBT alone and CBT in combination with fluoxetine were administered unblinded. Societal cost per unit of improvement on the Children’s Depression Rating Scale—Revised and cost per quality-adjusted life year (QALY) were compared. RESULTS: Results ranged from an incremental cost over placebo of $24,000 per QALY for treatment with fluoxetine to $123,000 per QALY for combination therapy treatment. The cost-effectiveness ratio for CBT treatment was not evaluable due to negative clinical effects. The models were robust on a variety of assumptions. CONCLUSIONS: Both fluoxetine and combination therapy are at least as cost-effective in the short-term as other treatments commonly used in primary care (using a threshold of $125,000/QALY). Fluoxetine is more cost-effective than combination therapy after 12 weeks of treatment.

[Articles] Stimulant Therapy and Risk for Subsequent Substance Use Disorders in Male Adults With ADHD: A Naturalistic Controlled 10-Year Follow-Up Study

2008-05-01

OBJECTIVE: The extant literature does not provide definite answers pertaining to whether stimulant treatment increases, decreases, or does not affect the risk for subsequent substance use disorders in youths with attention deficit hyperactivity disorder (ADHD). The authors examined the association between stimulant treatment in childhood and adolescence and subsequent substance use disorders (alcohol, drug, and nicotine) into the young adult years. METHOD: The authors conducted a 10-year prospective follow-up study. One hundred forty male Caucasian children with ADHD, ages 6 to 17, were examined at baseline. Of these, 112 (80%) were reassessed at the 10-year follow-up (mean age at follow-up=22 years). Assessments were made using Cox proportional hazards survival models. All models were adjusted for conduct disorder, since conduct disorder is a potent predictor of subsequent substance use disorders. RESULTS: Of the 112 ADHD subjects who were reassessed at the 10-year follow-up, 82 (73%) had been treated previously with stimulants and 25 (22%) were undergoing stimulant treatment at the time of the follow-up assessment. There were no statistically significant associations between stimulant treatment and alcohol, drug, or nicotine use disorders. CONCLUSIONS: The findings revealed no evidence that stimulant treatment increases or decreases the risk for subsequent substance use disorders in children and adolescents with ADHD when they reach young adulthood.

[Articles] Age of Methylphenidate Treatment Initiation in Children With ADHD and Later Substance Abuse: Prospective Follow-Up Into Adulthood

2008-05-01

OBJECTIVE: Animal studies have shown that age at stimulant exposure is positively related to later drug sensitivity. The purpose of this study was to examine whether age at initiation of stimulant treatment in children with attention deficit hyperactivity disorder (ADHD) is related to the subsequent development of substance use disorders. METHOD: The authors conducted a prospective longitudinal study of 176 methylphenidate-treated Caucasian male children (ages 6 to 12) with ADHD but without conduct disorder. The participants were followed up at late adolescence (mean age=18.4 years; retention rate=94%) and adulthood (mean age=25.3; retention rate=85%). One hundred seventy-eight comparison subjects also were included. All subjects were diagnosed by blinded clinicians. The Cox proportional hazards model included the following childhood predictor variables: age at initiation of methylphenidate treatment, total cumulative dose of methylphenidate, treatment duration, IQ, severity of hyperactivity, socioeconomic status, and lifetime parental psychopathology. Separate models tested for the following four lifetime outcomes: any substance use disorder, alcohol use disorder, non-alcohol substance use disorder, and stimulant use disorder. Other outcomes included antisocial personality, mood, and anxiety disorders. RESULTS: There was a significant positive relationship between age at treatment initiation and non-alcohol substance use disorder. None of the predictor variables accounted for this association. Post hoc analyses showed that the development of antisocial personality disorder explained the relationship between age at first methylphenidate treatment and later substance use disorder. Even when controlling for substance use disorder, age at stimulant treatment initiation was significantly and positively related to the later development of antisocial personality disorder. Age at first methylphenidate treatment was unrelated to mood and anxiety disorders. CONCLUSIONS: Early age at initiation of methylphenidate treatment in children with ADHD does not increase the risk for negative outcomes and may have beneficial long-term effects.

[Articles] Association of the Neurotrophic Tyrosine Kinase Receptor 3 (NTRK3) Gene and Childhood-Onset Mood Disorders

2008-05-01

OBJECTIVE: Genome scans have revealed significant evidence for linkage of depression to chromosome 15q25.3-q26.2. The gene for neurotrophic tyrosine kinase receptor 3 (NTRK3), the receptor for neurotrophin-3 (trkC) and a key gene in neurotrophin signaling, is located within this region and, given evidence for synaptic plasticity as a mechanism in mood disorders, was considered a prime candidate. The authors investigated NTRK3 as a susceptibility gene for childhood-onset mood disorders. METHOD: The study sample consisted of 603 families with 723 affected children and adolescents diagnosed with a mood disorder with onset of the first episode by age 15. The authors genotyped 18 polymorphic markers across the NTRK3 gene in this sample and tested for association. RESULTS: Results identified significant evidence for association for five of the markers using the transmission disequilibrium test. Four of the five markers were located in a region of strong linkage disequilibrium and were highly correlated. Haplotype results provided significant evidence for association to haplotypes composed of markers located in two haplotype blocks. CONCLUSIONS: The results for NTRK3 as well as the authors’ previous finding for association to brain-derived neurotrophic factor in this sample support synaptic plasticity as a mechanism contributing to mood disorders that begin during childhood and adolescence and specifically implicate the NTRK3 gene as a contributing factor in the 15q-linked region.

[Articles] A 6-Week Randomized, Placebo-Controlled Trial of CP-316,311 (a Selective CRH1 Antagonist) in the Treatment of Major Depression

Binneman, B., Feltner, D., Kolluri, S., Shi, Y., Qiu, R., Stiger, T. — 2008-05-01

OBJECTIVE: The corticotropin-releasing hormone (CRH) system is implicated in the pathogenesis of several psychiatric disorders, including major depressive disorder. This study was designed to evaluate the safety and efficacy of CP-316,311, a selective nonpeptide antagonist of corticotropin-releasing hormone type 1 (CRH₁) receptors, in the treatment of recurrent major depressive disorder. METHOD: Of a total of 167 patients with recurrent major depression who were screened, 123 were randomly assigned to receive 400 mg of CP-316,311 twice daily, or 100 mg of sertraline daily, or placebo in a 6-week fixed-dose, double-blind, double-dummy, parallel-group, placebo- and sertraline-controlled trial. The primary efficacy analysis compared the change in score from baseline to endpoint on the 17-item Hamilton Depression Rating Scale (HAM-D) between the CP-316,311 and placebo groups. A group sequential design was used to support early trial termination based on efficacy or futility at a planned interim analysis. RESULTS: The evaluable data set for the interim analysis included 28 patients in the CP-316,311 group, 31 patients in the placebo group, and 30 patients in the sertraline group. In the interim analysis, the change from baseline in the HAM-D score at the final visit was not significantly different between the CP-316,311 and placebo groups, while change from baseline between the sertraline and placebo groups was significantly different. Given these results, futility was declared for CP-316,311 and the trial was terminated. CONCLUSIONS: Although CP-316,311 was safe and well tolerated in this study population, it failed to demonstrate efficacy in the treatment of major depression.

[Articles] A Randomized, Controlled Trial of Cognitive-Behavioral Therapy for Augmenting Pharmacotherapy in Obsessive-Compulsive Disorder

2008-05-01

OBJECTIVE: Although serotonin reuptake inhibitors (SRIs) are approved for the treatment of obsessive-compulsive disorder (OCD), most OCD patients who have received an adequate SRI trial continue to have clinically significant OCD symptoms. The purpose of this study was to examine the effects of augmenting SRIs with exposure and ritual prevention, an established cognitive-behavioral therapy (CBT) for OCD. METHOD: A randomized, controlled trial was conducted at two academic outpatient clinics to compare the effects of augmenting SRIs with exposure and ritual prevention versus stress management training, another form of CBT. Participants were adult outpatients (N=108) with primary OCD and a Yale-Brown Obsessive Compulsive Scale total score ≥16 despite a therapeutic SRI dose for at least 12 weeks prior to entry. Participants received 17 sessions of CBT (either exposure and ritual prevention or stress management training) twice a week while continuing SRI pharmacotherapy. RESULTS: Exposure and ritual prevention was superior to stress management training in reducing OCD symptoms. At week 8, significantly more patients receiving exposure and ritual prevention than patients receiving stress management training had a decrease in symptom severity of at least 25% (based on Yale-Brown Obsessive Compulsive Scale scores) and achieved minimal symptoms (defined as a Yale-Brown Obsessive Compulsive Scale score ≤12). CONCLUSIONS: Augmentation of SRI pharmacotherapy with exposure and ritual prevention is an effective strategy for reducing OCD symptoms. However, 17 sessions were not sufficient to help most of these patients achieve minimal symptoms.

[Articles] 8-Year Follow-Up of Patients Treated for Borderline Personality Disorder: Mentalization-Based Treatment Versus Treatment as Usual

Bateman, A., Fonagy, P. — 2008-05-01

OBJECTIVE: This study evaluated the effect of mentalization-based treatment by partial hospitalization compared to treatment as usual for borderline personality disorder 8 years after entry into a randomized, controlled trial and 5 years after all mentalization-based treatment was complete. METHOD: Interviewing was by research psychologists blind to original group allocation and structured review of medical notes of 41 patients from the original trial. Multivariate analysis of variance, chi-square, univariate analysis of variance, and nonparametric Mann-Whitney statistics were used to contrast the two groups depending on the distribution of the data. RESULTS: Five years after discharge from mentalization-based treatment, the mentalization-based treatment by partial hospitalization group continued to show clinical and statistical superiority to treatment as usual on suicidality (23% versus 74%), diagnostic status (13% versus 87%), service use (2 years versus 3.5 years of psychiatric outpatient treatment), use of medication (0.02 versus 1.90 years taking three or more medications), global function above 60 (45% versus 10%), and vocational status (employed or in education 3.2 years versus 1.2 years). CONCLUSIONS: Patients with 18 months of mentalization-based treatment by partial hospitalization followed by 18 months of maintenance mentalizing group therapy remain better than those receiving treatment as usual, but their general social function remains impaired.

[Articles] The Other-Race Effect in Face Processing Among African American and Caucasian Individuals With Schizophrenia

2008-05-01

OBJECTIVE: Studies of emotion recognition abilities in schizophrenia show greater impairment for non-Caucasians with schizophrenia compared with Caucasians. These studies, however, included only Caucasian faces as stimuli. There is evidence from healthy individuals for a performance disadvantage on face memory and emotion recognition when processing faces from a different ethnicity. The authors sought to measure the "other-race effect" in schizophrenia, which could account for previous findings and provide information about sensitivity to such social cues in patients. METHOD: The study included 540 participants from four groups: African Americans with schizophrenia (N=135), Caucasians with schizophrenia (N=135), African American community comparison subjects (N=135), and Caucasian community comparison subjects (N=135). All participants completed face recognition and facial emotion identification tasks that included both Caucasian and African American faces as stimuli. RESULTS: Although comparison participants performed better than individuals with schizophrenia across all tasks, both comparison participants and participants with schizophrenia exhibited a strong and significant other-race effect for face memory and emotion recognition. The magnitude of the other-race effect did not differ between these two groups. CONCLUSIONS: These findings reveal an intact other-race effect in patients with schizophrenia and highlight a methodological concern in the measurement of face processing abilities in schizophrenia, namely, that findings of greater impairment in African American patients are spurious when Caucasian faces are used as stimuli. Despite overall impairments in face memory and emotion recognition, the presence of a normative other-race effect in schizophrenia may reflect typical experiences with faces during development.

[Letters to the Editor] Delving Further Into Discontinuation Risk: Addressing the Use of Mood Stabilizers During Pregnancy

ISAKOVICH, N., SMITH, E. — 2008-05-01

[Letters to the Editor] Mood Stabilizer Discontinuation in Pregnant Women With Bipolar Disorder

MAZER-POLINE, C., RIFKIN, A., GEISLER, S., WALCH, T. — 2008-05-01

[Letters to the Editor] Dr. Viguera Replies

VIGUERA,, A. C. — 2008-05-01

[Letters to the Editor] Application of the Seasonal Pattern Assessment Questionnaire in Detecting Seasonal Affective Disorder

GUPTA, N., SHARMA, P. — 2008-05-01

[Letters to the Editor] Ms. Sullivan and Dr. Payne Reply

SULLIVAN, B., PAYNE, T. W. — 2008-05-01

[Letters to the Editor] Argyria as a Result of Somatic Delusions

ANDERSON, E. L., JANOFSKY, J., JAYARAM, G. — 2008-05-01

[Letters to the Editor] Stabilization of Hypomania Following Initiation of Tamoxifen

PALMER, J. T., PAYNE, J. L. — 2008-05-01

[Letters to the Editor] Poor Neonatal Adaptation After in Utero Exposure to Duloxetine

EYAL, R., YAEGER, D. — 2008-05-01

[Letters to the Editor] Cingulate Gyrus Tumor Presenting as Panic Attacks

TAMBURIN, S., CACCIATORI, C., BONATO, C., ZANETTE, G. — 2008-05-01

[Corrections]

2008-05-01

[Book Forum] Changing American Psychiatry: A Personal Perspective

ROBINOWITZ, C. B. — 2008-05-01

[Book Forum] Dialectical Behavior Therapy With Suicidal Adolescents

JACOBSON, G. R. — 2008-05-01

[Book Forum] Magical Moments of Change: How Psychotherapy Turns Kids Around

HARTMANN, L. — 2008-05-01

[Book Forum] Clinical Topics in Addiction: Updates From Advances in Psychiatric Treatment

WOODY, G. E. — 2008-05-01

[Book Forum] The Confabulating Mind: How the Brain Creates Reality

FINEBERG, N. A. — 2008-05-01

[Books Received]

2008-05-01