You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 63 No. 6, June 2006 TABLE OF CONTENTS
  Archives
  •  Online Features
  This Month in Archives of General Psychiatry
 This Article
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal

This Month in Archives of General Psychiatry

Arch Gen Psychiatry. 2006;63:601.

Epidemiological comorbidity seems common with psychiatric disorders. However, psychiatric researchers have often assessed comorbidity using lifetime prevalence in mixed-age samples, which can produce pseudocomorbidity. Kraemer et al (SEE ARTICLE) discuss why such statistical artifacts occur and how researchers might better avoid them.

Corlett et al (SEE ARTICLE) report findings from ketamine-treated subjects, linking brain responses while taking placebo to the emergence of delusions at higher doses in the same subjects. The central findings, that frontal lobe responses to error-dependent associate learning are disrupted by ketamine and that delusional ideas are more likely to arise in subjects showing increased frontal sensitivity to such learning, suggest a link between frontal function, associate learning, and delusions.

In a randomized, double-blind study Krakowski et al (SEE ARTICLE) compared the efficacy of 2 atypical antipsychotic agents, clozapine and olanzapine, with one another and with haloperidol in the treatment of aggressive behaviors in physically assaultive patients with schizophrenia. Clozapine was superior to olanzapine and haloperidol and olanzapine was superior to haloperidol in reducing the number and severity of physical assaults as well as overall aggression. This antiaggressive effect is distinct from the antipsychotic and sedative actions of these medications.

Nicotinic receptors have been implicated in the pathophysiology of schizophrenia, and nicotine itself, which is heavily abused by persons with schizophrenia, has some positive neurocognitive effects in the illness. Olincy et al (SEE ARTICLE) found that selective stimulation of {alpha}7 nicotinic acetylcholine receptors in 12 persons with schizophrenia, using the investigational drug 3-[(2,4 dimethoxy)benzylidene]-anabaseine, resulted in improved performance on neuropsychological testing. Participants in the double-blind, placebo-controlled study reported increased attentiveness and concentration.

Dwivedi et al (SEE ARTICLE) studied a small guanine nucleotide triphosphate–binding protein, Rap-1, crucial for neuroprotection and plasticity, and its important activator, Epac, in the postmortem brain of depressed suicide subjects. They found reduced activation and expression of Rap-1, along with increased expression of 1 of the isoforms of Epac (ie, Epac-2), in the prefrontal cortex and hippocampus without any change in the cerebellum in depressed subjects.

Giesen-Bloo et al (SEE ARTICLE) conducted a randomized trial of 3 years of biweekly sessions of schema-focused therapy (SFT) or transference-focused psychotherapy (TFP) for patients with borderline personality disorder. More TFP patients dropped out than SFT patients. In both conditions, there was improvement in borderline personality disorder–specific and general psychopathologic dysfunction, measures of SFT and TFP concepts, and quality of life. For all measures, SFT was more effective than TFP, with more than twice as much recovery.

Using functional magnetic resonance imaging combined with heat pain stimulation, Schmahl et al (SEE ARTICLE) visualized disturbed pain processing in patients with borderline personality disorder. Patients had higher pain thresholds, increased pain-induced response in the dorsolateral prefrontal cortex, and deactivation in the anterior cingulate and amygdala in comparison with healthy controls.

Kessler et al (SEE ARTICLE) used the National Comorbidity Survey Replication to show the first national data on DSM-IV intermittent explosive disorder. Intermittent explosive disorder is much more common than previously realized (lifetime prevalence, 7.3%; 12-month prevalence, 3.9%). Most cases reported early onset, persistent course, high comorbidity with temporally secondary disorders, substantial impairment, and lack of treatment.

Olfson et al (SEE ARTICLE) report that there has been a sharp national increase in antipsychotic treatment of children and adolescents with a variety of mental disorders. Office-based medical visits by children and adolescents that included antipsychotic medications increased from approximately 201 000 in 1993 to 1 224 000 in 2002. During 2000 to 2002, a larger proportion of the child and adolescent visits with antipsychotic medications were to treat disruptive behavior disorders or mood disorders than developmental disorders or psychotic disorders.

Munson et al (SEE ARTICLE) prospectively examined relationships between magnetic resonance imaging morphometry at age 3 years and development of social and communication skills in 45 children with autism spectrum disorder. Using growth curve modeling, enlarged right amygdalar volume, but not left amygdalar, hippocampal, or total cerebral volume, was associated with a more severe clinical course and worse outcome at age 6 years even when controlling for effects of IQ.

In a longitudinal study following up 2 large cohorts of children referred for autism assessments at age 2 years through age 9 years, Lord et al (SEE ARTICLE) found that a parent interview, a structured clinician observation, and clinical judgment predicted the stability of diagnosis with odds ratios of 6.6, 6.8, and 12.8, respectively. Verbal IQ; repetitive behaviors, both as described in the parent interview and as observed; and observations of social behavior all contributed to predictions. Clinical judgment significantly added to other sources of information to predict autism at age 9 years.







HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2006 American Medical Association. All Rights Reserved.