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Thirty-nine children from intact families with a manic-depressive parent were evaluated by a semi-structured clinical interview and a number of rating scales for the presence or absence of psychopathology. This sample represents a larger one than in an earlier study, which showed minimal offspring psychopathology compared with reports of other investigators. The current study also examines the inter-relationships between the presence or absence of offspring psychopathology with both genetic loading and a number of psychosocial variables including measures of parental marital adjustment, severity and chronicity of proband parent illness and early exposure of children to parental illness. Nine of the thirty-nine children, (23%) received a positive DSM-III diagnosis, with depression of the dysthymic type being the most common. There was no significant correlation between genetic loading and offspring psychopathology. However, there were significant associations between children with psychopathology and paternal marital dissatisfaction and the age and chronicity of illness of the proband parent as compared with the children with no psychopathology.

Children with attention deficit hyperactivity disorder (ADHD) display higher rates of sleep problems such as bedtime resistance, sleep onset difficulties, night awakenings, difficulties with morning awakenings, sleep disordered breathing and daytime sleepiness. There has been a dramatic increase in new research of clinical significance to provide clinicians with the opportunity to better understand the association and possible causal relationships between sleep and ADHD. The objective of this paper is to provide an update on this literature over the past 3 years by examining any aspect of childhood ADHD and sleep and how it may inform clinical practice. As suggested by multiple lines of evidence, results from this review show that at the group level, there is a bidirectional impact of sleep and ADHD on each other and that both sleep and ADHD impairments may stem from common pathways. As hoped, effective intervention for either sleep or ADHD impacts both disorders thus opening the door to better treatment that goes beyond core symptoms to quality of life and functioning. Keywords Attention deficit hyperactivity disorder (ADHD). Sleep disordered breathing. Sleep onset difficulties. Neurobehavioural. Neurocognitive This article is part of the Topical Collection on Sleep and Psychological Disorders

Introduction Stimulant medication is a well-researched treatment for attention deficit hyperactivity disorder (ADHD) and is among the most effective treatments in psychiatry. Parents often want to know more about the long-term risks and benefits of medication. Our objective was to review the seminal papers on long-term outcomes of stimulant treatment for ADHD for the purpose of providing clinicians with the background they need to interpret these findings for patients. Methods We reviewed key articles on long-term outcome of symptoms, comorbidity, substance use, executive functioning, academics, side effects, neurobiology, functioning, and quality of life. Results Stimulants are very effective medications in the short term when used optimally. Long-term randomized, placebocontrolled studies are not feasible. Long-term naturalistic studies are limited by absence of controls.Discussion When administered properly with careful titration, follow-up, and dose adjustment, stimulants are a safe and effective treatment for ADHD with minimal long-term risk and possible long-term benefit.

Objective. We present a narrative review of pediatric catatonia and a case report illustrating the complexity of management of psychosis in a child with catatonia. Method. The literature search used the text terms pediatric, catatonia, and antipsychotics and the search engines PubMed and EBSCO. All references from peer-reviewed journals were reviewed for treatment strategies specific to management in children who are also psychotic. Findings. This 8-year-old girl presented with psychotic symptoms which were initially treated with antipsychotics and evolved into life-threatening catatonia that was eventually stabilized with a total daily dose of 46 mg of lorazepam. Lower doses led to recurrence. Once catatonia improved, she tolerated combined benzodiazepine and antipsychotic treatment. Long-term maintenance over 5 years required maintenance treatment with both benzodiazepines and antipsychotics to prevent relapse. Conclusions. The extraordinary doses of benzodiazepines found to be optimal for management of catatonia in this child led to improved alertness and orientation, without evident sedation. Catatonia did not recur with later management of psychosis using neuroleptics when added to lorazepam. The current literature on pediatric catatonia does not provide guidance on dose maintenance or when and if to rechallenge with antipsychotics.