Research examining the role of pharmacological therapy in the treatment of children and adolescents with clinical disorders is growing. Clinical disorders that present with comorbid aggression can add a challenge to treatment. Child and adolescent neuropsychiatric disorders associated with aggression include attention-deficit hyperactivity disorder, various mood disorders and in particular bipolar disorders/pediatric mania, schizophrenia, mental retardation, oppositional defiant disorder, conduct disorder, and autism spectrum disorders. This review describes the psychopharmacy to treat these disorders and the aggression that often appears comorbidly. Existing literature regarding the efficacy and safety of psychotropics for youth with neuropsychiatric disorders also is discussed. In addition, general guidelines for psychopharmacy of aggression in children and adolescents are presented. Studies reviewed in this article provide evidence for the use of psychostimulants, alpha-2 agonists, beta blockers, lithium, anticonvulsant mood-stabilizers, atypical antipsychotics, traditional antipsychotics, and selective serotonin reuptake inhibitors in treating pediatric aggression with the choice of medication dependent on symptomology. Despite increased support for pediatric psychotropic use, there is a need for more long-term safety and efficacy studies of existing medications and newer, safer, and more effective agents with fewer side effects for the pharmacological treatment of all childhood disorders in which aggression is prominent.
The literature examining social anhedonia, emotion regulation, and symptoms of depression in psychiatric inpatients has been limited. However, some studies have shown that difficulties in emotion regulation and social anhedonia were independently associated with depression. The current study attempted to examine the effects of these two potential predictors of unipolar depressed mood. Fifty-nine (73% female) psychiatric inpatients were given the measures of emotion regulation, symptoms of anxiety and depression, and social anhedonia. Results showed that difficulties in emotion regulation, specifically dysfunctional emotion regulation strategies and emotional clarity, served as significant predictors of depressive symptoms above and beyond contributions from social anhedonia. These results highlight the importance of attending to emotion regulation in the study and treatment of depression in inpatient samples.
Pharmacological intervention with methylphenidate to address the neurobehavioural deficits associated with various neurological disorders has increased during the past decade. One potential effect of methylphenidate use is its possible influence on serum glucose. This case report illustrates a significant post-intervention decrease in blood glucose levels subsequent to initiation of methylphenidate to address neurocognitive deficits, status post-acute cerebellar tumour resection, in a 38-year-old female with type 2 diabetes mellitus. A decrease of 26% in serum glucose values was seen from the pretreatment to the post-treatment phase (p = 0.003). Hypotheses concerning drug-drug interactions are offered to explain this unusual outcome. Although anecdotal, this finding has important implications for use of methylphenidate in the treatment of persons with diabetes and should be considered in light of the recent vote of the Drug Safety and Risk Management Advisory Committee of the US FDA urging 'black box' warnings on stimulant medications used to treat attention-deficit/hyperactivity disorder.
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