ADHD adversely affects long-term academic outcomes. A greater proportion of achievement test outcomes improved with treatment compared with academic performance. Both improved most consistently with multimodal treatment.

Accurate ADHD diagnosis in women and girls requires establishing a symptom history and an understanding of its gender-specific presentation. Coexisting anxiety and depression are prominent in female patients with ADHD; satisfactory academic achievement should not rule out an ADHD diagnosis.

Objective: Cognitive impairment frequently accompanies major depressive disorder (MDD) and can persist during remission. This review examined pharmacotherapy effects on cognitive function in MDD.Data Sources: PubMed and EMBASE searches were conducted on July 30, 2013, for English language reports of cognitive assessments following pharmacologic monotherapy or augmentation therapy in MDD.Study Selection: A total of 43 research reports were identified (31 monotherapy [8 placebo-controlled, 11 active-comparator, 12 open-label], 12 augmentation therapy [7 placebo-controlled, 5 open-label]). Data Extraction: Results reported in each publicationwere examined for open-label and placebo-or active comparator-controlled studies.Results: Studies varied widely in terms of size (median, 50 participants; interquartile range, 21-143 participants), populations examined, duration (median, 8 weeks; interquartile range, 6-12 weeks), and neurocognitive assessments used. Most individual studies reported some benefit to cognition with pharmacotherapy, but there was no pattern of response in specific domains and only 12% of individually analyzed changes favored active treatment over placebo or untreated healthy controls. Sample weighted mean effect sizes revealed that verbal memory improved with monotherapy, while the largest treatment effect with augmentation therapy was for visual memory. Conclusions:Pharmacotherapy may have benefit in reducing cognitive impairment in MDD, with augmentation therapy being a potential approach for addressing cognitive deficits that persist after monotherapy has brought about clinical response or remission. However, given the wide variability in study design and treatment duration across studies, these findings should be interpreted cautiously. More definitive research is required before firm conclusions can be reached. 2014;75(8):864-876 © Copyright 2014 Physicians Postgraduate Press, Inc. Submitted: May 31, 2013; accepted January 17, 2014. Online ahead of print: July 8, 2014 J Clin Psychiatry It is now recognized that individuals with major depressive disorder (MDD) may exhibit deficits in cognition, including cognitive inefficiency.1,2 However, of the 9 diagnostic criteria for MDD in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), 3 "diminished ability to think or concentrate, or indecisiveness, " is the only disturbance that is clearly cognitive in nature. Other symptoms, such as diminished energy and sleep disturbances, can also adversely affect cognitive function.Cognition may be impaired in several domains, including processing speed, psychomotor skills, attention, memory, and executive functions. The domains of memory and executive function tend to show the most severe impairment, especially in elderly people with MDD. 1 For most people with MDD, it is unclear whether cognitive impairment varies with the severity of depressive symptoms or persists during times of euthymia. The degree of correlation between the severity of cognitive impairment an...

Evaluate lisdexamfetamine dimesylate (LDX) augmentation of antidepressant monotherapy for executive dysfunction in partially or fully remitted major depressive disorder (MDD). This randomized, placebo-controlled study (NCT00985725) enrolled 143 adults (18-55 years) with mild MDD (Montgomery-Å sberg Depression Rating Scale (MADRS) score p18) and executive dysfunction (Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A) Self-Report Global Executive Composite (GEC) T score X60) on stable antidepressant monotherapy for X8 weeks. After 2 weeks of screening, participants were randomized to 9 weeks of double-blind LDX (20-70 mg/day) or placebo augmentation, followed by 2 weeks of single-blind placebo. The primary end point was change from baseline to week 9/end of study (EOS) in BRIEF-A Self-Report GEC T score; secondary assessments included the BRIEF-A Informant Report, MADRS, and treatment-emergent adverse events (TEAEs). Of 143 randomized participants, 119 completed double-blind treatment (placebo, n ¼ 59; LDX, n ¼ 60). Mean±standard deviation (SD) BRIEF-A GEC T scores decreased from baseline (placebo, 74.2±8.88; LDX, 76.8±9.66) to week 9/EOS (placebo, 61.4±14.61; LDX, 55.2±16.15); the LS mean (95% CI) treatment difference significantly favored LDX ( À 8.0 ( À 12.7, À 3.3); P ¼ 0.0009). The LS mean (95% CI) treatment difference for MADRS total score also significantly favored LDX ( À 1.9 ( À 3.7, 0.0); P ¼ 0.0465). TEAE rates were 73.6% with placebo and 78.9% with LDX; serious TEAE rates were 4.2 and 2.8%. In this trial, LDX augmentation significantly improved executive dysfunction and depressive symptoms in participants with mild MDD. The safety profile of LDX was consistent with prior studies in adults with attention-deficit/hyperactivity disorder.

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