The present review addresses the question of whether and how neuropsychological tests assessing cognition in attention-deficit/hyperactivity disorder (ADHD) can contribute to clinical and scientific issues concerning ADHD. Neuropsychological studies have shown various though inconsistent cognitive deficits in patients with ADHD. While patients with ADHD, at group level, may differ from healthy participants in regard to cognitive functioning, there is no distinct psychometric cognitive test or profile allowing an individual diagnosis of ADHD or the identification of subtypes according to DSM. Psychometric neuropsychological tests may provide a precise description of the cognitive problems in individual patients and offer specific information for individualized treatment planning. In addition, neuropsychological assessment may contribute to neuroscientific research by providing endophenotypes or biological markers of ADHD. Cognitive neuropsychological assessment appears to be at present of limited clinical use and confined to individual descriptions.

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Attention-deficit hyperactivity disorder (ADHD) is a common behavioral disorder in children and adolescents and may persist into adulthood. Insufficient nutritional supply of long-chain polyunsaturated fatty acids (LC-PUFAs) and other components including various minerals has been suggested to play a role in the development of ADHD symptoms. This review presents the evidence regarding the role of nutritional PUFA, zinc, iron, and magnesium supplements in the treatment of ADHD with a focus on the critical evaluation of the relevant literature published from 2014 to April 2016. The evaluation of therapeutic nutritional LC-PUFA supplementation in ADHD has shown mixed and inconclusive results and at best marginal beneficial effects. The benefits of PUFAs are much smaller than the effect sizes observed for traditional pharmacological treatments of ADHD. The effectiveness of PUFA supplements in reducing medication dosage has been suggested but needs to be confirmed. Zinc, iron, and magnesium supplementation may reduce ADHD symptoms in children with or at high risk of deficiencies in these minerals. However, convincing evidence in this regard is lacking.

The origin of ADHD is multifactorial and both the aetiology and pathophysiology of ADHD are as yet incompletely understood. The monoamine deficit hypothesis of ADHD postulates a dysbalance in the interaction of the neurotransmitters dopamine, noradrenaline and serotonin. Pathophysiological mechanisms involved in ADHD include alterations in fronto-striatal circuits. The currently proposed animal models of ADHD are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. Some evidence points to a genetic basis for ADHD which is likely to involve many genes of small individual effects. In summary, specific neurobiological substrates of ADHD are unknown and multiple genetic and environmental factors appear to act together to create a spectrum of neurobiological liability.

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