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Concepts of cognitive control (CC) and executive function (EF) are defined in terms of their relationships with goal-directed behavior versus habits and controlled versus automatic processing, and related to the functions of the prefrontal cortex (PFC) and related regions and networks. A psychometric approach shows unity and diversity in CC constructs, with 3 components in the most commonly studied constructs: general or common CC and components specific to mental set shifting and working memory updating. These constructs are considered against the cellular and systems neurobiology of PFC and what is known of its functional neuroanatomical or network organization based on lesioning, neurochemical, and neuroimaging approaches across species. CC is also considered in the context of motivation, as “cool” and “hot” forms. Its Common CC component is shown to be distinct from general intelligence (g) and closely related to response inhibition. Impairments in CC are considered as possible causes of psychiatric symptoms and consequences of disorders. The relationships of CC with the general factor of psychopathology (p) and dimensional constructs such as impulsivity in large scale developmental and adult populations are considered, as well as implications for genetic studies and RDoC approaches to psychiatric classification.

Key Points Although also being a characteristic of normal behaviour, excessive impulsivity is an important symptom of several neuropsychiatric and neurological disorders, including addiction, attention-deficit hyperactivity disorder and Parkinson disease. However, impulsivity may comprise several apparently related forms that depend on distinct neuropsychological processes and neural systems. Of particular importance are interactions between frontostriatal systems and their neurochemical modulation, which are also providing new insights into the functions of these systems in behaviour. The psychological and neural basis of impulsivity can be studied in a mutually profitable way in experimental animals and in humans. Striking parallels can be observed in the underlying neurobehavioural systems, allowing both macro- and micro-definition of functional circuits. The dissection of impulsivity in this Review may represent a way in which complex behaviour relevant to psychiatric disorders can be broken down into its constituent parts, thus allowing for improved genetic understanding and more-precise treatments at the level of symptoms rather than according to categorical diagnoses of mental health disorders. Impulsivity comes in various forms, with some forms considered more or less advantageous than others. Dalley and Robbins review the different types of impulsivity and their underlying neural mechanisms, and comment on the applicability of measures of impulsivity in research into psychiatric disorders. The ability to make decisions and act quickly without hesitation can be advantageous in many settings. However, when persistently expressed, impulsive decisions and actions are considered risky, maladaptive and symptomatic of such diverse brain disorders as attention-deficit hyperactivity disorder, drug addiction and affective disorders. Over the past decade, rapid progress has been made in the identification of discrete neural networks that underlie different forms of impulsivity — from impaired response inhibition and risky decision making to a profound intolerance of delayed rewards. Herein, we review what is currently known about the neural and psychological mechanisms of impulsivity, and discuss the relevance and application of these new insights to various neuropsychiatric disorders.

Obsessive–compulsive disorder (OCD) has become a paradigmatic case of goal-directed dysfunction in psychiatry. In this article, we review the neurobiological evidence, historical and recent, that originally led to this supposition and continues to support a habit hypothesis of OCD. We will then discuss a number of recent studies that have directly tested this hypothesis, using behavioural experiments in patient populations. Based on this research evidence, which suggests that rather than goal-directed avoidance behaviours, compulsions in OCD may derive from manifestations of excessive habit formation, we present the details of a novel account of the functional relationship between these habits and the full symptom profile of the disorder. Borrowing from a cognitive dissonance framework, we propose that the irrational threat beliefs (obsessions) characteristic of OCD may be a consequence, rather than an instigator, of compulsive behaviour in these patients. This lays the foundation for a potential shift in both clinical and neuropsychological conceptualization of OCD and related disorders. This model may also prove relevant to other putative disorders of compulsivity, such as substance dependence, where the experience of ‘wanting’ drugs may be better understood as post hoc rationalizations of otherwise goal-insensitive, stimulus-driven behaviour.

Hemispheric lateralization constitutes a core architectural principle of human brain organization underlying cognition, often argued to represent a stable, trait-like feature. However, emerging evidence underlines the inherently dynamic nature of brain networks, in which time-resolved alterations in functional lateralization remain uncharted. Integrating dynamic network approaches with the concept of hemispheric laterality, we map the spatiotemporal architecture of whole-brain lateralization in a large sample of high-quality resting-state fMRI data ( N = 991, Human Connectome Project). We reveal distinct laterality dynamics across lower-order sensorimotor systems and higher-order associative networks. Specifically, we expose 2 aspects of the laterality dynamics: laterality fluctuations (LF), defined as the standard deviation of laterality time series, and laterality reversal (LR), referring to the number of zero crossings in laterality time series. These 2 measures are associated with moderate and extreme changes in laterality over time, respectively. While LF depict positive association with language function and cognitive flexibility, LR shows a negative association with the same cognitive abilities. These opposing interactions indicate a dynamic balance between intra and interhemispheric communication, i.e., segregation and integration of information across hemispheres. Furthermore, in their time-resolved laterality index, the default mode and language networks correlate negatively with visual/sensorimotor and attention networks, which are linked to better cognitive abilities. Finally, the laterality dynamics are associated with functional connectivity changes of higher-order brain networks and correlate with regional metabolism and structural connectivity. Our results provide insights into the adaptive nature of the lateralized brain and new perspectives for future studies of human cognition, genetics, and brain disorders.

Cognitive impairment in patients with Parkinson's disease is gaining increased clinical significance owing to the relative success of therapeutic approaches to the motor symptoms of this disorder. Early investigations contributed to the concept of subcortical dementia associated with bradyphrenia and cognitive rigidity. For cognition in parkinsonian disorders, this notion developed into the concept of mild cognitive impairment and fronto-executive dysfunction in particular, driven mainly by dopaminergic dysmodulation and manifesting as deficits in flexibility, planning, working memory, and reinforcement learning. However, patients with Parkinson's disease could also develop a syndrome of dementia that might depend on non-dopaminergic, cholinergic cortical dysfunction. Recent findings, supplemented by advances in neuroimaging and genetic research, reveal substantial heterogeneity in the range of cognitive deficits in patients with Parkinson's disease. Remediation and management prospects for these cognitive deficits are based on neuropharmacological and cognitive rehabilitation approaches.

Background Prognosis in Parkinson's disease (PD) remains poorly understood due to a lack of unbiased data on the natural history of treated PD. The CamPaIGN study has been the first to prospectively track disease evolution from diagnosis in an unselected population-representative incident cohort. We now report the 10-year follow-up data, focusing on three key irreversible milestones: postural instability (Hoehn and Yahr 3), dementia and death. Methods The cohort was collected between December 2000 and 2002. Those meeting diagnostic criteria (n=142) were followed-up until 1 January 2012. Clinical, neuropsychological and genetic testing were performed. Progression to key milestones was evaluated using Kaplan–Meier and Cox regression survival analyses. Results At 10 years, 55% had died, 68% had postural instability and 46% dementia. 23% had a good outcome at 10 years (surviving free of dementia/postural instability). Death rate was comparable with the UK population (standardised mortality ratio 1.29 (0.97–1.61)). Death certificates indicated PD was a substantial contributor in only 20%, with pneumonia being the commonest cause of death. Age, non-tremor-dominant motor phenotype and comorbidity predicted earlier postural instability. Baseline predictors of dementia were age, motor impairment, ‘posterior-cortical’ cognitive deficits and MAPT genotype. Conclusions (1) outlook in PD is heterogeneous, with most dying or developing dementia or postural instability by 10 years from diagnosis, but a quarter still doing well, with preserved mobility and intact cognition; (2) death is not directly related to PD in the majority; (3) baseline clinical and genetic variables are predictive of outcome and may be helpful in selecting patients for clinical trials.

Research into the heterogeneous nature of cognitive impairment documented in patients with Parkinson’s disease (PD) has focused on disentangling deficits that vary between individuals, evolve and respond differentially to pharmacological treatments, and relate differentially to PD dementia (PDD). We summarise studies conducted in our laboratory over the last 2 decades, outlining the incremental development of our hypotheses, the starting point for which is our early work on executive deficits mirroring fronto-striatal dysfunction. We present subsequent findings linking these deficits to a model of dopaminergic function that conforms to an inverted curvilinear function. We review studies that investigated the range of dopamine-independent attentional and visuospatial memory deficits seen in PD, demonstrating that abnormalities in these domains more accurately predict PDD. We conclude with an exposition of the dual syndrome hypothesis, which distinguishes between dopaminergically mediated fronto-striatal executive impairments and a dementia syndrome with distinctive prodromal visuospatial deficits in which cholinergic treatments offer some clinical benefits.

Aversive emotional reactions to real or imagined social harms infuse moral judgment and motivate prosocial behavior. Here, we show that the neurotransmitter serotonin directly alters both moral judgment and behavior through increasing subjects' aversion to personally harming others. We enhanced serotonin in healthy volunteers with citalopram (a selective serotonin reuptake inhibitor) and contrasted its effects with both a pharmacological control treatment and a placebo on tests of moral judgment and behavior. We measured the drugs' effects on moral judgment in a set of moral 'dilemmas' pitting utilitarian outcomes (e.g., saving five lives) against highly aversive harmful actions (e.g., killing an innocent person). Enhancing serotonin made subjects more likely to judge harmful actions as forbidden, but only in cases where harms were emotionally salient. This harm-avoidant bias after citalopram was also evident in behavior during the ultimatum game, in which subjects decide to accept or reject fair or unfair monetary offers from another player. Rejecting unfair offers enforces a fairness norm but also harms the other player financially. Enhancing serotonin made subjects less likely to reject unfair offers. Furthermore, the prosocial effects of citalopram varied as a function of trait empathy. Individuals high in trait empathy showed stronger effects of citalopram on moral judgment and behavior than individuals low in trait empathy. Together, these findings provide unique evidence that serotonin could promote prosocial behavior by enhancing harm aversion, a prosocial sentiment that directly affects both moral judgment and moral behavior.

We hypothesize that drug addiction can be viewed as the endpoint of a series of transitions from initial voluntary drug use through the loss of control over this behaviour, such that it becomes habitual and ultimately compulsive. We describe evidence that the switch from controlled to compulsive drug seeking represents a transition at the neural level from prefrontal cortical to striatal control over drug-seeking and drug-taking behaviours as well as a progression from ventral to more dorsal domains of the striatum, mediated by its serially interconnecting dopaminergic circuitry. These neural transitions depend upon the neuroplasticity induced by chronic self-administration of drugs in both cortical and striatal structures, including long-lasting changes that are the consequence of toxic drug effects. We further summarize evidence showing that impulsivity, a spontaneously occurring behavioural tendency in outbred rats that is associated with low dopamine D2/3 receptors in the nucleus accumbens, predicts both the propensity to escalate cocaine intake and the switch to compulsive drug seeking and addiction.