This review focuses on eye movement control by the cerebral cortex, mainly in humans. Data have emerged based on the important contribution of recent techniques such as transcranial magnetic stimulation and functional magnetic resonance imaging, which provide complementary results to those of the classical lesion and electrical stimulation studies. The location of the human frontal eye field and its role in pursuit eye movement control were recently detailed. Cumulative evidence for the role of the dorsolateral prefrontal cortex in unwanted reflexive saccade inhibition, short-term spatial memory and prediction suggests that this area controls decisional processes governing ocular motor behaviour. The organization of spatial memory in the dorsolateral prefrontal cortex (short-term), the parahippocampal cortex (medium-term) and the hippocampal formation (long-term) is also reviewed with the results of recent transcranial magnetic stimulation studies. The relatively complicated anatomy of the posterior parietal cortex in humans is briefly described followed by some additional results concerning the location of the parietal eye field - within the posterior half of the intraparietal sulcus - and its role in visuo-spatial integration and attention. The other areas involved in spatial attention are also examined in the light of several recent contributing reports. Lastly, there are also new functional magnetic resonance imaging findings concerning the posterior cingulate cortex, which appears to be mainly involved in the control of externally guided eye movements and attentional mechanisms. Many new findings on the organization of saccades and pursuit eye movements at the cortical level have recently been reported. Furthermore, eye movements are increasingly used as a tool to elucidate relatively complex neuropsychological processes such as attention, spatial memory, motivation and decisional processes, and a considerable number of reports dealing with these questions have been observed.

Humankind faces a plethora of environmental problems, many of which are directly influenced by individual human behaviour. To better understand pro-environmental behaviour, we here try to identify interindividual markers that explain variance in the frequency of every-day pro-environmental behaviour. So far, research on this topic has mainly relied on subjective self-report measures and has yielded mixed results. In this study, we applied a neural trait approach to assess stable, objective individual differences. Using source-localised electroencephalography, we measured cortical activation at rest and combined our neural task-independent data with an ecologically valid assessment of everyday pro-environmental behaviour. We find whole-brain-corrected evidence that task-independent baseline activation in the right lateral prefrontal cortex, a brain area known to be involved in cognitive control and self-control processes, explains individual differences in pro-environmental behaviour. The higher the cortical baseline activation in this area, the higher the frequency of everyday pro-environmental behaviour. Implications for the promotion of pro-environmental behaviour are discussed.

Phantom limbs are traditionally conceptualized as the phenomenal persistence of a body part after deafferentation. Previous clinical observations of subjects with phantoms of congenitally absent limbs are not compatible with this view, but, in the absence of experimental work, the neural basis of such “aplasic phantoms” has remained enigmatic. In this paper, we report a series of behavioral, imaging, and neurophysiological experiments with a university-educated woman born without forearms and legs, who experiences vivid phantom sensations of all four limbs. Visuokinesthetic integration of tachistoscopically presented drawings of hands and feet indicated an intact somatic representation of these body parts. Functional magnetic resonance imaging of phantom hand movements showed no activation of primary sensorimotor areas, but of premotor and parietal cortex bilaterally. Movements of the existing upper arms produced activation expanding into the hand territories deprived of afferences and efferences. Transcranial magnetic stimulation of the sensorimotor cortex consistently elicited phantom sensations in the contralateral fingers and hand. In addition, premotor and parietal stimulation evoked similar phantom sensations, albeit in the absence of motor evoked potentials in the stump. These data indicate that body parts that have never been physically developed can be represented in sensory and motor cortical areas. Both genetic and epigenetic factors, such as the habitual observation of other people moving their limbs, may contribute to the conscious experience of aplasic phantoms.

Neurodegeneration in Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) affect cortical and subcortical networks involved in saccade generation. We therefore expected impairments in saccade performance in both disorders. In order to improve the pathophysiological understanding and to investigate the usefulness of saccades for differential diagnosis, saccades were tested in age- and education-matched patients with PDD (n = 20) and DLB (n = 20), Alzheimer's disease (n = 22) and Parkinson's disease (n = 24), and controls (n = 24). Reflexive (gap, overlap) and complex saccades (prediction, decision and antisaccade) were tested with electro-oculography. PDD and DLB patients had similar impairment in all tasks (P > 0.05, not significant). Compared with controls, they were impaired in both reflexive saccade execution (gap and overlap latencies, P < 0.0001; gains, P < 0.004) and complex saccade performance (target prediction, P < 0.0001; error decisions, P < 0.003; error antisaccades: P < 0.0001). Patients with Alzheimer's disease were only impaired in complex saccade performance (Alzheimer's disease versus controls, target prediction P < 0.001, error decisions P < 0.0001, error antisaccades P < 0.0001), but not reflexive saccade execution (for all, P > 0.05). Patients with Parkinson's disease had, compared with controls, similar complex saccade performance (for all, P > 0.05) and only minimal impairment in reflexive tasks, i.e. hypometric gain in the gap task (P = 0.04). Impaired saccade execution in reflexive tasks allowed discrimination between DLB versus Alzheimer's disease (sensitivity ≥60%, specificity ≥77%) and between PDD versus Parkinson's disease (sensitivity ≥60%, specificity ≥88%) when ±1.5 standard deviations was used for group discrimination. We conclude that impairments in reflexive saccades may be helpful for differential diagnosis and are minimal when either cortical (Alzheimer's disease) or nigrostriatal neurodegeneration (Parkinson's disease) exists solely; however, they become prominent with combined cortical and subcortical neurodegeneration in PDD and DLB. The similarities in saccade performance in PDD and DLB underline the overlap between these conditions and underscore differences from Alzheimer's disease and Parkinson's disease.