In order to characterise the overall clinical picture of chronic obstructive pulmonary disease (COPD) a better understanding of all relevant comorbidities is required. It is increasingly recognised that COPD is a multi-component disease, but little attention has been paid to its effects on cognitive function.Cognitive dysfunction is associated with increased mortality and disability; however, it remains poorly understood in COPD. This review examines mechanisms of injury and dysfunction to the brain and considers the methods used to evaluate cognition, and assembles evidence concerning the nature and level of cognitive impairment in COPD.Our main findings are: 1) there may be a pattern of cognitive dysfunction specific to COPD; 2) cognitive function is only mildly impaired in patients without hypoxaemia; 3) the incidence of cognitive dysfunction is higher in hypoxaemia; 4) hypoxaemia, hypercapnia, smoking and comorbidities (such as vascular disease) are unlikely to account for all of the cognitive dysfunction seen in COPD; 5) there is weak or no association between cognitive function and mood, fatigue or health status; 6) cognitive dysfunction may be associated with increased mortality and disability; and 7) there is limited evidence for a significant effect of treatment on cognitive function.

It has been proposed that two major axes, dominance and trustworthiness, characterize the social dimensions of face evaluation. Whether evaluation of faces on these social dimensions is restricted to conscious appraisal or happens at a preconscious level is unknown. Here we provide behavioral evidence that such preconscious evaluations exist and that they are likely to be interpretations arising from interactions between the face stimuli and observer-specific traits. Monocularly viewed faces that varied independently along two social dimensions of trust and dominance were rendered invisible by continuous flash suppression (CFS) when a flashing pattern was presented to the other eye. Participants pressed a button as soon as they saw the face emerge from suppression to indicate whether the previously hidden face was located slightly to the left or right of central fixation. Dominant and untrustworthy faces took significantly longer time to emerge (T2E) compared with neutral faces. A control experiment showed these findings could not reflect delayed motor responses to conscious faces. Finally, we showed that participants' self-reported propensity to trust was strongly predictive of untrust avoidance (i.e., difference in T2E for untrustworthy vs neutral faces) as well as dominance avoidance (i.e., difference in T2E for dominant vs neutral faces). Dominance avoidance was also correlated with submissive behavior. We suggest that such prolongation of suppression for threatening faces may result from a passive fear response, leading to slowed visual perception.

Background and AimsKIF1A-related disorders (KRD) were first described in 2011 and the phenotypic spectrum has subsequently expanded to encompass a range of central and peripheral nervous system involvement. Here we present a case series demonstrating the range of clinical, neurophysiological and radiological features which may occur in childhood-onset KRD. MethodsWe report on all the children and young people seen at a single large tertiary centre. Data was collected through a retrospective case-notes review. Results12 individuals from 10 families were identified. Eight different mutations were present, including four novel mutations. Two patients displayed a very severe phenotype including congenital contractures, severe spasticity and/or dystonia, dysautonomia, severe sensorimotor polyneuropathy and optic atrophy, significant white matter changes on brain MRI, respiratory insufficiency, and complete lack of neurodevelopmental progress. The remaining 10 patients represented a spectrum of severity with common features including a movement disorder with spasticity and/or dystonia, subtle features of dysautonomia, sensory axonal neuropathy, varying degrees of optic atrophy and of learning and/or behavioural difficulties, and subtle or absent -but sometimes progressive -changes in white matter on MRI. Epilepsy was common among the more severely-affected children. InterpretationThis case series demonstrates that KRD comprise a range of neurological disorders, with both the milder and the more severe forms combining central and peripheral (including autonomic) nervous system deficits.

Social cues conveyed by the human face, such as eye gaze direction, are evaluated even before they are consciously perceived. While there is substantial individual variability in such evaluation, its neural basis is unknown. Here we asked whether individual differences in preconscious evaluation of social face traits were associated with local variability in brain structure. Adult human participants (n = 36) monocularly viewed faces varying in dominance and trustworthiness, which were suppressed from awareness by a dynamic noise pattern shown to the other eye. The time taken for faces to emerge from suppression and become visible (t2e) was used as a measure of potency in competing for visual awareness. Both dominant and untrustworthy faces resulted in slower t2e than neutral faces, with substantial individual variability in these effects. Individual differences in t2e were correlated with gray matter volume in right insula for dominant faces, and with gray matter volume in medial prefrontal cortex, right temporoparietal junction and bilateral fusiform face area for untrustworthy faces. Thus, individual differences in preconscious social processing can be predicted from local brain structure, and separable correlates for facial dominance and untrustworthiness suggest distinct mechanisms of preconscious processing.