Curiosity is often portrayed as a desirable feature of human faculty. However, curiosity may come at a cost that sometimes puts people in a harmful situation. Here, with a set of behavioural and neuroimaging experiments using stimuli that strongly trigger curiosity (e.g., magic tricks), we examined the psychological and neural mechanisms underlying the motivational effect of curiosity. We consistently demonstrated that across different samples, people were indeed willing to gamble, subjecting themselves to physical risks (i.e. electric shocks) in order to satisfy their curiosity for trivial knowledge that carries no apparent instrumental value. Also, this influence of curiosity shares common neural mechanisms with that of extrinsic incentives (i.e. hunger for food). In particular, we showed that acceptance (compared to rejection) of curiosity/incentive-driven gambles was accompanied by enhanced activity in the ventral striatum (when curiosity was elicited), which extended into the dorsal striatum (when participants made a decision).

We contrasted the neuroanatomical substrates of sub-acute and chronic visuospatial deficits associated with different aspects of unilateral neglect using computed tomography scans acquired as part of routine clinical diagnosis. Voxel-wise statistical analyses were conducted on a group of 160 stroke patients scanned at a sub-acute stage. Lesion-deficit relationships were assessed across the whole brain, separately for grey and white matter. We assessed lesions that were associated with behavioural performance (i) at a sub-acute stage (within 3 months of the stroke) and (ii) at a chronic stage (after 9 months post stroke). Allocentric and egocentric neglect symptoms at the sub-acute stage were associated with lesions to dissociated regions within the frontal lobe, amongst other regions. However the frontal lesions were not associated with neglect at the chronic stage. On the other hand, lesions in the angular gyrus were associated with persistent allocentric neglect. In contrast, lesions within the superior temporal gyrus extending into the supramarginal gyrus, as well as lesions within the basal ganglia and insula, were associated with persistent egocentric neglect. Damage within the temporo-parietal junction was associated with both types of neglect at the sub-acute stage and 9 months later. Furthermore, white matter disconnections resulting from damage along the superior longitudinal fasciculus were associated with both types of neglect and critically related to both sub-acute and chronic deficits. Finally, there was a significant difference in the lesion volume between patients who recovered from neglect and patients with chronic deficits. The findings presented provide evidence that (i) the lesion location and lesion size can be used to successfully predict the outcome of neglect based on clinical CT scans, (ii) lesion location alone can serve as a critical predictor for persistent neglect symptoms, (iii) wide spread lesions are associated with neglect symptoms at the sub-acute stage but only some of these are critical for predicting whether neglect will become a chronic disorder and (iv) the severity of behavioural symptoms can be a useful predictor of recovery in the absence of neuroimaging findings on clinical scans. We discuss the implications for understanding the symptoms of the neglect syndrome, the recovery of function and the use of clinical scans to predict outcome.

This study reports the validation of the Hong Kong version of Oxford Cognitive Screen (HK-OCS). Seventy Cantonese-speaking healthy individuals participated to establish normative data and 46 chronic stroke survivors were assessed using the HK-OCS, Albert's Test of Visual Neglect, short test of gestural production, and Hong Kong version of the following assessments: Western Aphasia Battery, MMSE, MoCA, Modified Barthel Index, and Lawton Instrumental Activities of Daily Living scale. The validity of the HK-OCS was appraised by the difference between the two participant groups. Neurologically unimpaired individuals performed significantly better than stroke survivors on the HK-OCS. Positive and significant correlations found between cognitive subtests in the HK-OCS and related assessments indicated good concurrent validity. Excellent intra-rater and inter-rater reliabilities, fair test-retest reliability, and acceptable internal consistency suggested that the HK-OCS had good reliability. Specific HK-OCS subtests including semantics, episodic memory, number writing, and orientation were the best predictors of functional outcomes.

Abstract:Objective: We examined the utility of the BCoS screen in discriminating cognitive profiles and recovery of function across stroke survivors. BCoS was designed for stroke-specific problems across 5 cognitive domains: controlled and spatial attention, language, memory, number processing and praxis. Methods: Based on specific inclusion criteria, this cross-section observational study analysed cognitive profiles of 657 sub-acute stroke patients, 331 of them reassessed at 9 months. Impairments on 32 measures were evaluated by comparison to 100 matched healthy controls.Measures of affect, apathy, and activities of daily living were also taken. Betweensubject group comparisons of mean performance scores and impairment rates, as well as within-subject examination of impairment rates over time were conducted. Logistic regressions and general linear modelling were used for multivariate analysis of domain level effects on outcomes. Results: Individuals with repeated stroke experienced significantly less cognitive recovery at 9 months than those with a first stroke (OR=6.18) despite similar initial level of cognitive performance. Individuals with left hemisphere lesions performed more poorly than those with right hemisphere lesions but both groups showed similar extent of recovery at 9 months (OR=0.62). BCoS also revealed lesion-side specific deficits as well as common areas of persistent problems. stroke-specific cognitive deficits. We validate the screen and then use it to predict functional recovery. We demonstrate differences in recovery for patients with first and second stroke, even when matched for their initial deficit. We also show how the cognitive profile for a patient, across several domains, helps to predict outcome. Response to Reviewers: Response to reviewers (comments are copied below and corresponding responses are followed by "-")Editor's comments 1) The imaging information was used as a method for inclusion and nothing else? -For the purpose of this paper, it is indeed used for inclusion of patients and categorisation of left lesion vs right lesion groups.2) Was the AES self or informant rated? -It was self rated. We have added this to the text.3) The use of "motivation" in the context of AES findings.-Thanks for your comment, we agree that we should adhere to the use of "apathy" to avoid confusion. We have amended the wordings accordingly.4) Patient effort to engage.-We have not formally measured the patients' effort in the assessment and therefore have included this as a limitation of the current study.5) Patient's ability to sustain attention for 30 mins as inclusion criteria.-This was based on clinical judgement of the treatment team in the research site whom we checked with as well as assessment by the researcher during the BCoS testing.Reviewer 1's comments Abstract 1) 2nd sentence: 5 'COGNITIVE?' domains -Added, thanks2) Talk about 'sub-acute' stroke -what does this mean exactly? How much time has passed since the stroke? 657 analysed, 331 reassessed at 9 months -half dropped out? Why so m...

We report a lesion–symptom mapping analysis of visual speech production deficits in a large group (280) of stroke patients at the sub-acute stage (<120 days post-stroke). Performance on object naming was evaluated alongside three other tests of visual speech production, namely sentence production to a picture, sentence reading and nonword reading. A principal component analysis was performed on all these tests' scores and revealed a ‘shared’ component that loaded across all the visual speech production tasks and a ‘unique’ component that isolated object naming from the other three tasks. Regions for the shared component were observed in the left fronto-temporal cortices, fusiform gyrus and bilateral visual cortices. Lesions in these regions linked to both poor object naming and impairment in general visual–speech production. On the other hand, the unique naming component was potentially associated with the bilateral anterior temporal poles, hippocampus and cerebellar areas. This is in line with the models proposing that object naming relies on a left-lateralised language dominant system that interacts with a bilateral anterior temporal network. Neuropsychological deficits in object naming can reflect both the increased demands specific to the task and the more general difficulties in language processing.