ORCID Profile
0000-0002-6850-9255
Current Organisation
University of Oxford
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Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-2006
DOI: 10.1097/01.WCO.0000198101.87670.7E
Abstract: Disorders of spatial awareness and balance following stroke are common but often under-diagnosed. They lead to poor outcome and frequently coexist. Here we focus on recent progress in the understanding of the mechanisms underlying these disorders and potential therapeutic advances. Right-hemisphere networks are important for both spatial attention and postural awareness. Neglect patients show multiple oculomotor impairments including reduced saccade litude and difficulty retaining spatial locations across saccades. There has been controversy regarding the brain regions associated with neglect, although most studies show the right inferior parietal lobe to be crucial and new imaging modalities have provided insight into neglect caused by subcortical stroke. The 'pusher syndrome' is a poorly understood balance disorder where patients push towards their paretic side, resulting in falls. It may involve impairment of subjective verticality but experimental studies have reported erse findings. Advances in treatment for neglect include the successful use of prism adaptation and pilot data suggesting noradrenergic stimulation may improve search in selected patients. New experimental techniques have provided insight into the debilitating disorders of spatial and postural awareness that often follow stroke. There are currently no widely used therapies for neglect but both new behavioural techniques and pharmacological methods are promising.
Publisher: Public Library of Science (PLoS)
Date: 24-02-2017
Publisher: Oxford University Press (OUP)
Date: 08-2000
Abstract: Left neglect after right-hemisphere damage may involve perceptual and/or motor impairments. Here we discuss the limitations of previous attempts to separate these components, and introduce a new method. Six neglect patients (three with right inferior parietal lesions and three with right inferior frontal lesions) moved their right hand to a target light, which appeared unpredictably on either the left or the right of central fixation. The target appeared alone or with a distractor light in the opposite hemifield. Any directional motoric bias was measured by comparing reaches from a central start position with those for the same visual displays, but starting from the left of both possible targets (thus requiring only rightward reaches) or from the right (requiring only leftward reaches). All patients were slower to initiate reaches to left than right targets from a central start, which could reflect perceptual and/or motor biases. Critically, in the parietal neglect group only, initiation speed for left targets improved when a rightward reach was required to these (from a left start) rather than a leftward reach. This suggests a deficit in programming leftward movements into left hemispace, in addition to any visual impairment, for parietal neglect. A control task confirmed that this effect of start position was due to the associated change in reach direction and not to afferent inputs from the hand as it rested at the start position. Frontal neglect patients were slow to execute reaches to left targets, regardless of movement direction. Right visual distractors slowed visual reaction times to left targets more than vice versa in frontal neglect patients, and likewise for reach execution times in parietal neglect patients, suggesting that visual distractors on the neglected side have less impact. Distractor effects were unaffected by start position in the frontal neglect group (suggesting a perceptual basis), but distractors slowed reach initiation in the parietal neglect group only from left and central starts. Taken together, these findings demonstrate a directional motor component to parietal but not frontal neglect, and suggest that in man the inferior parietal lobe plays a role not only in perception but also in the programming of selective reaches. These conclusions are related to recent single-unit data from the monkey parietal lobe.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 29-05-2006
Publisher: Public Library of Science (PLoS)
Date: 14-07-2022
DOI: 10.1371/JOURNAL.PMED.1004039
Abstract: Brain iron deposition has been linked to several neurodegenerative conditions and reported in alcohol dependence. Whether iron accumulation occurs in moderate drinkers is unknown. Our objectives were to investigate evidence in support of causal relationships between alcohol consumption and brain iron levels and to examine whether higher brain iron represents a potential pathway to alcohol-related cognitive deficits. Observational associations between brain iron markers and alcohol consumption ( n = 20,729 UK Biobank participants) were compared with associations with genetically predicted alcohol intake and alcohol use disorder from 2-s le mendelian randomization (MR). Alcohol intake was self-reported via a touchscreen questionnaire at baseline (2006 to 2010). Participants with complete data were included. Multiorgan susceptibility-weighted magnetic resonance imaging (9.60 ± 1.10 years after baseline) was used to ascertain iron content of each brain region (quantitative susceptibility mapping (QSM) and T2*) and liver tissues (T2*), a marker of systemic iron. Main outcomes were susceptibility (χ) and T2*, measures used as indices of iron deposition. Brain regions of interest included putamen, caudate, hippoc i, thalami, and substantia nigra. Potential pathways to alcohol-related iron brain accumulation through elevated systemic iron stores (liver) were explored in causal mediation analysis. Cognition was assessed at the scan and in online follow-up (5.82 ± 0.86 years after baseline). Executive function was assessed with the trail-making test, fluid intelligence with puzzle tasks, and reaction time by a task based on the “Snap” card game. Mean age was 54.8 ± 7.4 years and 48.6% were female. Weekly alcohol consumption was 17.7 ± 15.9 units and never drinkers comprised 2.7% of the s le. Alcohol consumption was associated with markers of higher iron (χ) in putamen (β = 0.08 standard deviation (SD) [95% confidence interval (CI) 0.06 to 0.09], p 0.001), caudate (β = 0.05 [0.04 to 0.07], p 0.001), and substantia nigra (β = 0.03 [0.02 to 0.05], p 0.001) and lower iron in the thalami (β = −0.06 [−0.07 to −0.04], p 0.001). Quintile-based analyses found these associations in those consuming units (56 g) alcohol weekly. MR analyses provided weak evidence these relationships are causal. Genetically predicted alcoholic drinks weekly positively associated with putamen and hippoc us susceptibility however, these associations did not survive multiple testing corrections. Weak evidence for a causal relationship between genetically predicted alcohol use disorder and higher putamen susceptibility was observed however, this was not robust to multiple comparisons correction. Genetically predicted alcohol use disorder was associated with serum iron and transferrin saturation. Elevated liver iron was observed at just units (88 g) alcohol weekly c.f. units (56 g). Systemic iron levels partially mediated associations of alcohol intake with brain iron. Markers of higher basal ganglia iron associated with slower executive function, lower fluid intelligence, and slower reaction times. The main limitations of the study include that χ and T2* can reflect changes in myelin as well as iron, alcohol use was self-reported, and MR estimates can be influenced by genetic pleiotropy. To the best of our knowledge, this study represents the largest investigation of moderate alcohol consumption and iron homeostasis to date. Alcohol consumption above 7 units weekly associated with higher brain iron. Iron accumulation represents a potential mechanism for alcohol-related cognitive decline.
Publisher: Wiley
Date: 22-12-2006
DOI: 10.1002/ANA.20701
Abstract: Visual neglect after stroke is often associated with a failure to explore contralesional space. Here, we show that guanfacine, a noradrenergic agonist that modulates dorsolateral prefrontal cortex, improves leftward space exploration in selected right-hemisphere patients with neglect. The positive effects of guanfacine were associated with extended ability to maintain attention on task. The results suggest that neuropharmacological targeting of intact frontal areas might be one way to enhance cognitive function after damage to posterior brain regions in selected in iduals.
Publisher: Springer Science and Business Media LLC
Date: 03-1998
DOI: 10.1038/32413
Abstract: The exact role of the parietal lobe in spatial cognition is controversial. One influential hypothesis proposes that it subserves spatial perception, whereas other accounts suggest that its primary role is to direct spatial movement. For humans, it has been suggested that these functions may be ided between inferior and superior parietal lobes, respectively. In apparent support of a purely perceptual function for the inferior parietal lobe (IPL), patients with lesions to this structure, particularly in the right hemisphere, exhibit unilateral spatial neglect (deficient awareness for the side of space opposite to that of their lesion). Here we show that patients with right IPL lesions also have a specific difficulty in initiating leftward movements towards visual targets on the left side of space. This motor impairment was not found in neglect patients with frontal lesions, contrary to previous proposals that motor aspects of neglect are particularly associated with anterior damage. Our results suggest that the human IPL operates as a sensorimotor interface, rather than subserving only perceptual functions.
Publisher: Elsevier BV
Date: 07-2013
Publisher: Frontiers Media SA
Date: 06-11-2014
Publisher: Society for Neuroscience
Date: 31-12-2013
DOI: 10.1523/JNEUROSCI.2899-13.2014
Abstract: Emerging evidence suggests that items held in working memory (WM) might not all be in the same representational state. One item might be privileged over others, making it more accessible and thereby recalled with greater precision. Here, using transcranial magnetic stimulation (TMS), we provide causal evidence in human participants that items in WM are differentially susceptible to disruptive TMS, depending on their state, determined either by task relevance or serial position. Across two experiments, we applied TMS to area MT+ during the WM retention of two motion directions. In Experiment 1, we used an “incidental cue” to bring one of the two targets into a privileged state. In Experiment 2, we presented the targets sequentially so that the last item was in a privileged state by virtue of recency. In both experiments, recall precision of motion direction was differentially affected by TMS, depending on the state of the memory target at the time of disruption. Privileged items were recalled with less precision, whereas nonprivileged items were recalled with higher precision. Thus, only the privileged item was susceptible to disruptive TMS over MT+. By contrast, precision of the nonprivileged item improved either directly because of facilitation by TMS or indirectly through reduced interference from the privileged item. Our results provide a unique line of evidence, as revealed by TMS over a posterior sensory brain region, for at least two different states of item representation in WM.
Publisher: Oxford University Press (OUP)
Date: 19-12-2020
DOI: 10.1093/BRAINCOMMS/FCAA219
Abstract: Female sex, age and carriage of the apolipoprotein E e4 allele are the greatest risk factors for sporadic Alzheimer’s disease. The hippoc us has a selective vulnerability to atrophy in ageing that may be accelerated in Alzheimer’s disease, including in those with increased genetic risk of the disease, years before onset. Within the hippoc al complex, subfields represent cytoarchitectonic and connectivity based isions. Variation in global hippoc al and subfield volume associated with sex, age and apolipoprotein E e4 status has the potential to provide a sensitive biomarker of future vulnerability to Alzheimer’s disease. Here, we examined non-linear age, sex and apolipoprotein E effects, and their interactions, on hippoc al and subfield volumes across several decades spanning mid-life to old age in 36 653 healthy ageing in iduals. FMRIB Software Library derived estimates of total hippoc al volume and Freesurfer derived estimates hippoc al subfield volume were estimated. A model-free, sliding-window approach was implemented that does not assume a linear relationship between age and subfield volume. The annualized percentage of subfield volume change was calculated to investigate associations with age, sex and apolipoprotein E e4 homozygosity. Hippoc al volume showed a marked reduction in apolipoprotein E e4/e4 female carriers after age 65. Volume was lower in homozygous e4 in iduals in specific subfields including the presubiculum, subiculum head, cornu ammonis 1 body, cornu ammonis 3 head and cornu ammonis 4. Nearby brain structures in medial temporal and subcortical regions did not show the same age, sex and apolipoprotein E interactions, suggesting selective vulnerability of the hippoc us and its subfields. The findings demonstrate that in healthy ageing, two factors—female sex and apolipoprotein E e4 status—confer selective vulnerability of specific hippoc al subfields to volume loss.
Publisher: MIT Press - Journals
Date: 06-2005
Abstract: We examined priming of visual search by repeated target location or color in two patients with left visual neglect and extinction, following strokes centered on the right inferior parietal lobe. Both patients, like the healthy controls we tested, showed intact priming, with performance speeded when either the location or color of a singleton target was repeated over successive trials in a standard search condition (Experiment 1). This was observed both from and to targets on the contralesional (left) side. Moreover, priming of search was still observed even when a return of fixation back to display-center was required between successive trials (Experiment 2). When briefer displays were used (Experiment 3), the patients often failed to detect left targets. This situation revealed an important dissociation: Whereas location priming only arose from preceding left targets that had been consciously detected, color priming (possibly arising within the intact ventral stream) did not depend on awareness of the preceding target. There was considerable color priming from missed targets. These findings demonstrate relatively intact priming of visual search by color and location in patients with right parietal damage, and also reveal that location priming may differ from color priming in requiring awareness.
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 07-09-2011
DOI: 10.1167/11.10.1
Abstract: It was recently shown that expert face perception relies on the extraction of horizontally oriented visual cues. Picture-plane inversion was found to eliminate horizontal, suggesting that this tuning contributes to the specificity of face processing. The present experiments sought to determine the spatial frequency (SF) scales supporting the horizontal tuning of face perception. Participants were instructed to match upright and inverted faces that were filtered both in the frequency and orientation domains. Faces in a pair contained horizontal or vertical ranges of information in low, middle, or high SF (LSF, MSF, or HSF). Our findings confirm that upright (but not inverted) face perception is tuned to horizontal orientation. Horizontal tuning was the most robust in the MSF range, next in the HSF range, and absent in the LSF range. Moreover, face inversion selectively disrupted the ability to process horizontal information in MSF and HSF ranges. This finding was replicated even when task difficulty was equated across orientation and SF at upright orientation. Our findings suggest that upright face perception is tuned to horizontally oriented face information carried by intermediate and high SF bands. They further indicate that inversion alters the s ling of face information both in the orientation and SF domains.
Publisher: Oxford University Press (OUP)
Date: 18-03-2021
Abstract: Patients with small vessel cerebrovascular disease frequently suffer from apathy, a debilitating neuropsychiatric syndrome, the underlying mechanisms of which remain to be established. Here we investigated the hypothesis that apathy is associated with disrupted decision making in effort-based decision making, and that these alterations are associated with abnormalities in the white matter network connecting brain regions that underpin such decisions. Eighty-two patients with MRI evidence of small vessel disease were assessed using a behavioural paradigm as well as diffusion weighted MRI. The decision-making task involved accepting or rejecting monetary rewards in return for performing different levels of physical effort (hand grip force). Choice data and reaction times were integrated into a drift diffusion model that framed decisions to accept or reject offers as stochastic processes approaching a decision boundary with a particular drift rate. Tract-based spatial statistics were used to assess the relationship between white matter tract integrity and apathy, while accounting for depression. Overall, patients with apathy accepted significantly fewer offers on this decision-making task. Notably, while apathetic patients were less responsive to low rewards, they were also significantly averse to investing in high effort. Significant reductions in white matter integrity were observed to be specifically related to apathy, but not to depression. These included pathways connecting brain regions previously implicated in effort-based decision making in healthy people. The drift rate to decision parameter was significantly associated with both apathy and altered white matter tracts, suggesting that both brain and behavioural changes in apathy are associated with this single parameter. On the other hand, depression was associated with an increase in the decision boundary, consistent with an increase in the amount of evidence required prior to making a decision. These findings demonstrate altered effort-based decision making for reward in apathy, and also highlight dissociable mechanisms underlying apathy and depression in small vessel disease. They provide clear potential brain and behavioural targets for future therapeutic interventions, as well as modelling parameters that can be used to measure the effects of treatment at the behavioural level.
Publisher: Elsevier BV
Date: 2007
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2004
DOI: 10.1097/00001756-200410050-00009
Abstract: Recent attention research suggests that factors other than low-level sensory processes modulate perception across the visual field, with right parieto-temporal cortex playing a critical role in directing visual attention to peripheral events. Here we examine how different degrees of attentional demand at fixation dynamically affect detection of abrupt visual onsets in the periphery. In young healthy subjects, peripheral detection was significantly disrupted bilaterally when there was high attention demand at fixation. Right parieto-temporal lesioned patients, tested with a simplified version of task, demonstrated bilateral shrinkage of their available visual field, worse to the contralesional side, under increased attentional demand at fixation. These findings demonstrate how the effective visual field is dynamically modulated by the deployment of attention in health and, more severely, following right parieto-temporal damage.
Publisher: Springer Science and Business Media LLC
Date: 08-08-2018
DOI: 10.1038/S41598-018-30220-3
Abstract: Effort can be perceived both cognitively and physically, but the computational mechanisms underlying the motivation to invest effort in each domain remain unclear. In particular, it is unknown whether intensive physical training is associated with higher motivation specific to that domain, or whether it is accompanied by corresponding changes in cognitive motivation. Here, we tested a group of elite Oxford University rowers, and compared their behaviour to matched non-athletic controls. We trained participants on two tasks involving cognitive or physical effort. They then decided between a baseline low level of effort for low reward, versus higher levels of effort for higher rewards. Separate choices were made for the cognitive and physical tasks, which allowed us to computationally model motivation in each domain independently. As expected, athletes were willing to exert greater amounts of physical effort than non-athletes. Critically, however, the nature of cognitive effort-based decisions was different between groups, with a concave pattern of effort discounting for athletes but a convex pattern for non-athletes. These data suggest that the greater physical drive in athletes is accompanied by fundamentally different patterns of cognitive effort discounting, and suggests a complex relationship between motivation in the two domains.
Publisher: Psychology Press
Date: 11-2004
Publisher: Oxford University Press (OUP)
Date: 22-12-2004
DOI: 10.1093/BRAIN/AWH372
Abstract: It has been proposed recently that a deficit in keeping track of spatial locations may contribute to the severity of unilateral neglect in some right hemisphere stroke patients. However, performance on traditional spatial working memory (SWM) tasks (e.g. Corsi blocks) might be confounded by failure to encode leftward locations, rather than a true deficit of maintaining locations in SWM. Here we introduced new procedures for circumventing this to measure SWM capacity in neglect. In a first experiment, 20 right hemisphere stroke patients (10 with and 10 without neglect) were tested on a computerized vertical variant of the Corsi task. Sequences of spatial locations in a vertical column were displayed and participants had to tap out the remembered sequence on a touchscreen. Patients with left neglect were impaired on this vertical SWM task compared with all control groups. However, poor performance on this task (as for Corsi blocks) might involve impaired memory for stimulus sequence, or poor visuomotor control of manual responding, rather than reduced SWM capacity per se. A second experiment therefore employed a purer measure of vertical SWM. After the displayed sequence, a single location was now probed visually, with observers judging verbally (yes/no) if it had been in the preceding sequence. Hence order no longer mattered, and no spatial motor response was required. Again, the neglect group was impaired relative to all others, now with very little overlap between the performances of in idual neglect patients versus in iduals in control groups. Poor performance on the second task, which provides a purer measure of SWM capacity, correlated with severity of left neglect on cancellation tasks (but not on line bisection), consistent with recent proposals that SWM deficits can exacerbate left neglect on visual search tasks when present conjointly. Lesion anatomy indicated that neglect patients with a SWM deficit were most likely to have damage to parietal white matter, plus, in the second experiment, to the insula also. These findings demonstrate that an impairment in SWM capacity can contribute to the neglect syndrome in patients with stroke involving regions within the right parietal lobe and insula.
Publisher: Oxford University Press (OUP)
Date: 24-07-2016
DOI: 10.1093/BRAIN/AWW188
Publisher: Wiley
Date: 05-04-2018
DOI: 10.1111/JNP.12122
Publisher: Springer Science and Business Media LLC
Date: 07-09-2020
DOI: 10.1038/S41467-020-18201-5
Abstract: Healthy cognitive ageing is a societal and public health priority. Cerebrovascular risk factors increase the likelihood of dementia in older people but their impact on cognitive ageing in younger, healthy brains is less clear. The UK Biobank provides cognition and brain imaging measures in the largest population cohort studied to date. Here we show that cognitive abilities of healthy in iduals (N = 22,059) in this s le are detrimentally affected by cerebrovascular risk factors. Structural equation modelling revealed that cerebrovascular risk is associated with reduced cerebral grey matter and white matter integrity within a fronto-parietal brain network underlying executive function. Notably, higher systolic blood pressure was associated with worse executive cognitive function in mid-life (44–69 years), but not in late-life ( years). During mid-life this association did not occur in the systolic range of 110–140 mmHg. These findings suggest cerebrovascular risk factors impact on brain structure and cognitive function in healthy people.
Publisher: Oxford University Press (OUP)
Date: 21-01-2009
DOI: 10.1093/BRAIN/AWN350
Publisher: Springer Science and Business Media LLC
Date: 23-11-2022
DOI: 10.3758/S13415-022-01048-2
Abstract: While apathy is broadly defined as a loss of motivation, it is increasingly recognised as a multidimensional syndrome spanning executive, emotional, and initiation domains. Emotional apathy is purportedly driven by deficits in using socioemotional rewards to guide behaviour, yet the link between these symptoms and reward processing, and their common neural correlates, has not been directly examined. Sixty-four patients (33 behavioural-variant frontotemporal dementia, 14 Alzheimer’s disease, 8 semantic dementia, 6 progressive nonfluent aphasia, 3 logopenic progressive aphasia) were classified into high (HEA n = 36) and low (LEA n = 28) emotional apathy groups based on emotional apathy subscale scores on the Dimensional Apathy Scale. Patients and age-matched healthy controls (n = 27) performed an instrumental reward learning task where they learned to associate cues with either social or monetary outcomes. HEA patients showed impaired learning on both the social and monetary reward conditions, relative to LEA patients ( p = 0.016) and controls ( p = 0.005). Conversely, the LEA group did not differ from controls ( p = 0.925). Importantly, multiple regression analyses indicated that social reward learning significantly predicted emotional apathy. Voxel-based morphometry analyses revealed that emotional apathy and social reward learning were both associated with orbitofrontal cortex, ventral striatum, and insula atrophy. Our results demonstrate a unique link between impaired social reward learning and emotional apathy in dementia and reveal a shared neurobiological basis. Greater understanding of these neurocognitive mechanisms of reward processing will help improve the identification of emotional apathy in dementia and inform the development of novel interventions to address these symptoms.
Publisher: BMJ
Date: 20-06-2010
Publisher: Elsevier
Date: 2016
DOI: 10.1016/BS.PBR.2016.05.007
Abstract: Disorders of diminished motivation, such as apathy, are common and prevalent across a wide range of medical conditions, including Parkinson's disease, Alzheimer's dementia, stroke, depression, and schizophrenia. Such disorders have a significant impact on morbidity and quality of life, yet their management lacks consensus and remains unsatisfactory. Here, we review laboratory and clinical evidence for the use of dopaminergic therapies in the treatment of apathy. Dopamine is a key neurotransmitter that regulates motivated decision making in humans and other species. A large corpus of evidence suggests that it plays an important role in promoting approach behavior by attributing incentive salience to reward stimuli, and facilitating the overcoming of effort costs. Furthermore, dopaminergic neurons innervate several frontostriatal structures that mediate reward-guided behavior. Based on these findings, there are a priori reasons for considering dopamine in the treatment of disorders of diminished motivation. We highlight key studies that have attempted to use dopamine to manage patients with apathy, and that collectively offer cautious evidence in favor of its efficacy. However, many of these studies are small, unblinded, and uncontrolled, and utilize subjective, questionnaire-based measures of apathy. Given the development of novel paradigms which are able to objectively dissect motivational dysfunction, we are now well positioned to quantify the effect of specific classes of dopaminergic medication on reward- and effort-based decision making in apathy. We anticipate that such paradigms will lay the foundation for future studies to evaluate new and existing treatments for disorders of motivation, using sensitive measures of apathy as primary quantifiable end points.
Publisher: Elsevier BV
Date: 08-2015
Publisher: Oxford University Press (OUP)
Date: 09-2003
DOI: 10.1093/BRAIN/AWG200
Publisher: Elsevier BV
Date: 05-2014
Publisher: Oxford University Press (OUP)
Date: 04-2004
DOI: 10.1093/BRAIN/AWH112
Publisher: Elsevier BV
Date: 06-2015
Publisher: BMJ
Date: 18-05-2006
Publisher: Elsevier BV
Date: 2004
DOI: 10.1016/S0010-9452(08)70163-1
Abstract: Both impaired spatial working memory (SWM) and unilateral neglect may follow damage to the right parietal lobe. We propose that impaired SWM can exacerbate visual neglect, due to failures in remembering locations that have already been searched. When combined with an attentional bias to the ipsilesional right side, such a SWM impairment should induce recursive search of ipsilesional locations. Here we studied a left neglect patient with a right temporoparietal haemorrhage. On a nonlateralised, purely vertical SWM task, he was impaired in retaining spatial locations. In a visual search task, his eye position was monitored while his spatial memory was probed. He recursively searched through right stimuli, re-fixating previously inspected items, and critically treated them as if they were new discoveries, consistent with the SWM deficit. When his recovery was tracked over several months, his SWM deficit and left neglect showed concurrent improvements. We argue that impaired SWM may be one important component of the visual neglect syndrome.
Publisher: Elsevier
Date: 2016
DOI: 10.1016/BS.PBR.2016.05.002
Abstract: Motivation can be characterized as a series of cost-benefit valuations, in which we weigh the amount of effort we are willing to expend (the cost of an action) in return for particular rewards (its benefits). Human motivation has traditionally been measured with self-report and questionnaire-based tools, but an inherent limitation of these methods is that they are unable to provide a mechanistic explanation of the processes underlying motivated behavior. A major goal of current research is to quantify motivation objectively with effort-based decision-making paradigms, by drawing on a rich literature from nonhuman animals. Here, we review this approach by considering the development of these paradigms in the laboratory setting over the last three decades, and their more recent translation to understanding choice behavior in humans. A strength of this effort-based approach to motivation is that it is capable of capturing the wide range of in idual differences, and offers the potential to dissect motivation into its component elements, thus providing the basis for more accurate taxonomic classifications. Clinically, modeling approaches might provide greater sensitivity and specificity to diagnosing disorders of motivation, for ex le, in being able to detect subclinical disorders of motivation, or distinguish a disorder of motivation from related but separate syndromes, such as depression. Despite the great potential in applying effort-based paradigms to index human motivation, we discuss several caveats to interpreting current and future studies, and the challenges in translating these approaches to the clinical setting.
Publisher: Oxford University Press (OUP)
Date: 24-05-2015
Publisher: Springer Science and Business Media LLC
Date: 21-12-2022
DOI: 10.1038/S41467-022-35321-2
Abstract: Medical imaging provides numerous insights into the subclinical changes that precede serious diseases such as heart disease and dementia. However, most imaging research either describes a single organ system or draws on clinical cohorts with small s le sizes. In this study, we use state-of-the-art multi-organ magnetic resonance imaging phenotypes to investigate cross-sectional relationships across the heart-brain-liver axis in 30,444 UK Biobank participants. Despite controlling for an extensive range of demographic and clinical covariates, we find significant associations between imaging-derived phenotypes of the heart (left ventricular structure, function and aortic distensibility), brain (brain volumes, white matter hyperintensities and white matter microstructure), and liver (liver fat, liver iron and fibroinflammation). Simultaneous three-organ modelling identifies differentially important pathways across the heart-brain-liver axis with evidence of both direct and indirect associations. This study describes a potentially cumulative burden of multiple-organ dysfunction and provides essential insight into multi-organ disease prevention.
Publisher: Oxford University Press (OUP)
Date: 04-2010
DOI: 10.1093/BRAIN/AWQ052
Abstract: Constructional apraxia refers to the inability of patients to copy accurately drawings or three-dimensional constructions. It is a common disorder after right parietal stroke, often persisting after initial problems such as visuospatial neglect have resolved. However, there has been very little experimental investigation regarding mechanisms that might contribute to the syndrome. Here, we examined whether a key deficit might be failure to integrate visual information correctly from one fixation to the next. Specifically, we tested whether this deficit might concern remapping of spatial locations across saccades. Right-hemisphere stroke patients with constructional apraxia were compared to patients without constructional problems and neurologically healthy controls. Participants judged whether a pattern shifted position (spatial task) or changed in pattern (non-spatial task) across two saccades, compared to a control condition with an equivalent delay but without intervening eye movements. Patients with constructional apraxia were found to be significantly impaired in position judgements with intervening saccades, particularly when the first saccade of the sequence was to the right. The importance of these remapping deficits in constructional apraxia was confirmed through a highly significant correlation between saccade task performance and constructional impairment on standard neuropsychological tasks. A second study revealed that even single saccades to the right can impair constructional apraxia patients' perception of location shifts. These data are consistent with the view that rightward eye movements result in loss of remembered spatial information from previous fixations, presumably due to constructional apraxia patients' damage to the right-hemisphere regions involved in remapping locations across saccades. These findings provide the first evidence for a deficit in remapping visual information across saccades underlying right-hemisphere constructional apraxia.
Publisher: Oxford University Press (OUP)
Date: 03-07-2012
DOI: 10.1093/BRAIN/AWS154
Publisher: Elsevier BV
Date: 11-2014
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Masud Husain.