Deficits in the ability to draw objects, despite apparently intact perception and motor abilities, are defined as constructional apraxia. Constructional deficits, often diagnosed based on performance on copying complex figures, have been reported in a range of pathologies, perhaps reflecting the contribution of several underlying factors to poor figure drawing. The current study provides a comprehensive analysis of brain-behavior relationships in drawing disorders based on data from a large cohort of subacute stroke patients (n = 358) using whole-brain voxel-wise statistical analyses linked to behavioral measures from a complex figure copy task. We found that (i) overall poor performance on figure copying was associated with subcortical lesions (BG and thalamus), (ii) lateralized deficits with respect to the midline of the viewer were associated with lesions within the posterior parietal lobule, and (iii) spatial positioning errors across the entire figure were associated with lesions within visual processing areas (lingual gyrus and calcarine) and the insula. Furthermore, deficits in reproducing global aspects of form were associated with damage to the right middle temporal gyrus, whereas deficits in representing local features were linked to the left hemisphere lesions within calcarine cortex (extending into the cuneus and precuneus), the insula, and the TPJ. The current study provides strong evidence that impairments in separate cognitive mechanisms (e.g., spatial coding, attention, motor execution, and planning) linked to different brain lesions contribute to poor performance on complex figure copying tasks. The data support the argument that drawing depends on several cognitive processes operating via discrete neuronal networks and that constructional problems as well as hierarchical and spatial representation deficits contribute to poor figure copying.
Spatial working memory problems are frequently reported following brain damage within both left and right hemispheres but with the severity often being grater in individuals with right hemisphere lesions. Clinically, deficits in spatial working memory have also been noted in patients with visuospatial disorders such as unilateral neglect. Here, we examined neural substrates of short-term memory for spatial locations based on the Corsi Block tapping task and the relationship with the visuospatial deficits of neglect and extinction in a group of chronic neuropsychological patients. Principal Component Analysis (PCA) was used to distinguish shared and dissociate functional components. The neural substrates of spatial short-term memory deficits and the components identified by PCA were examined using whole brain voxel-based morphometry and tract-wise lesion deficits analyses. We found that bilateral lesions within occipital cortex (middle occipital gyrus) and right posterior parietal cortex, along with disconnection of the right parieto-temporal segment of arcuate fasciculus, were associated with low spatial memory span. A single component revealed by PCA accounted for over half of the variance and was linked to damage to right posterior brain regions (temporo-parietal junction, the inferior parietal lobule and middle temporal gyrus extending into middle occipital gyrus). We also found link to disconnections within several association pathways including the superior longitudinal fasciculus, arcuate fasciculus, inferior fronto-occipital fasciculus and inferior longitudinal fasciculus. These results indicate that different visuospatial deficits converge into a single component mapped within posterior parietal areas and fronto-parietal white matter pathways. Furthermore, the data presented here fit with the role of posterior parietal cortex/temporo-parietal junction in maintaining a map of salient locations in space, with Corsi Block performance being impaired when the spatial map is damaged.
People make faster familiarity decisions for their own face compared with a familiar other. Lesion studies diverge on whether this self-face prioritization (SFP) effect is associated with functional processes isolated in the left or right hemispheres. To assess both decreases (hypo-) and increases (hyper-) in SFP after brain lesion, we asked patients with chronic deficits to perform familiarity judgments to images of their own face, a familiar other, or unfamiliar faces. Of 30 patients, 7 showed hypo- and 6 showed hyper-self-bias effects, comparing responses with their own faces versus responses with a familiar other. Hyper-self-bias correlated with reduced executive control function and, at a neural level, this was associated with lesions to the left prefrontal and superior temporal cortices. In contrast, reduced self-prioritization was associated with damage to the right inferior temporal structures including the hippocampus and extending to the fusiform gyrus. In addition, lesions affecting fibers crossing the right temporal cortex, potentially disconnecting occipital-temporal from frontal regions, diminished the self-bias effect. The data highlight that self-prioritized face processing is linked to regions in the right hemisphere associated with face recognition memory and it also calls on executive processes in the left hemisphere that normally modulate self-prioritized attention.
Limited information processing capacity in the brain necessitates task prioritisation and subsequent adaptive behavioural strategies for the dual-task coordination of locomotion with severe concurrent cognitive loading. Commonly observed strategies include prioritisation of gait at the cost of reduced performance in the cognitive task. Alternatively alterations of gait parameters such as gait velocity have been reported presumably to free processing capacity for the benefit of performance in the cognitive task. The aim of this study was to describe the neuroanatomical correlates of adaptive behavioural strategies in cognitive-motor dual-tasking when the competition for information processing capacity is severe and may exceed individuals capacity limitations.
We examined the frequency and severity of visual versus tactile extinction based on data from a large group of sub-acute patients (n=454) with strokes affecting different vascular territories. After right hemisphere damage visual and tactile extinction were equally common. However, after left hemisphere damage tactile extinction was more common than visual. The frequency of extinction was significantly higher in patients with right compared to left hemisphere damage in both visual and tactile modalities but this held only for strokes affecting the MCA and PCA territories and not for strokes affecting other vascular territories. Furthermore, the severity of extinction did not differ as a function of either the stimulus modality (visual versus tactile), the affected hemisphere (left versus right) or the stroke territory (MCA, PCA or other vascular territories). We conclude that the frequency but not severity of extinction in both modalities relates to the side of damage (i.e. left versus right hemisphere) and the vascular territories affected by the stroke, and that left hemisphere dominance for motor control may link to the greater incidence of tactile than visual extinction after left hemisphere stroke. We discuss the implications of our findings for understanding hemispheric lateralization within visuospatial attention networks.
The default mode network (DMN) is one of the most studied resting-state networks, and is thought to be involved in the maintenance of consciousness within the alert human brain. Although many studies have examined the functional connectivity (FC) of the DMN, few have investigated its underlying structural connectivity (SC), or the relationship between the two. We investigated this question in fifteen healthy subjects, concentrating on connections to the precuneus/posterior cingulate cortex (PCC), commonly considered as the central node of the DMN. We used group independent component analysis (GICA) and seed-based correlation analysis of fMRI data to quantify FC, and streamline and probabilistic tractography to identify structural tracts from diffusion tensor imaging (DTI) data. We first assessed the presence of structural connections between the DMN regions identified with GICA. Of the 15 subjects, when using the probabilistic approach 15 (15) demonstrated connections between the PCC and mesial prefrontal cortex (mPFC), 11 (15) showed connections from the PCC to the right inferior parietal cortex (rIPC) and 8 (15) to the left IPC. Next, we assessed the strength of FC (magnitude of temporal correlation) and SC (mean fractional anisotropy of reconstructed tracts (streamline), number of super-threshold voxels within the mask region (probabilistic)). The lIPC had significantly reduced FC to the PCC compared to the mPFC and rIPC. No difference in SC strength between connections was found using the streamline approach. For the probabilistic approach, mPFC had significantly lower SC than both IPCs. The two measures of SC strength were significantly correlated, but not for all paired connections. Finally, we observed a significant correlation between SC and FC for both tractography approaches when data were pooled across PCC-lIPL, PCC-rIPL and PCC-mPFC connections, and for some individual paired connections. Our results suggest that the streamline approach is advantageous for characterising the connectivity of long white matter tracts (PCC-mPFC), whilst the probabilistic approach was more reliable at identifying PCC-IPC connections. The direct comparison of FC and SC indicated that pairs of nodes with stronger structural connections also had stronger functional connectivity, and that this was maintained with both tractography approaches. Whilst the definition of SC strength remains controversial, our results could be considered to provide some degree of validation for the measures of SC strength that we have used. Direct comparisons of SC and FC are necessary in order to understand the structural basis of functional connectivity, and to characterise and quantify the changes in the brains functional architecture that occur as a result of normal physiology or pathology.
In visual search, the detection of pop-out targets is facilitated when the target-defining dimension remains the same compared with when it changes across trials. We tested the brain regions necessary for these dimensional carry-over effects using a voxel-based morphometry study with brain-lesioned patients. Participants had to search for targets defined by either their colour (red or blue) or orientation (right- or left-tilted), and the target dimension either stayed the same or changed on consecutive trials. Twenty-five patients were categorized according to whether they showed an effect of dimensional change on search or not. The two groups did not differ with regard to their performance on several working memory tasks, and the dimensional carry-over effects were not correlated with working memory performance. With spatial, sustained attention and working memory deficits as well as lesion volume controlled, damage within the right inferior parietal lobule (the angular and supramarginal gyri) extending into the intraparietal sulcus was associated with an absence of dimensional carry-over (P < 0.001, cluster-level corrected for multiple comparisons). The data suggest that these regions of parietal cortex are necessary to implement attention shifting in the context of visual dimensional change.
Extinction is diagnosed when patients respond to a single contralesional item but fail to detect this item when an ipsilesional item is present concurrently. Extinction has been studied mainly in the visual modality but it occurs also in other sensory modalities (touch, audition) and hence can be considered a multisensory phenomenon. The functional and neuroanatomical relations between extinction in different modalities are poorly understood. Here, we used voxel-based mophometry (VBM) to examine the neuronal substrates of visual versus tactile extinction in a large group of sub-acute patients (n = 454) with strokes affecting different vascular territories. We found that extinction deficits in tactile and visual modalities were significantly correlated (r = 0.341; p < 0.01). Several lesions within the right hemisphere were linked to extinction including the inferior parietal lobule, the superior parietal lobule, the middle frontal and occipital gyri, while lesions involving the superior temporal gyrus, inferior temporal gyrus and putamen were associated with tactile extinction. Damage within the middle temporal gyrus and superior temporal sulcus was linked to both deficits. We conclude that extinction in different modalities emerges after damage to both common (supra-modal) and distinct (modality specific) brain regions, and that contrasting sites emerge after damage to different vascular territories. We discuss the implications for understanding extinction as a multisensory disorder.
Because of our limited processing capacity, different elements of the visual scene compete for the allocation of processing resources. One of the most striking deficits in visual selection is simultanagnosia, a rare neuropsychological condition characterized by impaired spatial awareness of more than one object at time. To decompose the neuroanatomical substrates of the syndrome and to gain insights into the structural and functional organization of visuospatial attention, we performed a systematic evaluation of lesion patterns in a group of simultanagnosic patients compared with patients with either (i) unilateral visuospatial deficits (neglect and/or extinction) or (ii) bilateral posterior lesions without visuospatial deficits, using overlap/subtraction analyses, estimation of lesion volume, and a lesion laterality index. We next used voxel-based morphometry to assess the link between different visuospatial deficits and gray matter and white matter (WM) damage. Lesion overlap/subtraction analyses, lesion laterality index, and voxel-based morphometry measures converged to indicate that bilateral parieto-occipital WM disconnections are both distinctive and necessary to create symptoms associated with simultanagnosia. We also found that bilateral gray matter damage within the middle frontal area (BA 46), cuneus, calacarine, and parieto-occipital fissure as well as right hemisphere parietal lesions within intraparietal and postcentral gyri were associated with simultanagnosia. Further analysis of the WM based on tractography revealed associations with bilateral damage to major pathways within the visuospatial attention network, including the superior longitudinal fasciculus, the inferior fronto-occipital fasciculus, and the inferior longitudinal fasciculus. We conclude that damage to the parieto-occipital regions and the intraparietal sulcus, together, with bilateral WM disconnections within the visuosptial attention network, contribute to poor visual processing of multiple objects and the loss of processing speed characteristic of simultanagnosia.
The present study examined the relations between the lesions linked to visual and tactile extinction (VE and TE), and those related to visual field defects and spatial neglect. Continuous variations in patients performance were used to assess the link between behavioural scores and integrity of both grey and white matter (GM and WM). We found both common and distinct neural substrates associated with extinction and neglect. Damage to angular and middle occipital gyri, superior temporal sulcus (STS) and insula were linked to VE. Lesions involving the supramarginal gyrus (SMG), intraparietal sulcus, middle frontal and superior temporal gyri (MFG and STG) were associated exclusively with spatial neglect. Lesions affecting the temporo-parietal junction (TPJ), the middle temporal region, middle frontal area (BA46) as well as the insula and putamen were linked to both spatial neglect and VE. Analysis of the relations between VE and TE highlighted the TPJ as the common site for both modalities. These findings suggest that the TPJ plays a general role in identifying salient events in the sensory environment across multiple modalities. Furthermore, WM analyses pointed to superior longitudinal fasciculus (SLF) as critical for interconnecting components of the visuospatial attention network. We demonstrated that functional disconnections resulting from SLF damage contribute to altered performance on attention tasks measuring not only neglect but also VE and TE. We propose that the SLF supports interactions between functionally specialized regions involved in attentional control across multiple sensory modalities.
Facial self-awareness is a basic human ability dependent on a distributed bilateral neural network and revealed through prioritized processing of our own over other faces. Using non-prosopagnosic patients we show, for the first time, that facial self-awareness can be fractionated into different component processes. Patients performed two face perception tasks. In a face orientation task, they judged whether their own or others faces were oriented to the left or right. In the cross experiment, they judged which horizontal or vertical element in a cross was relatively longer while ignoring a task-irrelevant face presented as background. The data indicate that impairments to a distinct task-based prioritization process (when faces had to be attended) were present after brain damage to right superior frontal gyrus, bilateral precuneus, and left middle temporal gyrus. In contrast, impairments to automatic prioritization processes (when faces had to be ignored) were associated only with left hemisphere damage (the cingulate gyrus, superior parietal lobe, and superior temporal gyrus). In addition, both automatic and task-based self-prioritizations were affected by damage to left supramarginal and angular gyrus. The results for the gray matter analyses also extended to the adjacent white matter fiber tracts including the inferior occipital-frontal fasciculus, cingulum, and optic radiation. The data provide the first empirical evidence for separate functional roles of the left and right hemispheres in different aspects of self-face perception and suggest distinct functional processes respectively for paying attention to and for ignoring self-related information.
Insights into the functional nature and neuroanatomy of spatial attention have come from research in neglect patients but to date many conflicting results have been reported. The novelty of the current study is that we used voxel-wise analyses based on information from segmented grey and white matter tissue combined with diffusion tensor imaging to decompose neural substrates of different neglect symptoms. Allocentric neglect was associated with damage to posterior cortical regions (posterior superior temporal sulcus, angular, middle temporal and middle occipital gyri). In contrast, egocentric neglect was associated with more anterior cortical damage (middle frontal, postcentral, supramarginal, and superior temporal gyri) and damage within subcortical structures. Damage to intraparietal sulcus (IPS) and the temporo-parietal junction (TPJ) was associated with both forms of neglect. Importantly, we showed that both disorders were associated with white matter lesions suggesting damage within long association and projection pathways such as the superior longitudinal, superior fronto-occipital, inferior longitudinal, and inferior fronto-occipital fascicule, thalamic radiation, and corona radiata. We conclude that distinct cortical regions control attention (a) across space (using an egocentric frame of reference) and (b) within objects (using an allocentric frame of reference), while common cortical regions (TPJ, IPS) and common white matter pathways support interactions across the different cortical regions.
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.
We investigated spatial and temporal deficits following brain injury using the temporal order judgement (TOJ) task. Patients judged the order in which two letters appeared to the left and right of fixation. We measured the extent of any spatial bias and the temporal resolution of the decision. Temporal and spatial deficits on the TOJ task were significantly correlated. The spatial bias on the TOJ task was also correlated with the spatial bias on a neglect task and with unilateral deficits on an extinction task, but not with extinction itself. These spatial deficits were all associated with damage to contralateral temporoparietal cortex. In contrast, the temporal resolution of TOJs was linked specifically to deficits in processing multiple stimuli on the neglect and extinction tasks and to damage to the right parietal lobe and the cerebellum. These data suggest that spatial and temporal deficits on the TOJ task reflect different underlying processes.
Unilateral visual neglect is commonly defined as impaired ability to attend to stimuli presented on the side of visual space contralateral to the brain lesion. However, behavioral analyses indicate that different neglect symptoms can dissociate. The neuroanatomy of the syndrome has been hotly debated. Some groups have argued that the syndrome is linked to posterior parietal cortex lesions, while others report damage within regions including the superior temporal gyrus, insula, and basal ganglia. Several recent neuroimaging studies provide evidence that heterogeneity in the behavioral symptoms of neglect can be matched by variations in the brain lesions, and that some of the discrepancies across earlier findings might have resulted from the use of different neuropsychological tests and/or varied measures within the same task for diagnosing neglect. In this paper, we review the evidence for dissociations between both the symptoms and the neural substrates of unilateral visual neglect, drawing on ALE (anatomic likelihood estimation) meta-analyses of lesion-symptom mapping studies. Specifically, we examine dissociations between neglect symptoms associated with impaired control of attention across space (in an egocentric frame of reference) and within objects (in an allocentric frame of reference). Results of ALE meta-analyses indicated that, while egocentric symptoms are associated with damage within perisylvian network (pre- and postcentral, supramarginal, and superior temporal gyri) and damage within sub-cortical structures, more posterior lesions including the angular, middle temporal, and middle occipital gyri are associated with allocentric symptoms. Furthermore, there was high concurrence in deficits associated with white matter lesions within long association (superior longitudinal, inferior fronto-occipital, and inferior longitudinal fasciculi) and projection (corona radiata and thalamic radiation) pathways, supporting a disconnection account of the syndrome. Using this evidence we argue that different forms of neglect link to both distinct and common patterns of gray and white matter lesions. The findings are discussed in terms of functional accounts of neglect and theoretical models based on computational studies of both normal and impaired attention functions.
Related JoVE Video
Journal of Visualized Experiments
What is Visualize?
JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.
How does it work?
We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.
Video X seems to be unrelated to Abstract Y...
In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.