Lesions Of Posterior Parietal Cortex Research Articles

More (corrective) consecutive saccades after a lesion to the posterior parietal cortex.

To reach a target, primary saccades (S1s) are often followed by (corrective) consecutive saccades (S2, and potentially S3, S4, S5), which are based on retinal and extraretinal feedback. Processing these extraretinal signals was found to be significantly impaired by lesions to the posterior parietal cortex (PPC). Recent studies, however, added a more nuanced view to the role of the PPC, where patients with PPC lesions still used extraretinal signals for S2s and perceptual judgements (Fabius et al., 2020; Rath-Wilson & Guitton, 2015). Hence, it seems that a PPC lesion is not disrupting extraretinal processing per se. Yet, a lesion might still result in less reliable processing of extraretinal signals. Here, we investigated whether this lower reliability manifests as decreased or delayed S2 initiation. Patients with PPC lesions (n = 7) and controls (n = 26) performed a prosaccade task where the target either remained visible or was removed after S1 onset. When S1 is removed, accurate S2s (corrections of S1 error) rely solely on extraretinal signals. We analysed S2 quantity and timing using linear mixed-effects modelling and additive hazards analyses. Patients demonstrated slower S1 execution and lower S1 amplitudes than controls, but their S2s still compensated the S1 undershoot, also when they only relied on extraretinal information. Surprisingly, patients showed an increased amount of S2s. This deviation from control behaviour can be seen as suboptimal, but given the decreased accuracy of the primary saccade, it could be optimal for patients to employ more (corrective) consecutive saccades to overcome this inaccuracy.

Trans-saccadic memory after right parietal brain damage

IntroductionSpatial remapping, the process of updating information across eye movements, is an important mechanism for trans-saccadic perception. The right posterior parietal cortex (PPC) is a region that has been associated most strongly with spatial remapping. The aim of the project was to investigate the effect of damage to the right PPC on direction specific trans-saccadic memory. We compared trans-saccadic memory performance for central items that had to be remembered while making a left- versus rightward eye movement, or for items that were remapped within the left versus right visual field. MethodsWe included 9 stroke patients with unilateral right PPC lesions and 31 healthy control subjects. Participants memorized the location of a briefly presented item, had to make one saccade (either towards the left or right, or upward or downward), and subsequently had to decide in what direction the probe had shifted. We used a staircase to adjust task difficulty (i.e., the distance between the memory item and probe). Bayesian repeated measures ANOVAs were used to compare left versus right eye movements and items in the left versus right visual field. ResultsIn both conditions, patients with right PPC damage showed worse trans-saccadic memory performance compared to healthy control subjects (for the condition with left- and rightward gaze shifts, BF10 = 3.79; and when items were presented left or right, BF10 = 6.77), regardless of the direction of the gaze or the initial location of the memory item. At the individual level, none of the patients showed a direction specific deficit after leftward versus rightward saccades, whereas two patients showed worse performance for items in the left versus right visual field. ConclusionDamage in the right PPC did not lead to gaze direction specific impairments in trans-saccadic memory, but instead caused more general spatial memory impairments.

Lesions to right posterior parietal cortex impair visual depth perception from disparity but not motion cues.

The posterior parietal cortex (PPC) is understood to be active when observers perceive three-dimensional (3D) structure. However, it is not clear how central this activity is in the construction of 3D spatial representations. Here, we examine whether PPC is essential for two aspects of visual depth perception by testing patients with lesions affecting this region. First, we measured subjects' ability to discriminate depth structure in various 3D surfaces and objects using binocular disparity. Patients with lesions to right PPC (N = 3) exhibited marked perceptual deficits on these tasks, whereas those with left hemisphere lesions (N = 2) were able to reliably discriminate depth as accurately as control subjects. Second, we presented an ambiguous 3D stimulus defined by structure from motion to determine whether PPC lesions influence the rate of bistable perceptual alternations. Patients' percept durations for the 3D stimulus were generally within a normal range, although the two patients with bilateral PPC lesions showed the fastest perceptual alternation rates in our sample. Intermittent stimulus presentation reduced the reversal rate similarly across subjects. Together, the results suggest that PPC plays a causal role in both inferring and maintaining the perception of 3D structure with stereopsis supported primarily by the right hemisphere, but do not lend support to the view that PPC is a critical contributor to bistable perceptual alternations.This article is part of the themed issue ‘Vision in our three-dimensional world’.

A visuomotor disorder in the absence of movement: Does Optic Ataxia generalize to learned isometric hand action?

Visuomotor deficits in parietal patients suffering from Optic Ataxia (OA) have been so far studied during natural reaching movements. We aimed at understanding if these disorders are also present when more abstract visuomotor transformations are involved. A patient with unilateral OA was tested during both standard reaches and isometric actions, therefore in the absence of hand displacement. Isometric action was affected similarly to standard reaches, with endpoint errors to visual targets that were found in both central and peripheral vision. The dissociation of perceptual and motor components of errors highlighted the existence of field, hand and hemispace effects, which depended on the type of error investigated. A generalization of the reaching disorder to learned isometric conditions would suggest that lesions of posterior parietal cortex (PPC) affect sensory-motor transformations not only for standard reaches, but also when visual signals need to be aligned with information from hand force receptors, therefore regardless of the specific remapping required to generate the directional motor output. The isometric impairment emerged with high and similar severity regardless of whether targets were in central or peripheral vision. Since under all isometric conditions gaze and hand position were decoupled, the spatial correspondence between the hand and the gaze seems to play a critical role in this syndrome. This indicates that regardless of the action to be performed and the specific remapping required, there exists in PPC an abstract representation of the directional motor output, where the computation of eye–hand alignment by parietal neurons plays a crucial role.

Inactivation of the Parietal Reach Region Causes Optic Ataxia, Impairing Reaches but Not Saccades

Lesions in human posterior parietal cortex can cause optic ataxia (OA), in which reaches but not saccades to visual objects are impaired, suggesting separate visuomotor pathways for the two effectors. In monkeys, one potentially crucial area for reach control is the parietal reach region (PRR), in which neurons respond preferentially during reach planning as compared to saccade planning. However, direct causal evidence linking the monkey PRR to the deficits observed in OA is missing. We thus inactivated part of the macaque PRR, in the medial wall of the intraparietal sulcus, and produced the hallmarks of OA, misreaching for peripheral targets but unimpaired saccades. Furthermore, reach errors were larger for the targets preferred by the neural population local to the injection site. These results demonstrate that PRR is causally involved in reach-specific visuomotor pathways, and reach goal disruption in PRR can be a neural basis of OA.

Neuroanatomical Dissections of Unilateral Visual Neglect Symptoms: ALE Meta-Analysis of Lesion-Symptom Mapping

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.

Insights from neuropsychology: pinpointing the role of the posterior parietal cortex in episodic and working memory

The role of posterior parietal cortex (PPC) in various forms of memory is a current topic of interest in the broader field of cognitive neuroscience. This large cortical region has been linked with a wide range of mnemonic functions affecting each stage of memory processing: encoding, maintenance, and retrieval. Yet, the precise role of the PPC in memory remains mysterious and controversial. Progress in understanding PPC function will require researchers to incorporate findings in a convergent manner from multiple experimental techniques rather than emphasizing a particular type of data. To facilitate this process, here, we review findings from the human neuropsychological research and examine the consequences to memory following PPC damage. Recent patient-based research findings have investigated two typically disconnected fields: working memory (WM) and episodic memory. The findings from patient participants with unilateral and bilateral PPC lesions performing diverse experimental paradigms are summarized. These findings are then related to findings from other techniques including neurostimulation (TMS and tDCS) and the influential and more abundant functional neuroimaging literature. We then review the strengths and weaknesses of hypotheses proposed to account for PPC function in these forms of memory. Finally, we address what missing evidence is needed to clarify the role(s) of the PPC in memory.

The relations between joint action and theory of mind: a neuropsychological analysis

We examined the relations between joint action and Theory of Mind (ToM) in neurological patients with impairments in ToM, in control patients (who passed ToM tasks) and non-lesioned controls. In two experiments, joint action was assessed in a "social Simon" procedure where spatial compatibility effects were tested under two-alternative forced-choice and under go/nogo conditions, which participants performed in isolation or alongside another participant (the joint action condition). In Experiment 1, patients with impaired ToM showed evidence of increased spatial compatibility effects under standard (two-alternative forced-choice) conditions but, unlike the control participants, these effects disappeared in the joint action condition. In Experiment 2, the ToM patients were asked to pay particular attention to their co-actor. With these instructions, ToM patients with lesions of posterior parietal cortex now showed a sustained spatial compatibility effect in the joint action condition, while ToM patients with lesions primarily involving frontal regions showed an initial effect of spatial compatibility that decreased across trials. The data suggest common processes involved in ToM processing and joint action effects, related to either the ability to attend to appropriate social cues (affected in posterior parietal patients) or the ability to recruit sufficient resources to code another's actions (affected in frontal patients).

The posterior parietal paradox: Why do functional magnetic resonance imaging and lesion studies on episodic memory produce conflicting results?

Recent functional magnetic resonance imaging (fMRI) studies addressing healthy subjects point towards posterior parietal cortex (PPC) involvement in episodic memory tasks. This is noteworthy, since neuropsychological studies usually do not connect parietal lesions to episodic memory impairments. Therefore an inventory of the possible factors behind this apparent paradox is warranted. This review compared fMRI studies which demonstrated PPC activity in episodic memory tasks, with findings with studies of patients with PPC lesions. A systematic evaluation of possible explanations for the posterior parietal paradox indicates that PPC activation in fMRI studies does not appear to be attributable to confounding cognitive/psychomotor processes, such as button pressing or stimulus processing. What may be of more importance is the extent to which an episodic memory task loads on three closely related cognitive processes: effort and attention, self-related activity, and scene and image construction. We discuss to what extent these cognitive processes can account for the paradox between lesion and fMRI results. They are strongly intertwined with the episodic memory and may critically determine in how far the PPC plays a role in a given memory task. Future patient studies might profit from specifically taking these cognitive factors into consideration in the task design.

At the intersection of attention and memory: The mechanistic role of the posterior parietal lobe in working memory

Portions of the posterior parietal cortex (PPC) play a role in working memory (WM) yet the precise mechanistic function of this region remains poorly understood. The pure storage hypothesis proposes that this region functions as a short-lived modality-specific memory store. Alternatively, the internal attention hypothesis proposes that the PPC functions as an attention-based storage and refreshing mechanism deployable as an alternative to material-specific rehearsal. These models were tested in patients with bilateral PPC lesions. Our findings discount the pure storage hypothesis because variables indexing storage capacity and longevity were not disproportionately affected by PPC damage. Instead, our data support the internal attention account by showing that (a) normal participants tend to use a rehearsal-based WM maintenance strategy for recall tasks but not for recognition tasks; (b) patients with PPC lesions performed normally on WM tasks that relied on material-specific rehearsal strategies but poorly on WM tasks that relied on attention-based maintenance strategies and patient strategy usage could be shifted by task or instructions; (c) patients’ memory deficits extended into the long-term domain. These findings suggest that the PPC maintains or shifts internal attention among the representations of items in WM.

Mental space travel: Damage to posterior parietal cortex prevents egocentric navigation and reexperiencing of remote spatial memories.

The ability to navigate in a familiar environment depends on both an intact mental representation of allocentric spatial information and the integrity of systems supporting complementary egocentric representations. Although the hippocampus has been implicated in learning new allocentric spatial information, converging evidence suggests that the posterior parietal cortex (PPC) might support egocentric representations. To date, however, few studies have examined long-standing egocentric representations of environments learned long ago. Here we tested 7 patients with focal lesions in PPC and 12 normal controls in remote spatial memory tasks, including 2 tasks reportedly reliant on allocentric representations (distance and proximity judgments) and 2 tasks reportedly reliant on egocentric representations (landmark sequencing and route navigation; see Rosenbaum, Ziegler, Winocur, Grady, & Moscovitch, 2004). Patients were unimpaired in distance and proximity judgments. In contrast, they all failed in route navigation, and left-lesioned patients also showed marginally impaired performance in landmark sequencing. Patients' subjective experience associated with navigation was impoverished and disembodied compared with that of the controls. These results suggest that PPC is crucial for accessing remote spatial memories within an egocentric reference frame that enables both navigation and reexperiencing. Additionally, PPC was found to be necessary to implement specific aspects of allocentric navigation with high demands on spontaneous retrieval.

Role of right posterior parietal cortex in maintaining attention to spatial locations over time

Recent models of human posterior parietal cortex (PPC) have variously emphasized its role in spatial perception, visuomotor control or directing attention. However, neuroimaging and lesion studies also suggest that the right PPC might play a special role in maintaining an alert state. Previously, assessments of right-hemisphere patients with hemispatial neglect have revealed significant overall deficits on vigilance tasks, but to date there has been no demonstration of a deterioration of performance over time—a vigilance decrement—considered by some to be a key index of a deficit in maintaining attention. Moreover, sustained attention deficits in neglect have not specifically been related to PPC lesions, and it remains unclear whether they interact with spatial impairments in this syndrome. Here we examined the ability of right-hemisphere patients with neglect to maintain attention, comparing them to stroke controls and healthy individuals. We found evidence of an overall deficit in sustaining attention associated with PPC lesions, even for a simple detection task with stimuli presented centrally. In a second experiment, we demonstrated a vigilance decrement in neglect patients specifically only when they were required to maintain attention to spatial locations, but not verbal material. Lesioned voxels in the right PPC spanning a region between the intraparietal sulcus and inferior parietal lobe were significantly associated with this deficit. Finally, we compared performance on a task that required attention to be maintained either to visual patterns or spatial locations, matched for task difficulty. Again, we found a vigilance decrement but only when attention had to be maintained on spatial information. We conclude that sustaining attention to spatial locations is a critical function of the human right PPC which needs to be incorporated into models of normal parietal function as well as those of the clinical syndrome of hemispatial neglect.

Lesion of posterior parietal cortex in rats does not disrupt place avoidance based on either distal or proximal orienting cues

A current topic in neurobiology is the study of the role of various brain structures in processing of spatial information. The present study was aimed at elucidating the role of the rat posterior parietal cortex in performing a place avoidance task. Two variants of the task were used: an arena frame task, in which animals were trained to avoid a sector defined by local cues bound to the surface of a rotating arena, and the room frame task, in which the shock sector was defined with respect to distal room landmarks. The results showed that both control and lesioned rats were able to efficiently solve both tasks, while locomotion was not altered. These results suggest that the posterior parietal cortex is not crucial for the processing of either proximal or distal cues in place avoidance.

Landmark control and updating of self-movement cues are largely maintained in head direction cells after lesions of the posterior parietal cortex.

Head direction (HD) cells discharge as a function of the rat's directional orientation with respect to its environment. Because animals with posterior parietal cortex (PPC) lesions exhibit spatial and navigational deficits, and the PPC is indirectly connected to areas containing HD cells, we determined the effects of bilateral PPC lesions on HD cells recorded in the anterodorsal thalamus. HD cells from lesioned animals had similar firing properties compared to controls and their preferred firing directions shifted a corresponding amount following rotation of the major visual landmark. Because animals were not exposed to the visual landmark until after surgical recovery, these results provide evidence that the PPC is not necessary for visual landmark control or the establishment of landmark stability. Further, cells from lesioned animals maintained a stable preferred firing direction when they foraged in the dark and were only slightly less stable than controls when they self-locomoted into a novel enclosure. These findings suggest that PPC does not play a major role in the use of landmark and self-movement cues in updating the HD cell signal, or in its generation.

Reaching errors in optic ataxia are linked to eye position rather than head or body position

When reaching towards a visual stimulus, spatial information about the target must be transformed into an appropriate motor command. Visual information is coded initially in retinotopic coordinates, while the reaching movement ultimately requires the specification of the target position in limb-centred coordinates. It is well established that the posterior parietal cortex (PPC) plays an important role in transforming visual target information into motor commands. Lesions in the PPC can result in optic ataxia, a condition in which the visual guidance of goal-directed movements is impaired. Here, we present evidence from two patients with unilateral optic ataxia following right PPC lesions, that the pattern of reaching errors is linked to an eye-centred frame of reference. Both patients made large errors when reaching to visual targets on the left side of space, while facing and fixating straight ahead. By varying the location of fixation and the orientation of the head and body, we were able to establish that these large errors were made specifically to targets to the left of eye-fixation, rather than to the left of head-, body-, or limb-relative space. These data support the idea that visual targets for reaching movements are coded in eye-centred coordinates within the posterior parietal cortex.

An exploration of the role of the superior temporal gyrus in visual search and spatial perception using TMS.

This study sought to investigate the recent claim by H.-O. Karnath and his colleagues that the crucial locus of neurological damage in neglect patients lies in the right superior temporal gyrus (STG), and not in the right posterior parietal cortex (PPC) as conventionally thought. Using transcranial magnetic stimulation (TMS), we first tested the involvement of the right STG in a task commonly used in the diagnosis of neglect, the landmark task. No evidence was found for a critical involvement of the right STG in the processing of this task, though evidence was found for the involvement of the right PPC. In contrast, however, when we examined the effects of TMS on exploratory search, a double dissociation between right STG and right PPC was found. When the processing of conjunction items was required, involvement of the right PPC (and not STG) was found in accordance with our previous research. When a difficult exploratory search through feature items was required, however, the right STG (not PPC) was found to be involved. A hitherto unknown role for right STG in visual search tasks was thus uncovered. These data suggest that conclusions about the area of brain damage resulting in neglect-like symptoms are highly dependent on the task used to diagnose them, with lesions in right PPC leading to deficits on the landmark task and conjunction visual search, and lesions in right STG resulting in deficits in feature based serial exploratory search tasks.

Early movement impairments in a patient recovering from optic ataxia

Since Balint’s first description, optic ataxia has been considered as a pure visuomotor impairment produced by a lesion of the posterior parietal cortex. Beyond general agreement on the parietal involvement in visually guided behaviour, the exact role of the dorsal posterior parietal cortex in the temporal aspects of visuomotor control remains unclear. Recent evidence has indicated a specific involvement of the parietal cortex in the on-line visual guidance of movement. Here, we report the motor performance of, GT, a patient recovering from an optic ataxia due to a right focal lesion of the dorsal posterior parietal cortex. When asked to reach and grasp, with his left contralesional hand, different sized objects, located at different positions from his body, GT showed an apparently complete recovery from optic ataxia. However, the early kinematic aspects of GTs prehension movement were not normally tuned either by intrinsic or extrinsic visual properties of objects. At variance with both an age-matched control group and a neurological patient with a right internal capsule lesion and no sign of optic ataxia, GTs latencies to peak wrist acceleration and peak velocity were not modulated by object location. A similar defective pattern was present in GTs grasping component where, despite the sparing of the classical scaling of grip aperture, object size did not modulate the peak velocity of grip aperture. These results constitute evidence that the posterior region of the dorsal parietal cortex, besides playing a role in the on-line control of movement execution may also be involved in the programming of early kinematics parameters.

Perceptual Attentional Set-Shifting Is Impaired in Rats with Neurotoxic Lesions of Posterior Parietal Cortex

The posterior parietal cortex (PPC) is believed to be involved in the representation of spatial information, including spatial attentional processing. Because the PPC is extensively interconnected with frontal cortical regions involved in attention and executive function, we sought to determine whether PPC was involved in nonspatial attentional processes such as those of the frontal areas to which it projects. Lesions of the medial frontal cortex (in rats) or lateral prefrontal cortex (in nonhuman primates) impair the ability to shift attention from one perceptual dimension of a stimulus to another (referred to as an extradimensional shift). Rats with neurotoxic lesions of the PPC tested in an attentional set-shifting paradigm demonstrated a pattern of impairment identical to that of rats with medial frontal cortex lesions: they were selectively impaired on the extradimensional shift phase of the task. Performance in other phases of the task was indistinguishable from that of control rats, including the ability to reverse a previously learned discrimination. These findings are consistent with models that assign the PPC a prominent role in cortical attentional processing networks, as well as a role for the PPC in processing information about expectancy and surprise. They also suggest, importantly, that the interaction between the PPC and the frontal cortex is not limited to spatial attentional processing.

Updating of locations during whole-body rotations in patients with hemispatial neglect.

Posterior parietal cortex lesions have been associated with both hemispatial neglect and spatial-updating deficits. Currently, the relation between these processes remains poorly understood. We tested the ability of parietal patients with neglect to update remembered target locations during passive whole-body rotations. The rotations and manual pointing responses were executed with and without vision. During the rotation, the remembered location stayed on the same side of the body midline or crossed the midline. Parietal patients generally underestimated rotations, as compared with control groups, but updated targets equally well on either side of the body midline, regardless of the amount of updating required. Once parietal patients have localized a target, they can use self-motion information to update its location, even if it passes into the region they typically neglect. This lack of contralesional updating effects contrasts with impairments in eye position updating found in previous work with parietal patients.

Combined deficits of saccades and visuo-spatial orientation after cortical lesions.

Functionally, saccadic eye movements are closely linked to visuo-spatial orientation. Anatomically, the network of cortical areas controlling saccades also seems to be involved in spatial attention and orientation. Consequently, lesions should cause deficits in both categories. We investigated this in 34 patients with focal unilateral lesions of the posterior parietal cortex (PPC), the frontal eye fields (FEF), the supplementary motor area (SMA), or the dorsolateral prefrontal cortex (PFC). Saccadic eye movements were recorded using infrared reflection oculography. Visual hemineglect or other visuo-spatial disorders were investigated by a series of standardized paper-pencil tests. Further, the internal spatial coordinates (subjective visual vertical and subjective straight ahead) were assessed psychophysically. Depending on the site of the lesion, different patterns of deficits were identified: lesions of the PPC impaired reflexive exploration of visual space in terms of delayed and hypometric visually triggered saccades into the contralesional hemifield, related to the severity of visual hemineglect. Further, PPC lesions specifically affected basic functions of the perceptual analysis of space, such as the internal spatial coordinates and spatial constancy across saccades. The latter was tested by applying visual double-step stimuli, where saccade-related extraretinal information had to be taken into account for achieving spatial accuracy. Frontal lesions left these functions intact. FEF lesions, however, impaired systematic intentional exploration of space, thus causing an exploratory-motor type of visual hemineglect. Prefrontal (PFC) lesions impaired the working memory for saccade-related spatial information, and SMA lesions affected temporal properties such as the timing of saccadic sequences, but did not cause specific visuo-spatial deficits. In conclusion, patients with frontal or parietal cortical lesions often exhibit combined saccadic and visuo-spatial disorders, most of which are topically specific.