Lesions Of Parietal Cortex Research Articles

Deficits and recovery of first- and second-order motion perception in patients with unilateral cortical lesions.

Unilateral lesions in the posterior parietal cortex can degrade motion perception in the contralesional visual hemifield. Our aim was to investigate whether deficits caused by cortical lesions may be different for first- and second-order motion perception, and to study the time scale of any potential recovery. In nine patients with circumscribed lesions mainly in the parietal and fronto-parietal cortex, thresholds for direction discrimination were measured for stimuli presented peripherally in their ipsi- and contralesional hemifield. Subjects had to identify the direction of a vertically moving object embedded in a background of dynamic random dot noise. The object consisted of various proportions of signal and noise dots. Signal dots were either (a) coherently moving in the same direction as the object (first-order), (b) stationary (second-order: drift-balanced), or (c) coherently moving in the opposite direction (second-order: theta). Noise dots were flickering. Two patients showed significant threshold elevations for all three types of motion stimuli presented in their contralesional hemifield, while thresholds for ipsilesional targets were unaffected. Neither showed any selective deficit of first- versus second-order motion perception, but second-order motion was more impaired. Their lesions probably included the motion area V5-MT, which was spared in the other seven patients. One of the patients, who was retested several times during a 27-month postlesional period, showed complete recovery for first- and second-order motion direction discrimination, as well as for the detection of speed differences.

Turn-signal utilization by rats with either unilateral or bilateral posterior parietal cortex injuries

Rats with sham, unilateral, or bilateral aspiration lesions of the posterior parietal cortex (PPC) were trained in a water T-maze to use flashing lights located along the starting alley (two each) and inner walls of the goal alleys (two each) to find a hidden escape platform. Thereafter, the performance of the spatial response was tested under several conditions. Rats with bilateral PPC lesions were significantly inferior to unilateral- and sham-injured rats in learning the “turn-signal” cued spatial task. Also, left-PPC-injured rats committed significantly more errors than did the control animals. After mastering the task, cue saliency was reduced and the amount of spatial discontiguity between the stimuli and escape site was increased in two stages. That is, the flashing light closest to the escape platform was turned off for one testing session. On the following day, animals were required to rely on information located within the starting alley to make the correct spatial response at the choice point. Animals with bilateral or left PPC lesions were significantly impaired on the task with cues located only in the starting alley. The animals were then tested with competing constant illumination of the lights on the side of the apparatus opposite the flashing-light cues. The performance of all animals dropped to chance and failed to improve with training. Finally, three of the sham-operated controls were retrained to criterion on the original discrimination and prepared with bilateral PPC injuries. Substantial savings was observed. The results reveal a greater role of the left PPC than the right in the use of local sensory cues for spatial navigation, and they show that the PPC is not the repository of the “engram” for this learned visuospatial behavior.

The effects of parietal cortex lesions on an object/spatial location paired-associate task in rats

The present experiment was conducted in order to test the hypotheses (1) that the posterior parietal cortex (PPC) serves as a neural system that is critical for binding spatial location and object information in long-term memory and (2) that even restricted lesions of the PPC would result in similar deficits. Long-Evans rats were given either a large or a small PPC lesion or a control surgery under Nembutal anesthesia. After a 1-week recovery period, the rats were tested on either an object or a spatial location go/no-go successive discrimination task. After reaching criterion (a minimum of a 5 sec difference between reward and nonreward trials), they were trained on the other discrimination. After reaching criterion on the second discrimination, all of the rats were trained on a successive discrimination go/no-go task in which they had to remember which object/spatial location pairs had been associated with reward. As compared with controls, neither the small nor the large PPC lesion impaired object or spatial location discrimination. In the paired-associate object/spatial location task, both large and small PPC lesioned rats were impaired, relative to controls. These data suggest that the rodent PPC is not involved in object or spatial location discrimination but rather is involved in discrimination and long-term memory for the combination of object and spatial location information.

Cortical Networks Underlying Mechanisms of Time Perception

Precise timing of sensory information from multiple sensory streams is essential for many aspects of human perception and action. Animal and human research implicates the basal ganglia and cerebellar systems in timekeeping operations, but investigations into the role of the cerebral cortex have been limited. Individuals with focal left (LHD) or right hemisphere (RHD) lesions and control subjects performed two time perception tasks (duration perception, wherein the standard tone pair interval was 300 or 600 msec) and a frequency perception task, which controlled for deficits in time-independent processes shared by both tasks. When frequency perception deficits were controlled, only patients with RHD showed time perception deficits. Time perception competency was correlated with an independent test of switching nonspatial attention in the RHD but not the LHD patients, despite attention deficits in both groups. Lesion overlays of patients with RHD and impaired timing showed that 100% of the patients with anterior damage had lesions in premotor and prefrontal cortex (Brodmann areas 6, 8, 9, and 46), and 100% with posterior damage had lesions in the inferior parietal cortex. All LHD patients with normal timing had damage in these same regions, whereas few, if any, RHD patients with normal timing had similar lesion distributions. These results implicate a right hemisphere prefrontal-inferior parietal network in timing. Time-dependent attention and working memory functions may contribute to temporal perception deficits observed after damage to this network.

Light deprivation produces a therapeutic effect on neglect induced by unilateral destruction of the posterior parietal cortex in rats

Light deprivation has been found to produce accelerated recovery from severe multimodal neglect induced by unilateral destruction of medial agranular cortex, the rat analog of area 8 in humans. However, neglect in humans is most often produced by destruction of the parietal association cortex. Therefore, the present study examined whether light deprivation would produce accelerated recovery from severe multimodal neglect induced by unilateral destruction of the rodent analog of the parietal association cortex. Subjects received unilateral parietal association cortex lesions, and 4 h after surgery were tested for neglect of visual, tactile, and auditory stimuli. If severe neglect was obtained, subjects experienced either light deprivation, constant light, or a 12:12 light/dark cycle for 48 h. The results indicated that, relative to the other groups, the light deprivation group demonstrated significant accelerated recovery from neglect. Recovery was evident on the first post-light deprivation behavioral test, and was maintained for the 3 weeks of behavioral testing. The results provide further support for the therapeutic effects of light deprivation on neglect induced by cortical lesions when light deprivation is administered in the immediate postoperative period.

Effects of hippocampal and parietal cortex lesions on the processing of multiple-object scenes.

Rats were taught 1 of 3 types of multiple-object scene discrimination. Manipulations included either replacing (object based), displacing (space based), or replacing and displacing (object/space based) 1 object in the scene. Once trained, rats received hippocampal, parietal cortex, or cortical control lesions and then were retested. Parietal cortex- and hippocampal-lesioned rats displayed deficits on both the space and object/space tasks but not the object task. The hippocampal-lesioned group's deficit on the object/space task was only transient, whereas the impairments of the parietal cortex-lesioned rats were stable for both tasks. The parietal cortex-lesioned rats sustained difficulty with the object/space task may indicate an inability to switch cognitive strategies.

Effects of hippocampal and parietal cortex lesions on the processing of multiple-object scenes.

Effects of hippocampal and parietal cortex lesions on the processing of multiple-object scenes.

Effects of hippocampal and parietal cortex lesions on memory for egocentric distance and spatial location information in rats.

Effects of hippocampal and parietal cortex lesions on memory for egocentric distance and spatial location information in rats.

Effects of hippocampal and parietal cortex lesions on memory for egocentric distance and spatial location information in rats.

To assess the working memory system for egocentric distance and place information, delayed matching-to-sample (DMTS) go/no-go tasks were run for each rat. To assess the reference memory system, and to serve as a control for nonmemory deficits, successive discrimination go/no-go tasks were then conducted using the same rats. Rats with hippocampal, but not parietal cortex, lesions were impaired relative to controls in the working memory (DMTS) task for both egocentric distance and place information, although the deficit observed in the working memory task for egocentric distance information by rats with hippocampal lesions was mild. Neither hippocampal nor parietal cortex lesioned rats were impaired relative to controls in the reference memory (successive discrimination) task for either cue. The hippocampus appears to be involved in working memory for egocentric distance and in spatial location information, whereas the parietal cortex is not.

Deficits in response initiation, but not attention, following excitotoxic lesions of posterior parietal cortex in the rat

Damage to posterior parietal cortex in humans is known to cause hemineglect, and specifically difficulty in disengaging attention in tests of covert orienting. Aspirative lesions of a region of cortex in rats which is thought to be homologous to primate posterior parietal cortex has also been reported to cause what appears to be multimodal neglect. In order to make an assessment of the nature of this disorder, a variety of tests were employed: (1) a test of somatosensory neglect after Schallert et al. (Pharmacol. Biochem. Behav., 16 (1982) 455–462); (2) a skilled paw-reaching test after Whishaw et al. (Brain 109 (1986) 805–843); (3) a visual reaction time task with peripheral cues analogous to Posner's test of covert orienting (Q. J. Exp. Psychol., 32 (1980) 3–25). Following the posterior parietal lesion there was a global increase in reaction time of responses made contralateral to the lesion in the reaction time task, but there was no evidence of a deficit in covert orienting. There was also no evidence of somatosensory neglect. There was a decrease in the number of attempted reaches with the contralateral paw and a tendency to spend a smaller proportion of time in the contralateral half of the reaching cage.

The Flexible Use of Multiple Cue Relationships in Spatial Navigation: A Comparison of Water Maze Performance Following Hippocampal, Medial Septal, Prefrontal Cortex, or Posterior Parietal Cortex Lesions

Rats prepared with lesions of the prefrontal cortex, posterior parietal cortex, hippocampus, or medial septal area were tested for acquisition of a number of variations of the open-field water maze using a version of place learning assessment described by Eichenbaum, Stewart, and Morris (1991). Specifically, the individual role of the aforementioned cortical and subcortical structures in tasks with differing representational demands on navigation were assessed. The results suggest that the sham-operated control, posterior parietal cortex-lesioned rats, and medial septal area-lesioned rats were able to navigate effectively under changing task conditions. Conversely, the navigational performances of the prefrontal cortex- and hippocampal formation-lesioned rats were impaired when task demands changed. The results are discussed in terms of the flexible use of multiple distal cues to guide navigation and the resulting loss of this flexibility after lesions to either the prefrontal cortex or the hippocampus.

Visual Discrimination Learning in Monkeys with Bilateral Parietal Cortex Lesions

The characteristics of visual discrimination learning were tested on rhesus monkeys during elaboration of an instrumental reflex after bilateral extirpation of the parietal cortex area 7. The animals were trained to discriminate stimuli with different visual attributes (shape, colour, orientation, size, spatial relationships). Their decisions and motor reaction times were recorded. Bilateral extirpation of area 7 did not influence learning characteristics for shape and colour discrimination. The duration of the learning process and the motor reaction time were shortest with these visual attributes. When monkeys were required to discriminate geometrical figures of different orientations and size, these learning characteristics slightly increased. However, learning to discriminate spatial relationships was dramatically impaired. As a result, the duration of the learning process and motor reaction time significantly increased and the level of correct decisions after training significantly decreased. Visual stimuli associated with identical learning characteristics formed distinct groups in a cluster analysis. These results support the suggestion that area 7 is a structural and functional component of mechanisms involved in evaluation of spatial relationships. The impairment of the learning to discriminate spatial relationships can be explained by a change of learning strategy upon disturbance of this mechanism, associated with visual-vestibular interactions and synchronisation processes which bind distributed neurons across different cortical areas into synchronised assemblies.

Distributed Cortical Network for Visual Attention

The contribution of prefrontal and posterior association cortex to voluntary and involuntary visual attention was as sessed using electrophysiological techniques in patients with focal lesions in prefrontal (n = 11), temporal-parietal (n = 10), or lateral parietal cortex (n = 7). Subjects participated in a task requiring detection of designated target stimuli embedded in trains of repetitive stimuli. Infrequent and irrelevant novel visual stimuli were randomly interspersed with the target and background stimuli. Controls generated attention dependent N1 (170 msec) and N2 (243 msec) potentials maximal over extrastriate cortex. Anterior and posterior association cortex lesions reduced the amplitude of both the N1 and N2 potentials recorded over extrastriate cortex of the lesioned hemisphere. The pattern of results obtained reveals that an intrahemispheric network involving prefrontal and posterior association cortex modulates early visual processing in extrastriate regions. Voluntary target detection generated a parietal maximal P300 response (P3b) and irrelevant novel stimuli generated a more frontocentrally distributed P300 (P3a). Cortical lesions had differential effects on P3a and P3b potentials. The P3b was not significantly reduced in any cortical lesioned group. Conversely, the P3a was reduced by both prefrontal and posterior lesions with decrements most severe throughout the lesioned hemisphere. These data provide evidence that an association cortex network involving prefrontal and posterior regions is activated during orientation to novel events. The lack of a significant effect on the visual target P3b in patients with novelty P3a reductions supports the notion that different neural systems are engaged during voluntary vs involuntary atten- tion to visual stimuli.

On-line brain potential correlates of right parietal patients' attentional deficit

EEG potentials evoked by cues and targets were recorded in Posner's visual cueing task from 10 patients with lesions of the right parietal cortex and from age-matched healthy subjects. The patients' N1 component evoked by left-side cues was reduced at the right-parietal recording site, suggesting a general impairment in processing left-side visual input. As usual, patients; keypress responses were delayed when left targets were preceded by right cues. There were two correlates of this delay in the patients' EEG potentials evoked by the critical combination of right cue/left target: their mean amplitude 160–280 ms after target onset (‘Nd’) was less negative than with other combinations of cue and target, and the following frontal P300 was enhanced. The Nd reduction seems to be an on-line measure of patients' momentary decrease of attention for the left hemifield, while the frontal P300 might reflect the patients' attempts at reorienting. In conclusion, different components were sensitive to different aspects of the patients; disorder, suggesting the utility of this approach for developing detailed hypotheses on the mechanisms of attentional deficits involved in visual extinction and neglect.

Effects of parietal cortex lesions on spatial problem solving in the rat

The Maier 3-table task was used to examine spatial representations in rats with lesions of the parietal cortex. Some animals had anteriorly placed lesions, some posteriorly placed in cortical areas, sometimes regarded as ‘parietal’ in earlier studies. After 5 days of familiarization, animals were given 18 days of testing on the standard Maier task. Both parietal groups were initially impaired, but reached the same level of performance as controls by the end of the test period. Learning occurred both within and between sessions for the anterior group, but only between sessions for the posterior group. There was no major functional differentiation apparent on this task between the two ‘parietal’ areas. Rate of exploration increased in both parietal groups across test sessions as task performance improved. It is argued that the change in exploratory activity across sessions in parietal groups may reflect the adoption of a compensatory strategy which improved performance, but that improvement could also have been due to neural changes, as structures, such as the frontal cortex or hippocampus, assume some functions normally mediated by the parietal area.

The differences shown by C57BL/6 and DBA/2 inbred mice in detecting spatial novelty are subserved by a different hippocampal and parietal cortex interplay

Inbred C57BL/6 (C57) and DBA/2 (DBA) mice with hippocampus, posterior parietal cortex or sham lesions were placed in an open-field containing five objects and their reactivity to the displacement (spatial novelty) or the substitution (object novelty) of some of these objects was examined. C57 mice reacted to spatial novelty by exploring more the displaced than the non-displaced objects while DBA mice did not show any consistent reaction. In the highly reactive C57 strain, the peak of exploratory responses directed towards the displaced objects was completely abolished by hippocampal and posterior parietal cortex lesions. In the non-reactive DBA strain, hippocampal lesions induced an aspecific decreased interest towards the two categories of objects while posterior parietal cortex lesions did not produce any behavioral modification. The high reactivity of C57 mice to spatial change appears to be subserved by the conjunctive participation of the hippocampus and the posterior parietal cortex. Conversely, the deficit shown by DBA mice in that situation seems to be related to: (i) a poorly functional hippocampus; and (ii) the non-involvement of the posterior parietal cortex. The present data suggest that the participation of the posterior parietal cortex to the detection of spatial novelty may depend on the degree of functionality of the hippocampus.

Insular Cortex Lesions Impair the Acquisition of Conditioned Immunosuppression

Conditioned immunosuppression can be readily obtained in animals by associating a taste with an immunosuppressive drug. On subsequent exposure to the conditioned taste, the animals show an attenuated immune response and also exhibit a conditioned taste aversion. It has been established that insular cortex lesions disrupt the acquisition of conditioned taste aversion. The effect of NMDA-induced lesions in either the insular cortex or the parietal cortex of male Wistar rats was evaluated in the acquisition of conditioned immunosuppression in two experiments. Unlesioned control rats showed the conditioned immunosuppressive response after reexposure to the taste, as indicated by lower hemagglutinating titers to sheep red blood cells in the first experiment and by a decreased IgM production to ovalbumin, measured by ELISA, in the second experiment. Insular cortex-lesioned rats did not show the conditioned immunosuppression in either experiment, while parietal cortex lesions and the sham-lesioned animals presented a clear decrease of hemagglutinating titer and a low IgM production. The insular cortex lesions did not affect the normal immune response, showing normal hemagglutinating titers and IgM production when compared to nonconditioned controls. The immunosuppressive action of cyclophosphamide also remained unaltered. In conclusion, these results show that the insular cortex is essential for the acquisition of conditioned immunosuppression.

Effects of lesions of the associative parietal cortex on the acquisition and use of spatial memory in egocentric and allocentric navigation tasks in the rat.

Effects of lesions of the associative parietal cortex on the acquisition and use of spatial memory in egocentric and allocentric navigation tasks in the rat.

The role of inferior parietal cortex and fornix in route following and topograhic orientation in cynomolgus monkeys

The effects of inferior parietal cortex lesions (Area 7a/PG) and bilateral transection of the fornix were compared within a single species (cynomolgus monkeys) and using a single paradigm of route running in a traditional (fixed entry and exit) whole-body maze. Experiment 1 showed that Area 7a/PG but not fornix lesions impaired post-operative retention of route running. Experiment 2 assessed the contribution of visual cues and proprioceptive/kinaesthetic guidance to route running and showed that in nonlesioned monkeys route running was influenced to varying degrees by proprioceptive guidance, visual extra-maze room cues and visual maze stimuli. Post-operative assessment of maze performance, including error patterns, retraining and misreaching (Experiment 1), suggested that monkeys in the Parietal Group were not topographically disoriented and did not have a spatial long-term memory deficit, but it was their difficulty responding to local spatial cues which initially impaired route running. Investigation of cue use (Experiment 2) also showed the sensitivity of the Parietal Group to local spatial cues; they were significantly impaired on entry through a new start position when the relationship between maze stimuli and extra-maze cues was changed. The Fornix Group showed no retrograde long-term memory deficit for route-running (Experiment 1). However, in Experiment 2, where a new goal position was learnt, the Fornix Group did show an anterograde memory deficit.

The effects of dorsal versus ventral hippocampal, total hippocampal, and parietal cortex lesions on memory for allocentric distance in rats.

To test for the contribution of the parietal cortex and hippocampus to memory for allocentric spatial cues, the authors trained rats on a go/no-go task that required the rat to remember the distance between two visual cues. Total hippocampal lesions impaired working-memory representation for allocentric distance, whereas parietal cortex lesions resulted in only a transient impairment. In a second experiment, neither hippocampal nor parietal cortex lesions impaired allocentric distance discrimination. A third experiment showed that both the dorsal and ventral areas of the hippocampal formation must be destroyed to impair working memory for allocentric distance information. There appears to be a dissociation between the hippocampus and parietal cortex in mediating memory for allocentric distance information.