Posterior Parietal Lesions Research Articles

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.

Selective inability to point to extrapersonal targets after left posterior parietal lesions: an objectivization disorder?

Selective inability to point to extrapersonal targets after left posterior parietal lesions: an objectivization disorder?

Selective Inability to Point to Extrapersonal Targets After Left Posterior Parietal Lesions: An Objectivization Disorder?

Selective Inability to Point to Extrapersonal Targets After Left Posterior Parietal Lesions: An Objectivization Disorder?

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.

Deficits and Recovery of First-Order and Second-Order Motion Perception in Patients with Unilateral Posterior Parietal Lesions

Our aim was to test whether unilateral posterior parietal lesions degrade first-order and second-order motion differentially, and to investigate the time course of any potential recovery. We tested ten patients with circumscribed parietal lesions. Thresholds were measured for the discrimination of the direction of motion of stimuli presented 5.5° peripherally in the ipsilesional and contralesional visual hemifields. Subjects had to indicate whether a rectangular region (1.6 deg × 3 deg) embedded in dynamic random noise background moved up or down. The region contained moving (signal) and flickering (background) dots and moved for 1 s at 2.36 deg s−1. Signal dots were either (a) coherently moving in the same direction as the region (first-order), (b) stationary (second-order), or (c) coherently moving in the opposite direction (theta). Thresholds were defined as percentage of signal dots within the region yielding 75% correct responses. All patients had higher thresholds for second-order than for first-order motion. When contralesional and ipsilesional thresholds were compared, three patients showed proportional threshold elevations for all three types of motion stimuli in the contralesional hemifield. Two of these three patients were tested again five months later. Both showed considerable recovery: in one patient, the contralesional deficit was no longer present; in the other, it was reduced by about half. None of our patients had lesions affecting first-order or second-order motion differentially; lesions always affected first-order and second-order motion similarly. Owing to recovery, these deficits might be detectable only for a short time.

Cortical control of double-step saccades: implications for spatial orientation.

To accurately localize a visual target in space despite eye movement-induced shifts of its retinal image, the brain must take into account both its retinal location and information about current eye position or at least the preceding eye displacement. We examined this ability with respect to saccadic eye movements by applying "double-step" stimuli, where the locations of two sequentially flashed target lights have to be fixated by two successive saccades performed after their disappearance. As the 2nd saccade will not start at the spatial location from which the 2nd target was seen, a dissonance arises between its retinal coordinates and the motor coordinates of the required 2nd saccade. Nevertheless, these saccades were performed quite accurately by 32 healthy human adults. To investigate the contribution of the cerebral cortex, we recorded horizontal double-step saccades in 35 patients with focal unilateral hemispheric lesions. Whereas frontal lesions impaired temporal properties, posterior parietal lesions caused spatial dysmetria or failure of even ipsiversive 2nd saccades following contraversive 1st saccades. This reflects an inability to compensate for retinospatial dissonance by using nonretinal information (corollary discharge) about eye displacement associated with a previous saccade into the contralesional hemifield. In conclusion, the parietal cortex is crucial for spatial constancy across saccades.

Parietal kinetic ataxia without proprioceptive deficit.

A patient with acute onset "classic" cerebellar ataxia of the right arm without clinically detectable deep sensory loss is reported, in relation to an acute posterior parietal infarct. Wild back and forth swaying of the arm, giving away, or worsening by suppression of vision were not seen. The lesion involved area 5, parts of area 7, the angular gyrus, the middle and posterior parieto-occipital gyri, and posterior parts of the superior and middle temporal gyri. The paracentral lobule, commonly thought to be responsible for parietal ataxia, was spared. Thus posterior parietal lesions can mimick cerebellar ataxia, possibly by severing specific projections to the ventrolateral thalamic nuclei. On the basis of previous studies in primates, the superior parietal gyrus may play a major part in the ataxia presented by this patient.

Ferrier's mistake revisited, or when it comes to the brain, nothing is simple.

To review the work of David Ferrier (1843-1928), the British pioneer in the localization of function in the cerebral cortex. In his experiments on monkeys, Ferrier mistakenly located the center for vision in the angular gyrus of the parietal lobe. What led him to this error? Ferrier included details of his technique and many of his original laboratory observations in his published papers and books; these published works have allowed a reconstruction of his thought processes as he struggled to assess vision in untrained animals. The occipital lobe lesions produced by Ferrier did not yield vision defects that were gross enough to be detected by observing a monkey's random behavior. On the other hand, the posterior parietal lesions produced by Ferrier did change a monkey's behavior in ways in which Ferrier misinterpreted as being due to induced blindness. Ferrier had probably induced visual neglect and a disinclination in the monkey to move its body, as well as actual vision disturbances in guiding voluntary limb movements.

A Selective Impairment of Hand Posture for Object Utilization in Apraxia

This study reports the case of an apraxic patient who was impaired in all aspects of gestural behavior following bilateral posterior parietal cortex lesions. The main impairment concerned manual prehension of objects during their utilization. The deficit contrasted with both normal movement trajectories of the arm during execution of such gestures, and with accurate manual prehension in the context of simple reaching movements. Although recognition of gestures and pantomimes made by the examiner was preserved, the patient showed a striking inability to visually discriminate or describe manual prehension associated with object utilization. We thus propose the existence of specialized cortical mechanisms for the representation and activation of the postural schemata of the hand required for complex actions.

Neurophysiological evidence for a role of posterior parietal cortex in redirecting visual attention.

Lesions of the posterior parietal cortex in humans and monkeys result in a spatial neglect syndrome characterized by defects in visual-spatial perception, oculomotor function, and directing visual attention. Although symptoms of spatial neglect can result from lesions to other cortical and subcortical areas, patients with posterior parietal lesions are particularly impaired in their ability to disengage and reorient visual attention. Neurophysiological experiments in area 7a of behaving monkeys reveal a large class of neurons that respond to visual stimuli and are powerfully modulated by states of attention. These cells respond better to passive visual stimuli presented during states of attentive fixation than to identical stimuli presented in nonattentive states. The responses of the majority of these cells are also influenced by covert shifts of attention away from the point of fixation; they respond to stimuli presented anywhere within their receptive fields except the covertly attended location. The combined effect of facilitation during attentive fixation and lack of response at the attended location results in a sensitivity for visual stimuli that appear at one location while attention is directed to another. The special sensitivity for unattended stimuli in this group of neurons in area 7a suggests that they may play a role in reorienting attention, possibly by providing signals of the spatial locations of novel stimuli.

Recovery from directional hypokinesia and bradykinesia in unilateral neglect

Patients with acute right hemisphere (RH) damage and left unilateral neglect may exhibit slowness in both the initiation and execution of goal-directed movements toward the contralesional side (respectively, directional hypokinesia and directional bradykinesia). We retested 13 patients with RH damage, who on initial testing 1 year earlier had shown these impairments on a visually cued sequential movement task. Initiation and execution times were measured separately for leftward and rightward movement sequences, performed in either hemispace and across the body midline. Patients with anterior/subcortical lesions exhibited directional hypokinesia and bradykinesia on initial testing, but no longer showed either after 12 months. It is suggested that the recovery exhibited by these patients was determined conjointly by residual functioning of flexible anterior/subcortical structures involved in response production, in addition to the resolution of transient secondary dysfunction (i.e., diaschisis) of posterior (parietal) areas responsible for attentional orienting and target selection. In contrast, patients with posterior (parietal) lesions continued to exhibit directional hypokinesia after 12 months, probably as a result of permanent damage to a region whose dedicated or specialised functions cannot readily be compensated by other brain areas. These results support the notion that spatial attention and goal-directed movement are subserved by a distributed network involving separate but interconnected brain regions. Distinct functional losses may be predicted, in both the acute and chronic stages postinjury, on the basis of temporary or permanent dysfunction of discrete components of this network.

Non-spatial learning following posterior parietal or hippocampal lesions.

Posterior parietal, hippocampal, or sham-lesioned rats were tested for the acquisition of a non-monotonic serial learning task. The performance of control rats and those with a posterior parietal lesion was similar, while those with hippocampal damage demonstrated a working memory deficit. The results are integrated with contemporary conceptualizations of hippocampal and posterior parietal cortex involvement in learning and memory for non-spatial tasks.

Spatial learning following posterior parietal or hippocampal lesions.

Rats with either posterior parietal (PPC) or dorsal hippocampal (HIP) lesions were tested for open-field activity, acquisition of a multiple T water maze habit, and presence of a 'cognitive map' of the water maze arena. The performances of control and PPC-lesioned rats were similar on all behavioral measures. However, the HIP-damaged rats demonstrated higher levels of general activity, severe deficits in both working and reference memory in the multiple T water maze task, and failed to develop a cognitive map of the water maze arena.

Impairment of grasping movements following a bilateral posterior parietal lesion

The observation of a patient (A.T.) with a bilateral posterior parietal lesion of vascular origin is reported. A.T. presented a bilateral (more marked on the right) deficit in grasping simple objects (neutral cylindrical dowels) without deficit in reaching toward the location of these objects. The major symptom was an exaggerated anticipatory opening of the fingers with poor correlation with object size, resulting in awkward grasps. It was present both when the hand was visible to the subject and when it was not. This deficit was much less marked if the neutral objects were replaced by usual objects of the same sizes. Finally, in tasks where she had to indicate with her fingers the size of visual objects presented as virtual images through a mirror, or the size of imagined usual objects, A.T. performed normally. These results are discussed within the framework of a dual representation of objects. Only the “pragmatic” representation for steering object-oriented actions would be impaired in this patient as a result of posterior parietal damage. By contrast the semantic representation for object identification would be intact.

Are Multiple Cerebral Infarcts Synergistic?

The goal of this study was to characterize the cumulative effects of multiple strokes on cognition. We conducted a prospective, longitudinal case study with neuropsychological, neurological, and radiological evaluations. Research was conducted at the Boston (Mass) Veterans Administration Medical Center, Neurology Service, on successive inpatient hospital admissions. We followed up a 66-year-old right-handed man with multiple subcortical lacunae during a 3.5-year period during which he suffered two additional cortical infarctions. Each evaluation included approximately 3 hours of neuropsychological testing spanning a range of cognitive domains (attention, language, memory, visuospatial functions, response inhibition, and mental flexibility), full neurological examination, and computed tomographic scan. The patient's stepwise cognitive decline was characterized by unexpected exacerbation of "frontal" neurobehavioral features following the occurrence of two posterior cortical lesions. At initial evaluation, the computed tomographic scan showed bilateral subcortical lacunae in basal ganglia and periventricular white matter, and symptoms included dysarthria and perseveration. The second evaluation, following a left posterior parietal lesion, revealed a range of new frontal features, including impulsivity, pull-to-stimulus, and difficulty shifting set. Following a subsequent right occipital infarct, further frontal lobe impairments emerged: forced grasp reflex and incontinence. We hypothesize that the cumulative effects of infarcts were synergistic. That is, the posterior cortical infarcts elicited frontal features that would not be expected from a simple sum of these lesions' effects.

Dissociation of the medial prefrontal, posterior parietal, and posterior temporal cortex for spatial navigation and recognition memory in the rat.

Rats with lesions of the medial prefrontal, posterior parietal, or posterior temporal cortex were tested in five spatial navigation tasks, which varied in egocentric or allocentric demands, a visual discrimination task, and two delayed nonmatching-to-sample tasks. Rats with prefrontal lesions were impaired at every spatial navigation task, whereas rats with posterior parietal lesions had selective spatial navigation impairments. Rats with prefrontal lesions were also impaired at a visual delayed nonmatching-to-sample task, as they were unable to learn the task, even with no delay. The results are consistent with the idea that the basic plan of mammalian cortex includes prefrontal, posterior parietal, and posterior temporal regions, each of which have generally similar functions across mammalian taxa. There are, however, species-typical differences that reflect specific ecological pressures on the development of the different regions.

Visual-spatial functions persist following temporal and posterior parietal cortex lesions in rat

Adult rats were prepared with either posterior parietal, temporal, or sham neocortical lesions. Gross kinetic functions and equilibrium were assessed on alternate days for 12 days following surgery by placing the animal on an elevated rod (3.5 cm diameter) oriented 20° to horizontal and rating locomotor functions. Although all groups improved with experience and time postsurgery, rats with posterior parietal lesions exhibited a greater kinetic disturbance throughout the testing period. After a 3-week recovery period, the animals were trained on a visual-spatial task in which a visual stimulus located at the choice point cued whether the escape platform was located in the left or right arm of a T-maze. Animals were trained at a rate of 20 trials per day until a criterion of 18 correct responses in a series of 20 trials was observed. This task differed from that used in a similar previous study in this laboratory (1) in that stimulus saliency was increased and rats were punished for errors by confinement to the incorrect alley for 15 s when errors were made. All rats learned the task, and although there were subtle differences in the rate of acquisition between the groups, there were no gross differences on any of several measures of learning and performance. It is concluded that, under appropriate conditions, rats with injuries in these posterior association regions can learn and perform a task requiring the execution of different spatial responses on the basis of visual landmark cues that are spatially discontiguous from the escape site.

Visual memory and visual spatial functions in the rat following parietal and temporal cortex injuries

Adult rats were prepared with either posterior parietal, temporal, or sham neocortical lesions, and after assessing gross locomotor functions, trained in cognitive visual tasks. Training was conducted in a modified circular water maze wherein the water was made opaque with a white nontoxic powder paint. The order of the tasks was counterbalanced within groups. One task was a visual matching-to-sample problem with an intertrial interval of 20 s. The second task was a visual spatial conditional problem in which visual stimuli (white or gray cards) cued spatial choices in a T maze that was inserted into the tank. After completing these tasks, the animals were trained on a simple visual pattern discrimination and a simple position habit. Both lesion groups demonstrated significant deficits on both cognitive tasks. Since gross visual perceptual, spatial, and motor abilities were found to be unaffected by the lesions, it is suggested that a generalized retardation in cognitive functions follows injuries in these sites. Also, qualitative evidence supported the conclusion that posterior parietal cortex plays an important role in integrating visuospatial stimuli with motor responses.

A case of peripheral dysgraphia

Abstract A 56-year-old right-handed man with 10 years of schooling, who suddenly developed writing problems, is described. An M.R.I. revealed a left posterior cortico-subcortical parietal lesion. The patient was not aphasic, had no neglect, and no apraxia. In contrast, spontaneous writing, written naming, writing to dictation, and copying of words and sentences showed a remarkable impairment. Letters were ill-formed; nonletters, stroke and letter repetitions, and omissions were present, both in words and nonwords; some letter substitutions were also found. There were no effects of word length, imageability, frequency, or word class. Oral spelling was normal. All these features are typical of a peripheral dysgraphia. An inability to use abstract motor patterns as input to neuromuscular routines is suggested as the major deficit, with minor impairment to the allographic conversion system.

Exploratory activity and response to a spatial change in rats with hippocampal or posterior parietal cortical lesions

Rats with bilateral lesions of posterior parietal cortex (PPC: Krieg's Area 7) or dorsal hippocampus (HIP) were compared with controls for their response to environmental change. In the first experiment, following subjects' exploration of a relatively homogeneous open-field environment, a stimulus-rat was introduced at a particular location beneath the glass floor. All groups selectively explored the location of the stimulus-rat, but only the control and PPC groups displayed habituation. On removal of the stimulus-rat, only the control group selectively re-explored the place where the stimulus-rat had been. A second experiment, similar to the first, used additional prominent visual cues beneath the floor. When the cues were spatially separate from the location of the stimulus-rat (Dissociated object condition), the same results were obtained as in the first experiment. When the additional cues were positioned close to the stimulus-rat location (Associated object condition), habituation occurred in all groups including the hippocampal group, and again the removal of the stimulus-rat resulted in a selective re-exploration of its former location in the control group only. However, a selective preference for staying at the stimulus-rat's previous location was found in PPC animals as in controls. Hippocampal rats failed to investigate the location of the missing stimulus in all conditions. The results confirm the role played by the hippocampus in spatial memory and suggest that the posterior parietal cortex is involved in the cognitive-demanding aspects of spatial encoding, particularly in environments that are poorly visually differentiated.