[Bilateral parietal lobe syndrome. Also a contribution to the understanding of layer-related cortico-griseo- and leuko-angiomatoses].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Lesion and electrophysiological studies indicate that the parietal lobes play a role in visual spatial attention and in computing the spatial coordinates of visual input. Fewer studies have investigated the role of the parietal lobe in auditory spatial processing, and an extensive comparison of visual and auditory spatial processing in humans with parietal lobe lesions has yet to be conducted. We have studied such localization abilities in a Balint's syndrome patient (RM) who has bilateral parietal lobe lesions. The results indicated that this patient had a significant deficit in both visual and auditory localization relative to age-matched controls. Unlike the controls, however, RM's auditory localization ability either matched or exceeded his visual localization ability depending on the task. Accordingly, RM exhibited "auditory capture," but not "visual capture" under conditions where control subjects showed the opposite pattern. These results are consistent with hypotheses that the parietal lobes are involved in creating multiple spatial representations and in shifting from one spatial reference point to another, but suggest that these parietal structures are not necessary for the integration of multiple sensory stimuli resulting in capture effects.
A large number of imaging studies have identified a role for the posterior parietal lobe, in particular Brodmann's area 7 and the intraparietal sulcus (IPS), in mental rotation. Here we investigated whether neural activity in the posterior parietal lobe is essential for successful mental rotation performance by observing the effects of interrupting this activity during the execution of a mental rotation task. Repetitive transcranial magnetic stimulation (rTMS) was applied to posterior parietal locations estimated to overlie Brodmann's area 7 in the right and the left hemisphere, or to a posterior midline location (sham condition). In three separate experiments, rTMS (four pulses, 20 Hz) was delivered at these locations either 200-400, 400-600, or 600-800 msec after the onset of a mental rotation trial. Disrupting neural activity in the right parietal lobe interfered with task performance, but only when rTMS was delivered 400 to 600 msec after stimulus onset. Stimulation of the left parietal lobe did not reliably affect mental rotation performance at any of the time points investigated. The time-limited effect of rTMS was replicated in a fourth experiment that directly compared the effects of rTMS applied to the right parietal lobe either 200-400 or 400-600 msec into the mental rotation trial. The results indicate that the right superior posterior parietal lobe plays an essential role in mental rotation, consistent with its involvement in a variety of visuospatial and visuomotor transformations.
Lesion studies show that a wide range of integrative sensorimotor functions can be selectively disturbed in patients with parietal lobe damage. Lesions restricted to the somatosensory representations on the anterior parietal lobe produce somatosensory deficits that resemble deafferentated states, including the secondary effects on motor control. Slightly more posterior lesions often are associated with impairment of more complex synthetic somatosensory functions similar to those observed after dorsal column lesions. Damage of the posterior parietal lobe can selectively interfere with virtually every aspect of somatosensory function. These perceptive and cognitive disturbances may or may not be associated with complex motor disturbances of the apractic type. The frequent association of astereognosia and tactile apraxia illustrate the mutual interdependence of the sensorimotor processes involved in active touch and the proximity of the respective processing modules. Parietal lobe function is critical for the control of force and posture, and for the formation of the body image and its relation to external space (the guidance of movements, including the eyes, to external objects). Imaging studies underscore the prominent role of the parietal cortex as a sensorimotor interface and provide complementary information about the interrelationship between perception and action. Action observation activates premotor cortex, but parietal cortex is also recruited whenever an action involves objects, thus emphasizing the significance of parietal cortex for object-directed motor behavior. In contrast to the ventral-dorsal route processing dichotomy in the visual system, both the perceptual-cognitive and motor aspects of somatosensory processing are compromised after parietal damage, demonstrating a different functional architecture of the two sensory systems. The preservation of the comprehension of the meaning of gestures or of object use in patients with lesions restricted to the parietal lobe reveals that the semantic aspects of motor behavior are mediated in the temporal lobe.
Disturbances stemming from lesions of the parietal lobes can produce the most wide-ranging and diagnostically ambiguous symptoms of any of the cortical regions. Currently, parietal assessment and research is hampered by the lack of a specific, brief battery which emphasizes sensory-perceptual rather than cognitive aspects of parietal lobe disease. The Neurological Tests of Parietal Impairment (NTPI) is a battery designed to fulfill this need, providing a broad but brief assessment of major neurobehavioral symptoms of parietal insult. The present study was a preliminary attempt to investigate the diagnostic validity of the NTPI, comparing 7 focal left and 7 focal right parietal lesion cases with 7 focal left and 4 focal right frontal lobe cases, and 5 cases with diffuse cortical disease. The NTPI was found correctly to lateralize right parietal patients and successfully to discriminate them from patients with both right and left frontal lesions on all NTPI subtests except those involving complex receptive speech. Diffuse lesion cases could not be differentiated from parietal patients on the NTPI, as expected. Left parietal patients were not correctly lateralized as effectively as right parietal cases by the NTPI, nor could their performance be differentiated from that of the frontal lesion cases. Possible reasons for this finding were discussed.
Turner syndrome, a genetic disorder that results from the complete or partial absence of an X chromosome in females, has been associated with specific impairment in visuospatial cognition. Previous studies have demonstrated a relationship between parietal lobe abnormalities and visuospatial deficits in Turner syndrome. We used high-resolution magnetic resonance imaging to measure parietal lobe subdivisions in 14 participants with Turner syndrome (mean age 13 years 5 months, SD 5 years) and 14 age-matched controls (mean age 13 years 5 months, SD 4 years 7 months) to localize neuroanatomical variations more closely. Scans were acquired and analyzed for 14 females with Turner syndrome. Analyses of variance were used to investigate differences in regional parietal lobes. Females with Turner syndrome showed a bilateral parietal lobe reduction, specifically in the superior parietal and postcentral gyri. Full-scale IQ scores were significantly positively correlated with postcentral tissue volume in the Turner syndrome group. Structural differences in the parietal lobe are localized specifically to the anterior and superior parietal lobe and might be related to the visuospatial and visuomotor deficits associated with Turner syndrome.
The exact role of the parietal lobe in spatial cognition is controversial. One influential hypothesis proposes that it subserves spatial perception, whereas other accounts suggest that its primary role is to direct spatial movement. For humans, it has been suggested that these functions may be divided between inferior and superior parietal lobes, respectively. In apparent support of a purely perceptual function for the inferior parietal lobe (IPL), patients with lesions to this structure, particularly in the right hemisphere, exhibit unilateral spatial neglect (deficient awareness for the side of space opposite to that of their lesion). Here we show that patients with right IPL lesions also have a specific difficulty in initiating leftward movements towards visual targets on the left side of space. This motor impairment was not found in neglect patients with frontal lesions, contrary to previous proposals that motor aspects of neglect are particularly associated with anterior damage. Our results suggest that the human IPL operates as a sensorimotor interface, rather than subserving only perceptual functions.
This study sought to determine the utility of an interlocking finger task in screening for parietal lobe dysfunction. The ability of 69 patients to imitate a standardised set of four interlocking finger figures was compared with concurrent performance on formal neurocognitive tests. Poor interlocking finger test scores correlated most highly with standard measures of parietal lobe dysfunction. In addition, an analytical model of parietal dysfunction indicated the interlocking finger test was similar to, if not better than, standard tests of parietal lobe dysfunction. Attempts to imitate these figures should serve as a fast and simple screen of parietal lobe dysfunction.
It is a commonly held view that numbers are represented in an abstract way in both parietal lobes. This view is based on failures to find differences between various notational representations. Here we show that by using relatively smaller voxels together with an adaptation paradigm and analyzing subjects on an individual basis it is possible to detect specialized numerical representations. The current results reveal a left/right asymmetry in parietal lobe function. In contrast to an abstract representation in the left parietal lobe, the numerical representation in the right parietal lobe is notation dependent and thus includes nonabstract representations. Our results challenge the commonly held belief that numbers are represented solely in an abstract way in the human brain.
OBJECT: The goal of this study is to report the incidence and clinical evolution of neurological deficits in patients who underwent resection of gliomas confined to the parietal lobe. METHODS: Patient demographics, findings of serial neurological examinations, tumor location and neuroimaging characteristics, extent of resection, and surgical outcomes were tabulated by reviewing inpatient and office records, as well as all pre- and postoperative magnetic resonance (MR) images obtained in 28 consecutive patients who underwent resection of a glial neoplasm found on imaging studies to be confined to the parietal lobe. Neurological deficits were correlated with hemispheric dominance, location of the lesion within the superior or inferior parietal lobules, subcortical extension, and involvement of the postcentral gyrus. The tumors were located in the dominant hemisphere in 18 patients (64%); had a mean diameter of 39 mm (range 14-69 mm); were isolated to the superior parietal lobule in six patients (21%) and to the inferior parietal lobule in eight patients (29%); and involved both lobules in 14 patients (50%). Gross-total resection, documented by MR imaging, was achieved in 24 patients (86%). Postoperatively, nine patients (32%) experienced new neurological deficits, whereas seven (25%) had an improvement in their preoperative deficit. A correlation was noted between larger tumors and the presence of neurological deficits both before and after resection. Postoperatively higher-level (association) parietal deficits were noted only in patients with tumors involving both the superior and inferior parietal lobules in the dominant hemisphere. At the 3-month follow-up examination, five of nine new postoperative deficits had resolved. CONCLUSIONS: Neurological deterioration and improvement occur after resection of parietal lobe gliomas. Parietal lobe association deficits, specifically the components of Gerstmann syndrome, are mostly associated with large tumors that involve both the superior and inferior parietal lobules of the dominant hemisphere. New hemineglect or sensory extinction was not noted in any patient following resection of lesions located in the nondominant hemisphere. Nevertheless, primary parietal lobe deficits (for example, a visual field loss or cortical sensory syndrome) occurred in patients regardless of hemispheric dominance.
1. We determined the effects of lesions of the parietal lobe on the capacities of monkeys to detect and discriminate between mechanical sinusoids delivered to the hand. Tests of discrimination measured the capacity to discriminate between frequencies of flutter (24--36 Hz) and the capacity to make gross discriminations of frequency of flutter-vibration over the range of 10--50 Hz. 2. A unilateral removal of the parietal lobe impaired sensory capacities only on the contralateral hand; detection threshold was elevated, the capacity to discriminate between frequenceis of flutter was permanently lost, and the capacity to discriminate between and identify frequencies of 10--50 Hz was grossly impaired. No defects were found on the hand ipsilateral to the lesion. Detection thresholds, but not discrimination thresholds, decreased during postoperative testing, but in most cases did not recover to preoperative values. The impairments in frequency discrimination remained through the last day of postoperative testing. 3. A unilateral, subtotal parietal lesion that completely destroyed the primary and secondary somatic areas and Brodmann's area 5 resulted in the same sensory impairments as those produced by total removal of the parietal lobe. In most cases, detection threshold was elevated; flutter-frequency discrimination was lost, and the capacity to discriminate between frequencies of 10--50 Hz over the extended range of flutter and vibration was impaired. 4. The loss in discriminative capacity following lesions of the somatosensory cortex is interpreted as due to the absence of a cortical mechanism that determined differences in the temporal pattern of cyclically entrained activity in the somatic afferent pathway. This loss was dissociated from the remaining capacity, although impaired, to detect the presence of any neural activity in the afferent pathways or to determine gross differences in the frequency of mechanical sinusoids by a mechanism of coding by the labeled line.
We report the clinical manifestations and outcome of 82 patients with nontumoural parietal lobe epilepsy treated surgically at the Montreal Neurological Institute between 1929 and 1988. Patients with extensive resections extending outside the parietal lobe were excluded. Ninety-four percent exhibited aurae: the most common were somatosensory, described by 52 patients; 13 of these also described pain. Other aurae included disturbances of body image, visual illusions, vertiginous sensations and aphasia or dysphasia. A few patients exhibited complex visual or auditory hallucinations and elementary visual hallucinations. Intraoperative cortical stimulation reproduced the habitual aurae in 44 patients. Often the clinical manifestations indicated ictal spread to the frontal, supplementary motor area, or temporo-limbic areas: 28% of patients exhibited tonic posturing of the extremities, 57% unilateral clonic activity, 17% oral or gestural automatisms and 4% complex automatisms. Sixty-one percent of patients with tonic posturing had epileptogenic zones which included the superior parietal lobe, and in 79% of patients with automatisms the epileptogenic zones extended to the inferior parietal lobe, suggesting different spread patterns. Forty-three patients underwent right, and 39 left parietal corticectomies. Postoperative sensory deficits were seen only when the corticectomy extended into the post-central gyrus. Early in the series extensive nondominant inferior parietal resections led to disturbances of body image in a few patients. Follow-up ranging from 2 to 50 years was available for 79 patients. Sixty-five percent had a complete or nearly complete cessation of seizures. Those patients with no post-resection electrocorticographic epileptiform discharges had a more favourable outcome.
Wave P 300 was studied in nine patients with parietal lobe lesions who had visual neglect but no hemianopia. Stimulation of the hemispace contralateral to the lesion showed a lengthening in latency and a decrease in amplitude of P 300, specifically related to visual stimulation. Comparison with results obtained in 14 normal subjects and four patients with localized hemispheric lesions without visual neglect showed that changes in P 300 were specifically related to visual neglect. The parietal lobe lesions may disturb cerebral processes involved in discrimination and visual stimulus evaluation required to perform a task, inducing disturbance of the system responsible for P 300.
Gelastic seizures have been described in various epilepsies arising from the temporal or frontal lobes, although the most commonly encountered form is related to the presence of an hypothalamic hamartoma. We report a patient with gelastic seizures involving the right parietal lobe. Our patient, a 32-year-old man, underwent video-EEG monitoring, interictal and ictal brain SPECTs during gelastic seizures. Subtraction ictal SPECT co-registered to MRI (SISCOM), was performed to localize any ictal hyperperfusion during these gelastic seizures. The seizures consisted of brief staring followed by smiling and laughing. Electroencephalography during the gelastic seizures showed rhythmic sharp waves in the right parietal lobe. SISCOM showed ictal hyperperfusion in the right parietal lobe and medial portions of right cerebellum. Our findings suggest that the right parietal lobe may actively participate in the particular epileptogenic network generating gelastic seizures.
We reported a case of an 86-year old woman with pure agraphia due to the left parietal lobe infarction. The characteristics of agraphia were as follows. Most errors in Kana and Kanji writing to dictation and copying were no response. She was able to write only numerals from 1 to 12 precisely. Most errors in numerals were substitution. One unrecognizable numeral was found. She succeeded in pointing to nine among ten single Kana letter named by the examiner with the systematic table of the Japanese syllabary, but missed in pointing to Kana words. It took more time for the patient to point to single Kana letter than the control. Magnetic resonance imaging showed a cerebral infarction in the left parietal lobe which included a part of superior parietal lobule and supramarginal gyrus. We classified pure agraphia with parietal lobe infarction into two types in our previous report. In one type (type 1), letters in writing are poorly formed, but the ability to make words with the methods other than writing are reserved. The only deficit of graphic motor pattern could cause Type 1 agraphia. In another type (type 2), letters in writing were well-formed, but spelling with anagram or typing was disturbed. The deficits of writing process other than graphic motor pattern could cause Type 2 agraphia. This typing seems to be effective not only in Kana but also in Kanji. In this report, we investigated the differences of lesion between two types out of some references. Type1 agraphia seems related to lesion of left superior parietal lobule, while Type 2 agraphia seems related to lesion of left supramarginal gyrus. This case had the features of type 2 agraphia at least, and the compatible lesions.
A case of agraphia due to cerebral infarction in the left parietal lobe was reported. A 63-year-old right-handed man was admitted to our hospital with writing disturbance. His spontaneous speech was fluent, and object naming, word fluency, repetition, verbal comprehension, and reading were fully preserved. However, his writing was slow and required effort. He showed hesitation in spontaneous writing and dictation. His power to copy was better than his power to write spontaneously or to take dictation, but he had some difficulty in copying letters and complex figures. The patient showed abnormal sequences of strokes and completed his strokes by piecing out of several fragments. CT scan and MRI showed a cerebral infarction in the left parietal lobe which included the superior parietal lobule. The amytal (Wada) test, which was performed via the left internal carotid artery, revealed that the left hemisphere was dominant for language. The characteristics of his agraphia much more closely resembled "apractic agraphia", as reported by Alexander et al (1992), than spatial agraphia or pure agraphia. Agraphia in this patient might result partially from the loss or unavailability of the memory of motor patterns necessary for writing letters.
Attentional control involves the factors, or cognitive parameters, that determine which environmental inputs receive attention and which do not. Cognitive studies of attentional control have highlighted two general classes of control parameters, bottom-up (data driven or exogenous) parameters and top-down (goal driven or endogenous) parameters. Which of these control parameters is affected following parietal-lobe damage? In parietal-damaged patients, it is possible that a disorder in one control parameter (e.g. goal driven) would appear as a disorder in another parameter (e.g. data driven). To investigate the control parameters that might be affected in parietal patients, we simulated neglect in normal participants by disrupting data-driven information processing. When half of a computer monitor was degraded by translucent tracing paper while normal participants performed a cued spatial attention task (Experiment 1), the normal participants showed a pattern of results similar to patients with unilateral parietal-lobe damage--the so-called "disengage deficit." This pattern of results replicated when neutral attentional cues were included in the experiment (Experiment 2). However, the disengage deficit was not simulated in normal participants with predictive central symbolic cues (Experiment 3) or predictive peripheral cues (Experiment 4). Because perceptual degradation influences data-driven attentional control parameters, we suggest that these control parameters may be disrupted following parietal-lobe damage.