[Brain tumors arising from frontal and parietal lobes].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the 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.
A woman who had spontaneous pain, hyperpathia and wasting of her left hand due to a subcortical lesion in the right parietal lobe is reported. The presentation and evaluation of this most unusual case are discussed.
We report a patient with selective short-term memory disturbance caused by a glioma in the left temporal-parietal lobe. The patient was a 40-year-old right-handed housewife who complained of difficulty in memorizing series of numbers. She was working as a car dealer. She was well until 6 months prior to the present admission when she noted a difficulty in memorizing series of numbers such when telephone numbers and car registration numbers. She had to write them down as her customers told them to her. On admission, she was alert and oriented to all spheres. She was mentally sound without dementia. She did not show aphasia, apraxia, or agnosia, except for brief periods of seizures in which she became unable to speech. Neuropsychological examination revealed that she had difficulty in repeating and dictating series of numbers and meaningless kana words. However, she could easily pick up the correct series of numbers or kana words among multiple choices presented visually. Thus it was clear that her problem was not the disturbance of auditory input nor expression, but a selective impairment of short-term memory. She could memorize the same stimuli when visually presented. Therefore, her problem was thought to be a disturbance of auditory short-term memory of meaningless words. After resection of her tumor, she developed transient amnesic aphasia, which improved a year later. She was examined again in her memory function. In the task of visual stimuli, we presented her a card in which a series of numbers or a nonsense syllable was written for 5 seconds and asked her to remember them.(ABSTRACT TRUNCATED AT 250 WORDS)
The perception threshold for trains of rapid tactile pulses, applied to the index finger, has been measured in patients with parietal lobe lesions and in patients with median nerve lesions. The former patients had increased perception thresholds for single tactile pulses on the abnormal side. With successively prolonged pulse trains, the threshold decreased exponentially to reach a stable level after 150-400 ms. In contrast, the median nerve patients had increased perception thresholds for tactile pulses irrespective of pulse train duration.
We reported a case of a 63-year-old right handed man with pure agraphia due to the left parietal lobe infarction. The characteristics of agraphia in the patient were as follows. 1) The written letters were generally recognizable and well formed. 2) He succeeded in pointing to single Kana letter named by the examiner from the Japanese syllabary, but missed in pointing to Kana words. 3) Further, it took more time for the patient to point to even single Kana letter than for the control. 4) Most errors in Kana writing was substitution. Errors in Kanji writing are partial lacking or no response. But his ability in Kanji writing was facilitated by visual cues. He was unable to describe the Hen (a left-hand radical) and Tsukuri (the body) of some Kanji letters and to name some Kanji letters when their Hen and Tsukuri were orally given. We classified pure agraphia into two types out of some references. In one type (Type 1), letters in writing are poorly formed, but the ability to make words with the methods other than writing, for example spelling with anagrams or typing are preserved. In another type (Type 2), letters in writing were well-formed, but spelling with anagrams or typing were abnormal. Type 1 agraphia could result from the only deficit of graphic motor engram, while type 2 agraphia could be caused by the deficits other than graphic motor engram. Agraphia in this case belongs to the type 2. The features of agraphia in this case suggested that his agraphia was caused by a disorder in recalling graphemes of letters, and in arranging at least of Kana-letters.
Explore the source record for details and available documents.
Optokinetic nystagmus (OKN) was studied by computer analysis in nine patients with lesions on the left unilateral parietal lobe (group A) and in five patients with lesions on the entire left hemisphere (group B), as confirmed by CAT or MRI scans. OKN stimulation and recordings were evaluated based on the optokinetic pattern (OKP). In group A, there was no directional preponderance. However, in group B, the Electronystagmography recordings showed typical asymmetry of OKP. This asymmetry was revealed by a low amplitude and a significantly impaired slow-phase eye velocity of the right OKP. Asymmetry of OKP resulted from the impaired slow-phase eye velocity of the contralateral OKN to the damaged hemisphere because of a slight change in fast-phase eye velocity.
The case of a 4 year old boy with a dysembryoplastic neuroepithelial tumor (DNT) of the left parietal lobe is reported. The DNT was located mainly in the cortex and showed no mass effect on magnetic resonance imaging (MRI). T1-weighted images of the DNT showed the characteristic findings of lesion hypointensity, but with a well preserved gyrus-like configuration. This lesion was isointense to the normal cortex on proton density imaging and hyperintense on T2-weighted imaging. The characteristic features on T1-weighted and proton density imaging in this patient were useful in differentiating DNT from other types of tumors. Histologic findings in DNTs, which include the presence of both glial and neuronal cells without atypia and no definite transitional zone between the adjacent disorganized cortical cell layers, suggest that DNT is not a true neoplasm but rather a dysplastic lesion. It is clinically important to differentiate this tumor both from other benign tumors and malignant tumors which have different prognoses and therapies. The distinctive MRI findings, as well as the histologic features of DNT, support the diagnosis in the clinical setting.
The authors described a case of multiple arteriovenous malformations of the left parietal lobe and the left cerebellar hemisphere, and presented a review of literature. A 42-year-old right-handed man was admitted to our Dept. of Neurosurgery on October 20, 1983, with left facial pain and occipitalgia. He had an episode of subarachnoid hemorrhage ten years ago, however, its etiology was not clear at neurological examination. This brief episode of pain began on the left side of his face about 9 years ago and has been gradually increasing. Although he has been treated with trigeminal nerve blocks several times, relapses were almost always evident within 6 months after those nerve blocks. On admission, there were no abnormal findings at neurological and physical examination. A CT scan with contrast medium infusion revealed two small AVMs on the left parietal region and on the left cerebellar hemisphere. A four-vessels cerebral angiogram confirmed the presence of two AVMs and fenestration of the left vertebral artery. The angiogram also revealed that his severe left trigeminal neuralgia had been caused by elongation of the anterior pontine segment of left SCA which was the main feeder of the cerebellar AVM. Two stages of surgical operations were carried out at two months interval. The first operation was total removal of the cerebellar AVM and microvascular decompression for the left trigeminal nerve. The second was total removal of the left parietal AVM. The postoperative course was uneventful, and angiographically the AVMs completely disappeared. The patient was discharged without any neurological deficits on March 11, 1984.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the neuropsychological mechanisms of kinesthetic alexia, we asked 7 patients who showed kinesthetic alexia with preserved visual reading after damage to the left parietal region to perform tasks consisting of kinesthetic written reproduction (writing down the same letter as the kinesthetic stimulus), kinesthetic reading aloud, visual written reproduction (copying letters), and visual reading aloud of hiragana (Japanese phonograms). We compared the performance in these tasks and the lesion sites in each patient. The results suggested that deficits in any one of the following functions might cause kinesthetic alexia: (1) the retrieval of kinesthetic images (motor engrams) of characters from kinesthetic stimuli, (2) kinesthetic images themselves, (3) access to cross-modal association from kinesthetic images, and (4) cross-modal association itself (retrieval of auditory and visual images from kinesthetic images of characters). Each of these factors seemed to be related to different lesion sites in the left parietal lobe.
In vitro influence of vanadate and vanadyl ions on the activities of Na,K- and Ca,Mg-ATPase from synaptosomal membranes of the parietal lobe of the human brain were compared. 1. Vanadate and vanadyl inhibit the enzymes activities in the investigated fraction. 2. Vanadate is a more effective inhibitor of both ATPases in the concentrations above 50 microM and vanadyl is an effective inhibitor in a very low concentration (10 nM). 3. Vanadate seems to be an uncompetitive inhibitor of Na,K-ATPase (K1 = 880 nM).
This paper reports on a case of a 70-year-old physician diagnosed with a parietal lobe abscess following such treatment. After stereotactic biopsy and drainage and a 6-week course of intravenous antibiotic treatment, the patient recovered with minimal neurologic deficits. Although brain abscesses are not commonly encountered in practice, clinicians must be aware of the potential virulence of the anaerobic components of the periodontal pocket and the possibility of resulting systemic infection, which can produce a life-threatening situation.
Patients with right parietal lesions often deny their paralysis (anosognosia), but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task (e.g., tying shoe laces) vs a unimanual one (e.g., threading a bolt). They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis (or, if such knowledge exists, it is not available for this particular task). Second, I used a "virtual reality box" to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM's left ear canal with cold water, a procedure that is known to shift that patient's spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of the paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also employ a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift." A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor.
At present there is hardly any appropriate therapy for central pain syndromes available. We report on a unique case of a central thalamic pain syndrome that did not respond to any therapy but disappeared after an additional contralateral parietal lobe lesion. This example indicates that lesions affecting the bilateral balance of thalamo-parietal circuits may lead to pain relief in patients with central pain syndrome, which probably constitutes a bilateral disorder of functional plasticity. This should be taken into account in chronic brain stimulation for persistent pain states.
Explore the source record for details and available documents.
This study assessed accuracy of visually perceived vertical and trunk median plane orientation in 41 subjects: 17 had unilateral brain lesions including the posterior parietal lobe (PPL), 8 had lesions outside PPL, and 16 were neurologically normal. Vertical perception errors clearly increased with size of unilateral lesions to PPL and posterior superior temporal gyrus (PSTG). Median plane perception errors increased only slightly with size of unilateral lesions to frontal lobe premotor areas and supramarginal gyrus. These results are compatible with the hypothesis that accurate visual vertical perception depends critically on intact PPL and PSTG in both cerebral hemispheres while accurate median plane perception likely involves a bihemispheric network that can compensate for lesions to one hemisphere.
Intracranial lesions may compromise structures critical for motor performance, and mapping of the cortex, especially of the motor hand area, is important to reduce postoperative morbidity. We investigated nine patients with parietal lobe tumours and used functional MRI sensitized to changes in blood oxygenation to define the different motor areas, especially the primary sensorimotor cortex, in relation to the localization of the tumour. Activation was determined by pixel-by-pixel correlation of the signal intensity time course with a reference waveform equivalent to the stimulus protocol. All subjects showed significant activation of the primary sensorimotor cortex while performing a finger opposition task with the affected and unaffected side. In five patients the finger opposition task additionally activated the ipsilateral sensorimotor cortex and the supplementary motor area (SMA). Extension and flexion of the foot, additionally performed in two patients, also activated the sensorimotor cortex, in one case within the perifocal oedema of the tumour. Tumour localization near the central sulcus induced displacement of the sensorimotor cortex as compared to the unaffected side in all patients with a relevant mass effect. The results of our study demonstrate that functional MRI at 1.5 T with a clinically used tomograph can reproducibly localize critical brain regions in patients with intracranial lesions.