Development of glioblastoma after medulloblastoma.
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Biomedical subjects
Publications and source records attributed to M Kushner.
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Local cerebral glucose metabolism was determined with 18-F-fluorodeoxyglucose using positron emission tomography in a sample of 12 unmedicated schizophrenics and 12 matched normal controls. The data were analyzed for absolute metabolic rates and region/whole-brain ratios using the cortical-subcortical, antero-posterior, and laterality dimensions. Lobar areas within cortical regions were also compared. Across groups, subcortical metabolism was higher than cortical metabolism. Patients had lower metabolism, cortically and subcortically, and a steeper subcortical to cortical gradient. Patients with higher scores on the Brief Psychiatric Rating Scale had higher absolute metabolism and higher left relative to right hemispheric metabolism than did patients with lesser severity. The results did not show "hypofrontality" in schizophrenia. These findings provide some support for cerebral dysfunction in schizophrenia and indicate the need for further examination of the cortical-subcortical dimension.
Cerebral glucose metabolism was measured twice in a sample of 15 schizophrenics and eight controls, using positron emission tomography (PET) with 18-F-fluorodeoxyglucose. Studies were separated by three to 33 weeks. Patients were unmedicated during the first study, and the majority were receiving neuroleptics during the second study. There were no changes from study 1 to study 2 in average whole-brain metabolic rates, regional cortical activity, or the gradient of subcortical to cortical activity. The steeper subcortical to cortical gradient in schizophrenics, present in the first study, persisted in the second. Changes in this gradient were uncorrelated with changes in clinical status. Laterality (right-left) was stable across studies, and changes toward higher right relative to left hemispheric metabolism were correlated with clinical improvement. The results support the hypothesis of abnormal hemispheric activity in schizophrenia and implicate the subcortical-cortical gradient as another dimension that merits further exploration.
We used [18F]fluoro-2-deoxyglucose positron emission tomography (PET) to study serial changes in the local cerebral metabolic rate of glucose in 5 patients with ischemic lesions of the posterior afferent visual system causing homonymous visual field defects. All 5 patients had striking impairment of glucose metabolism in the striate cortex shortly after ictus. In 2 patients, visual field defects abated, and repeat PET scans showed reduced size of the metabolic lesion and improvement of striate metabolism. Three patients did not recover vision, and repeat PET scans did not show improvement. Patients who recovered vision had ischemic lesions outside the occipital lobe, while those who did not experience improvement had primary damage to the occipital lobe itself.
Local cerebral metabolism was determined in a patient suffering aphemia following cerebral infarction using the 18FDG-PET technique. The syndrome was characterized by profound ictal nonfluency with sparing of other language functions. Speech subsequently improved so that content and grammar were appropriate but mild dysprosody persisted. Conventional CT showed no lesion of the left hemisphere while PET revealed a discrete focus of hypometabolism on the left which partially resolved on serial studies. The metabolic lesion could be localized to the region of the inferior precentral gyrus and the adjacent subcortical space.
Positron emission tomography (PET) studies with 18F deoxyglucose were completed in 35 patients with acute ischemic strokes. Twelve cases were studied within 72 h, 23 between 4 and 14 days. Results indicate the functional and prognostic significance of early tomography studies of metabolism, and anticipate possible use of metabolic imaging in the evaluation of treatment.
We studied cerebral metabolism, anatomy, and clinical status in 36 patients with acute cerebral ischemia. Results from FDG-PET were compared with CT to find the relationships between the metabolic, anatomic, and clinical findings. Metabolic abnormalities seen on PET frequently were more extensive than the corresponding CT findings. The pattern of metabolic abnormality was significantly related to both the type of clinical syndrome and the degree of eventual recovery. No such relationships were found for the CT results. We conclude that studies of cerebral metabolism are of value in establishing prognosis after acute cerebral ischemia. Also, knowledge of the patterns of cerebral dysmetabolism provides a powerful means for the localization of clinical function.
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We studied cerebellar metabolism in 118 subjects including young and elderly controls and patients suffering from stroke, supratentorial brain tumor and Alzheimer's disease using fluorine-18 fluorodeoxyglucose ([18F]FDG) and position emission tomography (PET). Alzheimer's disease and normal aging did not alter mean cerebellar metabolism. In stroke and tumor mean cerebellar metabolism was lower in the hemisphere contralateral to the supratentorial lesion. In tumor bilaterally significant reductions in absolute cerebellar metabolism also were noted, unlike stroke. Primary sensory stimulation did not alter absolute or relative cerebellar metabolism. These results show that absolute and relative values for cerebellar metabolism vary depending on the process under study. Thus analysis schemes employing normalization of regional metabolic data to cerebellar values may be subject to error.
Slowly progressive aphasia without generalized dementia is a degenerative syndrome selectively affecting dominant hemisphere language areas. We report changes in regional glucose metabolism measured by positron emission tomography in two patients with this condition. Striking abnormalities of glucose utilization in the left cerebral cortex were demonstrated in both patients. The findings of other neurodiagnostic studies were relatively unremarkable. The first patient had a 3-year history of progressive anomia and impaired auditory verbal recall. An electroencephalogram was normal, and computed tomography showed mild left perisylvian atrophy. Positron emission tomography revealed profound hypometabolism in the left temporal regions. The second patient also had a 3-year history of progressive anomia. Electroencephalography, computed tomography, and magnetic resonance imaging scans were normal. Positron emission tomography showed a major reduction in left parietal glucose utilization, with a lesser decrement in left temporal metabolism. Neither patient demonstrated significant contralateral or global abnormalities such as those reported in positron emission tomographic studies of Alzheimer's disease with or without focal clinical features. These observations support the concept of adult-onset progressive aphasia without dementia as a clinical syndrome distinct from Alzheimer's disease.
The (F-18) fluorodeoxyglucose (FDG) technique to measure local cerebral metabolic rate for glucose (LCMRglu) is well accepted and widely used by many institutions around the world. A large number of studies has been carried out in normal volunteers and patients with a variety of CNS disorders. Several investigators have noted that no significant age-related changes in cerebral glucose use occur with normal aging. Some important and interesting findings have been revealed following sensory, motor, visual, and auditory stimulations. Functional imaging with FDG in certain neurologic disorders has dramatically improved our understanding of their underlying pathophysiologic phenomena. Some abnormalities detected on the positron emission tomography (PET) images have no corresponding changes on either x-ray computed tomograms (XCT) or magnetic resonance images (MRI). In patients with Alzheimer's disease, primary sensorimotor, visual, and cerebellar metabolic activity appears relatively preserved. In contrast, parietal, temporal, and to some degree, frontal glucose metabolism is significantly diminished even in the early stages of the disease. Patients with Huntington's disease and those at risk of developing this disorder have a typical pattern of diminished CMRglu in the caudate nuclei and putamen. In patients with stroke, PET images with FDG have demonstrated abnormal findings earlier than either XCT or MRI and with a wider topographic distribution. FDG scans have revealed interictal zones of decreased LCMRglu in approximately 70% of patients with partial epilepsy. The location of the area of hypometabolism corresponds to the site of the epileptic focus as determined by electroencephalography and microscopic examination of the resected tissue. Ictal scans during partial seizures demonstrate areas of hypermetabolism corresponding to the sites of seizure onset and spread. Several investigators have reported relative hypofrontal CMRglu in patients with schizophrenia. In our center, FDG scans from patients with schizophrenia were successfully differentiated from those obtained in normal controls. Finally, our preliminary data (using PET, XCT, and MRI) in patients with CNS disorders indicate that MRI provides excellent delineation of the structural abnormalities. It may prove to be superior to XCT in the evaluation of certain diseases such as cerebral ischemia and infarcts, head injury, tumors, and white matter lesions. Metabolic imaging with FDG provides functional information not obtainable with either MRI or NMR spectroscopy. Therefore, PET studies will play a complementary role to the anatomic imaging in the management of patients with CNS disorders.
A 56-year-old man developed sinus node dysfunction culminating in 27 seconds of asystole during a thrombotic stroke. Bradyarrhythmias resolved over a period of 96 hours, at which time sinus node recovery times were normal. Sinus node dysfunction has not recurred during the two years of follow-up. We suggest that cardiac rhythm be closely monitored in acute stroke patients.
This work describes the determination of CBF in eight normal human subjects with positron emission tomographic (PET) imaging using the continuous intravenous infusion of H2(15)O. A whole-brain CBF model is described that permits the comparison of the CBF values determined using PET with those obtained using other methods. This model includes a correction for whole-brain recovery coefficient, a correction for the underestimation of flow due to the nonlinearity of the CBF model when considering tissue that includes both gray and white matter, the use of in vitro-determined brain-blood partition coefficients for gray and white matter, and a variation of the equilibrium model that permits the arterial concentration to vary. CBF values using this method compare well with values determined previously. Regional determinations using a brain overlay atlas are presented. Radiation dosimetry for the continuous infusion of H2(15)O is also included.
Superficial vasomotor tone in the forearm has been thought to be dependent mostly on vasodilatation rather than vasoconstriction. Despite this view we report now that a mechanism for profound vasoconstriction exists in the forearm surface. This phenomenon was observed in normal subjects undergoing elective radial artery catheterization and the stimulus for the vasoconstriction consisted of the intra-arterial infusion of normal saline (rate of 0.5 - 6.0 ml/min). Two components to this reaction were observed. A stable pericatheter zone of pallor varied in extent proportional to the rate of infusion. The second component consisted of distal patches of vasoconstriction over the whole anterior forearm surface which first appeared 5 to 10 seconds after the infusion rate was increased. These satellite areas tended to coalesce with sustained infusion but they were unstable over time. Local changes in vascular intrinsic regulation can account for the pericatheter vasoconstriction but this does not readily explain the observed distal changes. The time latency, distribution and evolution of the distal vasoconstriction suggests the operation of an autonomic vasomotor reflex arc.
In 44 patients, we studied the effects of superficial temporal-middle cerebral artery anastomosis on cerebral blood flow (CBF), neurologic examination, and cognitive functions. At 3 months, there was significant improvement in all variables. At 9 months, CBF was no longer significantly greater, but neurologic examination and cognitive functions had further improved. Patients with TIA had significant postoperative decreases in TIA frequency and did not progress to stroke, but had no significant changes in any variable. In stroke patients, we could not separate the effects of surgery from the natural evolution of changes in CBF and examination after stroke. None of the preoperative measurements predicted postoperative clinical improvement.
We used 18-F-fluoro-2-deoxyglucose positron emission tomography (PET) and computed tomography (CT) to study eight patients with homonymous hemianopias or quadrantanopias due to ischemic lesions of the visual pathways. Four patients with ischemic damage to all or part of the occipital lobe had decreased glucose metabolism in the affected region. Three patients with ischemic damage limited to the optic radiations had decreased glucose metabolism in the portion of striate cortex appropriate for the visual field defect. Changes in glucose metabolism frequently occurred in the undamaged ipsilateral thalamus and visual association areas.
The size and orientation of the spikes produced by a pacemaker are often used by clinicians as an index of the pacemaker's function. Following implantation, the pacemaker spikes ordinarily remain constant in size; alterations suggest electrical or mechanical malfunction. We describe a patient in whom giant spikes from a pacemaker were recorded on a digital electrocardiograph shortly after implantation. An electrocardiogram taken the following day, using an analog machine, showed marked diminution in the pacemaker spike. Because of a different type of signal processing, digital electrocardiographs show much larger spikes from pacemakers than do analog machines.
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