Hemiballismus: detection of focal hemorrhage in subthalamic nucleus by CT scan.
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Biomedical subjects
Publications and source records attributed to E Melamed.
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Data from recent studies in experimental animals suggest that central dopaminergic mechanisms may be involved in regulation of the regional cerebral blood flow (rCBF) in the mammalian brain. In order to evaluate possible effects of dopaminergic stimulation on human cerebral circulation, rCBF was measured by the 133Xenon inhalation technique in 26 patients with Parkinson's disease before and after the chronic oral administration of levodopa combined with a peripheral Dopa-decarboxylase inhibitor. Treatment with levodopa did not induce significant alterations in the mean brain, mean hemispheric or regional flow values in these patients. These findings suggest that the dopaminergic system does not play an important role in modulation of the rCBF in man.
Measurement of the regional cerebral blood flow (rCBF) by the 133Xenon inhalation method and computerised tomography were performed in 25 patients with presenile and senile dementia. Reduction of rCBF and various degrees of ventricular enlargement and cortical sulcal widening were demonstrated in the majority of demented subjects. However, there was no correlation between rCBF values and the severity of ventricular dilatation or cortical atrophy. These findings suggest that loss of brain substance is not an important factor in the reduction of rCBF in dementia.
In two patients, lesions in the non-dominant parietal lobe were associated with global anaesthesia to all sensory modalities affecting the opposite half of the body. A striking inconsistency existed between the complaints of limb anaesthesia and the grossly preserved motor and postural control of the involved limb. The gross discrepancy between complaint and functional ability prompted early consideration of a "non-organic" diagnosis. It is suggested that this unusual sensory deficit may be due to distorted perception of somatosensory stimuli, representing another disorder of body schema associated with parietal lobe lesions. The diagnosis of non-organic illness may then be avoided by focusing on a search for parietal disease.
A new fluorescent beta-adrenergic antagonist, 9-amino-acridin propranolol (9-AAP), was administered intravenously to living mice. In the cerebral cortex, the highest concentration of 9-AAP was noted in the hippocampal formation, where it distinctly labeled the hippocampal pyramidal cell layer and the granule cell layer of the dentate gryus. High uptake occurred in the pyramidal cell layer of the piriform cortex. In the neocortex, fluorescence was less dense and more diffuse but confined to the basal layers. A similar pattern was observed in the basal layers of the cingulate cortex, but an additional high-density dotted fluorescence labeled its layer II. In the cerebellar cortex, 9-AAP was localized within the Purkinje cell layer. In the spinal cord, the highest density of fluorescence was observed in the nuclear collections of alpha-motoneurons. The findings were similar to those observed in the central nervous system of the rat and support the reproducibility of the method. 9-AAP may be used in vivo as a fluorescent probe to map out the central beta-adrenergic receptor system.
A fluorescent analogue of propranolol, 9-AAP, was injected intravenously in order to detect beta-adrenergic receptors in the anterior segment of the albino rat eye. Specific 9-AAP fluorescence was noted along cell membranes of the ciliary epithelium and to lesser extent in the walls of blood vessels in the ciliary processes and episclera at the limbus. The iris showed maximum 9-AAP binding in the region of the sphincter muscle. These data suggest that 9-AAP may label beta receptors in the anterior segment of the rat eye.
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A new fluorescent beta-adrenergic blocker, 9-amino-acridin propranolol (9-AAP), was administered intravenously to albino rats. Fluorescent aggregates of 9-AAP binding sites were concentrated in the vascular poles of the glomeruli in association with the preglomerular afferent arterioles. 9-AAP fluorescence was reduced following pretreatment with (+/-)- and (-)-propranolol and was less affected in rats pretreated by the (+)-racemic isomer. 9-AAP binding sites were also observed on the lining epithelium of the renal collecting system. Our data suggest that 9-AAP may label beta-adrenergic receptors in rat kidney.
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A new fluorescent beta-blocker, 9-amino-acridin propranolol (9-AAP), was administered i.v. to rats. Multiple fluorescent 9-AAP binding sites were observed on cardiac muscle cells in frozen sections. Intensity and density of cardiac 9-AAP fluorescence were markedly reduced following pretreatment with (+/-)- and (-)-propranolol but not with (+)-propranolol. Our findings suggest that 9-AAP may label beta-adrenergic receptor sites in rat myocardium.
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The corneal copper content was measured by X-ray excitation spectrometry in two controls and in seven patients with Wilson's disease. Patients who were treated irregularly or not treated at all showed a high corneal copper content. Those who were adequately treated had low levels, comparable to the controls. In one case the corneal copper content declined 45%, after a course of dimercaprol. The corneal copper measured showed no correlation with the slit-lamp appearance of the Kayser-Fleischer ring. It is suggested that non-invasive X-ray excitation spectrometry can provide a fast and reliable method for the early diagnosis of Wilson's disease and for the objective evaluation of the efficacy of the treatment of this disease.