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Biomedical subjects

G Yasargil

Publications and source records attributed to G Yasargil.

8 recordsLinked to original sources
PubMed1997

The anterior and posterior selective temporal lobe amobarbital tests: angiographic, clinical, electroencephalographic, PET, SPECT findings, and memory performance.

The techniques, results, and problems of three types of selective temporal lobe (TL) amobarbital procedures (balloon technique with temporary occlusion of the internal carotid artery distal to the origin of the anterior choroidal artery (acha) [n = 19]; selective anterior catheterization of the acha [n = 20]; and selective catheterization of the peduncular P2-segment of the posterior cerebral artery [n = 5]) are described in a group of 40 patients with medically refractory complex partial seizures of mesial TL origin. Selective amobarbital tests were carried out before surgery to predict the memory deficit after an intended selective amygdalohippocampectomy. The effects of selective anaesthetization of TL were correlated with clinical data, pattern and duration of amobarbital induced EEG changes, and performance on verbal and nonverbal memory tasks measured during the test. In 4 patients the effect of selective amobarbital injection on regional and global metabolism was studied with 18F-FDG-PET, with the PET tracer being injected intravenously immediately after amobarbital. More recently in 2 patients the vascular territory perfused by amobarbital in the acha test was studied with SPECT using 99m Tc ECD injected immediately prior to the amobarbital into the acha. Whereas the PET studies showed a rather widespread and bilateral amobarbital-induced decrease of metabolism, the SPECT studies confirmed the selective distribution of the tracer in the vascular territory of the acha, i.e., in amygdala and hippocampus. The comparison of selective TL amobarbital test performance with postoperative neuropsychological performance showed that the predictive value of this test is rather good for the postoperative verbal memory but underestimates postoperative nonverbal ("figural") memory performance.

Adult↗
PubMed1990

Neuropathology of a human hippocampus following long-term treatment with vigabatrin: lack of microvacuoles.

Vigabatrin (gamma-vinyl-GABA), an irreversible inhibitor of gamma-aminobutyric acid transaminase, has been reported to be effective in the treatment of refractory epilepsies. Animal toxicology studies have shown that long-term application of vigabatrin induces intramyelinic edema and microvacuolation of the white matter in non-primate species. However, clinical and neuropathological studies of patients exposed to long-term vigabatrin treatment have, so far, provided no evidence for microvacuolation in the human brain. We report on the histopathological findings of selective amygdalohippocampectomy specimens from a 36-year-old female patient treated with vigabatrin for a period of 11.5 months, and from 2 control patients with chronic refractory temporal lobe seizures. All specimens showed changes associated with chronic epileptic seizures including focal neuronal loss and hippocampal gliosis. Microvacuoles, intramyelinic edema or other manifestations of neurotoxic damage were not observed in vigabatrin exposed tissue, supporting the view that this compound may not exert hippocampal neurotoxicity in humans.

Adult↗
PubMed1988

Simultaneous demonstrations of neuropeptide Y gene expression and peptide storage in single neurons of the human brain.

A combination of in situ hybridization for neuropeptide Y mRNA that used a 32P-labeled complementary RNA probe and immunocytochemistry with polyclonal antibodies against neuropeptide Y were applied to human cortical brain samples to simultaneously localize neuropeptide Y and its mRNA. These two techniques allowed simultaneous identification of neuropeptide Y gene expression and peptide storage in single neurons of the human brain.

Brain↗
PubMed1987

Localization of neuropeptide Y mRNA in neurons of human cerebral cortex by means of in situ hybridization with a complementary RNA probe.

The distribution of mRNA encoding neuropeptide Y (NPY) in neurons of the normal human cerebral cortex in surgical biopsy specimens and postmortem brain was studied by in situ hybridization techniques. A 32P-labeled complementary RNA (cRNA) probe was used on cryostat sections of 13 formaldehyde-fixed cortical biopsy specimens. Hybridization to NPY mRNA was found in all samples: after autoradiography, discrete deposits of silver granules were observed on neuronal cell bodies abundantly distributed in the deep layers of the cortex, particularly laminae IV and VI, and on smaller cell bodies in the white matter. The localization of the neurons hybridized for NPY mRNA was comparable to that of NPY-immunoreactive cells as shown in sections from the same tissue blocks immunostained by using NPY antibodies. The specificity of the in situ hybridization technique was confirmed by blot hybridization analysis of electrophoretically fractionated RNA. This study clearly demonstrated the consistent localization of NPY gene transcription and expression in normal mature human cortical neurons.

Antibodies↗
PubMed1986

Distribution of neurons and axons immunoreactive with antisera against neuropeptide Y in the normal human hippocampus.

The detailed distribution of neuropeptide tyrosine (neuropeptide Y; NPY) immunoreactive neurons and fibers is given for the normal human hippocampus. These neuronal elements are detected by a polyclonal antibody raised against the unconjugated peptide and controls were obtained by using liquid phase absorption immunocytochemistry. The description covers the distribution in the area dentata, the hippocampal subfields CA3 and CA1, the subicular complex, and the entorhinal area. Each region is distinct in its NPY content. In general, the hippocampal NPY immunoreactive neurons fall into distinct classes--large hilar neurons; cortical small bipolar or bitufted neurons; medium-sized multipolar neurons in the deep cortical layers; and finally the distinct, small bipolar NPY neurons of the white matter bundles. None of the NPY neurons are pyramidal; many are likely to be local circuit neurons, but some appear to have extrinsic connections. The NPY immunoreactive axonal innervation is dense throughout the hippocampus but shows distinct regional differences in the hippocampal subdivisions. The area dentata has hilar NPY immunoreactive neurons and radial varicose fibers scattered throughout without a clear laminar preference. Subfield CA3 is comparatively the weakest NPY-containing region and contrasts with CA1, which is well endowed with reactive neurons and a rich and unusual axonal innervation, with distinct laminar axonal specializations. The subicular complex is well endowed with cells and fibers and the parasubiculum consistently displays unusually heavy NPY innervation. The entorhinal area exhibits a rich cortical distribution pattern, like that previously described for the human cerebral cortex (Chan-Palay et al; J. Comp. Neurol. 238:382-390, '85a,b). The fimbria, alveus, and angular bundle have NPY neurons embedded within the white matter. Like the NPY immunoreactive innervation of the hippocampal regions of laboratory animals, the human NPY innervation seems to follow a common fundamental pattern with respect to cell locations, cell morphology, and axonal innervation. The difference, however, is the greater complexity and profusion of the NPY-immunoreactive axonal plexuses in the human hippocampus. This rich peptide network within the hippocampus with likely extrahippocampal interconnections raises questions concerning coexistence with other neuroactive substances, the functions of such substantial networks, and how they are altered in human neurological disease.

Aged↗
PubMed1986

Distribution of altered hippocampal neurons and axons immunoreactive with antisera against neuropeptide Y in Alzheimer's-type dementia.

This paper provides detailed information on the distribution of neuropeptide tyrosine (neuropeptide Y; NPY) immunoreactive neurons and fibers in the hippocampal region of eight neuropathologically confirmed cases of Alzheimer's-type dementia (ATD) at postmortem. These neuronal networks are detected by a polyclonal antibody raised against the unconjugated peptide and controls were obtained by using liquid phase absorption immunocytochemistry. The description covers the subfields area dentata, CA3 and CA1, the subicular complex, and the entorhinal area. The hippocampal regions in which the NPY-i neuron networks are most severely affected are the hilus, CA1, the parasubiculum, and the entorhinal cortex. Less obvious reductions occurred in CA3, subiculum, and the presubiculum. Parallel semiquantitative estimates were made of the numbers of neuritic plaques and neurofibrillary tangles in the other hippocampus of the brains in every ATD case. The areas of heaviest pathological changes by these indices are CA1 and the entorhinal cortex. The subicular complex CA3 and the area dentata are less affected. These findings show that the areas with the most severe loss of NPY-i neurons and axons, CA1 and the entorhinal cortex, are the same as those areas most severely affected by the other indices of ATD. Thus NPY-i networks are involved in the ATD disease process. However, other NPY-i networks survive, in some subfields better than in others. The cumulative evidence suggests a population of hippocampal peptide neurons that are remarkably resistant in terminal neurological disease. These neurons have the capability to participate in the maintenance of minimal functioning circuits in target areas of the disease and as such hold significant links for our understanding of synaptic plasticity in disease.

Aged↗
PubMed1986

Immunocytochemistry of human brain tissue with a polyclonal antiserum against neuropeptide Y.

NPY-containing neuronal structures in the cerebral cortex of surgical tissue samples were compared to those in postmortem material by immunocytochemical methods. However, the quality of preservation of individual neurons and axonal and dendritic plexuses in the neuropil is unusually fine in the surgical specimens. This result is most likely attributable to the excellent fixation that can be regularly achieved by rapid and careful handling of tissue during and after surgical removal. The tissue is suitable for both light and electron microscopy, and the superior preservation also leads to intense, reliable antibody reactions. Postmortem tissue samples can provide good specimens for immunocytochemistry when properly handled as previously described. However the postmortem delays prior to fixation disrupt neuronal integrity in the immunostained structures. Nevertheless, postmortem material from carefully studied subjects of neurological diseases compared with age matched controls can provide valuable information.

Adolescent↗