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Sid Gilman - One of the best experts on this subject based on the ideXlab platform.
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ORIGINAL ARTICLES Cerebellar and Brainstem Hypometabolism in Olivopontocerebellar Atrophy Detected with Positron Emission Tomography
2014Co-Authors: Sid Gilman, Larry Junck, Dorene S Markel, Karen J Kluin, Stephen S Gebarski, S Stephen, Richard D HichwaAbstract:We studied local cerebral metabolic rates for glucose (ICMRglc) with '8F-2-fluoro-2-deoxy-~glucose and positron emission tomography (PET) in 30 patients with Olivopontocerebellar Atrophy (OPCA) and 30 age-matched control subjects without neurological disease. The diagnosis of OPCA was based on the history and physical findings and on the exclusion of other causes of cerebellar ataxia by means of laboratory investigations. Computed tomographic scans revealed some degree of Atrophy of the cerebellum in most patients with OPCA, and many also had Atrophy of the brainstem. PET studies in these patients revealed significant hypometabolism in the cerebellar hemispheres, cerebellar vermis, and brainstem in comparison with the normal control subjects. A significant relationship was found between the degree of Atrophy and the level of ICMRglc in the cerebellum and brainstem. Nevertheless, several patients had minimal Atrophy and substantially reduced ICMRglc, suggesting that Atrophy does not fully account for the finding of hypometabolism. ICMRglc was within normal limits for the thalamus and cerebral cortex. The data suggest that PET/ ICMRglc may be useful as a diagnostic test in patients with the adult onset of cerebellar ataxia
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patterns of neuropsychological performance in multiple system Atrophy compared to sporadic and hereditary Olivopontocerebellar Atrophy
Brain and Cognition, 2002Co-Authors: Stanley Berent, Sid Gilman, Bruno Giordani, Larry Junck, Karen J Kluin, Roderick J A Little, C L Trask, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Abstract Although neuropsychological symptoms are associated with multiple system Atrophy (MSA), sporadic Olivopontocerebellar Atrophy (sOPCA), and dominantly inherited Olivopontocerebellar Atrophy (dOPCA), the differences between these groups have not been explored. We compared 28 MSA patients on psychiatric rating scales and neuropsychological measures to 67 sOPCA patients, 42 dOPCA patients, and 30 normal controls. Patients with dOPCA, sOPCA, and MSA all exhibited significant deficits on motor-related tasks, as well as relatively mild deficits in cognitive functioning. Patients with MSA had greater neuropsychological dysfunction, particularly in memory and other “higher order” cognitive processes, than patients with either sOPCA or dOPCA.
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evolution of sporadic Olivopontocerebellar Atrophy into multiple system Atrophy
Neurology, 2000Co-Authors: Sid Gilman, Larry Junck, Karen J Kluin, Roderick J A Little, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Objective: To determine the percentage of sporadic Olivopontocerebellar Atrophy (sOPCA) patients who later develop multiple system Atrophy (MSA). Methods: Observations of the course of 51 sOPCA patients 20 years of age or older initially evaluated in an ataxia clinic over 14 years and followed at 3- to 6-month intervals for 3 months to 10 years (median 2.5 years, interquartile range 5 months to 4 years). Results: Seventeen patients evolved to develop MSA, whereas the remaining 34 manifested only progressively worsening cerebellar ataxia. The features of the MSA cases included autonomic failure and parkinsonism in 10 patients, autonomic failure without parkinsonism in six, and parkinsonism without autonomic failure in one. Using survival analysis methods, the authors estimated that 24% of subjects in this population will evolve to MSA within 5 years of the onset of sOPCA symptoms (95% CI 10% to 36%). An older age at onset of symptoms and a shorter time from onset of symptoms to first presentation in a neurology specialty clinic were both highly predictive of evolution to MSA. Six of the 17 patients who evolved to MSA died 4 months to 5 years after they had met diagnostic criteria for MSA. The estimated median survival time from time of transition was 3.5 years. In contrast, death occurred in only one of the 34 patients with sOPCA who did not evolve to MSA. Autopsy examination of all six patients with MSA who died confirmed the diagnosis. Conclusions: Approximately one-fourth of sporadic Olivopontocerebellar Atrophy patients will evolve to multiple system Atrophy within 5 years, and this transition carries a poor prognosis for survival. Older age at onset of ataxia and earlier presentation in a neurologic specialty clinic predicted transition to MSA.
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reply from the authors mri in sporadic Olivopontocerebellar Atrophy and striatonigral degeneration
Neurology, 1997Co-Authors: Sid Gilman, Ann Arbor, Niall QuinnAbstract:Reply from the Authors: We thank Dr. Savoiardo et al for their interest in our review and acknowledge their group's major contribution to the delineation of multiple system Atrophy (MSA), particularly the neuroradiologic features. On clinical presentation, most MSA patients predominantly have signs of extrapyramidal disease with or without accompanying signs of cerebellar disorder. We use the term striatonigral degeneration (SND)-type MSA for these patients. A smaller proportion show chiefly signs of cerebellar disease, and some of these patients show additional signs of extrapyramidal disorder. We use the term Olivopontocerebellar Atrophy (OPCA)-type MSA for these patients. Our review [1] deliberately addressed the difficult subject of the diagnosis of sporadic OPCA (sOPCA) and the question of whether some, most, or all of these patients have MSA. In SND-type MSA, which we did not address specifically, putaminal hypointensity (relative to globus pallidus) on 1.0- to …
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decreased striatal monoaminergic terminals in Olivopontocerebellar Atrophy and multiple system Atrophy demonstrated with positron emission tomography
Annals of Neurology, 1996Co-Authors: Sid Gilman, Larry Junck, Robert A Koeppe, Kirk A Frey, Roderick J A Little, Thierry Vander Borght, Mary Lohman, Susan Martorello, Lihsueh C LeeAbstract:We used [11C]dihydrotetrabenazine, a new ligand for the type 2 vesicular monoamine transporter (VMAT2), with positron emission tomography to study striatal monoaminergic presynaptic terminals in 4 patients with multiple system Atrophy, 8 with sporadic Olivopontocerebellar Atrophy, and 9 normal control subjects. Specific binding in the striatum was significantly reduced in the multiple system Atrophy patients as compared with the normal control group, with average reductions of 61% in the caudate nucleus (p = 0.002) and 58% in the putamen (p = 0.009). Smaller reductions were found in the sporadic Olivopontocerebellar Atrophy group, averaging 26% in the caudate nucleus (p = 0.05) and 24% in the putamen (p = 0.11). Mean blood-to-brain [11C]dihydrotetrabenazine transport (K1) was significantly different between groups only in the cerebellum, with values for the sporadic Olivopontocerebellar Atrophy group diminished compared with the normal control group. Cerebellar K1 was not significantly decreased in the multiple system Atrophy group. The finding of reduced striatal VMAT2 in sporadic Olivopontocerebellar Atrophy patients suggests nigrostriatal pathology, indicating that some may later develop symptomatic extrapyramidal disease.
Robert A Koeppe - One of the best experts on this subject based on the ideXlab platform.
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patterns of neuropsychological performance in multiple system Atrophy compared to sporadic and hereditary Olivopontocerebellar Atrophy
Brain and Cognition, 2002Co-Authors: Stanley Berent, Sid Gilman, Bruno Giordani, Larry Junck, Karen J Kluin, Roderick J A Little, C L Trask, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Abstract Although neuropsychological symptoms are associated with multiple system Atrophy (MSA), sporadic Olivopontocerebellar Atrophy (sOPCA), and dominantly inherited Olivopontocerebellar Atrophy (dOPCA), the differences between these groups have not been explored. We compared 28 MSA patients on psychiatric rating scales and neuropsychological measures to 67 sOPCA patients, 42 dOPCA patients, and 30 normal controls. Patients with dOPCA, sOPCA, and MSA all exhibited significant deficits on motor-related tasks, as well as relatively mild deficits in cognitive functioning. Patients with MSA had greater neuropsychological dysfunction, particularly in memory and other “higher order” cognitive processes, than patients with either sOPCA or dOPCA.
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evolution of sporadic Olivopontocerebellar Atrophy into multiple system Atrophy
Neurology, 2000Co-Authors: Sid Gilman, Larry Junck, Karen J Kluin, Roderick J A Little, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Objective: To determine the percentage of sporadic Olivopontocerebellar Atrophy (sOPCA) patients who later develop multiple system Atrophy (MSA). Methods: Observations of the course of 51 sOPCA patients 20 years of age or older initially evaluated in an ataxia clinic over 14 years and followed at 3- to 6-month intervals for 3 months to 10 years (median 2.5 years, interquartile range 5 months to 4 years). Results: Seventeen patients evolved to develop MSA, whereas the remaining 34 manifested only progressively worsening cerebellar ataxia. The features of the MSA cases included autonomic failure and parkinsonism in 10 patients, autonomic failure without parkinsonism in six, and parkinsonism without autonomic failure in one. Using survival analysis methods, the authors estimated that 24% of subjects in this population will evolve to MSA within 5 years of the onset of sOPCA symptoms (95% CI 10% to 36%). An older age at onset of symptoms and a shorter time from onset of symptoms to first presentation in a neurology specialty clinic were both highly predictive of evolution to MSA. Six of the 17 patients who evolved to MSA died 4 months to 5 years after they had met diagnostic criteria for MSA. The estimated median survival time from time of transition was 3.5 years. In contrast, death occurred in only one of the 34 patients with sOPCA who did not evolve to MSA. Autopsy examination of all six patients with MSA who died confirmed the diagnosis. Conclusions: Approximately one-fourth of sporadic Olivopontocerebellar Atrophy patients will evolve to multiple system Atrophy within 5 years, and this transition carries a poor prognosis for survival. Older age at onset of ataxia and earlier presentation in a neurologic specialty clinic predicted transition to MSA.
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decreased striatal monoaminergic terminals in Olivopontocerebellar Atrophy and multiple system Atrophy demonstrated with positron emission tomography
Annals of Neurology, 1996Co-Authors: Sid Gilman, Larry Junck, Robert A Koeppe, Kirk A Frey, Roderick J A Little, Thierry Vander Borght, Mary Lohman, Susan Martorello, Lihsueh C LeeAbstract:We used [11C]dihydrotetrabenazine, a new ligand for the type 2 vesicular monoamine transporter (VMAT2), with positron emission tomography to study striatal monoaminergic presynaptic terminals in 4 patients with multiple system Atrophy, 8 with sporadic Olivopontocerebellar Atrophy, and 9 normal control subjects. Specific binding in the striatum was significantly reduced in the multiple system Atrophy patients as compared with the normal control group, with average reductions of 61% in the caudate nucleus (p = 0.002) and 58% in the putamen (p = 0.009). Smaller reductions were found in the sporadic Olivopontocerebellar Atrophy group, averaging 26% in the caudate nucleus (p = 0.05) and 24% in the putamen (p = 0.11). Mean blood-to-brain [11C]dihydrotetrabenazine transport (K1) was significantly different between groups only in the cerebellum, with values for the sporadic Olivopontocerebellar Atrophy group diminished compared with the normal control group. Cerebellar K1 was not significantly decreased in the multiple system Atrophy group. The finding of reduced striatal VMAT2 in sporadic Olivopontocerebellar Atrophy patients suggests nigrostriatal pathology, indicating that some may later develop symptomatic extrapyramidal disease.
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psychological factors and pet measured glucose metabolism in Olivopontocerebellar Atrophy
Assessment, 1996Co-Authors: Stanley Berent, Sid Gilman, Bruno Giordani, Larry Junck, Karen J Kluin, Robert A KoeppeAbstract:We compared 29 Olivopontocerebellar Atrophy (OPCA) patients on psychiatric rating scales, cognitive tests, and positron emission tomography to 12 normal volunteers with similar age and sex distributions. The patients were generally comparable to normals in cognitive function, but poorer on psychomotor tasks. They had significantly different scores on formal self-report scales than the normals, indicating a greater degree of self-complaint. Analyses of the components of self-complaint suggested that illness-related concerns accounted for most of the differences between the groups. The magnitude of self-complaint was significantly and specifically correlated with the level of glucose metabolism in the frontal cerebral cortex of OPCA patients. These results may be attributed to a combination of biological and experiential factors. The level of patient complaint may be influenced by organic brain dysfunction reflected in metabolism and emotional disturbance, whereas the content of complaint may be specific to...
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a comparison of cerebral blood flow and glucose metabolism in Olivopontocerebellar Atrophy using pet
Neurology, 1995Co-Authors: Sid Gilman, Larry Junck, Karen J Kluin, Robert A Koeppe, Roy T St Laurent, Mary LohmanAbstract:Objective In sporadic cases of Olivopontocerebellar Atrophy (OPCA), to determine whether local cerebral blood flow (ICBF) is reduced, whether lCBF is coupled to local cerebral metabolic rate for glucose (lCMRglc), and whether lCBF measurements are potentially useful in diagnosing OPCA. Design Positron emission tomography was used with [ 15 O]H 2 O to measure lCBF and with [ 18 F]fluorodeoxyglucose to measure lCMRglc in 17 patients with OPCA and 21 normal control subjects. Results In OPCA patients, lCBF was significantly decreased in the cerebellum, but not in the cerebral cortex, basal ganglia, thalamus, or brainstem. In the same patients, lCMRglc was significantly decreased in the cerebellum and brainstem, where the largest changes were observed, and also in the cerebral cortex, basal ganglia, and thalamus. The ratio of lCBF to lCMRglc, an indicator of the coupling of blood flow to metabolism, was similar in OPCA patients and normal subjects for all regions except the brainstem, where the ratio was marginally decreased in OPCA patients. Using logistic discriminant analysis to assess the ability of lCBF and lCMRglc to differentiate OPCA patients from normal subjects, we found the cross-validated sensitivity of absolute lCMRglc as a predictor of OPCA was 82% with a corresponding specificity of 71%; the sensitivity of absolute lCBF was 71% and the specificity 76%. Conclusions In sporadic cases of OPCA, lCBF is reduced in the cerebellum, CBF remains coupled to lCMRglc, and the lCBF pattern is a useful predictor of the diagnosis.
Roger F. Butterworth - One of the best experts on this subject based on the ideXlab platform.
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Selective Loss of Expression of Glutamate GluR2/R3 Receptor Subunits in Cerebellar Tissue from a Patient with Olivopontocerebellar Atrophy
Metabolic Brain Disease, 2002Co-Authors: Gregoire Dirson, Paul Desjardins, Tony Tannenberg, Peter Dodd, Roger F. ButterworthAbstract:Expression of the mRNAs encoding the astrocytic (EAAT1, EAAT2) and neuronal (EAAT3, EAAT4) excitatory amino acid transporters and the AMPA-type glutamate receptor subunits GluR2 and GluR3 was investigated in postmortem cerebellar extracts from a patient with Olivopontocerebellar Atrophy (OPCA) and in material from three age-matched controls. Decreased expression in the steady state level of EAAT4 mRNA in the OPCA sample was correlated with the selective loss of Purkinje cells. Neuropathological evaluation revealed reactive gliosis and concomitantly increased expression of the mRNA encoding astrocytic glial fibrillary acidic protein (GFAP). Expression of the mRNAs encoding the AMPA receptor subunits GluR2 and GluR3 subunits was found to be decreased in OPCA suggesting that excitotoxic mechanism could play a role in the pathogenesis of the selective neuronal cell death in this disorder.
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selective loss of expression of glutamate glur2 r3 receptor subunits in cerebellar tissue from a patient with Olivopontocerebellar Atrophy
Metabolic Brain Disease, 2002Co-Authors: Gregoire Dirson, Paul Desjardins, Tony Tannenberg, P R Dodd, Roger F. ButterworthAbstract:Expression of the mRNAs encoding the astrocytic (EAAT1, EAAT2) and neuronal (EAAT3, EAAT4) excitatory amino acid transporters and the AMPA-type glutamate receptor subunits GluR2 and GluR3 was investigated in postmortem cerebellar extracts from a patient with Olivopontocerebellar Atrophy (OPCA) and in material from three age-matched controls. Decreased expression in the steady state level of EAAT4 mRNA in the OPCA sample was correlated with the selective loss of Purkinje cells. Neuropathological evaluation revealed reactive gliosis and concomitantly increased expression of the mRNA encoding astrocytic glial fibrillary acidic protein (GFAP). Expression of the mRNAs encoding the AMPA receptor subunits GluR2 and GluR3 subunits was found to be decreased in OPCA suggesting that excitotoxic mechanism could play a role in the pathogenesis of the selective neuronal cell death in this disorder.
Larry Junck - One of the best experts on this subject based on the ideXlab platform.
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ORIGINAL ARTICLES Cerebellar and Brainstem Hypometabolism in Olivopontocerebellar Atrophy Detected with Positron Emission Tomography
2014Co-Authors: Sid Gilman, Larry Junck, Dorene S Markel, Karen J Kluin, Stephen S Gebarski, S Stephen, Richard D HichwaAbstract:We studied local cerebral metabolic rates for glucose (ICMRglc) with '8F-2-fluoro-2-deoxy-~glucose and positron emission tomography (PET) in 30 patients with Olivopontocerebellar Atrophy (OPCA) and 30 age-matched control subjects without neurological disease. The diagnosis of OPCA was based on the history and physical findings and on the exclusion of other causes of cerebellar ataxia by means of laboratory investigations. Computed tomographic scans revealed some degree of Atrophy of the cerebellum in most patients with OPCA, and many also had Atrophy of the brainstem. PET studies in these patients revealed significant hypometabolism in the cerebellar hemispheres, cerebellar vermis, and brainstem in comparison with the normal control subjects. A significant relationship was found between the degree of Atrophy and the level of ICMRglc in the cerebellum and brainstem. Nevertheless, several patients had minimal Atrophy and substantially reduced ICMRglc, suggesting that Atrophy does not fully account for the finding of hypometabolism. ICMRglc was within normal limits for the thalamus and cerebral cortex. The data suggest that PET/ ICMRglc may be useful as a diagnostic test in patients with the adult onset of cerebellar ataxia
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patterns of neuropsychological performance in multiple system Atrophy compared to sporadic and hereditary Olivopontocerebellar Atrophy
Brain and Cognition, 2002Co-Authors: Stanley Berent, Sid Gilman, Bruno Giordani, Larry Junck, Karen J Kluin, Roderick J A Little, C L Trask, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Abstract Although neuropsychological symptoms are associated with multiple system Atrophy (MSA), sporadic Olivopontocerebellar Atrophy (sOPCA), and dominantly inherited Olivopontocerebellar Atrophy (dOPCA), the differences between these groups have not been explored. We compared 28 MSA patients on psychiatric rating scales and neuropsychological measures to 67 sOPCA patients, 42 dOPCA patients, and 30 normal controls. Patients with dOPCA, sOPCA, and MSA all exhibited significant deficits on motor-related tasks, as well as relatively mild deficits in cognitive functioning. Patients with MSA had greater neuropsychological dysfunction, particularly in memory and other “higher order” cognitive processes, than patients with either sOPCA or dOPCA.
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evolution of sporadic Olivopontocerebellar Atrophy into multiple system Atrophy
Neurology, 2000Co-Authors: Sid Gilman, Larry Junck, Karen J Kluin, Roderick J A Little, Jewel R Johanns, Mary Heumann, Robert A KoeppeAbstract:Objective: To determine the percentage of sporadic Olivopontocerebellar Atrophy (sOPCA) patients who later develop multiple system Atrophy (MSA). Methods: Observations of the course of 51 sOPCA patients 20 years of age or older initially evaluated in an ataxia clinic over 14 years and followed at 3- to 6-month intervals for 3 months to 10 years (median 2.5 years, interquartile range 5 months to 4 years). Results: Seventeen patients evolved to develop MSA, whereas the remaining 34 manifested only progressively worsening cerebellar ataxia. The features of the MSA cases included autonomic failure and parkinsonism in 10 patients, autonomic failure without parkinsonism in six, and parkinsonism without autonomic failure in one. Using survival analysis methods, the authors estimated that 24% of subjects in this population will evolve to MSA within 5 years of the onset of sOPCA symptoms (95% CI 10% to 36%). An older age at onset of symptoms and a shorter time from onset of symptoms to first presentation in a neurology specialty clinic were both highly predictive of evolution to MSA. Six of the 17 patients who evolved to MSA died 4 months to 5 years after they had met diagnostic criteria for MSA. The estimated median survival time from time of transition was 3.5 years. In contrast, death occurred in only one of the 34 patients with sOPCA who did not evolve to MSA. Autopsy examination of all six patients with MSA who died confirmed the diagnosis. Conclusions: Approximately one-fourth of sporadic Olivopontocerebellar Atrophy patients will evolve to multiple system Atrophy within 5 years, and this transition carries a poor prognosis for survival. Older age at onset of ataxia and earlier presentation in a neurologic specialty clinic predicted transition to MSA.
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decreased striatal monoaminergic terminals in Olivopontocerebellar Atrophy and multiple system Atrophy demonstrated with positron emission tomography
Annals of Neurology, 1996Co-Authors: Sid Gilman, Larry Junck, Robert A Koeppe, Kirk A Frey, Roderick J A Little, Thierry Vander Borght, Mary Lohman, Susan Martorello, Lihsueh C LeeAbstract:We used [11C]dihydrotetrabenazine, a new ligand for the type 2 vesicular monoamine transporter (VMAT2), with positron emission tomography to study striatal monoaminergic presynaptic terminals in 4 patients with multiple system Atrophy, 8 with sporadic Olivopontocerebellar Atrophy, and 9 normal control subjects. Specific binding in the striatum was significantly reduced in the multiple system Atrophy patients as compared with the normal control group, with average reductions of 61% in the caudate nucleus (p = 0.002) and 58% in the putamen (p = 0.009). Smaller reductions were found in the sporadic Olivopontocerebellar Atrophy group, averaging 26% in the caudate nucleus (p = 0.05) and 24% in the putamen (p = 0.11). Mean blood-to-brain [11C]dihydrotetrabenazine transport (K1) was significantly different between groups only in the cerebellum, with values for the sporadic Olivopontocerebellar Atrophy group diminished compared with the normal control group. Cerebellar K1 was not significantly decreased in the multiple system Atrophy group. The finding of reduced striatal VMAT2 in sporadic Olivopontocerebellar Atrophy patients suggests nigrostriatal pathology, indicating that some may later develop symptomatic extrapyramidal disease.
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psychological factors and pet measured glucose metabolism in Olivopontocerebellar Atrophy
Assessment, 1996Co-Authors: Stanley Berent, Sid Gilman, Bruno Giordani, Larry Junck, Karen J Kluin, Robert A KoeppeAbstract:We compared 29 Olivopontocerebellar Atrophy (OPCA) patients on psychiatric rating scales, cognitive tests, and positron emission tomography to 12 normal volunteers with similar age and sex distributions. The patients were generally comparable to normals in cognitive function, but poorer on psychomotor tasks. They had significantly different scores on formal self-report scales than the normals, indicating a greater degree of self-complaint. Analyses of the components of self-complaint suggested that illness-related concerns accounted for most of the differences between the groups. The magnitude of self-complaint was significantly and specifically correlated with the level of glucose metabolism in the frontal cerebral cortex of OPCA patients. These results may be attributed to a combination of biological and experiential factors. The level of patient complaint may be influenced by organic brain dysfunction reflected in metabolism and emotional disturbance, whereas the content of complaint may be specific to...
Dikran S. Horoupian - One of the best experts on this subject based on the ideXlab platform.
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Olivopontocerebellar Atrophy in carbohydrate deficient glycoprotein syndrome
Pediatric Pathology & Laboratory Medicine, 1995Co-Authors: Dikran S. HoroupianAbstract:(1995). Case 4 Olivopontocerebellar Atrophy in Carbohydrate-Deficient Glycoprotein Syndrome. Pediatric Pathology & Laboratory Medicine: Vol. 15, No. 1, pp. 175-179.
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Striatonigral degeneration, Olivopontocerebellar Atrophy and "atypical" Pick disease
Acta neuropathologica, 1991Co-Authors: Dikran S. Horoupian, Dennis W. DicksonAbstract:A 75-year-old woman with parkinsonism plus was found at autopsy to have striatonigral degeneration (SND), Olivopontocerebellar Atrophy (OPCA) and intracytoplasmic neuronal inclusions, mostly confined to the hippocampus and pontine nuclei. These inclusions were intensely argyrophilic, ubiquitinated and expressed variable immunoreactivity for neurofilament but not for tau-1 and Alz 50 proteins. Ultrastructurally, they were formed of skeins of intermediate filaments averaging 11 nm in diameter. They were considered to represent Pick bodies. There was no cortical Atrophy, gliosis or sponginess. To our knowledge, SND and OPCA in association with Pick's disease has not been previously reported. In addition, intracytoplasmic oligodendroglial inclusions were present in the deeper layers of the cortex, especially the pericentral gyri, the striatum and the white matter of certain regions of the cerebral hemispheres, as well as in the cerebellum. These inclusions which have been previously reported in multisystem Atrophy, had to be distinguished from cortical Lewy bodies, Pick bodies, and the nonspecific ubiquitinated bodies in the white matter of the aged brain, mainly by their topographical distribution and immunostaining properties.
