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Biomedical subjects

J Rotrosen

Publications and source records attributed to J Rotrosen.

At least 91 records · Page 5Linked to original sources
PubMed1985

Persistence of cerebral metabolic abnormalities in chronic schizophrenia as determined by positron emission tomography.

Local cerebral metabolic rates were determined by positron emission tomography and the deoxyglucose method in a group of 10 chronic schizophrenic subjects before and after somatic treatment and in eight normal subjects. Before treatment, schizophrenic subjects had markedly lower absolute metabolic activity than did normal controls in both frontal and temporal regions and a trend toward relative hyperactivity in the basal ganglia area. After treatment, their metabolic rates approached those seen in normal subjects in nearly all regions except frontal. Persistence of diminished frontal metabolism was manifested as significant relative hypofrontality. These findings suggest specific loci of aberrant cerebral functioning in chronic schizophrenia and the utility of positron emission tomography in characterizing these abnormalities.

Adult↗
PubMed1985

Efficacy of propranolol in neuroleptic-induced akathesia.

The effects of propranolol, 20 to 30 mg/day, on neuroleptic-induced akathesia were compared with those of lorazepam, 2 mg/day, and periods of no treatment. Raters were blind to treatment condition. As reported in prior open studies, propranolol was found to be dramatically effective in reducing akathesia induced by neuroleptic treatment.

Adult↗
PubMed1984

Patterns of metabolic activity in the treatment of schizophrenia.

Six patients with chronic schizophrenia were studied with positron emission tomography (PET) before and after neuroleptic treatment, using fluorine-18-labeled fluorodeoxyglucose. After treatment, the mean whole-slice glucose metabolic rate at the level of the basal ganglia showed a 25% increase. However, patterns of frontal hypometabolism observed with the schizophrenic patients were not altered by medication. Pattern analysis using the fast Fourier transform was applied to a set of 422 images from a mixed group of normal, depressed, and schizophrenic subjects. Reconstruction of the images with low-frequency coefficients was excellent, reducing considerably the number of variables needed to characterize each image. Hierarchical cluster analysis categorized the transformed images according to anatomical level and subject group (patient versus control). The results suggest the utility of this procedure for the classification and characterization of metabolic PET images from psychiatric patients.

Adult↗
PubMed1984

CSF somatostatin in Alzheimer's disease.

Studies have previously demonstrated low somatostatin levels in autopsy cortical tissue from Alzheimer's disease (AD) patients and low somatostatin levels in CSF obtained from subjects with dementia. We evaluated levels of this peptide in 21 non-depressed subjects, 10 with AD, 2 with Parkinson's disease (PD), and 9 with other neurological conditions. The AD patients had significantly lower mean CSF somatostatin than the "other" neurological patients (14.6 +/- 1.5 S.E.M. versus 26.7 +/- 3.2 pg/ml, p less than 0.005). A demented PD subject had a level in the range of the AD group, while the non-demented PD patient had a value above this range. Thus, all 11 patients with AD or PD dementia, analogous disorders, had levels below 21.8 mg/ml, while 7 of the 10 remaining patients had values above 21.8 pg/ml. Age did not explain this finding.

Age Factors↗
PubMed1984

TRH test abnormalities in psychiatric disorders.

Blunted responses to thyrotropin-releasing hormone (TRH) stimulation have been found consistently in depressed patients, and have been reported in other affective disorders as well. In a smaller number of schizophrenic subjects, TRH tests have generally been normal. Thus, it has been suggested that this test may have diagnostic utility in distinguishing schizophrenia from affective disorders. In the present study the TRH test was performed upon a sample of 51 subjects that included 17 schizophrenics in order to further study the diagnostic or symptom specificity of this endocrine test. Abnormal TRH tests were present in both schizophrenic and affectively disturbed patients. There were no correlations with ratings of depression or other aspects of psychopathology. Factors which may have previously obscured abnormal TRH tests in schizophrenia are discussed.

Bipolar Disorder↗
PubMed1984

Murine lymphocytes lack clearly defined receptors for muscarinic and dopaminergic ligands.

[3H]Quinuclidinyl benzilate and [3H]spiperone binding to murine lymphocytes is displaceable but differs from binding to brain receptor sites for these ligands: (1) binding to intact lymphocyte preparations was not saturable; (2) disruption of intact lymphocytes was associated with a marked loss of displaceable ligand binding; (3) drugs differentially displace these ligands in lymphocytes compared to brain. Displaceable binding was increased following incubation of lymphocytes under phospholipid methylating conditions; however, marked effects on cell viability and cell recovery make it difficult to interpret these binding changes. If dopaminergic and cholinergic receptors do exist on lymphocytes, their binding characteristics are profoundly different from comparable cns receptors.

Animals↗
PubMed1983

Norepinephrine stimulation of phospholipid methylation in rat cortical synaptosomes: fact or artifact?

Synaptosomes from rat cerebral cortex incubated with 3H-S-adenosyl-L-methionine (3H-SAM) displayed an increase in chloroform- extractable tritium when norepinephrine was added to the reaction mixture. The products of this mixture were maximally generated from intact synaptosomes, only partially inhibited by propranolol, and not enhanced by exogenous phospholipids. Thin layer chromatographic analysis of these chloroform extracts in three solvent systems yielded large norepinephrine- stimulated peaks of radioactivity that did not consistently co-chromatograph with authentic methylated phospholipid standards: phosphatidylmonomethylethanolamine (PME), phosphatidyldimethylethanolamine (PDE), and phosphatidylcholine (PC). Further, attempts to identify these peaks of radioactivity using as standards several putative methylated products of varied chemical classes, failed to elucidate likely candidates. It appears that while norepinephrine markedly stimulates the amount of tritium extracted into the chloroform phase, careful and positive structural elucidation of formed products is required before it can be concluded that these are indeed methylated phospholipids.

Animals↗
PubMed1982

Red cell phospholipids in schizophrenia.

Phospholipids in red blood cells (RBCs) of schizophrenics and controls were determined. Three different RBC preparations and two different extraction methods were used. Phospholipids were separated by thin layer chromatography and by high pressure liquid chromatography, and were quantified by phosphorus analysis and by ultraviolet absorption. Findings were consistent with values previously reported for normals. However, in contrast to recent reports of elevated phosphatidylserine levels in schizophrenics' RBCs, we observed no differences between populations.

Adult↗
PubMed1982

Partial improvement in negative schizophrenic symptoms after amphetamine.

In stable schizophrenic outpatients with predominantly "defect state" symptomatology amphetamine caused a reduction in negative symptoms that was statistically significant but not complete (i.e. these symptoms remained clinically discernible). The possibility that dopaminergic hypofunction contributes some elements to the schizophrenic defect state is presented, along with some limited data compatible with this concept. These findings are compared to prior studies in recently hospitalized schizophrenic subjects, and discussed with respect to recent theoretical concepts regarding the role of dopamine in schizophrenic psychopathology.

Adult↗