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Biomedical subjects

J E Kleinman

Publications and source records attributed to J E Kleinman.

At least 145 records · Page 8Linked to original sources
PubMed1984

Muscarinic binding in suicides.

Supersensitive muscarinic cholinergic receptors may underlie mood, neuroendocrine, and sleep disturbances in depression. To test this hypothesis, we examined muscarinic binding sites in the brains of suicides and controls in a matched-pair design, using the radioligand 3H-quinuclidinyl benzilate (QNB) and focusing on regions (frontal cortex, hypothalamus, and pons) mediating those functions. Receptor densities and binding affinities did not differ between suicide and control brains in any brain region studied, although there was a trend for both density and affinity to be lower in hypothalami from suicides. We discuss the implications of these findings for the cholinergic-adrenergic balance hypothesis of depression and the methodological limitations of our preliminary study.

Acetylcholine↗
PubMed1984

Eye-blinking and cerebral ventricular size in chronic schizophrenic patients.

Spontaneous eye-blinking, a possible measure of central dopaminergic activity, was studied in 55 drug-free chronic schizophrenic patients subdivided by cerebral ventricular size. Blink rates were higher in schizophrenic patients than in normal control subjects, regardless of cerebral ventricle size. Neuroleptics lowered blink rates in patients with normal ventricles but did not affect blink rates in patients with large ventricles. Insofar as blinking is a dopaminergic parameter, these findings suggest that the dopamine hypothesis of schizophrenia is most relevant in patients with normal ventricles.

Adult↗
PubMed1984

Postmortem studies in psychiatry.

Neurochemical postmortem examination of brain tissue may never be completely replaced as a research tool in psychiatry. This method has already provided support for the hypotheses relating norepinephrine, dopamine, serotonin, peptides, and hemisphere asymmetries to psychiatric syndromes.

Alcoholism↗
PubMed1983

Coupling of dopamine D1 recognition sites with adenylate cyclase in nuclei accumbens and caudatus of schizophrenics.

Sodium fluoride, guanylimidodiphosphate, and the D1 dopamine receptor agonist SKF 38393 elicited a greater activation of adenylate cyclase in homogenates of caudate nucleus in schizophrenic than in nonschizophrenic subjects used as controls. Similarly, a greater activation of adenylate cyclase by sodium fluoride was observed in the nucleus accumbens of schizophrenics. These findings suggest that the coupling of dopamine D1 recognition sites with adenylate cyclase is more efficient in the brain of the schizophrenic, presumably because of an increased affinity of the G/F protein for guanosine 5'-triphosphate.

Adenylyl Cyclases↗
PubMed1983

Apomorphine response and subtyping of schizophrenia.

(1) We conducted a double-blind study of acute effects of low-dose apomorphine (0.01 mg/kg) in 12 chronic schizophrenic patients. (2) Overall, there was no significant difference in therapeutic response to apomorphine versus placebo. (3) Of the individual subscales of the Brief Psychiatric Rating Scale, anxiety and depression syndromes showed significant improvement with apomorphine. (4) On dividing the schizophrenic patients into two groups on the basis of computed tomography (CT) scans, it was found that there was a significant difference in their responsiveness to apomorphine. (5) Patients with abnormal CT scans (primarily, large ventricles) tended to have improvement or no change with apomorphine, whereas those with normal CT scans tended to have worsening of symptoms. (6) Possible implications of our findings are discussed.

Adult↗
PubMed1983

An inverse correlation between spontaneous eye-blink rate and platelet monoamine oxidase activity.

An inverse correlation between platelet monoamine oxidase activity and spontaneous eye-blink rate, a putative measure of central dopaminergic activity, was found in medication-free chronic schizophrenic patients without tardive dyskinesia (n = 20, rs = -.47, P less than .025). A similar correlation was found when patients with tardive dyskinesia were included but was weaker (n = 27, rs = -.35, P less than .05). Normal controls and patients with tardive dyskinesia did not demonstrate this relationship. This report confirms a previous finding of a significant platelet monoamine oxidase-blink rate correlation in chronic schizophrenic patients. Insofar as this relationship is mediated by dopamine, it suggests that dopaminergic relations are more readily demonstrated in schizophrenic subjects than normals. Moreover, tardive dyskinesia appears to obscure this dopaminergic relationship.

Adult↗
PubMed1982

Plasma prolactin concentrations and psychopathology in chronic schizophrenia.

Plasma prolactin concentrations in 17 drug-free chronic schizophrenic patients correlated inversely with ratings of their psychopathology. An inverse relationship between psychotic symptoms and plasma prolactin concentrations was particularly clear in patients with normal cerebral ventricular size as determined by computed tomography. The psychosis-prolactin relationship did not hold for schizophrenic patients with large ventricular size. These data suggest that the degree of psychosis is related to dopaminergic activity insofar as this is reflected by plasma prolactin concentrations, especially in schizophrenic patients with normal ventricular size. These findings lend further support to the hypothesis that ventricular size is a meaningful factor in subtyping chronic schizophrenic patients.

Adult↗
PubMed1982

Naloxone in chronic schizophrenic patients: neuroendocrine and behavioral effects.

Naloxone produced improvement in abnormal thought content in medicated chronic schizophrenic patients, but not in drug-free patients. In contrast, drowsiness and increases in plasma prolactin concentrations were seen only in drug-free schizophrenic patients. Although growth hormone concentrations increased in drug-free and medicated schizophrenic patients, the time course was different in the two groups. Neuroleptics appear to alter naloxone's clinical and neuroendocrine effects in chronic schizophrenic patients.

Adult↗
PubMed1982

Haloperidol-induced changes in blink rates correlate with changes in BPRS score.

Spontaneous eye blink rates, psychiatric symptoms and response to neuroleptic medication may all be mediated by dopamine. Fixed doses of haloperidol, a dopamine blocking agent, were administered for six weeks to 17 chronic schizophrenic patients who had been previously withdrawn from all medications. The change in blink rates caused by haloperidol corresponded to a change in the thought disturbance syndrome which measures positive symptoms (r = .48, P less than .05). The relationship was particularly clear in patients with normal cerebral ventricles (r = .74, P less than .01).

Adult↗
PubMed1982

Ex uno multi: subtyping the schizophrenic syndrome.

We studied 93 chronic schizophrenic inpatients, who met the Research Diagnostic Criteria for schizophrenia. Data on a number of historical, epidemiologic, phenomenologic, biochemical, neuropathological, and treatment-response variables were analyzed, using univariate and multivariate statistical analyses. Patients were classified into pairs of subgroups, according to each of the following seven dimensions: (1) ventricle/brain ratio (VBR) assessed on computed tomography scans (normal vs. abnormal); (2) premorbid adjustment (good vs. poor); (3) therapeutic response to neuroleptics (good vs. poor); (4) platelet monoamine oxidase (MAO) activity (low vs. high); (5) paranoid features (present vs. absent); (6) tardive dyskinesia (present vs. absence); and (7) hemispheric asymmetry on computed tomography scans (normal vs. abnormal). These seven dimensions were chosen because earlier studies had shown that the variables involved were operationally definable and were of potential relevance to the subgrouping of schizophrenic patients. Our results suggested that two biological variables, viz., VBR and platelet MAO activity, might be useful in identifying two rather distinct subgroups among chronic schizophrenic patients. A subgroup with large VBR was associated with poor premorbid adjustment, neurological impairment, and poor therapeutic response to neuroleptics, while the subgroup with low platelet MAO activity was characterized by the presence of paranoid features and tardive dyskinesia. Possible explanations, implications, and limitations of our findings are discussed.

Adult↗
PubMed1981

Speaking, thinking, and blinking.

The effect of several mental tasks on the spontaneous eye blink rate in 36 normals was examined. The blink rate during silence was 19.0 blinks/minute. This was significantly lower than the mean blink rate during speech (24.7 blinks/minute) and while listening to a paragraph to be memorized (27.6 blinks/minute). Reading reduced the blink rate to 12.3 blinks/minute. Men were more able to suppress and speed up blinking than women.

Adult↗
PubMed1981

The schizophrenia syndrome. Examples of biological tools for subclassification.

Six biological variables-platelet monoamine oxidase activity, urine phenylethylamine concentration, brain norepinephrine concentration, abnormalities on computerized tomography, lateralization asymmetries, and the presence or absence of tardive dyskinesia-are used to discriminate possible biological groups of schizophrenic patients. All variables successfully subclassify patients, some into divisions consistent with phenomological, psychosocial, or biochemical descriptions or hypotheses of schizophrenia. None of the measures, however, has sufficiently stood the test of time to be of clinical utility.

Amphetamine↗
PubMed1981

Drug effect on blink rates in rhesus monkeys: preliminary studies.

Various drugs that alter central monoamine activity were given to monkeys to determine effects on blink rate. Chronic pargyline treatment raised the mean +/- SD blink rate slightly to 18.2 +/- 5.3 blinks/90 sec. When phenylethylamine was added to chronic pargyline treatment, blinks increased from a base line of 16.8 +/- 7.6 blinks/90 sec to 37 +/- 15 blinks/90 sec. Apomorphine (0.36 mg/kg) raised blinks from a base lone of 12.2 +/- 2.8 blinks/90 sec. to 41.9 +/- 10.3 blinks/90 sec. and reversed a decrease in blinking caused by haloperidol. The neurochemical basis of blinking and implications for tardive dyskinesia are discussed.

Animals↗