Receptors and the mechanism of action of ECT.
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Biomedical subjects
Publications and source records attributed to B Lerer.
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Although numerous studies have suggested that depression may be associated with a reduction in synaptic noradrenaline in the brain, direct beta-adrenergic receptor agonist have only recently been tested in the treatement of depression. Moreover, newer theories of antidepressant action suggest that a reduction in beta-adrenergic receptor sensitivity is a better correlate of antidepressant treatment than noradrenaline turnover changes. Eleven depressed patients were treated with salbutamol, a beta-2-adrenergic agonist, and beta-2-adrenergic receptor sensitivity was evaluated before, during, and after treatment. beta-Adrenergic receptor sensitivity was evaluated by measuring the plasma cyclic AMP increase after an IV dose of salbutamol. The beta-adrenergic agonist exhibited antidepressant efficacy and induced subsensitivity of the beta-adrenergic adenylate cyclase with a time course paralleling the antidepressant effects. The results support the concept that receptor sensitivity changes occur during antidepressant therapy.
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Haloperidol levels were measured by radioreceptor assay in 12 schizophrenic patients during gradual dosage reduction (at 10-day) intervals) from 60 to 0 mg/day. Serum levels were highly correlated with the oral dose in each patient, but poorly correlated across patients. Clinical deterioration appeared only 10-20 days after total cessation of the oral drug, and so it was not possible to determine an optimal blood level for chronic maintenance. Below oral dosage of 10 mg/day of haloperidol many patients' blood levels are undetectable by the radioreceptor method.
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Neither the acute nor the chronic i.p. administration of delta-6-tetrahydrocannabinol affected the passage of lithium from blood to brain in normal rats.
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The physician in hospital practice may be faced with a situation in which a patient under his care suffers a bereavement or some other unexpected tragedy but is unaware of the fact. Three such cases encountered in the context of our psychiatric sonsultation service are presented. Factors influencing the decision as to whether, when and how the patient should be informed are considered. The complex psychodynamic situation which arises and involves the patient, his family and the medical staff is described. Stress is laid on the role played by archaic fears of being the bearer of evil tidings. The situation is seen as being ideally handled by the direct treating physician in conjunction with the family, the extent of psychiatric intervention being dictated by the needs of each of the parties concerned. Ideally the patient should be told as soon as his physical and mental condition are seen as conducive and preferably before he leave hospital.
As an index of central serotonergic function, plasma prolactin response to fenfluramine (60 mg orally) and placebo challenge was examined in 10 depressed patients before and after treatment with imipramine 200 mg/day for 3 weeks. Although baseline prolactin levels were not altered by imipramine, the prolactin response to fenfluramine was significantly (P = 0.01) increased compared to the response in the untreated state. The response to placebo was also enhanced but this effect was of lesser magnitude and not statistically significant. These findings complement previous reports and suggest that tricyclic antidepressant treatment enhances serotonergically mediated neuroendocrine responses.
Neuroendocrine and mood responses to a 60 mg oral dose of the serotonin-releasing agent, fenfluramine, were assessed in ten neuroleptic-free, chronic schizophrenic patients and in age- and sex-matched normal control subjects. The prolactin (PRL) response to fenfluramine was significantly blunted in the schizophrenic subjects. Growth hormone and cortisol levels were not differentially affected by the challenge. There was no significant effect of fenfluramine on mood in either group. The blunted PRL response in the schizophrenic group suggests serotonergic dysfunction; possible mechanisms of this finding and implications for treatment are considered.
A case control investigation was performed to examine the relatively high rate of unrecognized psychotic illness within an extended family with a high-density of psychotic illness and identify factors related to nonrecognition. The study was conducted within the catchment area of a Regional Mental Health Center in central Israel. Subjects were recruited using clinic records indicating multiple family members with mental illness. Additional subjects were recruited in the homes of the subjects through family members. A total of 247 subjects were recruited, 111 of whom were determined to suffer from a psychotic disorder based on criteria in standard use. Sixty-six subjects were members of a single extended family (clan) and 181 subjects were members of nonrelated families residing in the same geographic area. While the rate of unrecognized psychotic illness was insignificant among the members of the families not related to the clan, among clan members the rate of unrecognized psychotic illness was 45%. Among this clan, recognition of psychotic illness appeared to be directly related to disruptive behavior. Additionally, it was found that, overall, subjects were more likely to recognized by the mental health system if they had fewer ill family members and more education. We conclude that although nonrecognition of mental illness does not appear to be a problem among the families in the area who are not related to the particular clan, within the clan a particular subculture appears to have developed in which perceived need for psychiatric services is related to disruptive behavior. A high density of psychotic illness within a family and less education may create a family environment that becomes tolerant of psychotic symptoms that are not disruptive to others, resulting in nonrecognition of nondisruptive illness by the mental health system.
To evaluate social adjustment and self-esteem in patients with unipolar (UP) and bipolar (BP) affective disorder and to examine demographic and clinical correlates of these variables, outpatients with UP and BP disorder in remission for at least 12 months were consecutively recruited and individually matched to control subjects with no personal or family history of psychiatric illness (UP-control matched pairs, n = 23; BP-control matched pairs, n = 27). Subjects completed the Rosenberg Self-Esteem scale (SES) and the self-report version of the Social Adjustment Scale (SAS). UP patients reported significantly worse overall social adjustment than their matched controls (P = .009), specifically in the area of social and leisure activities (P = .0003) and poorer self-esteem (P = .02). When separated by gender, only the female UP group manifested significant findings on the SAS. BP patients reported poorer self-esteem than their controls (P = .04), but were not significantly different on the SAS. Although the patients were not clinically depressed, a worse social adjustment was significantly associated with a higher score on the Hamilton Depression Scale (HAM-D) in both groups. In the UP group, this association was absent when the analysis was limited to patients receiving antidepressant pharmacotherapy. The findings indicate that (1) UP patients, particularly women, experience substantial difficulties in social adjustment, primarily in social and leisure activities, even during stable clinical remission, and (2) in both UP and BP patients, adjustment problems are related to depressive symptoms even though these are minimal in severity.