Biomedical subjects
Publications and source records attributed to M G Gelder.
The research evidence strongly suggests that the most effective form of treatment for panic disorder is cognitive therapy. It is more practical, however, to initiate treatment with alprazolam or with imipramine. Either drug will suppress symptoms and even a half of the patients will stay well.
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The endocrine responses to the 5-hydroxytryptamine (5HT) precursor, L-tryptophan, were assessed in 10 depressed patients before and after at least 4 weeks of treatment with amitriptyline. Overall, amitriptyline did not alter either prolactin or growth hormone responses to L-tryptophan. When three subjects with severe pretreatment weight loss were excluded, however, the remaining seven patients showed a significant increase in the prolactin response to L-tryptophan, consistent with other published studies. The findings suggest that severe recent weight loss may alter the effects of tricyclic antidepressants on 5HT-mediated prolactin release.
A National Committee for the Ethics of Research could consider new questions arising from innovations in research or practice, deal with multi-centre trials, adjudicate when separate local committees give conflicting advice about similar projects, or oversee the work of district committees. The value of each of these functions is assessed and it is concluded that a national committee would be most valuable in providing detailed evaluations of difficult or controversial issues. Though it could offer useful advice about multi-centre trials, local committees would probably wish to continue to consider research involving patients within their health districts even though approval had been given by a central committee. A national committee could usefully oversee the working of a system of quality control throughout the country, but the detailed monitoring of district committees would be done more effectively at regional level.
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Anxiety attacks were included in the first descriptions of the syndrome of anxiety neurosis. Recently it has been suggested that such attacks (now usually called panic attacks) characterize a distinct form of anxiety disorder--panic disorder. It has also been proposed that panic attacks result from a biochemical disorder and require pharmacological treatment. Some of the evidence for these ideas is presented, and two other explanations for panic attacks are reviewed: that they are caused by hyperventilation, and that they result from a cognitive disorder. It is concluded that although it is not possible on the present evidence to choose between the three theories, there is strong indirect support for the cognitive theory and good reason to investigate cognitive factors more thoroughly. Future work on biochemical causes of, and pharmacological treatments for panic attacks should take account of such factors.
Seventy-seven patients with diagnosis of schizophrenia (62) or schizoaffective disorder (15) were studied 2-20 years since onset of illness, when in a stable condition. The investigation included clinical assessment, measurement of plasma concentrations of neuroleptics and prolactin, computed tomography brain scan, neuropsychological and neurological examination. Outcome of illness was classified according to the presence of chronic psychiatric symptoms and social impairment, and response to neuroleptics according to the effect of treatment in the most recent psychotic episode. Neither outcome nor response to neuroleptics was related to duration of illness. The groups with good and poor outcome differed in premorbid adjustment, age at onset and symptoms of the initial episode, but not in drug bio-availability or prolactin response. Large cerebral ventricles and cognitive impairment, but not neurological 'soft' signs, were associated with unfavourable outcome. The three measures of organicity were not inter-related. No clinical differences were found between chronic patients with and without signs of organic dysfunction. The findings suggest that schizophrenia with good and unfavourable outcome may be separate sub-types. However, the role of organic factors in the latter group remains unclear.
Platelet alpha 2-adrenoceptor binding characteristics were investigated in 28 healthy women during the peripartum period. The number of platelet alpha 2-adrenoceptors fell after childbirth, corresponding to a fall in the circulating levels of oestrogen and progesterone. Two-thirds of the women had an episode of maternity blues. At 7-10 days post partum the platelet alpha 2-adrenoceptor capacity in these subjects was significantly higher than in those women who did not show signs of maternity blues and significantly higher than a control group of normally menstruating women. We conclude that platelet alpha 2-adrenoceptors may be affected by the circulating levels of endogenous oestrogen and progesterone and that a delayed or diminished fall in platelet alpha 2-adrenoceptor capacity after childbirth may be associated with the development of maternity blues.
The growth-hormone (GH) response to subcutaneous administration of the dopamine agonist, apomorphine (0.005 mg/kg), was assessed in 15 depressed patients at the beginning and at the end of a course of electroconvulsive therapy (ECT). After ECT there was a significant increase in the GH response to apomorphine, supporting the hypothesis that ECT produces an enhancement of dopamine-mediated responses in the brain. Additional studies in depressed patients receiving other antidepressant treatment suggested that the increase in apomorphine response following ECT was not attributable either to concurrent antidepressant medication or to clinical recovery from depressive illness.
1 The effects of treatment with a range of neuroleptic drugs on 5-hydroxytryptamine (5-HT) induced platelet aggregation in vivo were examined in a group of recently admitted psychiatric patients and in a larger group of chronic schizophrenic patients. 2 Five of seven recently admitted patients treated with chlorpromazine showed enhanced aggregation. Four of seven patients treated with fluphenazine, flupenthixol, trifluoperazine and haloperidol showed enhancement. 3 Enhanced aggregation responses were observed in only 20% of chronic schizophrenic patients being treated with a neuroleptic drug. 4 The relationship between changes in platelet aggregation and clinical changes in recently admitted patients was variable and platelet aggregation responses were not predictive of response to treatment. 5 Chronic schizophrenic patients with enhanced aggregation showed significant week to week variation in platelet aggregation response. Variability of responses was not related to the drug used or to the dose administered. There was some evidence that higher plasma concentrations of neuroleptic drugs were associated with enhanced platelet aggregation responses. 6 Treatment with neuroleptic drugs leads to enhancement of platelet aggregation responses induced by 5-HT. The frequency and reliability with which such responses can be elicited is unpredictable and the value of platelet aggregation responses as an empirical guide to treatment with neuroleptic drugs is therefore open to question.
1 The reliability of 5-hydroxytryptamine induced platelet aggregation responses in psychiatric patients treated with neuroleptic drugs was investigated by examining the effects of a number of technical factors which could account for the variability of responses observed in some patients. 2 Variation in incubation time, temperature, aggregometer stirrer speed, and in the time interval between withdrawal of the blood sample and testing, had no significant effects on the consistency of responses. 3 Dilution of platelet rich plasma (PRP) led to enhanced platelet aggregation responses becoming non-enhanced. 4 Overcentrifugation of blood samples during the preparation of PRP caused a decrease in the incidence of enhanced platelet aggregation responses observed in chronic schizophrenic patients receiving chlorpromazine. 5 The reliability of platelet aggregation responses as indices of the action of neuroleptic drugs in psychiatric patients remains doubtful.
1 Using a radioimmunoassay, plasma fluphenazine (FPZ) concentrations were examined in 33 schizophrenic patients during 38 intervals between injections of FPZ decanoate. Doses ranged from 12.5 to 150 mg and intervals from 1 to 5 weeks. At least three blood samples were taken between injections from each subject; also in 26 subjects additional samples were taken during the first 24 h post-injection. 2 FPZ was measurable in all plasma samples. 3 Each injection was followed by a rapid rise in plasma FPZ concentration to a maximum at 1-8 h. The height of this peak varied considerably. Within the next 12-36 h plasma FPZ fell to a level slightly above that found before injection and then remained stable until the next injection, thus confirming the steady release of FPZ from the depot over this period. 4 For the group, dose and mean plasma FPZ levels correlated strongly. 5 Despite this, there was a four-fold variation in plasma FPZ concentration among subjects receiving the same dose. 6 The FPZ level on the last day of an interval between injections was a satisfactory estimate of the mean FPZ level for the interval. 7 In one subject examined in this way, a positive correlation was found (r = 0.76) between plasma FPZ (by radioimmunoassay) and plasma prolactin levels.
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