Countries of origin of patients and professional staff in a mental hospital.
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Biomedical subjects
Publications and source records attributed to E Persad.
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Rapid cycling affective disorder is characteristically unresponsive to conventional interventions. In bipolar rapid cycling affective disorder, the manic episodes may be controlled with either neuroleptics or electroconvulsive therapy, but the depressive episodes are highly intractable. This report describes the successful treatment of a patient with a bipolar rapid cycling affective disorder using a combination of valproic acid and lithium carbonate.
After a 7-day washout period, 16 subjects suffering from unipolar depression were randomly assigned to either desipramine (DMI) or DMI plus propranolol treatment for 21 days. Both groups showed a significant improvement in their scores on the Hamilton Rating Scale for Depression (HRSD) after 21 days of drug treatment. However, there was no significant difference in the improvement in HRSD scores between the two groups. The results of this pilot study support the need to reevaluate the popular belief that propranolol induces or worsens depression.
The authors present a case of a 40-year-old female with a history of recurrent unipolar depression in which combined treatment with cognitive therapy and medication was associated with significant clinical improvement. Rather than providing a straightforward example of combined interventions for depressed inpatients, it is hoped that some of the complexities involved in such an endeavour will be highlighted. Specifically, issues concerning planned communication between relevant staff, orientation of ward staff to nonorganic treatments, choice of treatment targets, and potential strains in the collaborative relationship between the cognitive therapist and treating physician are explored.
Electroconvulsive therapy (ECT) has been in use for over 50 years and remains one of the most effective treatments in psychiatry. Effectiveness rates for ECT in depression range between 80% and 90%; no comparative study has shown any other intervention to be superior to ECT. ECT is also recommended for mania, schizophrenia and as a safe treatment for the elderly or medically ill depressed patient. This paper will deal with the use of ECT in depression. The areas to be covered are the clinical indications, the factors predictive of response, the evidence for the efficacy of ECT, as well as theories of the mechanism of its action, side effects and guidelines for prescribing the procedure. Notwithstanding the efficacy, the safety and perhaps an improved public acceptance, some observers have noted that there is a decline in the use of ECT. Others have suggested that such a decline may be evident only in the public sectors such as state and provincial psychiatric hospitals. Ongoing research is necessary to achieve further refinement of ECT, as well as enhance our understanding of this important treatment procedure.
The Toronto-Rochester Depression study consisted of 116 pedigrees ascertained for multiple cases of major affective disorders. Among the 857 psychiatrically evaluated family members, of whom more than 85% were given a structured interview, 363 had major affective disorder by Research Diagnostic Criteria and 385 had no history of psychological aberration. HLA region genes were typed in 804 of these persons.
Unipolar affective disorders are highly recurrent. Indicators of risk for recurrence can be established for the individual patient. These may include severity of episode, number of episodes, older age of onset, and preexisting other psychiatric conditions. The continuation treatment phase is necessary for all patients with depression in order to prevent relapse or breakthrough symptoms. Preventative treatment should be offered for the patients at risk for recurrences. The drugs in the continuation phase are usually the same ones used to treat the acute phase. The dose should be very gradually decreased while the patient is closely monitored. The choice of drug is also a matter of individual choice, though some general guidelines are available. For example, for a patient who is clearly unipolar and whose index episode is severe, an antidepressant may be preferable to lithium.
HLA typing was conducted on 577 family members of 86 families having at least two first-degree family members with a lifetime history of major depression or bipolar disorder. The results were combined with a follow-up study of 10 Newfoundland kindreds and with the data obtained from our previous studies, giving a total cohort of 117 families of diverse ethnic and geographic origin. There was increased sharing of HLA haplotypes, as compared with random expectation, over all possible pairwise comparisons both in the follow-up studies (P less than 0.025) and in the total data (P less than 0.01). The increase in HLA haplotype sharing over random expectation was greater if comparisons within heavily loaded sibships (by prior convention, sibships with three or more affected siblings) were omitted from the analysis (P less than 0.002). There was also non-random transmission of HLA haplotypes in 50 families selected for a low-load, unaffected parent (P less than 0.005). Thus, we conclude that genes in the HLA region of chromosome 6 constitute one of the elements in the multifactorial etiology of affective disorder. This conclusion does not depend on any assumption concerning genetic heterogeneity or epistasis or on specific modes of transmission, penetrance values or linkage distances. In addition, the data suggest that chromosome 6 region genes may have a different effect in unipolar and bipolar illness.
This study compared the morbidity risk for affective disorder in relatives of probands who had bipolar (BP) or major depression (UP). Other risk factors were also evaluated. 112 consecutively admitted inpatients yielded 621 relatives with diagnostic information based on either the Renard diagnostic interview, hospital records or information from at least two reliable relatives using the Feighner diagnostic criteria. Similar age corrected morbid risk estimates were found for family members of UP and BP probands of 0.243 and 0.246. There was a 50% increase in morbidity risk for women in all three generations but no relationship to the diagnosis of the proband. A proportional hazards (life table) analysis demonstrated that probands with onset prior to age 40 had relatives with younger onset and higher risk. None of the analyses, including logistic regression and proportional hazards, differentiated UP from BP illness.
This report constitutes the Newfoundland component of a large scale replication study to assess the relationship of HLA to affective disorders; the Ontario component will be published subsequently. In a collaborative study between the University of Toronto, Memorial University and the University of Rochester, first degree family members of Probands with major affective disorder in Newfoundland were assessed for the lifetime presence of psychiatric disorder; their blood was also typed for Human Leucocyte Antigens (HLA). Because of the high rate of refusal to participate, only 10 Newfoundland families could be assessed completely. While this number of families is too small to evaluate the role of HLA as a marker of susceptibility to affective disorder, the results will be added to those of the larger Ontario component. Some problems of conducting research in communities similar to those found in Newfoundland are briefly discussed in the context of characteristics of the Probands in the study group as compared with those of subjects who refused entry into the study.
This data would suggest that psychiatric training programs may not be organized according to the interest or needs of many trainees. The emphasis on fulltime research in neurobiological psychiatry is centre stage in most programs, and yet according to our survey, few residents view this as a desirable career path. Our data from 8 years of trainees at the University of Toronto indicates that a new model of training streams would best suit the needs of the trainee, the profession and the community. This report is a continuation of a study into the recruitment process. An earlier report was published in the Canadian Journal of Psychiatry Vol. 29, December 1984. Our present data is on two groups of trainees as well as from faculty.
Urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), 3-4-dihydroxyphenylethyleneglycol (DHPG), 5-hydroxyindoleacetic acid (5-HIAA), plasma thyroid stimulating hormone (TSH), prolactin (PRL) and growth hormone (GH) were measured before and after the injection of thyrotropin releasing hormone (TRH) in healthy subjects and depressed patients with primary affective disorder. The TSH response to TRH did not differ in depressed compared with control subjects. A trend (.05 less than p less than .10) toward a lower PRL response appeared in male depressed compared with male control subjects. GH levels did not consistently change after TRH. In all subjects the TSH response correlated positively with pre- and post-TRH urinary MHPG. The PRL response correlated negatively with pre-TRH urinary 5-HIAA. Pre-TRH daytime urinary 5-HIAA levels were elevated in depressed subjects.
Urinary and plasma DHPG and MHPG were estimated in patients with MADD and showing DST non-suppression as compared to those with normal suppression. Day and night 12h urine collections and morning plasma samples were analyzed by GC-MS for total MHPG and DHPG and free MHPG levels. Urinary DHPG excretion was significantly elevated in DST non-suppressors compared to suppressors, but no differences were found in urinary MHPG or plasma glycol levels. Elevated DHPG excretion in DST non-suppressors suggests that increased peripheral sympathetic NE activity occurs in association with dexamethasone resistance in MADD.
Recent findings of reduced 3H-imipramine binding in platelets of depressed patients compared to healthy controls have been proposed as a biological marker of depression. However, these studies failed to consider the possible occurrence of seasonal variation in the binding characteristics. Our results show a highly significant seasonal variation in platelet 3H-imipramine binding which occurs in both normal and depressed populations. Furthermore, when annual rhythms are taken into account, there is no difference in the binding parameters in the two populations.
Plasma levels of desipramine (DMI) and the unconjugated form of its principal metabolite 2-hydroxydesipramine (OH-D) were measured under steady-state conditions in nine depressed inpatients during treatment with 75 mg DMI every 12 hr and after at least 1 wk of an increased dose of DMI (after steady state). When DMI dosage was raised after an initial steady state had been reached, the rise in plasma DMI level was proportionately greater than the increase in dosage, suggesting saturation of DMI elimination pathways. Levels of OH-D rose in proportion to dose, suggesting saturation of DMI elimination by 2-hydroxylation could not explain DMI plasma level changes. In contrast, there were no dose-dependent effects on the disposition of amitriptyline or its metabolite nortriptyline in subjects receiving the same amitriptyline dose.
This is a report of an open clinical trial of Carbamazepine in the treatment of patients who suffered from affective disorders and who did not have an adequate response to Lithium or other medications. Our findings suggest that Carbamazepine can be a useful adjunctive medication when used in combination with Lithium and other psychotropic medications. The characteristics of the patients who responded were examined. The clinical state of the patients at the point of intervention varied; eight patients were manic and four patients were depressed. Four patients were judged to have had markedly effective responses, four showed an effective response and in four there was a slightly effective response. From the duration of the trials it was evident that in cases where Carbamazepine produced a good response its effect was seen as early as two weeks. The mean daily dose used varied from 300-1300 mgs. Because of the open nature of this trial, Carbamazepine was not withdrawn except in one instance.