[Epidemiology and mental health].
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Biomedical subjects
Publications and source records attributed to D Widlöcher.
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The aim of this paper is to focus on methodological problems related to clinical studies on the onset of action of antidepressants, especially moclobemide. The methodological discussion proposed focuses on: --global efficacy as a function of time; --proposals for a specific approach to the study of the onset of action; --quality of the response and onset of action; --the dimensional level and the onset of action.
This study examines the concordance of clinical subtypes and age at onset of schizophrenia in 42 sibships of multiply affected schizophrenic patients. Subtypes were defined by four major diagnostic systems (DSM-III, DSM-III-R, ICD-10, and Tsuang-Winokur criteria) and rated both for the first hospitalization and long-term diagnosis. When a sibship method was used, no concordance for subtypes was found in siblings. Age at onset, analyzed as a continuous variable with the intraclass correlation method, was found to be correlated in siblings. This finding suggest that the search for continuous traits distributed in families of schizophrenic patients might constitute an alternative to discrete category-based family studies.
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The extent to which patients' reports of maladjustment is influenced by depressive symptoms was estimated in 25 acute depressed patients responding to pharmacotherapy. Their social adjustment over the same four-month period immediately prior to hospitalization was assessed on two separate occasions: firstly when they were acutely depressed, and again a mean of 20 days later when clinically recovered. Significant differences between the two reports were found in mean score of maladjustment in four out of five fields of social adjustment (work, social/leisure life, family of origin, marriage, and sex). The reduction in depressive symptoms scores (of pessimism considered separately), correlated significantly with changes in the total maladjustment score. The reduction in pessimism scores correlated with changes in the scores for both work and social/leisure fields, and also accounted for 40% of the total variance in maladjustment score. These results indicate that impaired social adjustment as assessed during the height of the depressive illness arises in part from a symptom--related overreporting bias leading patients to make a harsh appraisal of themselves.
Potential biases due to acute depressive symptomatology on raters' assessments of social maladjustment derived from patients' reports were assessed in 25 patients responding to pharmacotherapy during medium-term hospitalization. Patients were questioned on two separate occasions about their social maladjustment covering the exact same period (the 4 months preceding hospitalization): the first was during the acute illness phase, and the second a mean of 20.5 days later, when symptoms remitted. In the second report, composite scores for all fields as a whole showed significantly fewer reports of social impairment than did the first. Significant differences from the first to the second evaluation concerning both subjective distress and observable behavior were found in four and three, respectively, of the five "fields" of social adjustment. Although subjective distress was most modified by remission of acute symptoms, even supposedly objective, observable disturbances were significantly affected. These results indicate that acutely depressed patients overreport social maladjustment, which they then more accurately reappraise when symptoms remit. Patients are completely unaware of both the initial bias and of the reappraisal.
A novel clinical and experimental situation has been created, based on the psychopathological concepts of 'pensée opératoire' and alexithymia and the contribution of recent trends in cognitive science as to the dual skills of the brain hemispheres: the Parallel Visual Information Processing Test. This test was validated in more than 100 subjects, and revealed that holistic visual attention is reduced during logical task performance; this impairment appeared to be typical of patients with poor fantasizing ability and operative behavior. Such findings are consistent with some authors' theory according to which there is a functional commissurotomy in alexithymic and psychosomatic patients.
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Twenty-five depressed inpatients were asked to report their adjustment at work during the 4-month period preceding their hospitalization. Two separate reports were given: the first during the acute illness phase and the second one 10-28 days later, after symptomatic remission following standardized pharmacotherapy. Thirty-two percent more patient ratings showed absence of adjustment problems on the second report compared with the first. Significant differences between the 2 reports were found in 7 of the 9 items on the Structured and Scaled Interview to Assess Maladjustment, which is designed to assess specific aspects of maladjustment at work. The changes in the scores of maladjustment correlated with the changes in the scores of depressive symptoms, and 40% of the variation in maladjustment scores was accounted for by the pessimism item of the Montgomery-Asberg Depression Rating Scale. Much of the poor work adjustment reported by the acutely depressed patients thus seems to be caused by symptom-related subjective bias.
Choice reaction time involves, at least two components of response latency, decision time and movement time. Studies of choice reaction time usually provide values of these two components averaged over a given number of trials. The aim of the present study of depressed subjects was to investigate changes across practice on Decision Time (DT) and Movement Time (MT) before and after clinical improvement. 19 depressed subjects were given two sessions of 50 trials each, one before treatment (Di) and one after recovery (Df). Decision time and movement time exhibited quite different patterns. Decision time significantly decreased with clinical improvement. No significant variation across trials was found, in either session. Movement time values varied across trials but the variations observed on Di and Df were significantly different, whereas before treatment latencies recorded at the end of the session were greater than those scored at the start, the contrary was observed after clinical recovery. No significant difference was found between values of movement time scored at the start of the two sessions.
The relationship between thyroid disorders and depression is well known. This type of endocrine disease is mainly observed in patients with depression resistant to appropriate antidepressor therapy. Three clinical forms of this association may be distinguished: hypothyroidism in a patient with depression but without a previous psychiatric history; a relapse of depression in a manico depressive patient who has developed hypothyroidism; the finding of slight thyroid dysfunction (increased TSH response after injection of TRH) in a patient with depression. The frequency of the association of hypothyroidism and resistant depression underlines the need to perform thyroid function tests in all depressed patients who do not respond normally to appropriate antidepressor therapy. The precise mechanism of the resistance of depressive symptoms to tricyclic antidepressors is unclear. Several arguments point to an effect of triiodothyronine on central noradrenergic receptors. In practice, significant hypothyroidism implies substitute therapy. Minor thyroid dysfunction (abnormal TRH test alone) may require the association of tricyclic antidepressors and thyroid hormone although the indications and precise dosages of this drug association have not been established.
To determine cognitive disturbances in recent demyelinating disease, we studied 21 patients with definite or probable multiple sclerosis (MS) of less than two years' duration and nine patients with recently isolated optic neuritis. None had any clinical or social evidence of cognitive impairment. Mild to moderate cognitive impairment. Mild to moderate cognitive impairment was present in 18 (60%) of 30 cases, affecting visual and/or verbal efficiency. These abnormalities were statistically significant when compared with the results of a control group of 29 patients. There was no correlation with a depressive status, between the presence of cognitive impairment and either the degree of handicap or the activity of the disease. The frequency of cognitive dysfunction (60%) appears to be comparable to that reported in other series in which MS evolution is over ten years. The natural history of cognitive functions in MS has to be identified. Neuropsychologic tests could be useful in the diagnosis of monosymptomatic or paucisymptomatic forms of MS (ie, visual or medullary).
The authors treated 24 newly hospitalized patients suffering from acute mania with 450-900 micrograms/day of clonidine, an alpha 2-adrenergic agonist, for 2 weeks. A marked decrease in manic symptoms was observed after 5 and 13 days of treatment in about half of the patients. Early response seemed to predict the final result. Patients with a family history of affective disorder and patients who had had a good response to neuroleptics during a previous manic episode tended not to respond to clonidine. At the doses given, the patients' tolerance to clonidine was excellent: sedation was markedly lower than it is with neuroleptic treatment.
Wrist motor activity was continuously recorded by a solid-state monitor in 12 patients with major depression throughout their stay in hospital; their clinical state was evaluated using three scales. During the day, activity troughs and immobility peaks occurred before noon and around 1500 hrs. Activity level progressively increased, while the duration of immobility decreased, with clinical improvement. The immobility measurement appeared to be a valuable index of depression and is more sensitive than the activity level, mainly for agitated depressed patients. Immobility episodes during the day could suggest the release of an ultradian sleep-wake rhythm in depression.
The association of involuntary motor disturbances and psychic symptoms is a salient feature of Gilles de la Tourette's disease. The frequency of the association is supported by recent epidemiological data. However, a clear distinction must be made between psychic symptoms dependent of the pathological process and psychological reactions to the disease. The link between motor and psychic symptoms raises a crucial and yet controversial question. Etiology, and particularly the role of psychological and social factors, is discussed. But mechanisms must be studied independently. Is there a causal relationship between motor and psychic symptoms? Is there a common neuro-chemical alteration? There is no evidence for clear conclusion but this questions must be clarified.
According to the author, psychomotor retardation, which influences all the activities of the individual, reflects an infraclinical disturbance, which--as well as the action systems revealed by the analytical investigation--reflects functional disturbances of the central nervous system. Antidepressants probably act on the monoaminergic systems regulating the fundamental cognitive processes, while psychotherapy would act on the action systems.
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