[Tardive dyskinesia and second generation antipsychotics: a review of four cases]. / Dyskinésies tardives et neuroleptiques atypiques : revue de quatre cas cliniques et discussion.

We report four cases of tardive dyskinesia (TD) with second generation antipsychotics (SGA). All of those cases where women, three of them had affective psychosis. The presentation of TD where choreo athetosis in one case, respiratory dyskinesia in another and a tardive dystonia in a third. The fourth one had a very precocious form after just a few weeks of treatment. All of them, except one, had a major form of the disorder, with a major impact on their quality of live. We discuss the necessity to remain aware of this dangerous side effect and to keep it in mind while prescribing SGA for bipolar disorders.

[Body dysmorphic disorder and psychosis. Case reports and discussion]. / Peur d'une dysmorphophobie corporelle et psychose. Cas cliniques et discussion.

INTRODUCTION: The diagnosis of patients who have a preoccupation about physical ugliness is not easy. Many diagnoses can be made. Body dysmorphic disorder (BDD) is defined as a preoccupation with an imaginary defect in physical appearance. What seems difficult in this diagnosis is to make the difference between the psychotic and the non-psychotic form of the disorder. If the patient becomes delusional, we have to make the diagnosis of delusional disorder, somatic subtype. Sometimes it is not easy to make the difference between the delusional and non-delusional form of the illness. A good example is the so-called "olfactory reference syndrome" (ORS), which involves the persistent preoccupation with one's body odour. To make it more difficult, the preoccupation with one's appearance can be seen in many other disorders, such as schizophrenia, or major depressive disorders. We present three cases of dysmorphophobic patients, to discuss their diagnosis and show how we have to be careful about this delusional versus non-delusional difference. CASE REPORTS: The first case is a young man, aged 20 year, who exhibits the typical picture of an ORS. He has probable olfactory hallucinations. He had good response to a treatment combining escitalopram 15mg and risperidone 1mg. The second case had a first appearance of BDD, but he had auditive hallucinations and the evolution showed a pattern more typical of schizophrenia, paranoid subtype. He responded initially to citalopram 20mg and ripseridone 2mg. Sleepy with risperidone, it was shifted to amisulpiride 200mg. After five years, it was possible to stop the amisulpiride, but we had to maintain it to avoid a relapse. The third case is typical of schizophrenia, with a pseudo neurotic aspect, and its course was terrible, with poor response to all neuroleptic therapy, including clozapine. DISCUSSION: These three cases are typical of a feature rarely reported in the literature: the delusional aspect of a dysmorphophobic concern. The literature mainly focuses on the more anxious pattern, and so emphasises the treatment with serotoninergic antidepressants. Our cases demonstrate a gradation in the delusional and psychotic aspect. The first case is dubitatively psychotic, the second is an "ambulatory" schizophrenia with a good response to treatment, the third a very destructive disease. In our cases, some features showed in the typical BDD are also present. We question the obsessive compulsive aspect of the disorder, which was present in our three cases. This supports the fact that the dysmorphophobic feature could be considered more like a symptom than a disorder itself. It reminds us to be always looking for the delusional features of a disorder so as to give the appropriate treatment.

[Influence of depressive history on biological parameters in major depression]. / Influence de l'histoire dépressive sur les paramètres biologiques dans la dépression majeure.

BACKGROUND: Major depressive disorder is associated with several biological abnormalities. Among them, sleep disturbances and alterations of hypothalamic structures and cortisol system have been largely studied. Most studies have found a relationship between depression and alteration of sleep. Electroencephalic sleep profiles during depression demonstrate abnormalities of sleep continuity, reduction of slow waves sleep and REM pressure (27). The cortisol system, investigated by the Dexamethasone Suppression Test (DST), is abnormal in about an half of the depressed subjects. We confirm a cortisol escape from suppression by dexamethasone (21). A complex dysregulation of the Hypothalamic Pituitary Adrenal axis (HPA) is thought to explain this escape (15, 33). The HPA has been first involved in the theory of stress. There are two ways to study this. First by looking at early adversities and genetic susceptibility to stress, and second by studying acute stressors and depressive reactions (8). The sensitization model postulated that the acute abnormalities of depression may leave biological scares. Those scares could make people more vulnerable to latter depressive triggers (34). We could then suppose that biological correlates of depression become more severe during the course of the illness. The present study further examines relationships between DST, polysomnography and some clinical and epidemiological characteristics of the depressive illness. We tried to examine if there were increasing biological disturbances during the course of the illness. We also examined the effect of the history of illness on the psychosocial stressors, and the effects of those stressors on the biological correlates of depression. METHODS: The DST and polysomnographic recordings were performed in a sample of 130 inpatients with primary major depressive disorder, unipolar form, as defined with the RDC (41). All of those patients have been consecutively admitted to the Sleep Laboratory of the Department of Psychiatry, Erasme Hospital, between 1981 and 1992. This population has been previously reported elsewhere (19, 20, 21). The depressive symptom severity was assessed with the 24-items HRSD (17). The Newcastle Endogenous Depression Diagnostic Index was used to assess the endogenous character of the depressive episode (5). The history of the illness and the impact of psychosocial stressors were assessed retrospectively using the interview associated with the RDC (41), the SADS (7). Psychosocial stressor has been assessed using the item 216 of the SADS. We must remind that it is not a precise measurement of stress. RESULTS: Table I shows clinical characteristics and biological variables in our 130 depressed patients. No correlation were found between number of depressive episodes and DST or EEG sleep records (table II). Age of onset was correlated with DST and all sleep EEG parameters (REM latency, REM density, awakening and slow wave sleep). But the age was a major confounding factor. When corrected the results for age, a significant correlation between age of onset and DST still remained, but no correlation between age of onset and EEG sleep results (table III). The psychosocial stressors were correlated only with awakening. A positive trend was found between an augmentation of psychosocial stressors and the number of episodes (p = 0.06). CONCLUSION: This study does not support the view that the biological correlates of depression are worsening with the course of the illness. We found only correlation between age of onset and DST, but a possible confounding effect of age cannot formerly be excluded. The impact of psychosocial stressors on the biological correlates of depression was minimal. The only significant correlation found was between awakening and psychosocial stressors. We found no correlation between psychosocial stressors and the course of depression. Those results do not support the view of sensitization of the illness, but it should be remember that evaluation of psychosocial stressors by item 216 of the SADS was probably not a sufficient sensitive measure. We suggest thus that the impact of the history of depression on biological correlates of depression is not very strong. An alternative explanation of the lack of correlation found is that we used inaccurate measurement of the course of depression. For example, we had no evaluation of the quality of remission between different episodes of depression and of subsyndromic depression. Recent works show the importance of this (6, 9). The major limitations of this work were the retrospective character of the study and the low precision of the evaluation of psychosocial stressors used.