[Neuroleptics and disinhibition].
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Biomedical subjects
Publications and source records attributed to J F Chevalier.
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Viloxazine administered as a unique antidepressant may in some cases cause an aggravation of anxiety and agitation or manic states. In order to control this effect, we thought of administering neuroleptics and anxiolytics: 1) Before Viloxazine for a few days. 2) Then during antidepressant treatment. The results were as follow: 1) Quick and efficient upon melancholic states in manic -- depressive psychoses. 2) Irregular and questionable upon other depressions.
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The SPECT (Single Photon Emission Computed Tomography), a new advance in medical imagery, allows the measure of cerebral blood flow and could be of interest in studying mental disorders. We report here a case of pseudo-dementia for which a SPECT has been performed before and after treatment. Mrs V., a 49 years old female, has been suffering from a dementia-like syndrome for several months. She is divorced, has two children, lives with a boy-friend, and has been working in a factory for 25 years. The first psychiatric disorders began three years ago with a gradual apragmatism and muteness. A neuroleptic treatment gave no result. One year later, without any reason, Mrs V. recovered a normal way of life. Nevertheless, from time to time, she had some periods of subexcitation. Few months later, she relapsed in her previous state of apragmatism and muteness. During a new hospitalization, neuroleptic treatment is tried again without any success. Mrs V. is then referred to us for medical screening of a dementia syndrome. In the Unit, it is difficult to communicate with her; she looks sad or amimic and has motor stereotypies (like rubbing her feet continuously against the floor). She has polidypsia and glutonny. Neurologic examination is normal, as well as EEG, X Scan, Nuclear Magnetic Resonance. The Folstein Mini Mental State score is 9/30.(ABSTRACT TRUNCATED AT 250 WORDS)
The association cotrimoxazole-tricyclic antidepressants seems to involve a rapid relapse of the depressive states continuously treated with the latter drugs. Five cases are reported. Mechanisms of this unknown drug interaction are discussed. The hypothesis of an enzymatic induction is not the most probable. A central inhibition of the tricyclic antidepressants seems to be possible but needs to be supported by further evidence.
The definition of schizophrenic patients communication disorders sets many problems (partly linked to the descriptive vagueness of the Bleuler mental dissociation syndrome) and leads today to give up those signals, considered as of little specification, for symptoms of easier definition. Nevertheless, french clinicians go on using the dissociation concept to make the diagnostic of schizophrenia, faithful to Bleuler teaching according to which the communication of these patients would be very specific. The object of this article is to take up with the Bleuler logic and to propose hypothesis of cognitive abnormalities that underlie the symptomatic expression of the communication troubles of these patients and point out, from these hypothesis, how a more specific rereading of the language, thought and communication disorders is possible. Two cognitive abnormalities are suggested by the literature data to explain some schizophrenic communication disorders, abnormalities which seem at least partly independent. The first one can be described in the terms of a model of action and brings down communication to its dimension of discursive action. The authors define it as a trouble of a mechanism of action supervision, of the action monitoring, or of the planning of discourse. The symptomatic expressions of this trouble may be described when the subject is under interview conditions soliciting it Examples of such clinical situations are given. The second abnormality may be described in the terms of the "Theory of Mind" and concern the difficulties of some schizophrenic patients to attribute mental states to their interlocuters. Here again, examples of clinical conditions are given, allowing us to investigate this abnormality.
The authors report a case of acute mania induced by perindopril (Coversyl) in a 57 year old man with no prior history of mental illness. This Angiotensin-Converting Enzyme Inhibitor (ACEI) had been introduced eight days prior to the first signs of excitation, in order to treat recently diagnosed arterial hypertension. Without proof of reintroduction, and on the basis of clinical observations, the attribution appears plausible. Similar observations have been made for other molecules in this class of medication, such as captopril (Lopril). A review of literature regroups recent data concerning psychotropic effects of ACEIs. Several reports claim that captopril clearly acts as an antidepressant. Studies on the mood or the quality of life of treated hypertensive patients show ACEIs to have an euphoric-type positive effect compared to other anti-hypertensive treatments. Captopril and perindopril also act like potential antidepressants in experimental models of antidepression. Furthermore, pharmacologic data confirm that the most lipophilic ACEIs penetrate the central nervous system and argue in favor of the role of these molecules in activating central opioides. As these data provide evidence of mood swing in some patients, but also of an overall benefit in hypertensive populations, the clinical importance of the antidepressant effect of ACEIs needs further investigations.
Idiopathic basal ganglia calcifications is a heterogeneous entity characterized by the association of bilateral and symmetric calcifications of the basal ganglia and the dentae nuclei in the cerebellum, polymorphous neuropsychiatric symptomatology. It is rare, of unknown etiology and often hereditary. We report the case of a 48 years old man, who presented with melancholic depression which has been steadily worsening for more than a year and which had led to a serious suicide attempt. Clinical observation revealed apragmatism, affective dullness and impoverished spontaneous expression; the theme of incapacity predominated but guilt feelings were absent. Neurologic examination was normal except for extra-pyramidal signs. CT-scan revealed the presence of bilateral and extensive calcifications of caudate nuclei, lenticular nuclei and thalamus, which indicated a diagnosis of idiopathic basal ganglia calcification characterized by depression. Moreover, MRI revealed an hypersignal of the white periventricular substance. Phospho-calcic results and the parathormone dosage were normal. Psychometric tests showed that although intellectual capacity seemed to be intact, it was not utilised in practice. Unresponsive to antidepressants and sismotherapy, the patient is still the same one and a half year later, and needs to remain in an institution. Subsequent tests indicate that intellectual deterioration has begun. This case poses the problem of the relationship between depressive syndrome and basal ganglia lesions. We look at studies bearing on this subject and on other clinically similar syndromes (athymhormia, loss of psychic self-activation), in which the interruption or cortico-striato-pallido-thalamo-cortical circuits (particularly the limbic loop), is a physiopathologic mechanism currently invoked.