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1.
Encephale ; 39(3): 224-31, 2013 Jun.
Artigo em Francês | MEDLINE | ID: mdl-23095594

RESUMO

INTRODUCTION: Acute catatonia is a non-specific, relatively frequent syndrome, which manifests itself through characteristic motor signs that enables its diagnosis. It occurs in association with mood disorders, psychotic disorders and several somatic or toxic diseases. Its short-term prognosis is of paramount importance. Without effective treatment, it is associated with high mortality. Despite the vital risk inherent in this disorder, it is not recognized as an independent diagnostic category by international rankings, which makes its diagnostic detection difficult and consequently does not allow adequate therapeutic care. However, if benzodiazepines and electroconvulsive therapy have proved effective in the treatment of acute catatonia, the role of atypical antipsychotics remains controversial. In fact, despite the progress made by the DSM-IV-TR and CIM 10 by the recognition of the etiologic diversity of catatonia, we deplore the absence to date of a consensus on clinical management and therapy of catatonia, which constitutes a source of confusion for practitioners in their approach to catatonic patients. To illustrate the difficulty in supporting these patients, we report here a clinical vignette. CLINICAL FEATURES: Mr. M. aged 21, without psychiatric history, has shown a functional acute psychotic episode involving a delirious and hallucinatory syndrome associated with a marked catatonic dimension. Olanzapine was initiated at a dose of 10mg/d on the nineth day of hospitalization; the clinical picture was complicated by a malignant catatonia justifying the halt of olanzapine and the institution, in intensive units, of 15mg per day of lorazepam. After 72hours, the patient has not responded to this treatment. ECT was expected, but the patient died on the 12th day. DISCUSSION: This case raises a threefold question: the crucial issue of immediate vital prognosis, that of the truthfulness of the positive diagnosis of this psychotic table and finally the issue of therapeutic care, primarily the well-founded or otherwise use of an atypical antipsychotic for the treatment of this type of psychotic disorder. For Mr. M., the clinical diagnosis that he has shown, according to the DSM IV-TR, is brief psychotic disorder "temporary diagnosis". This diagnosis - brief psychotic disorder - does not actually allow for a specific clinical approach to this type of psychotic table. The immediate vital prognosis inherent in the catatonic dimension may not be properly evaluated and the therapeutic conduct may miss the application of the specific treatment of the catatonic syndrome. The proper diagnosis for this type of psychotic disorder would be "catatonia" as proposed by Taylor and Fink, instead of "brief psychotic disorder" if the international rankings have included this disorder as a separate and independent diagnosis. The identification by international rankings of the catatonic syndrome as an independent diagnostic category seems essential for clinicians to allow: its clinical detection, the establishment of a syndromic diagnosis of catatonic disorder, appropriate prognostic evaluation and finally, the application of a suitable therapeutic strategy. Conventional treatment, benzodiazepine- and/or ECT-based, can solve the catatonic episode in a few days, irrespective of its etiology and its severity. Moreover, while all authors agree that conventional antipsychotics may induce a catatonic state or worsen a preexisting catatonia into a malignant catatonia and should thus be avoided for catatonic patients or with prior catatonic episodes, recent data from the literature emphasize the frequent and successful use of atypical antipsychotics, including olanzapine, in various clinical forms of benign catatonia. However, our patient did not respond to treatment with olanzapine and got even more complicated. Was the malignant catatonia that this patient has shown induced by olanzapine ? The answer to this question seems difficult since some authors report the efficacy of olanzapine in malignant catatonia. We wonder if we should have kept olanzapine and strengthen its dosage like Cassidy et al. in 2001 and Suzuki et al. in 2010 for the treatment of the malignant form constituted in this patient rather than having stopped it and used lorazepam as indicated by Taylor and Fink in 2003. IN CONCLUSION: The non-recognition of catatonia as an independent entity, the lack of a therapeutic consensus and the pending issue on the safety and efficacy of atypical antipsychotics in the treatment of catatonia are at the origin of the difficulties of therapeutic support of catatonic patients.


Assuntos
Antipsicóticos/efeitos adversos , Antipsicóticos/uso terapêutico , Benzodiazepinas/efeitos adversos , Benzodiazepinas/uso terapêutico , Catatonia/induzido quimicamente , Catatonia/tratamento farmacológico , Transtornos Psicóticos/tratamento farmacológico , Doença Aguda , Catatonia/diagnóstico , Catatonia/psicologia , Evolução Fatal , Hospitalização , Humanos , Masculino , Olanzapina , Prognóstico , Transtornos Psicóticos/diagnóstico , Transtornos Psicóticos/psicologia , Falha de Tratamento , Adulto Jovem
2.
Rev Neurol (Paris) ; 167(3): 221-4, 2011 Mar.
Artigo em Francês | MEDLINE | ID: mdl-20822785

RESUMO

INTRODUCTION: Psychotic symptoms are a rare but well-known complication of epilepsy. The prevalence is estimated between 4 and 9%. PATIENT: We report a case of a 40-year-old patient, unrecognized epileptic, who presented an acute psychotic syndrome which seemed to be of functional origin, the EEG performed during the episode, and the cerebral CT scan being normal. Nevertheless, the clinical presentation, especially the sudden ending of delusions, led to further investigations. Careful history taking and repeated EEG recordings allowed the diagnosis of partial epilepsy that had begun 17 years earlier and symptomatic of a dysembryoplastic tumour of the left hippocampus revealed by MRI. DISCUSSION AND CONCLUSION: Search for an epileptic origin of an acute psychotic syndrome must always be undertaken by systematic EEG. The possibility of a symptomatic temporal tumor must not be overlooked.


Assuntos
Epilepsias Parciais/diagnóstico , Hipocampo/patologia , Transtornos Psicóticos/etiologia , Neoplasias Supratentoriais/diagnóstico , Teratoma/diagnóstico , Doença Aguda , Adulto , Anticonvulsivantes/uso terapêutico , Antipsicóticos/uso terapêutico , Diagnóstico Diferencial , Eletroencefalografia , Epilepsias Parciais/tratamento farmacológico , Epilepsias Parciais/etiologia , Alucinações/etiologia , Hipocampo/fisiopatologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Transtornos Paranoides/etiologia , Agitação Psicomotora/etiologia , Transtornos Psicóticos/tratamento farmacológico , Neoplasias Supratentoriais/complicações , Teratoma/complicações , Ácido Valproico/uso terapêutico
3.
Med Trop (Mars) ; 56(4 Pt 2): 441-4, 1996.
Artigo em Francês | MEDLINE | ID: mdl-9379872

RESUMO

The authors describe two case reports involving Moroccan patients that illustrate the essence of Existence in both health and illness. The principle is universal but there are cultural aspects. However such differences do not prevent management by caretakers from different cultures: other people are not like me but they are not so different except in societies based on deep racial segregation. As shown by our two patients, symptoms are but a mask. The manifestation is somatic in name only and depends on psychic experience. Manifestations cover neurotic conflicts. Cultural aspects can be misleading but the origin is guilt, the common factor for everyone.


Assuntos
Árabes/psicologia , Características Culturais , Transtornos Mentais/etnologia , Relações Profissional-Paciente , Adulto , Etnopsicologia , Família/psicologia , Culpa , Humanos , Masculino , Transtornos Mentais/terapia , Marrocos
4.
Plant Cell Rep ; 9(9): 471-4, 1991 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-24213782

RESUMO

A protocol for direct organogenesis from internodal segments of in vitro grown shoots obtained from mature apple cv. Golden delicious trees is presented. Adventitious buds were initiated on Murashige and Skoog medium (1962) containing various combinations of benzylaminopurine (BAP) and 2,3,5-triiodobenzoic acid (TIBA). Low concentration of BAP (4.4 µM) in combination with TIBA (1 µM) gave the best percentage of regeneration. Three repeated cycles of culture and regeneration produced an increase of adventitious budding up to 23%. Although no auxin was used in the organogenic medium, callus was always obtained. The regenerated shoots were micropropagated and rooted. Cytological studies revealed that proliferating buds originated directly from the superficial layers of the internodal explants without an intermediate callus phase.

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