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1.
Encephale ; 42(4): 340-5, 2016 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-27216588

RESUMEN

INTRODUCTION: Catatonia is a psychomotor syndrome which can include motor, mental, behavioral and vegetative symptoms. Exclusively associated with schizophrenia until the 1970s, catatonia still remains an under-diagnosed syndrome with significant morbidity and mortality. LITERATURE FINDINGS: As a result of its different forms and developments, catatonic syndrome can be associated with many organic and psychiatric etiologies and confused with a variety of diagnoses. In addition to its organic complications, malignant catatonia can also be extremely severe. Several diagnostic scales are described, those of Bush and Peralta being the most widely used. Despite the recent development of the DSM-5, we can regret the lack of progress in the international classifications concerning both the recognition of the etiological diversity of this syndrome and in the clinical and therapeutic approaches to it. The diagnosis is based solely on clinical data, and needs to be completed by information from paraclinical settings, particularly with respect to detecting organic etiology. The first-line treatment is still based on the use of certain benzodiazepines or benzodiazepine-like agents such as lorazepam, diazepam and zolpidem. If the first or second line fails, or in case of malignant catatonia, electroconvulsive therapy is recommended. For the periodic form, no large-sample study has been performed on long-term treatment. A few case reports suggest the use of lithium in periodic catatonia, specifically to prevent recurrent episodes or at least to extend the inter-episode intervals. Other studies are in favor of the use of benzodiazepines, with disagreement between gradual discontinuation and long-term treatment. Concerning the management of catatonia in patients with schizophrenia, for whom first-line benzodiazepines are often insufficient, certain atypical antipsychotics such as clozapine or quetiapine appear efficient. These data are also applicable to children and adolescents. CONCLUSION: Often neglected by practitioners, catatonic syndrome remains a common entity of which it is important to be aware, especially in case of rapid installation of the symptoms. Diagnostic scales should be used and a lorazepam test should be performed to avoid delaying the diagnosis. Second-line therapy requires further study. This concerns in particular diazepam, anti-NMDA (N-methyl-D-aspartate) and rTMS (repetitive transcranial magnetic stimulation). Some specificities of catatonia, such as the periodic form and cases in patients with schizophrenia, also require further evaluations.


Asunto(s)
Catatonia/diagnóstico , Catatonia/terapia , Adolescente , Adulto , Niño , Humanos , Hipnóticos y Sedantes/farmacología , Lorazepam/farmacología , Escalas de Valoración Psiquiátrica , Síndrome
2.
Encephale ; 40(1): 86-94, 2014 Feb.
Artículo en Francés | MEDLINE | ID: mdl-23928066

RESUMEN

BACKGROUND: Hyperprolactinemia is a frequent but neglected adverse effect observed in patients treated with antipsychotic-drugs. In this review, we summarize its physiopathogenetic mechanism, its clinical manifestations in men and women, and the way to manage it. LITERATURE FINDINGS: Prolactin is a hormone secreted by lactotroph cells in the anterior pituitary. Its synthesis and release are under the control of peptides, steroids and neurotransmitters. The main inhibitory regulation is made by dopamine, which binds dopamine receptors D2 on the membrane of lactotroph cells. Antipsychotic-drugs block these receptors and thus remove the inhibitory effect of dopamine on prolactin secretion. All antipsychotic-drugs block D2 receptors and all can induce hyperprolactinemia. Nonetheless, it seems that the faster the antipsychotic-drug dissociates from D2 receptors, the lesser the increase of prolactin in the plasma. Another way to explain hyperprolactinemia is the ability of antipsychotic-drugs to cross the blood-brain barrier. The role of their metabolites should also be considered. For these reasons, one can distinguish prolactin-raising (conventional neuroleptics, amisulpride, risperidone) and prolactin-sparing (clozapine, aripiprazole, olanzapine) antipsychotics. An English study showed that 18% of men and 47% of women treated with antipsychotics for severe mental illness had a prolactin level above the normal range. Hyperprolactinemia is in fact more frequent in women than in men. Sometimes it is asymptomatic, but the higher the prolactin level is, the more patients have clinical manifestations. Some symptoms are due to the hypogonadism caused by prolactin, which disturbs hypothalamic-pituitary axis function, and others are due to direct effects on target tissues. Consequently, patients can suffer from sexual dysfunction, infertility, amenorrhea, gynecomastia or galactorrhoea. Data suggest that these symptoms are common, but patients don't mention them spontaneously and clinicians underestimate their prevalence. In the long-term, hypogonadism involves a premature bone loss in men and women. Klibanski and colleagues showed that this loss is significant only in women with hyperprolactinemia associated with amenorrhea. That suggests that prolactin is not directly responsible for this clinical feature. Nevertheless, prolactin seems to be involved in the development of breast cancer, but its role is unclear for prostate cancer. DISCUSSION: Our review promotes a check-up before beginning a treatment with antipsychotic agents. First, a baseline prolactin level should be measured. It should also include the research on previous treatment with antipsychotic-drugs and the assessment of adverse effects suggestive of hyperprolactinemia. Questioning should finally look for any contra-indication to antipsychotics. Monitoring during antipsychotic treatment has been studied by a group of international experts in psychiatry, medicine, toxicology and pharmacy who made a critical review of clinical guidance on hyperprolactinemia. Experts notify that it is important to check whether patients have any sexual dysfunction, such as loss of libido or menstrual irregularity, and galactorrhoea. Prolactin level should also be controlled after three months of stable dose treatment, or if any clinical feature of hyperprolactinemia appears. If a patient prescribed antipsychotic-drugs has a confirmed prolactin level above the normal range, it is necessary to exclude other causes of hyperprolactinemia. If antipsychotics are really involved, the management should be adapted with the prolactin level and the patient him/herself. To summarize, clinicians can decrease the dose of the antipsychotic or switch to a prolactin-sparing drug. Oral contraceptives can be added whether to prevent pregnancy or to prevent bone loss and osteoporosis. Finally, experts recommend reserving dopamine agonists to treat antipsychotic-induced hyperprolactinemia in very exceptional circumstances as it can worsen the mental illness.


Asunto(s)
Antipsicóticos/efectos adversos , Antagonistas de los Receptores de Dopamina D2 , Hiperprolactinemia/inducido químicamente , Hiperprolactinemia/fisiopatología , Adenohipófisis/efectos de los fármacos , Antipsicóticos/uso terapéutico , Densidad Ósea/efectos de los fármacos , Densidad Ósea/fisiología , Dopamina/fisiología , Femenino , Humanos , Hipogonadismo/inducido químicamente , Hipogonadismo/fisiopatología , Sistema Hipotálamo-Hipofisario/efectos de los fármacos , Sistema Hipotálamo-Hipofisario/fisiopatología , Masculino , Adenohipófisis/fisiopatología , Sistema Hipófiso-Suprarrenal/efectos de los fármacos , Sistema Hipófiso-Suprarrenal/fisiopatología , Prolactina/sangre , Receptores de Dopamina D2/fisiología , Factores de Riesgo , Factores Sexuales
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