Evaluatie van de activiteit van capsules droogextract van passiebloem, volgens een "ster"-model.

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DULOXETINE IN MAJOR DEPRESSED PATIENTS RESISTANT TO SSRIS AND/OR VENLAFAXINE

Several acute depression trials suggest that only 35% of the patients achieve remission state with antidepressant monotherapy. An increasing body of evidence is emerging suggesting that multi-action antidepressants might be more effective in treatmentresistant depressed patients than single-action agents. In this context, the purpose of the study was to assess the effectiveness of duloxetine in treatment-resistant major depressed outpatients. We performed a retrospective study assessing the efficacy of duloxetine in major depressed outpatients who did not achieve full symptom remission (CGI-S (severity) ≥ 3) after treatment of adequate dose and duration (more than 8 weeks) with at least either one SSRI or the SNRI venlafaxine. We excluded patients with a severe medical illness and a personality disorder. CGI-S was used as a measure of symptom severity and administered before the prescription of duloxetine and 6 weeks later. The sample included 29 patients (9 M, 20 F). We observed a very significant decrease in CGI-S scores (4,86 ± 0.51 to 2,17 ± 1,44, p<0.0001) after treatment with duloxetine (dose between 60 and 120 mg). Remission was achieved in 48 % of the patients. The tolerance was excellent. This study suggests the potential interest of duloxetine in some treatment-resistant depressed patients

Dépression et neuroplasticité.

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The lack of relationship between DST nonsuppression in the dexamethasone suppression test and EEG abnormalities.

peer reviewedAs a recent study suggested a relationship between cortisol escape following dexamethasone suppression test (DST) and electroencephalogram (EEG) abnormalities, we tried to replicate these findings in 52 major depressive inpatients. A total of 23 patients exhibited DST nonsuppression (44%) and 18 patients had EEG abnormalities (35%). No relationship existed between DST and EEG results

Les antidépresseurs tricycliques et les IMAO ont-ils encore une place dans le traitement de la dépression?

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Dépression et neuroplasticité : des découvertes neuroanatomiques aux nouvelles stratégies thérapeutiques.

peer reviewedThe antidepressants action cannot be understood only by the neurochemical approach and the monoaminergic theory. In particular, that model does not explain the time lag between the acute chemical modulations induced by the antidepressants and the delayed clinical response. Many hypothesis have been developped to specify the antidepressants action, each of them implicating different mechanisms of receptors regulation. In the same way, the advanced knowledge in neuroanatomy leads towards the existence of specifical lesions in this pathology. Indeed, there is, in depression, a neuronal loss focused on some regions forming the cortico-striato-pallido-limbic-thalamic tract. These anatomical changes are reduced after antidepressant treatment. Accordingly, in the last decade, a new pathophysiological concept of affective disorders has emerged. This concept integrates preferentially molecular and cellular antidepressants-induced changes leading to rehabilitation of synaptic activity and neuronal trophism. In this article, we synthesize the current knowledge about the anatomical abnormalities observed in depression, and about the pathophysiological mechanisms that account for these ones. The central phenomenon in neuroplasticity turns around neurogenesis. This process takes place in the dentelate gyrus of hippocampus, where promoter cells enter in division, differentiate and become able to migrate to specifical regions of the central nervous system and to integrate into it. Neurogenesis is stimulated by neurotrophic factors, including the BDNF (brain derived neurotrophic factor) and by a lot of environmental situations. An inhibition of neurogenesis is attributed to the excess of glucocorticoids seen in stress situations like depression. Moreover, the neuronal loss in major depression is also caused by an excessive concentration of glutamate in synapsis that can lead cells to apoptotic process. Recently, it has been demonstrated that the clinical effects of the antidepressants are correlated to an elevation of neurogenesis in the dentelate gyrus. In this article, we finally present some potentially therapeutic straregies actually being studied, being aware that neuroplasticity is still a new concept (if the anxio-depressive pathology is considered) and that it thus must be seen with that reserve

Dopamine-glutamate reciprocal modulation of release and motor responses in the rat caudate-putamen and nucleus accumbens of "intact" animals

peer reviewedFunctional interactions between dopaminergic neurotransmission and glutamatergic neurotransmission are well known to play a crucial integrative role in the striatum, the major input structure of the basal ganglia now widely recognized to contribute to the control of motor activity and movements but also to the processing of cognitive and limbic functions. However, the nature of these interactions is still a matter of debate and controversy. This review (1) summarizes anatomical data on the distribution of dopaminergic and glutamatergic receptors in the striatum-accumbens complex, (2) focuses on the dopamine-glutamate interactions in the modulation of each other's release in the striatum-accumbens complex, and (3) examines the dopamine-glutamate interactions in the entire striatum involved in the control of locomotor activity. The effects of dopaminergic and glutamatergic receptor selective agonists and antagonists on dopamine and glutamate release as well on motor responses are analyzed in the entire striatum, by reviewing both in vitro and in vivo data. Regarding in vivo data, only findings from focal injections studies in the nucleus accumbens or the caudate-putamen of "intact" animals are reviewed. Altogether, the available data demonstrate that dopamine and glutamate do not uniformly interact to modulate each others' release and postsynaptic modulation of striatal output neurons. Depending on the receptor subtypes involved, interactions between dopaminergic and glutamatergic transmission vary as a multiple and complex combination of tonic, phasic, facilitatory, and inhibitory properties. (c) 2005 Elsevier B.V. All rights reserved

Anxiety Disorders and Organic Pathology: A Differential Diagnosis Difficulty

peer reviewedThe diagnostic criteria for panic disorder include symptoms commonly experienced by patients with organic diseases. We report a case of coronary artery spasm in a patient with chest pain, exhibiting atypical characteristics, and accompanied by symptoms of nervousness. The approach and the management of anxiety disorders are discussed

Cognitive topography imbalance in alcoholism and psychiatric comorbidity

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