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Objective To determine the characteristics of the activation syndrome (AS) that predict the emergence or worsening of suicidal ideation (SI) in the first month of antidepressant treatment with tianeptine, as well as the temporal relationship between both conditions. Method A naturalistic sample of 2422 depressed outpatients starting a new antidepressant treatment with tianeptine was assessed at 2, 4 and 6 weeks of follow-up using validated questionnaires. Four main dimensions of AS were examined: impulsivity, sleep problems, anxiety and agitation. Results The emergence of an AS was more likely in long-lasting depressive episodes, but less likely if the patient responded to the antidepressant or benzodiazepines were added as an add-on treatment. Treatment-emergent SI was strongly associated to the presence of an AS, particularly in case of sleep problems (OR = 8.42) or impulsivity upsurges (OR = 3.89), even after adjustment for all relevant confounding factors. Conclusions Our findings suggest a dose-effect mechanism modulating the relationship between treatment-related SI and AS. AS symptoms may need to be monitored closely in the weeks that follow the introduction of an antidepressant treatment.

International audience; Autism spectrum disorders comprise a range of neurodevelopmental disorders characterized by deficits in social interaction and communication, and by repetitive behaviour. Mutations in synaptic proteins such as neuroligins, neurexins, GKAPs/SAPAPs and ProSAPs/Shanks were identified in patients with autism spectrum disorder, but the causative mechanisms remain largely unknown. ProSAPs/Shanks build large homo- and heteromeric protein complexes at excitatory synapses and organize the complex protein machinery of the postsynaptic density in a laminar fashion. Here we demonstrate that genetic deletion of ProSAP1/Shank2 results in an early, brain-region-specific upregulation of ionotropic glutamate receptors at the synapse and increased levels of ProSAP2/Shank3. Moreover, ProSAP1/Shank2(-/-) mutants exhibit fewer dendritic spines and show reduced basal synaptic transmission, a reduced frequency of miniature excitatory postsynaptic currents and enhanced N-methyl-d-aspartate receptor-mediated excitatory currents at the physiological level. Mutants are extremely hyperactive and display profound autistic-like behavioural alterations including repetitive grooming as well as abnormalities in vocal and social behaviours. By comparing the data on ProSAP1/Shank2(-/-) mutants with ProSAP2/Shank3αβ(-/-) mice, we show that different abnormalities in synaptic glutamate receptor expression can cause alterations in social interactions and communication. Accordingly, we propose that appropriate therapies for autism spectrum disorders are to be carefully matched to the underlying synaptopathic phenotype.

International audience; OBJECTIVES: The cessation of sedation in brain-injured patients may result in severe agitation and/or acute withdrawal syndrome related to the prolonged administration of large doses of benzodiazepines and/or opioids. The aim of the present study was to assess the clinical efficacy of a written protocol to withdraw sedation for these patients. STUDY DESIGN: Observational prospective study. PATIENTS AND METHODS: After approval by the Institutional Review Board, 40 severely brain-injured patients were included. They had received continuous administration of midazolam and sufentanil or fentanyl for median 15 days. On cessation of midazolam infusion, patients were given clorazepate for 3 days. On cessation of opioid infusion and clorazepate, clinical data were collected for 48 hours: heart rate, systolic blood pressure, respiratory rate, agitation, and pupil diameter. If an opioid withdrawal syndrome occurred, patients received a 48-hour continuous infusion of buprenorphine. RESULTS: Of 40 patients, there were 10 who did not require buprenorphine. An agitation occurred 5 hours (1-21) after cessation of opioid, associated with tachycardia, arterial hypertension, and tachypnea. After 6 hours buprenorphine treatment, these parameters were normalized. No patient needed the reintroduction of the initial sedation. CONCLUSION: The cessation of sedation in severely brain-injured patients can be successfully managed with the use of clorazepate, associated with buprenorphine in the presence of agitation.

International audience; In this study we have quantified the "epileptogenicity" of several brain regions in seizures originating in the posterior parietal cortex in 17 patients investigated by intracerebral recordings using stereotactic EEG (SEEG). Epileptogenicity of brain structures was quantified according to the "epileptogenicity index" (EI), a way to quantify rapid discharges at seizure onset. Seven patients had maximal epileptogenicity in the superior parietal lobule-BA area 7 (Gr1), 2 patients in the superior parietal lobule-area 5 (Gr2), 4 patients in inferior parietal lobule (Gr3) and 4 in the opercular region (Gr4). A large majority of patients (15/17 (88%)) reported to have at least one aura during the course of their disease. Somato-sensory manifestations were reported in the four groups. Vestibular disturbance was observed mainly in seizures from the superior parietal lobule (Gr1 and 2). Ipsilateral version was the most frequent objective manifestation (64%). Hyperkinetic behaviour (motor agitation) was found to be frequent, observed in 4/17 cases (23%) and observed in seizures from inferior parietal regions. In conclusion, the electrophysiological organization and the clinical manifestations of PLS are various and complex. The subjective manifestations are frequent and often suggestive, therefore must be actively sought.

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International audience; The two missions of an emergency psychiatric intervention are firstly diagnostic, and then if possible, therapeutic. The therapeutic aims are thus dominated by two potential cases, one not exclusive of the other: hospitalisation and/or the obtainment of anxiolysis, if not sedation. In a psychiatric emergency, everything comes together in such a way that can induce serious errors, in terms of prescription, for the outcome for the patient: 1) not to appreciate the situation of the crisis, and above all, 2) to "over-estimate" the intensity of the problems, in confusing the gravity of the clinical picture with the intensity of the psychomotor agitation. A sedative and anxiolytic molecule proves to be necessary when faced with a patient in whom the agitation doesn't settle, who remains threatening and oppositional, or in whom the anxious character of the life-like delirium is manifest. Physical containment may be necessary and is then considered a prescribed therapeutic act that necessitates the surveillance of the subject. Therapeutic prescriptions are led by two cases which are not reciprocally exclusive non exclusive.

International audience; Agitation is one of the diagnostic features of catatonia in the DSM IV classification, but permanent forms of agitated catatonia have occasionally been described. We report the case of a 43-year-old man who had already suffered from undifferentiated schizophrenia for 7 years, and in whom we diagnosed agitated catatonia. While our patient was being treated with a neuroleptic during a second episode of paranoia, a state of agitation was observed which persisted for a further 8 months. During this period, he was treated with several different neuroleptics and benzodiazepines, either alone or in association, without any improvement. No organic cause was found. He was then transferred to our electroconvulsive therapy (ECT) unit, with a diagnosis of schizophrenic agitation resistant to drug therapy. ECT was begun, and he was only given droperidol in case of agitation and alimemazine for insomnia, neither of which had any effect. In view of his persistent agitation without any purpose, echolalia and echopraxia, stereotyped movements with mannerisms and marked mimicking and grimacing, we diagnosed him as having agitated catatonia. After the fourth session of ECT, we decided to stop all treatment and gave him lorazepam at a dose of 12.5 mg daily. Twenty-four hours later, all symptoms of agitation had disappeared. In our opinion, permanent catatonic agitation is not rare. In our case, the neuroleptic treatment maintained and may even have worsened the symptomatology. Lorazepam can be used as a therapeutic test for this type of agitation, especially if it does not respond to neuroleptics. This also allows the patient to be sedated rapidly and effectively, thus preventing him from injuring himself further.