[The neuroplastic effects of electroconvulsive therapy]. / Les effets neuroplastiques de la sismothérapie.

Major depressive disorder is an important cause of disability around the world, with a tremendous psychological burden and extensive socioeconomic consequences. Whilst both psychotherapy and psychopharmacology are effective in treating a depressive episode, often there is a delay of several weeks between the start of treatment and the first beneficial effects. More importantly, approximately 30 % of patients do not remit, even after several treatment attempts. As the oldest biological treatment in psychiatry that is still available, electroconvulsive therapy (ECT) remains the most potent of antidepressant interventions, today achieving a staggering 70-80 % response and a 50-60 % remission rate. In treatment-resistant patients, response rates are even as high as 50 %-70 %. Despite its effectiveness, the neurobiological mechanisms of ECT remain unclear. A large body of research suggests that ECT induces widespread changes in both brain structure and function. A key factor behind these powerful therapeutic properties appears to be the important neuroplastic effects of this treatment. This review of the literature will discuss the importance of neuroplasticity in the pathophysiology of depression and then bring up the neuroplastic effects of ECT.

Le trouble dépressif majeur est une cause importante d'invalidité dans le monde, avec des conséquences psychologiques et socio-économiques notables. Bien qu'un épisode dépressif soit généralement traité par différentes formes de psychothérapies ou de pharmacothérapies, il y a souvent un délai de plusieurs semaines entre le début de ces traitements et leurs premiers effets bénéfiques. Plus important encore, environ 30 % des patients n'entrent pas en rémission, même après plusieurs tentatives de traitement. L'électroconvulsivothérapie (ECT) reste la plus puissante des interventions antidépressives, atteignant une réponse de 70 à 80 % et un taux de rémission de 50 à 60 %. Chez les patients résistant au traitement, des taux de réponse de 50 à 70 % sont atteints. Malgré son efficacité, les mécanismes neurobiologiques de l'ECT restent flous. Un grand nombre de recherches suggère que l'ECT induit des changements généralisés à la fois dans la structure et le fonctionnement du cerveau. L'un des facteurs clé derrière ces puissantes propriétés thérapeutiques semble être les importants effets neuroplastiques de ce traitement. Dans cette revue de la littérature, nous aborderons l'importance de la neuroplasticité dans la physiopathologie de la dépression pour, ensuite, aborder les effets neuroplastiques de l'ECT.

Hair cortisol in patients with a depressive episode treated with electroconvulsive therapy.

BACKGROUND: There is substantial evidence showing changes in hypothalamic pituitary adrenal (HPA)-axis activity in patients with major depressive disorder (MDD). Also, there seem to be differences in HPA-axis functioning between MDD subgroups. It is however unclear whether hair cortisol concentrations (HCC), which are a stable marker of long-term cortisol levels, are suitable as a biomarker for identifying subgroups in MDD. METHODS: We were able to attain valid HCC from a scalp hair sample of sixty-two patients with a major depressive episode right before electroconvulsive therapy (ECT). HCC were our main biological outcome measure. We created subgroups using depression severity as defined by the Hamilton Depression Rating Scale, the presence/absence of psychotic symptoms, the presence of melancholia as defined by the CORE and catatonia as defined by the Bush-Francis Catatonia Rating Scale. RESULTS: Our analyses of the total group showed a median HCC of 4.4 pg/mg. We found patients with catatonia (N = 10) to have substantially higher median HCC (8.3 pg/mg) than patients without catatonia (3.8 pg/mg). Although presence of melancholia and depression severity were not significantly associated with HCC, more severe psychomotor agitation was associated with higher HCC. Pre-treatment HCC was not associated with ECT outcome. STRENGTHS AND LIMITATIONS: A complicating factor in interpretation of our results was the large variability in HCC. This could be related to potential confounders such as cardiometabolic and other comorbidities, that were however addressed to the extent possible. CONCLUSIONS: HCC is a potential biomarker for MDD patients with severe agitation and/or catatonia. CLINICALTRIALS.GOV: Identifier: NCT02562846.

Impaired facial and vocal emotion decoding in schizophrenia is underpinned by basic perceptivo-motor deficits.

INTRODUCTION: Emotional decoding impairments have been largely demonstrated in schizophrenia for facial and prosodic stimuli, when presented separately. Nevertheless, the exploration of crossmodal integration has been far less considered, despite its omnipresence in daily social interactions. Moreover, the role played by basic visuo-motor impairments in unimodal and crossmodal decoding remains unexplored. METHODS: Thirty-two patients were compared with 32 matched controls in an emotional decoding task including unimodal (visual and auditory) and crossmodal (congruent and incongruent) conditions. A control perceptive task was also conducted to take potential low-level perceptual deficits into account. RESULTS: Schizoprenic patients presented lower performance and higher reaction times for both unimodal tasks (visual and auditory) and crossmodal conditions. Moreover, reaction times for the visuo-perceptive task were also significantly longer for patients compared to controls. CONCLUSIONS: The consistency of the results across unimodal and crossmodal tasks suggests a globalised emotional impairment in schizophrenia, independent of the sensorial modality and crossmodal nature of the stimuli. Centrally, given the results in the visuo-perceptive task, the impairments observed for emotional recognition appears at least partly explained by primary cognitive deficits, namely reduced processing speed.