Cardiophénoménologie

En croisant l’interprétation d’enregistrements cardiovasculaires avec le recueil de l’expérience émotionnelle, au lieu de chercher les oscillations cérébrales corrélatives des illusions perceptives, on remédie à la différence d’échelle qui hypothéquait la méthode des contraintes mutuelles de Varela. La cardiophénoménologie propose un modèle dynamique de la surprise associant les variations d’indices physiologiques à une analyse husserlienne des phases du vécu. Une expérimentation avec des patientes dépressives soumises à une tâche émotionnelle combinée à l’entretien d’explicitation semble devoir valider une hypothèse d’hyporéactivité de la dépression en réaction à la surprise.By crossing the interpretation of cardiovascular recordings with the collection of emotional experience, instead of seeking correlative brain oscillations of perceptual illusions, one overcomes the difference in scale that hampered Varela’s method of mutual constraints. Cardiophenomenology provides a dynamic model of surprise associating variations in physiological indices to a Husserlian analysis of lived phases. An experiment with depressive patients undergoing an emotional task combined with the interview of explicitation seems to validate a hypothesis of hyporesponsiveness of depression in response to surprise

Assessment of Translocator Protein Density, as Marker of Neuroinflammation, in Major Depressive Disorder: A Pilot, Multicenter, Comparative, Controlled, Brain PET Study (INFLADEP Study)

Background: Major depressive disorder (MDD) is a serious public health problem with high lifetime prevalence (4.4–20%) in the general population. The monoamine hypothesis is the most widespread etiological theory of MDD. Also, recent scientific data has emphasized the importance of immuno-inflammatory pathways in the pathophysiology of MDD. The lack of data on the magnitude of brain neuroinflammation in MDD is the main limitation of this inflammatory hypothesis. Our team has previously demonstrated the relevance of [18F] DPA-714 as a neuroinflammation biomarker in humans. We formulated the following hypotheses for the current study: (i) Neuroinflammation in MDD can be measured by [18F] DPA-714; (ii) its levels are associated with clinical severity; (iii) it is accompanied by anatomical and functional alterations within the frontal-subcortical circuits; (iv) it is a marker of treatment resistance.Methods: Depressed patients will be recruited throughout 4 centers (Bordeaux, Montpellier, Tours, and Toulouse) of the French network from 13 expert centers for resistant depression. The patient population will be divided into 3 groups: (i) experimental group—patients with current MDD (n = 20), (ii) remitted depressed group—patients in remission but still being treated (n = 20); and, (iii) control group without any history of MDD (n = 20). The primary objective will be to compare PET data (i.e., distribution pattern of neuroinflammation) between the currently depressed group and the control group. Secondary objectives will be to: (i) compare neuroinflammation across groups (currently depressed group vs. remitted depressed group vs. control group); (ii) correlate neuroinflammation with clinical severity across groups; (iii) correlate neuroinflammation with MRI parameters for structural and functional integrity across groups; (iv) correlate neuroinflammation and peripheral markers of inflammation across groups.Discussion: This study will assess the effects of antidepressants on neuroinflammation as well as its role in the treatment response. It will contribute to clarify the putative relationships between neuroinflammation quantified by brain neuroimaging techniques and peripheral markers of inflammation. Lastly, it is expected to open innovative and promising therapeutic perspectives based on anti-inflammatory strategies for the management of treatment-resistant forms of MDD commonly seen in clinical practice.Clinical trial registration (reference: NCT03314155): https://www.clinicaltrials.gov/ct2/show/NCT03314155?term=neuroinflammation&cond=depression&cntry=FR&rank=

Physiologie cardiaque et cérébrovasculaire dans la dépression

Dépression et maladies cardiovasculaires sont liées mais la physiopathologie de cette association est mal connue. Les mécanismes de la variabilité de la fréquence cardiaque (VFC) et de la dysfonction endothéliale (DE) pourraient rendre compte de cette association mais leur implication demeure controversée et seuls certains symptômes de la dépression, l’anhédonie et l’hyporéactivité émotionnelle (HE), semblent leur être associés. En outre, certains obstacles méthodologiques ont, jusqu’à présent, limité l’étude de la réactivité cardiaque et cérébrovasculaire dans l’anhédonie et l’HE. Dans ce travail, nous établissons par deux protocoles expérimentaux distincts 1) qu’une nouvelle technique d'échographie cérébrale (Tissue Pulsatility Imaging - TPI) permet de mettre en évidence des modifications de la réactivité cérébrovasculaire dans la dépression et 2) qu’il est possible d’associer la VFC et l’anticipation émotionnelle, processus clef dans l’HE. Nos résultats suggèrent que l’anhédonie et l’HE de la dépression peuvent être caractérisées par un trouble de l’anticipation émotionnelle, lui-même associé à une VFC diminuée et une DE cérébrale.Depression and cardiovascular diseases are related but the physiopathology of this association is unclear. Heart rate variability (HRV) and endothelial dysfunction (ED) could account for this association but their involvement remains controversial and only some symptoms of depression, anhedonia and emotional hyporeactivity (EH), seem to be involved. In addition, some methodological obstacles have so far limited the assessment of cardiac and cerebrovascular reactivity in anhedonia and EH. In this work, we establish using two distinct protocols 1) that cerebrovascular changes in depression can be assessed using a new ultrasound technique (Tissue Pulsatility Imaging - TPI) and 2) that HRV and emotional anticipation, as a key process in EH, are associated. Our results suggest that anhedonia and EH in depression can be characterized by a blunted emotional anticipation which is associated with a decreased HRV and a cerebral ED

Influence de la personnalité dans la réponse émotionnelle de sujets dépressifs

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Le modèle vasculaire de la maladie d'Alzheimer (revue de la littérature scientifique et étude pilote utilisant la mesure échographique de la pulsatilité cérébrale)

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Système cardiovasculaire et expérience émotionnelle (la dynamique temporelle de l'émergence émotionnelle)

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Dépendance aux hypnotiques et connaissance du traitement par le patient (existe-t-il un lien ?)

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Depression and Emotion

International audienc

Endothelial dysfunction: A potential therapeutic target for geriatric depression and brain amyloid deposition in Alzheimer's disease?

International audienceDepression and Alzheimer's disease (AD) are among the most prevalent mental disorders in the elderly. Strong evidence suggests that vascular diseases and vascular risk factors are associated with both depression and AD, and could partially explain the coexistence or the concurrent onset of these two diseases. In particular, endothelial dysfunction appears to play a critical role in the neurobiology of depression and amyloid deposition in the brains of patients with AD. Antidepressants have a significant impact on endothelial function. In addition, several drugs used to treat vascular disease or vascular risk factors, such as calcium-channel blockers, angiotensin-converting enzyme inhibitors and statins, have, to variable extents, significant clinical effects on depressive symptomatology or amyloid deposition in AD. Furthermore, preclinical and clinical data suggest that the nitric oxide and VEGF signaling pathways may be of value for the treatment of depression and AD

The temporal dynamic of emotional emergence

International audienceFollowing the neurophenomenological approach, we propose a model of emotional emergence that identifies the experimental structures of time (i.e., anticipation, crisis, and aftermath) involved in emotional experience and their plausible components in terms of cognition, physiology, and neuroscience. We argue that surprise, as a lived experience, and its physiological correlates of the startle reflex and cardiac defense are the core of the dynamic, and that the heart system sets temporally in motion the dynamic of emotional emergence. Finally, in reference to Craig’s model of emotion, we propose an integrative model of the temporal dynamic of emotional emergence that allows emotions to be distinguished depending on each temporal phase and that involves the following three systems: the brain (3rd person), the consciousness (1st person), and the doubled-sided (subjective/objective) continuum of the body-heart context, with the heart as the focus within the body during emotion. This model provides the framework for future developments in 1st- and 3rd-person approaches for an integrative understanding of the science of emotion, including the fields of psychophysiology and psychopathology