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Thèse (M.Ps.)--Université Laval, 2004. / Bibliogr.: f. 65-70. Publié aussi en version électronique.

Background: The fetal origins hypothesis poses that adverse intrauterine conditions predispose to cardiovascular and metabolic diseases in adulthood. Evidence is accumulating that similar mechanisms to those identified for physical disorders may also apply to psychiatric disorders. Focusing on the activity of neurophysiological systems thought to regulate emotions from very early in life may be key to understanding how maternal stress in pregnancy impacts on the developing baby with possible long-lasting consequences for behaviour and psychopathology. Respiratory Sinus Arrhythmia (RSA), "vagal tone", is thought to reflect autonomic regulatory capabilities that may underpin emotion regulation. However, little is known about possible fetal origins of vagal tone. Animal studies increasingly point to sex differences in the effects of prenatal stress, and this is supported by human studies of the prenatal origins of cardiovascular functioning and psychopathology. The current investigation examines whether prenatal depression and anxiety predict vagal tone in infancy, and whether the associations are modified by infant sex. Method: Two hundred mothers and infants from a high-risk consecutive community sample were examined prospectively from the first trimester of pregnancy until 29 weeks postnatal. Maternal self-reports of stress (EPDS and STAI) were collected in pregnancy (20 and 32 weeks) and postnatally (5 weeks and 29 weeks). Vagal tone was ascertained across five procedures, the "Helper-Hinderer" social evaluation task, toy exploration and the "Still Face" paradigm (2 minutes of social engagement, followed by 2 minutes of maternal unresponsiveness and concluded by 2 minutes of social reunion). Results: Principal Component Analysis of the RSA scores yielded a one-factor solution explaining over 70% of the variance, and so mean of RSA scores was used as the index of overall vagal tone, and the difference between overall and RSA during the Still Face as the estimate of vagal withdrawal. There were no main effects of prenatal maternal depression or anxiety on vagal tone or vagal withdrawal. However, there were significant prenatal stress by sex of infant interactions. Follow-up analyses revealed that increasing maternal depression and anxiety at 20 weeks gestation were associated with decreasing vagal tone in males and increasing vagal tone in females. Vagal withdrawal in response to the still face showed similar patterns i.e. decreased in males and increased in girls with elevated maternal anxiety at 32 weeks gestation. These associations were not explained by possible confounding variables assessed in pregnancy, nor by postnatal maternal depression and anxiety. Conclusions: The findings support the fetal origins hypothesis for vagal tone and vagal withdrawal, but only in interaction with sex of the infant. Longitudinal study is required to determine conditions under which increasing vagal tone and withdrawal in girls associated with prenatal depression and anxiety, and decreasing vagal tone and withdrawal in boys, are associated with later resilience or vulnerability to psychopathology.

Alzheimer’s disease is the most common cause of dementia worldwide. As the disease course progresses, it can be debilitating to the patient and provide a large burden for their families and caregivers alike. As our population ages, it more important than ever to find safe and efficacious strategies to combat the cognitive effects of Alzheimer’s disease. While there have been many recent advances surrounding early identification of the disease including the use of PET imaging with specific targeted ligands or CSF analysis for biomarkers, there has been less progress in the development of disease modifying therapies to halt or reverse the symptoms. Vagus nerve stimulation has been a standard in therapy for drug-resistant epilepsy and depression for many years. It has been proven to be effective and has led to drastic improvement in many patients’ lives whose diseases were refractory to standard medications. There is evidence that stimulation of the vagal nerve leads to a physiologic response that also supports long term potentiation of memory within the hippocampus, though trials have been limited by sample size in the past due to the necessity of surgical implantation of the vagal nerve stimulator device. The recent development of non- invasive vagal nerve stimulation removes this limitation. This non-invasive strategy takes advantage of the auricular branch of the vagus nerve innervation of the ear to access the vagal pathway. The following work includes a proposal for a randomized control study to investigate the cognitive benefits of non-invasive vagal nerve stimulation of the auricular branch of the vagus nerve in a cohort of patients with MCI due to Alzheimer’s disease. This trial is planned for patients of neurology or gerontology practices associated with Boston Medical Center, Massachusetts General Hospital, Beth Israel Hospital, and Brigham and Women’s Hospital. Outcomes of this study will be the change in Mini- Mental State Examination (MMSE) and Alzheimer’s Disease Assessment Scale-cognitive subscale (ADAS-Cog) score over a two-year intervention time.

Cardiovascular disease (CVD) is the leading cause of death worldwide and is expected to increase in prevalence. As a result of the individual and systemic healthcare impacts of CVD, heart failure, and its subsets, focusing on the alleviation of cardiac dysfunction and restoration of autonomic imbalance is paramount. Most research regarding cardiovascular disease is focused on mitigating heart failure from a cardiovascular perspective. However, this review will investigate heart failure from a neuroscientific perspective, highlighting the influence of the renin-angiotensin-aldosterone system, autonomic imbalance, and neuroinflammation on the progression of heart failure. By doing so, this research will bring light to how neuroscience may be applied to the cardiovascular system, and how interventions, such as vagal nerve stimulation, may be an untapped resource in mitigating the progression of heart failure. This review examined current relevant research to understand the brain regions implicated in the progression of heart failure, and to better understand how the nervous system may be modulated to improve heart failure outcomes through vagal nerve stimulation. This review sets the conceptual framework for future research to examine the structural changes observed in research animals who receive vagal nerve stimulation.

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