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La prévalence des personnes âgées atteintes de troubles bipolaires augmente et leurs troubles cognitifs sont associés à une perte d’autonomie et un risque d’institutionnalisation précoce. Les troubles cognitifs dans la bipolarité sont présents dès le début de la maladie et se majorent avec l’avancée en âge, soulevant la question du diagnostic différentiel de démence spécifique au trouble bipolaire et d’autres troubles cognitifs majeurs d’origine neurodégénérative. L’évolution démentielle du patient bipolaire est discutée en abordant les notions d’endophénotype cognitif, de vieillissement cognitif physiologique, de réserve cognitive et de neuroprogression pour comprendre l’hétérogénéité des troubles cognitifs et de faire le lien entre le caractère cyclique et l’évolution délétère progressive du trouble bipolaire. L’enjeu thérapeutique est d’identifier les troubles cognitifs réversibles d’origine thymique de ceux d’origine lésionnelle. La prévention des épisodes thymiques et la recherche de thérapeutiques neuroprotectrices devraient permettre d’améliorer le pronostic fonctionnel des patients bipolaires âgés.

Bipolar disorder is a severe, recurrent mood disorder, associated with a higher rate of morbidity and mortality. A new population of aging bipolar patients is emerging for which specific studies are scarce. There seem to be an association between bipolar disorder and major cognitive disorder, significantly affecting patients’ psychosocial outcomes. Though the neuropathological mecanisms underlying such an evolution have yet to be found, there are three paradigms that can help us understand the clinical heterogeneity within the aging bipolar group. First, there seem to be different cognitive endophenotypes within the bipolar spectrum, related to different neurodevelopmental abnormalities. Each of these endophenotypes will interact with the normal cognitive aging process which is associated with a decline in certain cognitive domains while others remain stable. Nevertheless this cognitive decline will be variable from one patient to another. This can be explained by cognitive reserve which reflects the brain's capacity to endure neuropathology, and minimize clinical manifestations. The second hypothesis is the neuroprogression paradigm that offers an explanation on how a cyclic disorder such as bipolar disorder could evolve progressively into a major cognitive disorder. According to this paradigm, each manic and depressive episode is associated to an allostatic load, a systemic response associated with the secretion of neuroinflammatory factors which will secondarily alter the brain's connectivity. The third paradigm suggests that bipolar patients may develop either vascular dementia which is coherent with their increased vascular risk factor or another neurodegenerative disease. All three paradigms are not exclusive, and many other factors are to be taken into account such as medication, sensory impairment, health related changes and residual mood symptoms, which can alter cognitive functions.