“…38 These findings have been replicated, with the addition of poststroke anxiety and functional capacity as relevant risk factors. 25,33,34,37,[39][40][41] Stroke location seems irrelevant for PSD despite early tentative evidence to the contrary. 33,37,[42][43][44] Other studies have reported associations between PSD and neuroinflammation, disruption of the hypothalamic-pituitary axis, oxidative stress, abnormal glutamatergic neurotransmission, disrupted production of neurotrophic factors, lower levels of monoaminergic transmission, and genetic susceptibility.…”