The scientific community is divided into two “camps” supporting opposing views: some propose a primary biological mechanism with<unk>  affecting neural circuits involved in mood regulation which in turn causes<unk> , while other researchers claim that<unk>  is caused by social and psychological stressors that emerge as a result of<unk> . While an integrated bio-psycho-social model including both biological and psychosocial aspects of<unk>  seems warranted, a number of studies clearly suggest that biological mechanisms play a major role in the development of<unk> .<unk>  patients show a higher rate of depression compared to orthopedic patients with disabilities of comparable severity. #Several studies proposed an association with specific lesions (left anterior and basal ganglia lesions and lesions close to frontal pole) and occurrence of<unk> . #Some studies reported an association between post-stroke mania and right orbital frontal, basotemporal, basal ganglia lesions. #It has been shown that patients with anosognosia who are unaware of their disability still develop<unk> . Despite this evidence, the association of<unk>  to specific brain lesions is still vague and needs replication from various independent groups. Furthermore, the cause of<unk>  at a functional level is not clear. The only biological model was proposed by Robinson and co-workers: They hypothesized that the depletion of monoaminergic amines occurring after<unk>  play a role in post<unk> -depression. They point out that norepinephrinergic and serotonergic nuclei send projections to the frontal cortex and arc posteriorly, running through the deep layers of the cortex, where they arborize and send terminal projections into the superficial cortical layers. These norepinephrinergic and serotoninergic pathways are disrupted in basal ganglia and frontal lobe lesions – sites that are shown to be associated with<unk> . Additionally, depletion in dopamine (due to pallidal lesions) can trigger anhedonia and avolition. However, this model is far from being universally accepted and there are serious objections both to their model and findings showing the association between<unk>  and lesion sites. Depression-like behaviors are demonstrated in a mouse model of cortical intracerebral hemorrhage.
Post-stroke depression
Excited delirium
Collective depression
Late life depression
Post-concussion syndrome
Mass psychogenic illness
Treatment-resistant depression
Masked depression