<unk>  <unk>  is considered as the most frequent and important neuropsychiatric consequence of<unk> , since approximately one-third of<unk>  survivors experience depression. Moreover this condition can have an adverse effect on cognitive function, functional recovery and survival.
The Diagnostic and Statistical Manual (DSM) IV  categorizes<unk>  as “mood disorder due to a general medical condition (i.e.<unk> ” with the specifiers of depressive features, major depressive-like episodes, manic features, or mixed features. Utilizing patient data from acute hospital admission, community surveys, or out patient clinics previous studies have identified two types of depressive disorders associated with cerebral ischemia: major depression, which occurs in up to 25% of patients; and minor depression, which has been defined for research purposes by DSM-IV criteria as a depressed mood or loss of interest and at least two but fewer than four symptoms of major depression. Minor depression occurs in up to 30% of patients following<unk> .
Prevalence clearly varies over time with an apparent peak 3-6 months after<unk>  and subsequent decline in prevalence at one-year reaches about to 50% of initial rates. Robinson and colleagues characterized the natural course of major depression after<unk>  with spontaneous remission typically 1 to 2 years after<unk>   However, it was also noted that in few cases depression becomes chronic and may persist more than 3 years following<unk>  . On the other hand, minor depression appeared to be more variable, with both short term and long term depression occurring in these patients .
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> .
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<unk> . They point our that norepinephrinergic and serotonergic nuclei send projections to the frontal cortex and arc<unk> eriorly, 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> .
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.
Post stroke depression
Post travel depression
Depression in elderly
Depression 
Schizophrenia risk factors
Clinical depression
Excited delirium
Suicide crisis