ABSTRACT
Our understanding of mood disorders has progressed from a notion of black bile causing melancholia to a realization that they develop from a complex interaction of genetic, psychological and social factors. That these disorders of the mind derive from some form of dysfunction of the brain is supported by evidence from clinical, neurochemical, neuroendocrine and histological studies. A high prevalence of depression has been observed in patients with neurological disorders, such as Parkinson’s and Huntington’s diseases,1,2 and in patients following a stroke.3-5 This clinical evidence of secondary mood disorders (i.e. a mood disorder that is secondary to a medical/neurological disorder) indicates an underlying pathology within the brain and further suggests some regions where the dysfunction may be localized. Researchers have been examining the expression of similar abnormalities in primary mood disorders using structural and functional neuroimaging techniques.
