Research suggests that depression is not simply due to having too much or too little of certain brain chemicals. Rather, there are many possible causes of depression, including faulty mood regulation by the brain, genetic vulnerability, and stressful life events. Finally, in terms of connectivity, corticolimbic connectivity abnormalities are often cited as a cause of depression or, for that matter, a number of other psychiatric illnesses. An implicit assumption of this hypothesis is that depression may imply how one region may affect the functioning of another region for example,.
Regulatory effects of the anterior cingulate cortex in limbic regions, such as the amygdala (2). This latter possibility also implies that some of the abnormalities in the brain regions may be secondary to abnormalities in another primary region. At this time, it is very difficult to determine which regional anomaly can be primary and which is secondary. The primary abnormality may be in the subcortical or brain stem regions and abnormalities in large cortical areas, such as the dorsolateral prefrontal cortex, may be secondary in nature.
However, neuropsychiatric studies suggest that depression could arise from primary abnormalities in cortical areas, such as the left frontal cortex as well. No one knows exactly what causes it, but it can happen for several reasons. Some people have depression during a serious medical illness. Others may have depression with life changes, such as a move or the death of a loved one.
Others have a family history of depression. Sufferers may have depression and be overwhelmed by sadness and loneliness for no known reason. There is no single cause of depression. It can occur for a variety of reasons and has many different triggers.
For example, the hippocampus, a small part of the brain that is vital for memory storage, appears to be smaller in some people with a history of depression than in those who have never been depressed. A review of neuroimaging, neuropsychiatric therapy and brain stimulation studies of depression indicates that, like other abnormalities of higher mental functions, it is difficult to determine the location of depression. Although depression and grief share some characteristics, depression is different from the pain you feel after losing a loved one or the sadness you feel after a traumatic life event. Drinking alcohol often can worsen symptoms of depression, and people who have depression are more likely to abuse or become dependent on alcohol.
The 1950s was an important decade in the treatment of depression, thanks to doctors noting that a tuberculosis drug called isoniazid seemed to be useful in treating depression in some people. Multiple genes that interact with each other in special ways are likely to contribute to the various types of depression that occur in families. The emergence of these cognitive models of depression played an important role in the development of cognitive behavioral therapy (CBT), which has been shown to be effective in treating depression. Mayberg and colleagues (1) first observed a reciprocal relationship between decreased metabolism in the prefrontal cortex and increased metabolism in limbic regions such as striatum and thalamus in depression, leading to the hypothesis that corticolimbic connectivity abnormality may be present in the depression.
For example, depression can cause disturbances in sleep, appetite, and activity levels; in turn, lack of sleep, diet, and exercise can aggravate symptoms of depression. Although melancholy remained the dominant diagnostic term, depression gained increasing popularity in medical treatises and was a synonym at the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as a general term, referring to different types of melancholy as depressive states. Based on neuroimaging findings of reduced prefrontal cortex metabolism in depression, EMT therapy for depression has so far been limited to the prefrontal cortex. Another strategy that has been suggested to preserve the hypothesis on a regional neuroanatomical basis of depression is not to treat depression as a unitary disease, but to divide it into its different symptoms while exploring its anatomical basis.
The common manifestation of depression and executive dysfunction in the context of vascular disease is common (7) and, therefore, may suggest the contribution of DLPFC involvement in the etiology of depression. Children, siblings, and parents of people with major depression are more likely to have depression than members of the general population. While ancient conceptualizations of depression emphasized the role of early experiences, more recent approaches increasingly emphasize the biopsychosocial model that analyzes the biological, psychological and social factors that play a role in depression. .