Depression and Anxiety Disorder
Depression affects more than 300 million people globally. Untreated depression can lead to suicide, the second cause of death in people between 15 and 29 years of age.
Chronic stress and trauma in the first years of life have been associated with vulnerability to depression. A complex interaction between the genetic and environmental factors is involved in the pathophysiology of the disease.
Among the obstacles that prevent efficient care are the following:
Lack of resources and trained health staff
Stigmatization of mental disorders
Inaccurate or erroneous clinical assessment
In countries with different income levels, the people with depression are frequently given an incorrect diagnosis, while others who are not afflicted by this condition are often diagnosed erroneously and treated with anti-depressants.
Better understanding and knowledge of the disease is required because more than half of those affected worldwide do not receive an efficacious treatment.
Several brain regions are involved in the depression etiology, including the hippocampus, the amygdala, the nucleus accumbens, the nucleus striatum, the insula, the medial thalamus, and regions of the frontal cortex.
The hippocampus and prefrontal cortex formation have a two-way interaction to regulate several cognitive functions and process the emotional information. There is a strong neural synchrony between both regions during behavior and their functional interaction is regulated by oscillations. The neural group made up by the hippocampus cells and the prefrontal cortex influence each other like a circuit in the modulation of emotional and cognitive processes.
The hippocampus plays a key role in the stress-induced deregulation of the hypothalamus-pituitary-adrenal axis.
The imaging studies in patients with depression have shown a reduction in the hippocampus volume and it represents the most frequent disorder in the brain structures in depression. Minor but consistent reductions have been reported as well in the frontopolar cortex.
The high corticosterone levels that result from the deregulation of the hypothalamus-pituitary-adrenal axis are considered to be contributing factors in the hippocampus reduction seen in patients with major depressive disorder.
The neurophysiological studies, especially during the event-associated potentials, show a severe voltage or power reduction in frontopolar and temporal regions during tasks that involve attention, verbal memory, and emotional process. This voltage deficit is related directly to hypoactivity of the dopaminergic circuit in charge of activating the memory, attention, and motivation circuits.
For the above reasons, the depression approach must be focused first on detecting the disorders of circuits and regions mentioned and on differentiating other depression types, like those seen in bipolar disorder and schizophrenia, which result from other causes.
The patients with major depressive disorder frequently show cognitive deficiencies, like difficulties in attention, information processing, work memory, and executive function. It is worth stressing that all of these traits are not present in all the depressed patients, because some abnormalities have been reported in certain specific subgroups.
However, before the persistence of these deficiencies despite their mood improvement requires further efforts to understand the interrelationship between the cognitive dysfunction and depression and to prescribe treatments targeted specifically to this aspect of the disease.
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