Melancholic depression is a severe form of depressive disorder or mental illness and is psychotic in nature. It is primarily caused by biological and genetic factors rather than psychological factors. It is a mental state that is characterized by feelings of extreme sadness, hopelessness and loss of interest and pleasure in almost everything. Person with Melancholic depression becomes non-responsive to happy incidents or surroundings even for the short period. Melancholic depression also leads to psychomotor disturbances such as low energy, poor concentration, slowed or agitated movements.
Causes of melancholia
It is believed that certain biological factors and genetic factors play an important role in development of this clinical depression. Studies also show that those who suffer from melancholia generally have a family history of depression disorders. Melancholia may not be an outcome of few negative incidents in life, but surely such events act as a trigger and initiate the problem. Biologically, melancholic depression is believed to be caused by a chemical imbalance or malfunctioning of the neurotransmitters in the brain.
Symptoms of Melancholia
A person is diagnosed as suffering from melancholia when constantly experiencing extreme sadness accompanied by any 3 or 4 features mentioned above.
Unlike situational depression which is caused by sad events in life, melancholia is caused by biological disorder. Hence counseling and psychotherapy is probably not the solution. Treatment requires physical intervention via antidepressant drugs and also Electroconvulsive therapy (ECT) or shock treatment in case of extreme severity. Electroconvulsive therapy is recommended only for the severest forms of depressions, when a patient is not responding to antidepressant treatment or is posing a threat to self or others. Electroconvulsive therapy has certain side effects like short and long-term memory loss, hence it is advised only when the situation demands.
Bibliography / Reference
Collection of Pages - Last revised Date: December 13, 2017