Distinction from major depressive disorder in adults
While there are many similarities to adult depression, especially in expression of symptoms, there are many differences that create a distinction between the two diagnoses. Research has shown that when a childs age is younger at diagnosis, typically there will be a more noticeable difference in the expression of symptoms from the classic signs in adult depression. One major difference between the symptoms exhibited in adults and in children is that children have higher rates of internalization; therefore, symptoms of child depression are more difficult to recognize. One major cause of this difference is that many of the neurobiological effects in the brain of adults with depression are not fully developed until adulthood. Therefore, in a neurological sense children and adolescents express depression differently. Treatment
Clinicians often divide treatment into three phases: In the acute phase, which usually lasts six to 12 weeks, the goal is to relieve symptoms. In the continuation phase, which can last for several more months, the goal is to maximize improvements. At this stage, clinicians may make adjustments to the dose of a medication. In the maintenance phase, the aim is to prevent relapse. Sometimes the dose of a drug is lowered at this stage, or psychotherapy carries more of the weight. Unique differences in life experience, temperament, and biology make treatment a complex matter; no single treatment is right for everyone. Psychotherapy and medications are commonly used treatment options. In some research, adolescents showed a preference for psychotherapy rather than antidepressant medication for treatment.
Glucocorticoid deficiency 1  is an adrenocortical failure characterized by low levels of plasma cortisol produced by the adrenal gland despite high levels of plasma ACTH. This is an inherited disorder with several different causes which define the type.FGD type 1 (FGD1 or GCCD1) is caused by mutations in the ACTH receptor (melanocortin 2 receptor; MC2R). FGD type 2 is caused by mutations in the MC2R accessory protein (MRAP). These two types account for 45% of all cases of FGD.Some cases of FGD type 3 are caused by mutations in the steroidogenic acute regulatory protein (StAR), with similarity to the nonclassic form of lipoid congenital adrenal hyperplasia. In this case, a general impairment in not just adrenal steroid production, but gonadal steroid production can affect sexual development and fertility. The causes of other cases of FGD type 3 not due to StAR are currently unknown. References
External links
GCCD1 Online Mendelian Inheritance in Man (OMIM): 202200
GCCD2 Online Mendelian Inheritance in Man (OMIM): 607398
GCCD3 Online Mendelian Inheritance in Man (OMIM): 609197