Signs and symptoms
In both the American Psychiatric Associations DSM-5 and the World Health Organizations ICD-10, the same criteria used to diagnose bipolar disorder in adults are used to make the diagnosis in children with some adjustments to account for differences in age and developmental stage. For example, the DSM-5 specifies that in children, depressive episodes can manifest as persistently irritable moods.In diagnosing manic episodes, it is important to compare the changes in mood and behavior to the childs normal mood and behaviors at baseline instead of to other children or adults. For example, grandiosity (i.e., unrealistic overestimation of ones intelligence, talent, or abilities) is normal at varying degrees during childhood and adolescence. Therefore, grandiosity is only considered symptomatic of mania in children when the beliefs are held despite being presented with concrete evidence otherwise or when they lead to a child attempting activities that are clearly dangerous, and most importantly, when the grandiose beliefs are an obvious change from that particular childs normal self-view in between episodes. Controversy
The diagnosis of childhood bipolar disorder is controversial, although it is recognized that bipolar disorder typical symptoms are dysfunctional and have negative consequences for minors with the condition. Main discussion is centered on whether what is called bipolar disorder in children refers to the same disorder than when diagnosing adults, and the related question on whether adults criteria for diagnosis are useful and accurate when applied to children.
Exposure to UV light from sunlight is maybe associated with an increased risk of developing AMD, although evidence is weaker than other causes. A digital screen does not radiate harmful energy against human eyes, but staring at the screen for a long time without pauses does increase eye strain. There is no evidence to support the claim that exposure to digital screens contributes to the risk of macular degeneration. Genetics
AMD is a highly heritable condition. Recurrence ratios for siblings of an affected individual are three- to six-fold higher than in the general population. Genetic linkage analysis has identified 5 sets of gene variants at three locations on different chromosomes (1, 6 and 10) as explaining at least 50% of the risk. These genes have roles regulating the immune response, inflammatory processes and homeostasis of the retina. Variants of these genes give rise to different kinds of dysfunction in these processes. Over time, this results in accumulation of intracellular and extracellular metabolic debris. This can cause scarring of the retina or breakdown of its vascularization. The list of genetic variations association with AMD include complement factors, apolipoprotein E, fibroblast growth factor 2, DNA excision repair protein, and age-related maculopathy susceptibility protein 2.Although genetic testing can lead to the identification of genetic variation which can predispose to AMD, the complex pathogenesis of the condition prevents the use of these tests in routine practice. Nevertheless, they can be useful in selecting patients for clinical trials and analysing their response to treatment.