Depression 105month according to ICD-10 and within three months according to DSM-
IV) and do not outlast the stressor by more than six months.
Associated features
1 Comorbidity. Over 50% of depressed children in epidemiological samples
have at least one other psychiatric disorder as well (typically an anxiety
or disruptive behavioural disorder), and the rate of comorbidity is often
even higher in clinic samples.
2 Friendship difficultiesare common during depressed episodes, and may
precede (and possibly precipitate) these episodes.
3 Biological features.A variety of neuroendocrine abnormalities such as
raised cortisol levels have been described, though none are sufficiently
consistent or marked to be useful diagnostic tests in everyday prac-
tice. Sleep studies do not consistently show the sorts of abnormalities
described in adults (but these abnormalities are less marked in young
adults too).
Differential diagnosis
1 Normal sadness, including normal bereavement reactions. It is worth
noting, though, that bereavement and depression can co-exist. DSM-
IV allows a depressive episode to be diagnosed if a depressive symptom
cluster persists for more than two months after a major bereavement
or is particularly severe, for example, with suicidal ideation, psychotic
symptoms or marked functional impairment.
2 Misery can occur as just one feature of another psychiatric disorder,
without the additional affective, cognitive and behavioural features
needed to diagnose a true depressive disorder. But remember that just
because a child or adolescent has some other disorder, this does not
mean that he or she cannot have depression too.
Causation
Depression runs in families. Depressed children are more likely than
children with other psychiatric disorders to have parents or siblings who
are themselves depressed. Conversely, parents with depression are more
likely to have depressed children. The relative importance of genetic and
environmental transmission is uncertain: twin studies suggest moderate
heritability, but this has not been replicated in adoption studies. There is
preliminary evidence that a genetic loading for depression may sometimes
act by increasing a young person’s vulnerability to adverse life events – if
so, this is an example of a gene–environment interaction.