Research on Child and Adolescent Mental Health

derived neurotrophic factor in the hippocampus and
cerebral cortex) (Duman et al., 1997). Clinical
studies also provide evidence for atrophy and cell
death in the hippocampus as well as the prefrontal
cortex in response to stress and impaired function
of these neurons in depression (Bowen, Najlerahim,
Procter, Francis & Murphy, 1989; Sapolsky, Uno,
Rebert & Finch, 1990; Rajkowska et al., 1999).
Thus, it is possible that various antidepressant
treatments could limit these adverse cellular events
that might be best conceptualized as a loss of
neuronal plasticity in the developing nervous
system of children and adolescents. The clinical
utility of these research findings lies not only in
their potential for developing safer and more
effective treatments for children whose nervous
systems are still developing, but also, as in Amy’s
case, for educating her and her family about the
potential benefits of antidepressant treatment at
both the behavioral and the brain level.
Amy appeared to do better over the next year, but
then her progress appeared to come to a halt.
During the summer of her sophomore high school
year when Amy was 16, her mother made a
decision to move from a house to a small apartment
in another neighborhood, due to significant
financial stress. Amy was extremely upset by the
move, became increasingly anxious about how her
friends might perceive her living situation, and
refused to socialize or engage in activities she used
to enjoy. She felt so dejected that she impulsively
attempted suicide by ingesting 30 Tylenol tablets.
She became scared of dying and told her mother,
who immediately took her to the emergency room.
Given the severity of her depression and the lethal
intent of her attempt, she was admitted to an
adolescent psychiatric inpatient unit for 4 days.
During this stay, she received intensive individual
therapy and family work and was switched from
fluoxetine to serzone (Nefazodone), a newer
generation of antidepressant with properties of both
an SSRI and a tricyclic antidepressant (TCA), to
target both depressive and anxiety symptoms. Amy
and her mother continued with outpatient
treatment over the next 6 months until her mother’s
work conflicts made it difficult for them to continue.
5. Suicide and Social Connectedness
Suicide is the third leading cause of death among
teenagers; nearly half of these suicides are
associated with depression. Several lines of
evidence indicate that suicidal behavior is linked to
a lack of social connectedness. Suicidal risk is
associated with interpersonal conflicts or losses
(e.g., romantic break-ups and parental divorce) in
adolescents (Brent et al., 1993; Gould, Fisher,
Parides, Flory & Shaffer, 1996). Another
phenomenon reported in the adolescent age group
is the clustering of teen suicides in close temporal
and geographic proximity to successful suicide
attempts, likely due to imitative behavior (Gould,
1990; Gould & Shaffer, 1986; Phillips &
Carstensen, 1986). In the case of Amy, these
findings argue for careful observation of social
behavior in teens predisposed to depression. Other
known risk factors for suicide that did not appear
to be present for Amy include substance abuse,
lifetime history of abuse, availability of a gun, and
past suicide attempts.
Primate studies suggest that the activity of the
serotonergic system helps regulate social
interactions and that social interactions can affect
serotonergic activity (Raleigh, McGuire, Brammer &
Yuwiler, 1984). For example, a dominant monkey
isolated from his social group can experience a
decrease in whole blood serotonin, while a
submissive monkey can be made dominant with
treatment using drugs such as fluoxetine and
tryptophan, which enhance serotonin function
(Rogeness & McClure, 1996). These findings offer
further indirect support for using serotonergic
antidepressants to treat adolescent depression and
improve social functioning in this developmentally
vulnerable period.
As adolescents transition to early adulthood, they
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