My blog has moved!

You should be automatically redirected in 6 seconds. If not, visit
and update your bookmarks.

Tuesday, July 24, 2007

Adolescents brain and Depression

Symptoms of depression in adolescents look like those of depression in adults. Before the late 1970s the existence of depression in adolescents was controversial. The last two decades research has shown that adolescents are capable of experiencing episodes of depression comparable to adults. As a beginning psychiatrist I wouldn't believe that adolescents could be depressed, all other diseases starting in young life such as ADHD, Autism I did accept. Depression such as adults can experience, no.

Epidemiological studies estimate the prevalence of depression in adolescents is 5-8%. Despite similarities there are also notable differences in treatment response of depressed adolescents compared to adults.In contrast to adults TCA do not appear effective for the treatment of depression in children and adolescents.
Recently I discussed the brain changes during adolescence.

There are notable neurobiological differences between depressed adolescents and adults:
1. Adolescents do not have subtle thyroid alterations as in adults with depression
2. Growth hormone probes in adolescents donot differ between depressed adolescents and healthy adolescents in contrast with most adult depressed patients. Adolescents do not differ in growth hormone secretion after administration of clonidine, L-Dopa and dextroamphetamine.
3. Cortisol hyper-secretion is rare in adolescent depressed patients in contrast to depressed adults.
4. There is no blunted corticotrophin secretion after CRH infusion with depressed adolescents compared to a not depressed groups. In adults 50% of depressed patients have a blunted corticotrophin release.
5. Depressed adults have changes in cellular immunity such as changes in lymphocytes or lymphocyte subset number. In adolescents no studies reported changes in lymphocyte or lymphocyte subset number.

Depressed adolescents share another similarity with depressed adults, EEG changes during sleep are comparable between these groups:
1. prolonged sleep latency
2. sleep continuity disorders
3. reduced time until rapid eye movement (REM) period
4. increased REM density
5. decreased alfa (stage 3 and 4) sleep (this last one not with adolescents)

Neuroanatomical differences between adults with depression and adolescents has hardly been a subject for research. In adults the most important findings in MRI research are abnormal amygdala volumes, although the direction of this abnormality varies across studies. Volumes of the hippocampus have been found to be reduced in most, though not all, studies of chronic or recurrent adult depressives.
MRI findings in 20 children and adolescents with depression:
1. smaller amygdalas in depressed children compared to healthy subjects, reduction of left and right amygdala volumes
2. Hippocampus volumes did not differ between the groups
3. No significant correlation were found between amygdala volumes and depressive symptom severity, age at onset, or illness duration

How can these differences between early onset depression and adult depression be explained? There are three kinds of factors that me contribute to these different findings.
1. Development factors
Many of the neurobiological systems implicated in the pathophysiology of adult depression are not fully devloped until adulthood. For instance serotonin content and synthetic activity matures relatively early, the serotonergic innervation of the prefrontal cortex is achieved at age 5-6 years. In contrast the development of norepinephrine and dopamine content and synthetic activity continues through puberty with dopamine innervation of the prefrontal cortex not finalised until to early adulthood. Corresponding with these changes there are developmental differences in sensitivity to various pharmacological agents.

2. Stages of illness
Biological correlates and treatment response of patients with recurrent episodes of depression may differ from a single episode. Most adolescents experience their first depression in this life-phase. There is also some evidence that HPA axis disturbances differ between recurrent illness and patients experiencing their first episode. Differences in the neurobiological correlates of depression across the life cycle may reflect course-of-illness factors and not fundamental differences in the pathophysiology of the disorder.

3. Heterogeneity in clinical outcome
Several studies have reported that as many as 20 to 40% of children and adolescents with depression experience a manic episode within 5 years of their initial episode of depression. Adolescents in normal control may also switch group status over time In a longitudinal study 23 % of the normal control subjects had an episode of depression during the 7 year interval follow-up. Studies that failed to use normal controls subjects at low familial risk for affective disorder may have obscured group differences in neurobiological studies with child and adolescent probands.
These findings highlight the need for careful characterization of normal control subjects and the importance of longitudinal follow-up data

There are many differences in the neurobiological correlates and treatment response of depressed adolescents and adults. We currently do not know if adolescent- and adult onset depression are one and the same disorder. Systematic longitudinal research is needed that accounts for:
1. developmental stage
2. stage of illness (number of episodes, total duration)
3. familial factors

The results suggest that early onset depression shares some but not all of the neuroanatomical features of adult onset depression. This raises the possibility that the pathophysiology of early onset depression may differ from adult onset depression, despite similarities in phenomenology. This in turn may have implications for the treatment of childhood depression.

No comments: