An 8 year-old boy with Asperger's syndrome had difficulties in communicating with his teachers and classmates. He occasionally stole out of the classroom. He could not sleep at night recalling his awful experience and kept crying every night and refused to go to school. The treatment with fluvoxamine was started at the dose of 25 mg daily. Four weeks after the treatment, his repetitive behavior and hyperactivity decreased and night crying diminished.

It is possible that the effects of reuptake antidepressant drugs and the effects of inositol may have a common final pathway.

Many autistic children may actually suffer from a genetically linked depression that is treatable with antidepressants such as Prozac. Recent studies point to a gene somewhere on chromosome 15 as a potential autism gene.

The cause of depression is not clearly understood. It is important for the clinician to recognize whether or not physical illness or the medications or treatments used for treating physical illness are inducing the depression.

About two-thirds of youngsters with the most common form of infantile autism actually have a treatable, genetically linked, early-onset form of severe depression.

Our findings are consistent with previous family history reports in autism which suggest an increased incidence of serotonergic mediated psychiatric illnesses in first-degree relatives of individuals with autism.

While autistic children have higher mean whole blood 5-HT content than controls matched for race and pubertal status, there is little or no evidence that blood 5-HT is associated with cognitive or behavioral traits in the normal population. (JAACAP)

The trials consistently found large improvements in placebo groups, with statistically significant additional benefits for active drug on some measures only. These results make a major benefit from newer antidepressants unlikely, but a small benefit remains possible.

Theoretical considerations underlying the rationale for the study of 5-HT in autism include 5-HT's role in neurodevelopment, its especially rich innervation of limbic areas critical for emotional expression and social behavior

Studies of GABA have resulted in a greater understanding of the possible role of this neurotransmitter amino acid in the actions of antidepressants, particularly phenelzine. This drug should be investigated for its usefulness as a neuroprotective agent.

It is clear that autistic individuals, as a group, exhibit significant increases in peripheral blood levels of serotonin, a central neurotransmitter involved in various regulatory neuronal systems that is also found in blood platelets and the digestive system.

After a brief introduction to serotonin neurobiology and a general discussion of appropriate genetic methodology, each of the major 5-HT-related genes and their encoded proteins are reviewed in turn.

A single hSERT gene is located at chromosome locus 17q11.2 (20) and has recently been implicated in anxiety traits (24), major depression (25), and autism (26).

Combining 20 mg of fluoxetine with 2 g of tryptophan daily at the outset of treatment for major depressive disorder appears to be a safe protocol that may have both a rapid antidepressant effect and a protective effect on slow-wave sleep.

The authors conclude that the risk of suicidal behavior is increased in the first month after starting antidepressants, especially during the first one to nine days.

Six articles met inclusion criteria. Only 2 studies claim efficacy by significant results in primary outcomes; both have since been contested in further analysis. Not one study adequately examines safety, particularly with respect to whether a link exists between antidepressant use and induction of suicidal ideation or attempts.

An association study was performed to elucidate the role of the serotonin transporter (5-HTT) gene as a susceptibility factor for autism as treatment of patients with antidepressant drugs which selectively target 5-HTT reduced autistic or concomitant symptoms, such as repetitive behavior and aggression, and ameliorate language use... In our study haplotype analysis of the 5-HTTLPR and the VNTR in intron 2 supplied evidence for an association of 5-HTT and autism in the stringent (P = 0.069) and extended patient group (P = 0.049). Overall, we were not able to replicate the findings of the first study on 5-HTT and autism and instead observed a tendency for association of the opposite genetic variant of the gene with the disorder. The implications for genetic variants of the serotonin transporter in the etiology of autism and possible subgroups of patients, therefore, needs clarification in further studies with other and larger patient samples.

There are similar symptoms between autism and OCD, such as the repetitive preoccupations and perseverative behaviors. The similarity between some of the above symptoms and that of OCD has led to the use of SSRI's in the management of PDDs.

Overlapping symptoms between OCD and autism prompted trials of SSRIs in autism. SSRIs work well in autism to reduce the frequency and intensity of repetitive, ritualized behaviors including motor stereotypies and more classic compulsive rituals.

Overlapping symptoms between OCD and autism prompted trials of SSRI's in autism. SSRI's work well in autism to reduce the frequency and intensity of repetitive, ritualized behaviors including motor stereotypies and more classic compulsive rituals.

A systematic review of randomized controlled trials of the use of atypical antipsychotics and selective serotonin reuptake inhibitors in the treatment of behavioural problems associated with pervasive developmental disorders is reported. A search through both published and unpublished literature, including contacting drug companies and known experts in the field was undertaken. Six trials met the criteria for inclusion in the review. They largely suffer from methodological weaknesses; only two trials had satisfactory methodological quality. The heterogeneity in outcome measurements prevented from conducting a meta-analysis. There is yet no coherent body of data concerning the effects of these medications across all sub-classifications of pervasive developmental disorders, across all age categories, and concerning their medium- and long-term effects, and their effects on quality of life. Atypical antipsychotics and selective serotonin reuptake inhibitors may be of benefit for behavioural problems associated with pervasive developmental disorders. Risperidone has been the best studied among these medications. Atypical antipsychotics appear to have a low risk of extrapyramidal symptoms during short-term treatment. The reviewed trials cannot provide data on the use of selective serotonin reuptake inhibitors in the treatment of children with pervasive developmental disorders. No firm conclusions for clinical practice can be drawn. Larger, well-conducted randomized controlled trials with long-term follow-up are needed.