What's New, What's Old and What's Next 1998-2000: Overview of Autism Research
Portia Iversen, Cure Autism Now (CAN) - March 1,2001

[This review of autism research is from the premiere issue of the Cure Autism Now newsletter, Advances. Portia Iversen is a founder of CAN and is a parent to an autistic child. There is some technical language.] http://www.canfoundation.org/

After forty years in the desert, major change has been underway in the field of autism research. The past two years in particular, have seen a major increase in autism research. Significant new data are beginning to accumulate, laying the ground work for discovering the causes, treatments and a cure for autism.

Autism research is increasing, both in the number of studies being conducted and in their scope and variety of approaches. We expect to see this trend continue and as scientific efforts continue to accelerate, we will experience the first medical breakthroughs in our understanding of the causes of autism and the development of treatments and a cure.
The following is a sampling of important autism research conducted over the past two years, which may be of particular interest to parents.
Note: The inclusion or omission of any study in this review does not constitute an opinion as to its relevance, importance or validity.

Continued Evidence of Serotonin Involvement in Autism Dr. Diane Chugani* of Wayne State University, Detroit has provided us with important new information through the use of PET scanning techniques on the abnormal capacity for serotonin synthesis in the brains of autistic children and adults.
While the children appear to have decreased serotonin levels, adults show increased levels. This data suggest that humans undergo a period of high brain serotonin synthesis capacity during childhood and that the developmental process may be disrupted in autistic children.
In a striking finding, Marion Leboyer* from the Faculte Jussieu in Paris reports on whole blood serotonin and plasma beta-endorphin in autistic probands and their first-degree relatives.
Whole blood serotonin is known to be elevated in autistic subjects and could be a possible marker of genetic liability to autism. The author confirms the previously reported familiality of hyperserotoninemia in autism as mothers (51%), fathers (45%) and siblings (87%) have elevated levels of serotonin and mothers (53%) also show elevated levels of C-ter-beta-EP-ir.
In other serotonin-related research, Robert DeLong of Duke University has completed a study on the use of low-doses of serotonin reuptake inhibitors (SSRI) in young children with autism.
Twenty-two of the 37 children who underwent fluoxetine treatment had a beneficial treatment response that was sustained during continuing treatment for 13 - 33 months (mean 21 months). Those children with positive response showed behavioral, language, cognitive, affective and social improvements.
In still another study involving SSRIs, Dr. D. Branford of the Southern Derbyshire Mental Health Trust in Derby, England undertook a retrospective case-note analysis of 37 adults with autism. The subjects were prescribed one of two selective serotonin re-uptake inhibitor antidepressants (fluoxetine or paroxetine). The SSRIs proved to be of no benefit for 15 subjects (40%) and led to a deterioration in nine additional cases (25%). However, some reduction of perseverative and maladaptive behaviors was achieved in 13 cases (35%).
A number of other pharmaceuticals have recently been under investigation for use in autism. Risperidone was investigated by Dr. R. Nicolson of the University of Toronto in his study titled, "An open trial of risperidone in young autistic children." Eight of the 10 children were considered to be responders. Dr. C.J. McDougle of Indiana University School of Medicine conducted a 12-week double-blind placebo-controlled study of risperidone in 31 adults with autistic spectrum disorders.
This study concluded that risperidone was superior to the placebo in reducing repetitive behavior, aggression, anxiety or nervousness, depression, irritability and the overall behavioral symptoms of autism. Nine (60%) of 15 patients who received treatment with open-label risperidone following the double-blind placebo phase responded. In another recent report,
Dr. A. Zuddas from the University of Cagliari, Italy, reports that risperidone is an effective and relatively safe drug for long-term treatment of behavioral disruption in autistic children and adolescents.
Dr. Eric Hollander,* from the Seaver Autism Research Center at the Mount Sinai School of Medicine, N.Y. conducted an open, retrospective clinical study with venlafaxine and evaluated its effect on core symptoms of autism as well as associated features of ADHD. He reports that Venlafaxine was effective in low dosages (mean, 24.37 mg/day; range, 6.25 to 50 mg/day) and was well tolerated.
Improvement was noted in repetitive behaviors and restricted interests, social deficits, communication and language function, inattention, and hyperactivity. Venlafaxine is both a serotonin and norepinephrine reuptake inhibitor.
Dr. P. G. Rossi, from the Neurological Institute, University of Bologna, Italy, reports promising results in its study of Niaprazine, a histamine H1-receptor antagonist with marked sedative properties. Niaprazine was administered at 1 mg/kg/day for 60 days to 25 subjects with autistic disorder.
A positive effect was found in 52% of patients, particularly on hyperkinesia, unstable attention, resistance to change and frustration, mild anxiety signs, heteroaggressiveness, and sleep disorders. No side effects were observed. Because of its sedative effects and good tolerability, niaprazine can be used as a first-choice drug to improve behavior and sleep disorders in patients with autistic disorder.