Neuropediatrics 2011; 42(05): 207-209
DOI: 10.1055/s-0031-1291242
Short Communication
© Georg Thieme Verlag KG Stuttgart · New York

Effects of Fluoxetine Treatment on Striatal Dopamine Transporter Binding and Cerebrospinal Fluid Insulin-Like Growth Factor-1 in Children with Autism

Authors

  • I. Makkonen

    1   Department of Pediatrics, Unit of Child Neurology, Kuopio University Hospital and School of Medicine, University of Eastern Finland, Kuopio, Finland
  • H. Kokki

    2   Department of Anesthesiology and Intensive Care, Kuopio University Hospital and School of Medicine, University of Eastern Finland, Kuopio, Finland
  • J. Kuikka

    3   Imaging Center, Kuopio University Hospital and School of Medicine, University of Eastern Finland, Kuopio, Finland
  • U. Turpeinen

    4   HUSLAB, Laboratory of Women’s Clinic, Helsinki, Finland
  • R. Riikonen

    1   Department of Pediatrics, Unit of Child Neurology, Kuopio University Hospital and School of Medicine, University of Eastern Finland, Kuopio, Finland
Further Information

Publication History

received 24 February 2011

accepted 21 September 2011

Publication Date:
20 October 2011 (online)

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Abstract

A positive effect of fluoxetine has been shown in some children with autism. The present study was undertaken to correlate striatal dopamine transporter (DAT) binding and cerebrospinal fluid insulin-like growth factor-1 (CSF-IGF-1) with clinical response in autistic children (n=13, age 5–16 years) after a 6-month fluoxetine treatment. Good clinical responders (n=6) had a decrease (p=0.031) in DAT binding as assessed using single-photon emission computed tomography with [123I]-nor-β-CIT, whereas poor responders had a trend to an increase. An increase in CSF-IGF-1 (p=0.003) was detected after the treatment period, but no correlation between the clinical response and CSF-IGF-1 was found. In conclusion, fluoxetine decreases DAT binding indicating alleviation of the hyperdopaminergic state and increases CSF-IGF-1 concentration, which may also have a neuroprotective effect against dopamine-induced neurotoxicity in autistic children.