Neurofeedback treatment in autism. Preliminary findings in behavioral, cognitive, and neurophysiological functioning

نویسندگان

  • Mirjam E.J. Kouijzer
  • Hein T. van Schie
  • Jan M.H. de Moor
  • Jan K. Buitelaar
چکیده

Effects of neurofeedback treatment were investigated in children with autism spectrum disorders (ASD). Sixty percent of the participants in the treatment group successfully reduced excessive theta power during neurofeedback treatment. Reduction of theta power was confirmed by preand post-QEEG measures. Parents of participants in the neurofeedback treatment group reported significant improvements in reciprocal social interactions and communication skills, relative to the parents of the control group. Setshifting skills improved following neurofeedback treatment relative to the control group. The reduction of theta power is assumed to reflect modulation of activity in the anterior cingulate cortex (ACC), which is known to be involved in social and executive dysfunctions in autism. 2009 Elsevier Ltd. All rights reserved. Autism spectrum disorders (ASD) have been defined as developmental disorders characterized by abnormalities in social interaction, communication skills, and behavioral flexibility (American Psychiatric Association, 1994). Although no evidence-based cure exists for ASD, psychosocial and pharmacologic interventions can improve the quality of life of children with ASD and their families. Psychosocial interventions in ASD include behavioral therapy, social skills training, and parental interventions. In general, psychosocial interventions appear to have limited effect sizes and maintenance of results over time. Recent research suggests that of all psychosocial interventions, intensive one-to-one behavioral therapy of at least 20 h per week at an early age is most effective (van Engeland & Buitelaar, 2008). Pharmacologic interventions such as atypical antipsychotics, serotonin reuptake inhibitors, and stimulants do no affect the core symptoms of ASD, but may be components of a comprehensive treatment program in temporarily reducing additional problem behavior. Both psychosocial and pharmacologic interventions provide no curative solution for the treatment of ASD, but might offer benefits for relieving ASD symptoms. A relatively new form of treatment for ASD is neurofeedback. The goal of neurofeedback is to influence or change abnormal oscillatory activity by making clients aware of this activity and reward the inhibition or enhancement of desired oscillatory activity. In 2002, Jarusiewicz started research on the effects of neurofeedback in childrenwith autism. She found a 26% decline in autistic behavior as reported by parents in 12 autistic children after inhibiting theta power and enhancing low beta power, compared to a 3% decline in a matched waiting list control group. Coben and Padolsky (2007) extended this * Corresponding author at: Behavioural Science Institute, Radboud University Nijmegen, P.O. Box 9104, 6500 HE Nijmegen, The Netherlands. Tel.: +31 243611167; fax: +31 243616211. E-mail address: [email protected] (Mirjam E.J. Kouijzer). Please cite this article in press as: Kouijzer, M. E. J, et al. Neurofeedback treatment in autism. Preliminary findings in behavioral, cognitive, and neurophysiological functioning. Research in Autism Spectrum Disorders (2009), doi:10.1016/ j.rasd.2009.10.007 1750-9467/$ – see front matter 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.rasd.2009.10.007 M.E.J. Kouijzer et al. / Research in Autism Spectrum Disorders xxx (2009) xxx–xxx 2 G Model RASD-216; No of Pages 14 research by comparing the outcomes of neurofeedback training in a treatment (n = 37) and control group (n = 12) on neuropsychological tests, behavior ratings, and neurophysiological measures. They showed improvement on all outcome measures for the treatment group but not for the control group. In our own study (Kouijzer, deMoor, Gerrits, Congedo, & van Schie, 2009) we evaluated neurofeedback treatment in seven children with ASD compared to a waiting list control group (n = 7) and found positive effects of inhibiting theta power and enhancing low beta power on behavioral, cognitive, and neurophysiological outcome measures. These results were maintained after one year, as was found in a follow-up study (Kouijzer, de Moor, Gerrits, Buitelaar, & van Schie, 2009). Compared to common psychosocial and pharmacological interventions, neurofeedback may be at an advantage with respect to shortened treatment duration, the absence of side effects, and long-termmaintenance of treatment results. These advantages suggest that neurofeedback may be a promising tool for the treatment of children with ASD. To further establish neurofeedback as an efficacious and specific treatment for ASD, the current study implemented several methodological improvements (cf. Heinrich, Gevensleben, & Strehl, 2007; Kouijzer, de Moor, Gerrits, Congedo, et al., 2009; LaVaque et al., 2002). First, our previous study reported positive results for children with pervasive developmental disorders – not otherwise specified (PDD-NOS), a relatively mild form of ASD. However, neurofeedback might also benefit children with more severe subtypes of ASD. The present study investigated neurofeedback treatment in children from the full autistic spectrum. Second, in contrast to the fixed treatment protocol that was used in our first study (Kouijzer, de Moor, Gerrits, Congedo, et al., 2009), i.e. reduction of 4–7 Hz power and increase of 12–15Hz power at location C4, frequency bands and electrode placement for treatment in this study were adjusted to the individual quantitative electroencephalogram (QEEG) of each participant, which is referred to as individualized or QEEG-guided neurofeedback (Coben & Padolsky, 2007; Heinrich et al., 2007;Walker & Kozlowski, 2005). Third, our first study found consistent changes in theta and low beta power over subsequent neurofeedback sessions, but no transfer of these changes in theta and low beta power to QEEG as measured during rest. In the present study, we extended analysis at the neurophysiological level by investigating transfer effects of neurofeedback on QEEG data during a variety of rest and task conditions. Fourth, evaluation of the procedure of the previous study revealed that the investment of time and energy of parents and children to visit the neurofeedback practice twice a week was extensive. In the present study, feasibility of neurofeedback treatment was increased by implementing neurofeedback treatment in the school programs of the participants. Finally, effects on behavior in our previous study were evaluated only by parents. However, behavior of children with ASD often is expressed differently across different contexts and improvement in behavior might vary across contexts as well. This study assessed behavioral effects of neurofeedback both at home and at school by enclosing parent and teacher questionnaires. This paper describes and discusses the results of individualized neurofeedback in ASD by comparing treatment and control groups before and after treatment. Participantswere randomly divided into treatment and control group. Sixmonths after treatment ended there was a follow-up for both treatment and control group. The present study has three aims. First, the effects of neurofeedback treatment on social behavior were investigated. We evaluated social interactions, communication skills, and stereotyped and repetitive behavior in the neurofeedback treatment and control group with behavior questionnaires filled out by parents and teachers. Second, the effects of neurofeedback treatment on executive functioning, i.e. attentional control, cognitive flexibility, goal setting, and speed and efficiency, were investigated using a range of neuropsychological tasks. Finally, the effects of neurofeedback treatment on brain activity were examined by investigating session data that were gathered during neurofeedback treatment and preand post-measures of QEEG.

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تاریخ انتشار 2009