Assessment-Guided Neurofeedback for Autistic Spectrum Disorder

Robert Coben, PhD Ilean Padolsky, PhD

ABSTRACT. Background. Research reviewing the epidemiology of Autism (Medical Research Council, 2001) indicated that approximately 60 per 10,000 children (1/166) are diagnosed with Autistic Spectrum Disorder (ASD). Jarusiewicz (2002) published the only controlled study docu- menting the effectiveness of neurofeedback for Autism based on one outcome measure. The pres- ent study extended these findings with a larger sample size, broader range of assessments, and physiological measures of brain functioning.

Methods. Assessment-guided neurofeedback was conducted in 20 sessions for 37 patients with ASD. The experimental and control groups were matched for age, gender, race, handedness, other treatments, and severity of ASD.

Results. Improved ratings of ASD symptoms reflected an 89% success rate. Statistical analyses revealed significant improvement in Autistics who received Neurofeedback compared to a wait list control group. Other major findings included a 40% reduction in core ASD symptomatology (indi- cated by ATEC Total Scores), and 76% of the experimental group had decreased hyper- connectivity. Reduced cerebral hyperconnectivity was associated with positive clinical outcomes in this population. In all cases of reported improvement in ASD symptomatology, positive treat- ment outcomes were confirmed by neuropsychological and neurophysiological assessment.

Conclusions. Evidence from multiple measures has demonstrated that neurofeedback can be an effective treatment for ASD. In this population, a crucial factor in explaining improved clinical outcomes in the experimental group may be the use of assessment-guided neurofeedback to reduce cerebral hyperconnectivity. Implications of these findings are discussed. doi:10.1300/J184v11n01_02 [Article copies available for a fee from The Haworth Document Delivery Serv 1-800-HAWORTH. E-mail address: <docdelivery@haworthpress.com> Website: <http://www.HaworthPress.com> © 2007 by The Haworth Press, Inc. All rights reserved.]

Patches of Disorganization in the Neocortex of Children with Autism

Rich Stoner, Ph.D., Maggie L. Chow, Ph.D., Maureen P. Boyle, Ph.D., Susan M. Sunkin, Ph.D., Peter R. Mouton, Ph.D., Subhojit Roy, M.D., Ph.D., Anthony Wynshaw-Boris, M.D., Ph.D., Sophia A. Colamarino, Ph.D., Ed S. Lein, Ph.D., and Eric Courchesne, Ph.D.

N Engl J Med 2014; 370:1209-1219March 27, 2014DOI: 10.1056/NEJMoa1307491

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BACKGROUND

Autism involves early brain overgrowth and dysfunction, which is most strongly evident in the prefrontal cortex. As assessed on pathological analysis, an excess of neurons in the prefrontal cortex among children with autism signals a disturbance in prenatal development and may be concomitant with abnormal cell type and laminar development.

METHODS

To systematically examine neocortical architecture during the early years after the onset of autism, we used RNA in situ hybridization with a panel of layer- and cell-type–specific molecular markers to phenotype cortical microstructure. We assayed markers for neurons and glia, along with genes that have been implicated in the risk of autism, in prefrontal, temporal, and occipital neocortical tissue from postmortem samples obtained from children with autism and unaffected children between the ages of 2 and 15 years.

RESULTS

We observed focal patches of abnormal laminar cytoarchitecture and cortical disorganization of neurons, but not glia, in prefrontal and temporal cortical tissue from 10 of 11 children with autism and from 1 of 11 unaffected children. We observed heterogeneity between cases with respect to cell types that were most abnormal in the patches and the layers that were most affected by the pathological features. No cortical layer was uniformly spared, with the clearest signs of abnormal expression in layers 4 and 5. Three-dimensional reconstruction of layer markers confirmed the focal geometry and size of patches.

CONCLUSIONS

In this small, explorative study, we found focal disruption of cortical laminar architecture in the cortexes of a majority of young children with autism. Our data support a probable dysregulation of layer formation and layer-specific neuronal differentiation at prenatal developmental stages. (Funded by the Simons Foundation and others.)