One of my publications just became available to the public on PubMed. The publication deals with the use of transcranial magnetic stimulation in autism spectrum disorders, more specifically, why I thought it could offer a good therapeutic intervention, and some of the results from our laboratory. Having had the idea and written the article I can only offer my eternal gratitude to a wonderful group of collaborators capable of making dreams come true.
In the following paragraphs I offer both the abstract and the conclusions to the article.
Despite growing knowledge about autism spectrum disorder (ASD), research findings have not been translated into curative treatment. At present, most therapeutic interventions provide for symptomatic treatment. Outcomes of interventions are judged by subjective endpoints (e.g., behavioral assessments) which alongside the highly heterogeneous nature of ASD account for wide variability in the effectiveness of treatments. Transcranial magnetic stimulation (TMS) is one of the first treatments that targets a putative core pathological feature of autism, specifically the cortical inhibitory imbalance that alters gamma frequency synchronization. Studies show that low frequency TMS over the dorsolateral prefrontal cortex (DLPC) of individuals with ASD decreases the power of gamma activity and increases the difference between gamma responses to target and non-target stimuli. TMS improves executive function skills related to self-monitoring behaviors and the ability to apply corrective actions. These improvements manifest themselves as a reduction of stimulus bound behaviors and diminished sympathetic arousal. Results become more significant with increasing number of sessions and bear synergism when used along with neurofeedback. When applied at low frequencies in individuals with ASD, TMS appears to be safe and to improve multiple patient-oriented outcomes. Future studies should be conducted in large populations to establish predictors of outcomes (e.g., genetic profiling), length of persistence of benefits, and utility of booster sessions.
In summary, the cerebral cortex’s inherent excitatory/inhibitory bias demands the presence of dampening mechanisms to maintain a proper set point when acquiring and processing stimuli. This bias is altered in ASD individuals and manifested as gamma oscillation abnormalities, deficits in executive function, and stimulus bound behaviors. TMS is a non-invasive therapeutic intervention capable of modulating evoked and induced gamma oscillations and altering maladaptive behaviors83. Recent reviews of the literature suggest that TMS is safe and effective when used in ASD54,84–91. Selecting appropriate outcome measures is of importance due to limitations in presently available sham procedures that help define differences between active and control populations92. It is therefore of importance that the selection process for outcome measures extends beyond subjective methods, such as behavioral screening, and into unbiased electrophysiological measures that maximize both internal and statistical validity. In addition, objective measures of quality care should be instituted and analyzed by themselves rather than being considered surrogate measures of outcomes. We have found that autonomic measures, themselves related to behavior problems and emotional regulation, help define functional changes associated with ASD while simultaneously monitoring adverse experiences80,81. At present, efforts should focus on developing large sample clinical trials with targeted inclusionary/exclusionary criteria and longitudinal follow-up. This will allow testing critical questions regarding possible predictors of outcome (e.g., genetic profiling), length of persistence of benefits, assessing outcome according to severity of phenotypic presentation, and utility of booster sessions.