27117
Magnetoencephalographic (MEG) Gamma Oscillations and Sensory Sensitivity in People with and without Autism Spectrum Disorders (ASD)

Poster Presentation
Thursday, May 10, 2018: 5:30 PM-7:00 PM
Hall Grote Zaal (de Doelen ICC Rotterdam)
E. V. Orekhova1, J. F. Schneiderman2,3, S. Lundström4, B. Riaz5, N. Hadjikhani4,6, O. V. Sysoeva1, T. A. Stroganova1 and C. Gillberg4, (1)MEG-Center, Moscow University of Psychology and Education, Moscow, Russian Federation, (2)Department of Clinical Neurophysiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, (3)MedTech West, Gothenburg, Sweden, (4)Gillberg Neuropsychiatry Centre, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, (5)Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, (6)MGH/ Martinos Center for Biomedical Imaging/ Harvard Medical School, Charlestown, MA
Background: People with ASD often demonstrate hypo- and hypersensitivity to sensory stimuli of different modalities. Altered balance between neural excitation (E) and inhibition (I) has been suggested as one of the mechanisms underlying ASD and is likely to contribute to the sensory sensitivity problems through affecting gain control properties of the neurons in sensory cortex (Isaacson and Scanziani, Neuron, 2011, 72:231-43). Neural oscillations in high-frequency (30-100 Hz, i.e. ‘gamma’) range are generated by local E-I circuits and are highly sensitive to changes in the E/I balance. Therefore, variations in gain control properties of the cortical circuitry may be reflected in intensity-related changes of gamma oscillations.

Objectives: In this study we sought to find E/I–related neurophysiological underpinning of abnormal sensory sensitivity in people with ASD by investigating properties of magnetoencephalographic (MEG) gamma oscillations and their modulation by intensity of visual stimulation (excitatory drive).

Methods: MEG was recorded in 20+20 high-functioning adults with and without ASD. Subjects watched high-contrast concentric gratings moving at 1.2, 3.6 or 6.0 deg/sec that effectively induced visual gamma oscillations in our previous study in children. We also recorded pupillary constriction as an indirect measure of excitatory drive. Sensory sensitivity was assessed in all participants using the Adolescent/Adult Sensory Profile questionnaire.

Results: Participants with ASD had higher sensory sensitivity (p<0.05). Increasing stimulus velocity led to stronger pupillary constriction - reflecting an increase in excitatory drive to the cortexboth in individuals with ASD and those without. The increase in excitatory drive was accompanied by highly significant acceleration of gamma oscillations and suppression of gamma response magnitude. The ASD group demonstrated weaker intensity-related suppression of gamma response, while no significant group differences in either amplitude or frequency of gamma response were found. In both groups the weaker suppression of gamma response correlated with higher sensory sensitivity.

Conclusions: The intensity-related changes in MEG gamma oscillations may be useful for characterization of E/I balance in the visual cortex and may provide biomarkers for clinical trial studies targeting E/I balance in ASD.