Available online at www.sciencedirect.com Neuroscience Letters 434 (2008) 218–223 Sensory gating in young children with autism: Relation to age, IQ, and EEG gamma oscillations Elena V. Orekhova a,∗ , Tatiana A. Stroganova b,c , Andrey O. Prokofyev c , Gudrun Nygren d , Cristopher Gillberg d , Mikael Elam a a Department of Clinical Neurophysiology, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden b Psychological Institute of Russian Academy of Education, 125009 Moscow, Russia c Moscow University of Psychology and Education, 103051 Moscow, Russia d Department of Child & Adolescent Psychiatry, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden Received 8 September 2007; received in revised form 23 January 2008; accepted 29 January 2008 Abstract Unusual reactions to auditory stimuli are often observed in autism and may relate to ineffective inhibitory modulation of sensory input (sensory gating). A previous study of P50 sensory gating did not reveal abnormalities in high-functioning school age children [C. Kemner, B. Oranje, M.N. Verbaten, H. van Engeland, Normal P50 gating in children with autism, J. Clin. Psychiatry 63 (2002) 214–217]. Sensory gating deficit may, however, characterize younger children with autism or be a feature of retarded children with autism, reflecting imbalance of neuronal excitation/inhibition in these cohorts. We applied a paired clicks paradigm to study P50 sensory gating, and its relation to IQ and EEG gamma spectral power (as a putative marker of cortical excitability), in young (3–8 years) children with autism (N = 21) and age-matched typically developing children (N = 21). P50 suppression in response to the second click was normal in high-functioning children with autism, but significantly (p < 0.03) reduced in those with mental retardation. P50 gating improved with age in both typically developing children and those with autism. Higher ongoing EEG gamma power corresponded to lower P50 suppression in autism (p < 0.02), but not in control group. The data suggest that ineffective inhibitory control of sensory processing is characteristic for retarded children with autism and may reflect excitation/inhibition imbalance in this clinical group. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Autism; Children; ERP; P50 sensory gating; Gamma oscillations Abnormal reactivity to sensory stimuli is commonly observed in young children with autism (CWA), pervasively presents in adult age [2,20], and is especially noticeable in the audi- tory modality. CWA may demonstrate both unresponsiveness to sound and acoustic hypersensitivity. It has been suggested that altered inhibitory control of sensory intake may cause sensory overload and disruption of higher order processing in autism, leading to active avoidance of external stimulation [12]. Suppression of processing of irrelevant repetitive sensory input is often studied using a ‘sensory gating’ paradigm. Pairs of clicks separated by short within-pair interstimulius inter- vals (ISIs) are presented with much longer inter-pair ISIs. The so-called ‘preattentive’ middle-latency P50 component ∗ Corresponding author. Tel.: +46 31 342 48 02; fax: +46 31 82 12 68. E-mail address: elena@neuro.gu.se (E.V. Orekhova). of the auditory event-related potential markedly decreases in amplitude with repetition of stimuli with short ISIs, reflecting inhibitory gating of repetitive auditory input. Sensory gating is usually defined as the ratio of P50 amplitude after the second click (S2) to the P50 amplitude after the first click (S1). The pronounced P50 suppression to the second click corresponds to a robust inhibitory function of the brain, i.e. a normal sensory gating [1,7,19]. The sensory gating paradigm has been widely used to study neurophysiologic mechanisms in schizophrenia. The reduced sensory gating that was found in schizophrenic patients may contribute to sensory overload experienced by these patients [19]. This gating deficit has been related to decreases in inhibitory interneurons found in schizophrenia [13]. Simi- larly to schizophrenic patients, individuals with autism often demonstrate increased sensitivity to sensory stimuli. Moreover, pathology of inhibitory interneurons [14] and imbalance of excitation and inhibition processes [25] has been implicated in 0304-3940/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.neulet.2008.01.066