Neural correlates of semantic activation spreading on the path to picture naming in adults who stutter Nathan D. Maxfield * , Jessica L. Huffman, Stefan A. Frisch, Jacqueline J. Hinckley University of South Florida, Department of Communication Sciences & Disorders, USA article info Article history: Accepted 23 March 2010 Available online 10 April 2010 Keywords: Stuttering Psycholinguistic Lexical Semantic Event-related potentials Adults abstract Objective: On the path to picture naming, words that relate semantically to the pictured object become activated in the mental lexicon. We used a neuroscientific approach to investigate this semantic activa- tion spreading process in adults who stutter (AWS). Methods: Fourteen AWS and 14 adults who do not stutter (AWNS) completed a picture–word priming task. On each trial, a picture was named at a delay. On some trials, an unattended auditory probe word was presented after the picture, before naming commenced. Event-related potentials recorded to probe words Semantically-Related to the picture labels, and to probe words Semantically- and Phonologically- Unrelated to the picture labels, were compared using spatial–temporal principal component analysis. Results: Posterior N400 amplitude was attenuated for Semantically-Related versus Unrelated probes in AWNS, while in AWS posterior N400 amplitude was enhanced for Semantically-Related versus Unrelated probes. Marginal albeit potentially relevant group differences in the morphology of other ERP compo- nents were also observed. Conclusions: The posterior N400 results point to a strategic, inhibitory influence on semantic activation spreading in AWS on the path to naming. Group differences in the amplitude of other ERP components tentatively suggest that AWS allocated attentional resources differently than the AWNS during the task. Preliminary ERP evidence of intact conceptual (as opposed to lexical-semantic) priming in the AWS is also discussed. Significance: This study contributes to a growing body of research describing linguistic performance in AWS. Ó 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. 1. Introduction Stuttering is a disorder of fluency that emerges during child- hood. The prevalence of stuttering in preschool children is 2% (Beitchman et al., 1986). Fewer people stutter persistently into school age (1%) and adulthood (<1%) (Bloodstein, 1995; Craig et al., 2002). Still, the impact on quality of life can be devastating for those whose stuttering persists (see Yaruss, 2007). For those individuals, the core deficit affecting verbal communication is the moment of stuttering, defined by Wingate (1964) as: 1. (a) Disruption in the fluency of verbal expression, which is (b) characterized by involuntary, audible or silent, repetitions or prolongations in the utterance of short speech segments, namely: sound, syllables, and words of one syllable. These dis- ruptions (c) usually occur frequently or are marked in character and (d) are not readily controllable. 2. Sometimes the disruptions are (e) accompanied by accessory activities involving the speech apparatus, related or unrelated body structures, or stereotyped speech utterances. These activ- ities give the appearance of being a speech-related struggle. 3. Also, there are not infrequently (f) indications or report of the presence of an emotional state, ranging from a general condi- tion of ‘‘excitement” or ‘‘tension” to more specific emotions of a negative nature such as fear, embarrassment, irritation, or the like (p. 488). Moments of stuttering potentially result from an interaction of several different factors. As summarized in a recent model (Conture et al., 2006), core deficits in psycholinguistic planning and/or speech motor control, which may have a genetic basis, limit a person’s capacity to produce speech fluently. According to this same model, when environmental demands on speech exceed one’s fluent capacity, stuttering may emerge, the severity of which 1388-2457/$36.00 Ó 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2010.03.026 * Corresponding author. Address: University of South Florida, Department of Communication Sciences & Disorders, USF, PCD1017, 4202 East Fowler Ave., Tampa, FL 33620, USA. Tel.: +1 813 9746190. E-mail address: nmaxfiel@cas.usf.edu (N.D. Maxfield). Clinical Neurophysiology 121 (2010) 1447–1463 Contents lists available at ScienceDirect Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph