Sensorimotor integration is an active domain of speech research and is characterized by two main ideas, that the auditory system is critically involved in speech production, and that the motor system is critically involved in speech perception. Despite the complementarity of these ideas, there is little crosstalk between these literatures. We propose an integrative model of the speech-related “dorsal stream” in which sensorimotor interaction primarily supports speech production, in the form of a state feedback control architecture. A critical component of this control system is forward sensory prediction, which affords a natural mechanism for limited motor influence on perception, as recent perceptual research has suggested. Evidence shows that this influence is modulatory but not necessary for speech perception. The neuroanatomy of the proposed circuit is discussed as well as some probable clinical correlates including conduction aphasia, stuttering, and aspects of schizophrenia.

Human subjects are known to adapt their motor behavior to a shift of the visual field brought about by wearing prism glasses over their eyes. The analog of this phenomenon was studied in the speech domain. By use of a device that can feed back transformed speech signals in real time, subjects were exposed to phonetically sensible, online perturbations of their own speech patterns. It was found that speakers learn to adjust their production of a vowel to compensate for feedback alterations that change the vowel's perceived phonetic identity; moreover, the effect generalizes across phonetic contexts and to different vowels.

Several behavioral and brain imaging studies have demonstrated a significant interaction between speech perception and speech production. In this study, auditory cortical responses to speech were examined during self-production and feedback alteration. Magnetic field recordings were obtained from both hemispheres in subjects who spoke while hearing controlled acoustic versions of their speech feedback via earphones. These responses were compared to recordings made while subjects listened to a tape playback of their production. The amplitude of tape playback was adjusted to match the amplitude of self-produced speech. Recordings of evoked responses to both self-produced and tape-recorded speech were obtained free of movement-related artifacts. Responses to self-produced speech were weaker than were responses to tape-recorded speech. Responses to tones were also weaker during speech production, when compared with responses to tones recorded in the presence of speech from tape playback. However, responses evoked by gated noise stimuli did not differ for recordings made during self-produced speech versus recordings made during tape-recorded speech playback. These data suggest that during speech production, the auditory cortex (1) attenuates its sensitivity and (2) modulates its activity as a function of the expected acoustic feedback.

Spoken language exists because of a remarkable neural process. Inside a speaker's brain, an intended message gives rise to neural signals activating the muscles of the vocal tract. The process is remarkable because these muscles are activated in just the right way that the vocal tract produces sounds a listener understands as the intended message. What is the best approach to understanding the neural substrate of this crucial motor control process? One of the key recent modeling developments in neuroscience has been the use of state feedback control (SFC) theory to explain the role of the CNS in motor control. SFC postulates that the CNS controls motor output by (1) estimating the current dynamic state of the thing (e.g., arm) being controlled, and (2) generating controls based on this estimated state. SFC has successfully predicted a great range of non-speech motor phenomena, but as yet has not received attention in the speech motor control community. Here, we review some of the key characteristics of speech motor control and what they say about the role of the CNS in the process. We then discuss prior efforts to model the role of CNS in speech motor control, and argue that these models have inherent limitations – limitations that are overcome by an SFC model of speech motor control which we describe. We conclude by discussing a plausible neural substrate of our model.

The control of vocalization is critically dependent on auditory feedback. Here, we determined the human peri-Sylvian speech network that mediates feedback control of pitch using direct cortical recordings. Subjects phonated while a real-time signal processor briefly perturbed their output pitch (speak condition). Subjects later heard the same recordings of their auditory feedback (listen condition). In posterior superior temporal gyrus, a proportion of sites had suppressed responses to normal feedback, whereas other spatially independent sites had enhanced responses to altered feedback. Behaviorally, speakers compensated for perturbations by changing their pitch. Single-trial analyses revealed that compensatory vocal changes were predicted by the magnitude of both auditory and subsequent ventral premotor responses to perturbations. Furthermore, sites whose responses to perturbation were enhanced in the speaking condition exhibited stronger correlations with behavior. This sensorimotor cortical network appears to underlie auditory feedback-based control of vocal pitch in humans.

Ocular dominance stripes in the striate cortex of a macaque monkey were labeled by autoradiography after injection of [3H]proline into one eye. The stripes were reconstructed on a representation of the flattened cortical surface by two independent techniques: one used computer graphics, and the other was the manual unfolding procedure of Van Essen and Maunsell (VanEssen, D. C., and J. H. R. Maunsell (1980) J. Comp. Neurol. 191: 255-281). The two reconstructions differed in many details of the pattern but were in agreement on its general features. As described in earlier studies, the stripes formed a system of parallel bands, with numerous branches and islands. They were roughly orthogonal to the Vl/V2 border throughout the binocular segment of the cortex. In the lateral part of the operculum, where the fovea is represented, the stripes were less orderly than elsewhere. In the calcarine fissure the stripes ran directly across the striate cortex from its dorsal to its ventral margin. In the far periphery the stripes for the ipsilateral eye became progressively narrower, eventually fragmenting into small islands at the edge of the monocular segment. The overall periodicity (width of a left-plus right-eye pair of stripes) averaged 0.88 mm but decreased by a factor of about 2 from center to periphery. This decrease was not accounted for solely by shrinkage of the ipsilateral eye stripes.The flattened cortical reconstruction was transformed back into visual field coordinates, using information about visual field topography obtained from the detailed mapping study of Van Essen et al. (Van Essen, D. C., W. T. Newsome, and J. H. R. Maunsell(1984) Vision Res. 24: 429-448), as well as from more limited mapping done in the same monkey that was used for the reconstruction.In the transformed map, the stripes increased in width about 40-fold from the fovea to the far periphery. As deduced previously (LeVay, S., D. H. Hubel, and T. N. Wiesel (1975) J. Comp. Neurol. 159: 559-576; Hubel, D. H., and D. C., Freeman (1977) Brain Res. 122: 336-343), there were portions of the map in which the stripes followed curves approximating isoeccentricity lines, but this relationship was not very exact or consistent. The pattern of stripes appears to be more meaningfully related to the geometry of the cortical surface. This has significant implications for understanding the developmental mechanisms involved in stripe formation.The striate cortex (area 17, Vl) is the first major site on the visual pathway at which information from the two eyes is integrated. In many species, geniculocortical afferents serving the left and right eyes terminate in layer 4C as alternating bands-ocular dominance stripes. Within a stripe, cells respond only to stimulation of the appropriate eye. By virtue of intracortical projections, which are predominantly vertical, this eye dominates the responses of cells in a slab of tissue extended from pia to white matter-an ocular dominance column (Hubel

These data support a connection between auditory verbal hallucinations and the imprecision of the corollary discharge heralding the sensory consequences of thoughts and actions.

Sensory responses to stimuli that are triggered by a self-initiated motor act are suppressed when compared with the response to the same stimuli triggered externally, a phenomenon referred to as motor-induced suppression (MIS) of sensory cortical feedback. Studies in the somatosensory system suggest that such suppression might be sensitive to delays between the motor act and the stimulus-onset, and a recent study in the auditory system suggests that such MIS develops rapidly. In three MEG experiments, we characterize the properties of MIS, by examining the M100 response from the auditory cortex to a simple tone triggered by a button press. In Experiment 1, we found that MIS develops for zero-delays but does not generalize to non-zero delays. In Experiment 2, we found that MIS developed for 100 ms delays within 300 trials and occurs in excess of auditory habituation. In Experiment 3, we found that unlike MIS for zero-delays, MIS for non-zero delays does not exhibit sensitivity to sensory, delay or motor-command changes. These results are discussed in relation to suppression to self-produced speech and a general model of sensory motor control.