Speech stimuli give rise to neural activity in the listener that can be observed as waveforms using magnetoencephalography. Although waveforms vary greatly from trial to trial due to activity unrelated to the stimulus, it has been demonstrated that spoken sentences can be discriminated based on theta-band (3-7 Hz) phase patterns in single-trial response waveforms. Furthermore, manipulations of the speech signal envelope and fine structure that reduced intelligibility were found to produce correlated reductions in discrimination performance, suggesting a relationship between theta-band phase patterns and speech comprehension. This study investigates the nature of this relationship, hypothesizing that theta-band phase patterns primarily reflect cortical processing of low-frequency (<40 Hz) modulations present in the acoustic signal and required for intelligibility, rather than processing exclusively related to comprehension (e.g., lexical, syntactic, semantic). Using stimuli that are quite similar to normal spoken sentences in terms of low-frequency modulation characteristics but are unintelligible (i.e., their time-inverted counterparts), we find that discrimination performance based on theta-band phase patterns is equal for both types of stimuli. Consistent with earlier findings, we also observe that whereas theta-band phase patterns differ across stimuli, power patterns do not. We use a simulation model of the single-trial response to spoken sentence stimuli to demonstrate that phase-locked responses to low-frequency modulations of the acoustic signal can account not only for the phase but also for the power results. The simulation offers insight into the interpretation of the empirical results with respect to phase-resetting and power-enhancement models of the evoked response.

Speech elicits a phase-locked response in the auditory cortex that is dominated by theta (3–7 Hz) frequencies when observed via magnetoencephalography (MEG). This phase-locked response is potentially explained as new phase-locked activity superimposed on the ongoing theta oscillation or, alternatively, as phase-resetting of the ongoing oscillation. The conventional method used to distinguish between the two hypotheses is the comparison of post- to prestimulus amplitude for the phase-locked frequency across a set of trials. In theory, increased amplitude indicates the presence of additive activity, while unchanged amplitude points to phase-resetting. However, this interpretation may not be valid if the amplitude of ongoing background activity also changes following the stimulus. In this study, we employ a new approach that circumvents this problem. Specifically, we utilize a fine-grained time–frequency analysis of MEG channel data to examine the co-modulation of amplitude change and phase coherence in the post-stimulus theta-band response. If the phase-locked response is attributable solely to phase-resetting of the ongoing theta oscillation, then amplitude and phase coherence should be uncorrelated. In contrast, additive activity should produce a positive correlation. We find significant positive correlation not only during the onset response but also throughout the response period. In fact, transient increases in phase coherence are accompanied by transient increases in amplitude in accordance with a “signal plus background” model of the evoked response. The results support the hypothesis that the theta-band phase-locked response to attended speech observed using MEG is dominated by additive phase-locked activity.

We examine lateralization in the evoked magnetic field response to a click stimulus, observing that lateralization effects previously demonstrated for tones, noise, frequency modulated sweeps and certain syllables are also observed for (acoustically simpler) clicks. These effects include a difference in the peak latency of the M100 component of the evoked field waveform such that the peak consistently appears earlier in the right hemisphere, as well as rightward lateralization of field amplitude during the rise of the M100 component. Our review of previous findings on M100 lateralization, taken together with our data on the click-evoked response, leads to the hypothesis that these lateralization effects are elicited by stimuli containing a sharp sound energy onset or acoustic transition rather than specific types of stimuli. We argue that both the latency and the amplitude lateralization effects have a common origin, namely, hemispheric asymmetry in the amplitude of the magnetic field generated by one or more sources active during the M100 rise. While anatomical asymmetry cannot be excluded as the cause of the amplitude difference, we propose that the difference reflects a rightward asymmetry in the processing of sound energy onsets that potentially underlies the lateralization of several functions.

The spatial frequency hypothesis contends that performance differences between the hemispheres on various visuospatial tasks are attributable to lateralized processing of the spatial frequency content of visual stimuli. Hellige has proposed that such lateralization could arise during infant development from the earlier maturation of the right hemisphere combined with the increasing sensitivity of the visual system to high spatial frequencies. This proposal is intuitively appealing but lacks an explicit theory with respect to the underlying visual system biology. In this paper, we develop such a theory based on knowledge of visual system processing and development. We then translate our theory into a computational model that serves as the basis for a series of development simulations. We find that the simulations produce spatial frequency lateralization effects consistent with those observed empirically. We relate the nature of the neural asymmetry implied by our theory to empirical findings on visual pathway bias and the relative spatial frequency lateralization effect.

While various functional and cognitive capabilities appear to differ in both degree and direction of lateralisation, the factors underlying these differences are poorly understood. It is hypothesised that time-varying asymmetry in plasticity between homologous regions in the cerebral hemispheres, coupled with asynchronous development of capabilities, may account for the lateralisation differences in two ways. First, the lateralisation of an earlier acquired behaviour may influence the lateralisation of a later developing behaviour. Second, temporal changes in the underlying plasticity asymmetry may also result in differences in lateralisation for functions acquired at different times. This study examines the plausibility of these hypotheses using a computational neural network model consisting of two interacting hemispheric regions and capable of learning two tasks. Lateralisation was measured while learning rates for the two hemispheres were changed independently over time to create a time-varying asymmetry in plasticity, and while the initiation of learning for each task was also varied over time. The results suggest that the lateralisation of one behaviour/function can affect the lateralisation of another in a fundamental way, and that experimentally observed temporal differences in hemispheric development can result in functional lateralisation differences, providing support for past theories of lateralisation based on asymmetric hemispheric growth and maturation.