Ken I. McAnally

Can contrast sensitivity functions in dyslexia be explained by inattention rather than a magnocellular deficit

We examined whether data demonstrating contrast sensitivity losses in dyslexia that have been interpreted as evidence for loss of magnocellular visual function could be explained by inattention. Computer simulations of observers with poor concentration yielded inflated estimates of threshold that were a constant proportion of the true threshold across spatial frequencies. Data from many, but not all, studies supporting the magnocellular deficit theory are well described by these simulations, which predicted no interaction between observer group and spatial frequency. Some studies have reported significant interactions, but suffer from statistical deficiencies. This compromises some of the evidence for a magnocellular deficit in dyslexia derived from studies of threshold contrast sensitivity.

Contrast sensitivity in subgroups of developmental dyslexia

It has been proposed that developmental dyslexia is associated with a deficit in the magnocellular pathway of the visual system. Other research focuses upon the heterogeneous nature of developmental dyslexia, and evidence that subgroups of dyslexia may be identified based on selective deficits in specific component reading skills. This study tested the hypothesis that visual processing deficits may be present in different subgroups of developmental dyslexia by comparing the visual contrast sensitivity of three subgroups of dyslexic children (phonological, surface and mixed) and controls. The stimulus designed to measure magnocellular visual function was a low spatial frequency Gaussian blob, flickered sinusoidally at a temporal frequency of 8.33 Hz. The control stimulus, designed to measure parvocellular visual function, was a relatively high spatial frequency Gaussian windowed grating (8 c/deg) slowly ramped on and off. There were no significant differences between the groups of dyslexic and control children in contrast sensitivity to either stimulus. The findings do not support the existence of a magnocellular system deficit in dyslexia.

Lapses of concentration and dyslexic performance on the Ternus task

Recently, Cestnick and Coltheart (Cognition 71 (1999) 231) have reported evidence of abnormal performance on the Ternus apparent motion task in dyslexics. We demonstrate that some aspects of their data may be accounted for by more frequent lapses of concentration in the dyslexic group than in controls. We then report on a study in which a modification of the Ternus procedure was employed to simplify the task and to control for the effects of inattention. The results suggest that dyslexics do genuinely differ from normal readers in their perceptual processing.

A gated differential amplifier for recording physiological responses to electrical stimulation

Artifact from electrical stimulation imposes a problem for the recording of physiological responses to electrical stimulation. Here we describe a simple, low-cost, gated differential amplifier for the recording of physiological responses to electrical stimulation. The gain of the amplifier is set to 1 during electrical stimulation by setting the gate input to a high logic state to avoid overloading of the amplifier by the artifact. Following electrical stimulation, the gate input is set to a low logic state, resulting in a gain of 1000 for frequencies between 300 Hz and 25 kHz (-3 dB points). The gain at low frequencies (0-0.2 Hz) is held constant at 1 to avoid transients in the output signal arising from changes in gain at these frequencies. The gain of the amplifier following stimulation (gate low) was independent of the magnitude of the artifact and was therefore suitable for the measurement of neural field potentials with low impedance electrodes.

Hair cell mediated responses of the auditory nerve to sinusoidal electrical stimulation of the cochlea in the cat.

Electrical stimulation of the cochlea elicits discharges of auditory nerve fibres which are mediated by the electrical or mechanical stimulation of inner hair cells (electrophonic responses). In order to isolate hair-cell mediated responses from those elicited by electrical stimulation of the nerve, the compound action potential (CAP) evoked by an acoustic probe was forward-masked by sinusoidal monopolar, or localized bipolar electrical stimulation of the base of the cochlea. The degree of masking of a given probe estimated the synaptically mediated response to the masker of the population of auditory nerve fibres innervating the cochlear location tuned to the probe. There was a peak of masking for probes close to the frequency of the electrical stimulus, suggesting a spatial tuning of the hair cell mediated response along the cochlea. This is consistent with excitation of the inner hair cells by a propagating mechanical response which is generated within the electrical field at the base of the cochlea. Furthermore, tuning curves for masking of a given probe were sharply tuned to electrical stimulation close to the probe frequency. This masking was not dependent upon the presence of functional outer hair cells close to the electrodes, suggesting an alternate transduction of electrical to mechanical energy.

Stimulation of residual hearing in the cat by pulsatile electrical stimulation of the cochlea

Electrical stimulation of the cochlea may excite residual inner hair cells, either by direct electrical stimulation or through a mechanical event. Hair cell mediated responses of the auditory nerve to electrical stimulation were estimated from forward masking of the compound action potential evoked by an acoustic probe. Masking by a fixed electrical masker peaked for probes equal in frequency to the pulse repetition rate and its second harmonic, suggesting a spatially tuned profile of excitation within the cochlea. Furthermore, the tuning curves for masking of a fixed acoustic probe peaked for masker pulse rates close to the frequency of the probe. A secondary peak of masking was commonly seen for electrical stimulation at one half of the probe frequency, suggesting masking of the probe by the second harmonic of the electrical stimulus. These results suggest that pulsatile stimulation at the base of the cochlea generates a spectrally rich mechanical disturbance in which each component propagates to its place of resonance in the cochlea.

A Test of the magnocellular deficit theory of dyslexia in an adult sample

An influential theory of dyslexia is based on the premise that individuals with the disorder have impaired sensitivity to rapidly changing stimuli in the visual and auditory modalities, due to a dysfunction in the magnocellular channel of the visual system and its analogue in the auditory pathway. The deficit in the auditory system is thought to cause difficulties in the segmentation of speech and the formation of accurate phonological representations, leading to problems in making the grapheme–phoneme correspondences necessary for reading. In a sample of 13 adults with a history of severe reading difficulty and 18 controls, visual contrast thresholds were measured in response to an 8-Hz flickering Gaussian blob as well as a slowly modulated 8 cycles/deg Gaussian windowed grating. Auditory thresholds were measured in response to a 4-s burst of white noise, the 2nd or 3rd second of which was amplitude modulated at 100 Hz or 1 Hz. The adult reading difficulty group exhibited normal thresholds to rapidly changing stimuli in both modalities and to the slowly modulated visual stimulus, but some showed reduced sensitivity to the 1-Hz amplitude-modulated auditory stimulus. Sensitivity to amplitude modulation at slower rates has been shown to be important for segmentation of the speech stream and so may be implicated in the reading difficulty of the affected individuals. A magnocellular deficit cannot explain this impaired sensitivity, which may be the result of a reduced echoic memory span.

Estimating mechanical responses to pulsatile electrical stimulation of the cochlea

This study estimated the mechanical response of the cochlea to pulsatile electrical stimulation of the scala tympani of the cat. The auditory nerve compound action potential evoked by an acoustic probe was forward-masked by a train of charge-balanced biphasic current pulses. Masking as a function of probe frequency reflected the excitation pattern of the response to the masker and resembled the spectrum of the electrical stimulus. Both pulse rate and pulse width influenced the degree of masking. The vibration of a region of the basilar membrane was estimated by recording the local cochlear microphonic evoked by biphasic pulses. The amplitude of the cochlear microphonic was proportional to the amplitude of the spectral component of the electrical stimulus to which the local cochlear microphonic was tuned. These results are consistent with the generation of a mechanical response to the electrical stimulus.

Acoustic and electric forward-masking of the auditory nerve compound action potential: evidence for linearity of electro-mechanical transduction.

We investigated electro-mechanical transduction within the cochlea by comparing masking of the auditory nerve compound action potential (CAP) by acoustical and electrical maskers. Forward-masking of the CAP reflects the response to the masker of the cochlear location tuned to the probe. Electrical stimulation was delivered through bipolar stimulating electrodes within the basal turn of the scala tympani. The growth of masking of high-frequency probes which excite cochlear locations close to the stimulating electrodes was similar for both acoustic and electrical maskers, suggesting a linear transduction of electrical energy to mechanical energy. Exposure to intense acoustic stimulation caused an equal loss of sensitivity to acoustic and electrical maskers. Masking of lower-frequency probes by electrical maskers increased rapidly with masker current, suggesting the direct electrical stimulation of neural elements. This masking was reduced by the administration of strychnine suggesting a contribution by the efferents towards masking of these low-frequency probes.

Source monitoring and proneness to auditory-verbal hallucinations: A signal detection analysis

Introduction. It has been suggested that a bias to misattribute self-generated thoughts to a nonself source underlies the experience of auditory-verbal hallucinations (AVH). We tested this hypothesis with healthy participants prone or not prone to AVH. Method. Participants (N=133) were presented with 96 words for subsequent recognition (half positively, half negatively valenced). For self-generated trials, participants generated a sentence containing the word. For other-generated trials, participants heard a prerecorded sentence containing the word. At test, studied words were re-presented visually, intermixed with 96 matched lures. Participants indicated the study status (old or new) and source (self or other) for each item. Sensitivity and bias measures were derived for item and source memory using signal detection theory. The 20 participants scoring highest on questions relating to AVH from the revised Launay-Slade Hallucination Scale formed the high-AVH group and the 20 scoring lowest formed the low-AVH group. Results. ANOVAs revealed no significant differences between the two participant groups in sensitivity or bias of source memory, regardless of item valence. There was a trend for the sensitivity of item memory to be lower in the high-AVH group, compared with the low-AVH group. The bias of item memory was not significantly different between groups. Conclusions. Although we found no evidence that source-monitoring problems underlie the experience of AVHs in the general population, we recommend that signal detection measures be applied in future investigations of source monitoring in at-risk and clinical populations.