1.7.3.3 ‘Magnosensitive’ tasks
4.6 Neural disorganization hypothesis
The results of this series of studies (I-IV) showed that develop-mentally dyslexic readers, as a group, suffer from a generalized impairment of temporal acuity, which does not support the sug-gestions that the deficits in developmental dyslexia are restrict-ed to the phonological or linguistic domains. Nor were the diffi-culties restricted to or most pronounced in modalities directly involved in reading (visual, auditory, audiovisual). However, the results do not support a purely perceptual impairment as a suffi-cient causal factor for dyslexia either, since the reading groups’
temporal acuities overlapped to a great extent, and temporal acu-ity thresholds could not be used in fully discriminating the read-ing groups. Not every dyslexic reader had poor temporal acuity but, generally, of the fluent readers only those with suggestive difficulties in some cognitive processes were misclassified as dyslexics. Also, the temporal acuity impairment was not confined to unimodal difficulties, but was observed in the crossmodal tasks in a way that could not fully be explained by the unimodal (per-ceptual) difficulties. Our results agree therefore better with mod-ified versions of the magnocellular impairment hypothesis, de-scribed in the introduction. According to these hypotheses, the magnocellular deficit may result in impaired perceptual tempo-ral acuity, but the underlying neutempo-ral deficit also affects, or is re-lated to, other more central functions, which may cause the dys-lexic difficulties more directly. Accordingly, an association was found between temporal acuity and phonological processing.
A multi-factor model was suggested in Study II (Virsu, 1998).
This model explains developmental dyslexia as a result of un-derdeveloped or deteriorated connectivity of central neurons in neural networks, which can be magnocellular or not. The signal-to-noise (S/N) ratio of the responses to rapidly changing percep-tual input is assumed to be defective. This does not result from increased latency or decreased response strength but is
suggest-ed to result from temporal diffusion of input activation, evoksuggest-ed by rapid changes. Although the total amount of neural energy contained in input signals can be the same, the response energy may spread differently in time. When the temporal dispersion increases, the signal amplitude decreases, and vice versa.
The rationale of the model is as follows. Multiple impulses converge into the same neuron or their parallel set at the same neuronal level, from many cells. The summation of these input activities, within a limited time window, evokes the responses of the specific neuron or set of neurons. Following a brief stimulus pulse or a sudden change in stimulation, the activation travel-ling several routes reaches the target set with some temporal dis-persion. In disorganized neural networks, as is suggested to be the case in developmental dyslexia, temporal dispersion is greater, and the signal energy of the evoked response distributes widely in time with a low amplitude and poor S/N ratio. This process of smoothing affects the onset and offset of every signal but is pro-nounced with rapidly presented stimulus onsets and offsets, and for brief stimuli in which the response S/N ratio decreases more as compared to long stimuli. Long sequences of brief stimuli, such as those used in the TPA tasks, which follow each other at short intervals in time, near threshold, are very sensitive to reveal the occurrence of the smoothing. Such a smoothing is assumed to cause a decrease of cognitive temporal acuity. The temporal spread in onset and offset signal activity, and the resulting de-crease in response S/N ratio to brief stimuli has been observed directly in developmentally dyslexic readers with evoked re-sponse techniques, like ERPs (McAnally & Stein, 1996) and MEG responses (Nagarajan et al., 1999).
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Acknowledgements
I wish to thank my supervisors Veijo Virsu and Elisabet Service;
my close collaborators Pekka Lahti-Nuuttila, Seppo Salminen, and Henna Oksanen; Jaana Tomma-Halme and other members of our research team; Will Hennah; Teija Kujala, Pekka Niemi, Timo Ahonen, Kimmo Alho, and Heikki Summala; Neuropsy-chology research group; Department of PsyNeuropsy-chology; Finnish Graduate School of Neuroscience; Markku, Paula, and Matti Laa-sonen; Helvi Poskiparta, Kirsi Saurén, Ulla Peltonen, Jaana Lind-holm, Rami Salle, Kantavat, and all my dearest friends.
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