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Data are presented from a neurological patient (M. P.) with an acquired deficit for naming words with atypical spelling-sound correspondences. In Experiment 1, the degree of consistency within neighborhoods of orthographically similar words had a parallel impact on M. P.'s pronunciations of regular and irregular words and nonwords. This result is more compatible with models in which the same basic procedure, sensitive in a graded fashion to both frequency and consistency, computes pronunciations for all types of letter strings than it is with models postulating separate lexical and nonlexical mechanisms. In Experiment 2, both correct and regularized pronunciations of exception words yielded response times significantly modulated by word frequency, a finding not predicted by any current model. Neuropsychological observations provide an important additional source of evidence regarding models of cognitive function.

We recorded the far-field EEG potential evoked by amplitude modulation of acoustic stimuli (the amplitude modulation following response, AMFR) in adults with developmental dyslexia and in a matched control group of adults with no history of reading problems. The mean AMFR recorded from participants with dyslexia was significantly smaller than that recorded from members of the control group. In contrast, the amplitude of the click-evoked auditory brainstem response (ABR) was not significantly different between participant groups. Also, there was no difference between participant groups in the latency of the AMFR or ABR. The reduced AMFR in listeners with dyslexia may reflect impaired ability of the auditory system to follow rapid changes in stimulus energy, a cue believed to be important in the perception of speech. KEY WORDS: dyslexia, evoked potentials, hearing, amplitude modulation

An experiment investigating two versions of the phonological representations hypothesis is conducted. The study aims to examine whether the accuracy of the phonological representations of words in the mental dictionary can provide explanation for dyslexic children's problems with segmental phonological awareness tasks. In the experiment, the subjects were asked to name pictorial stimuli. Each dyslexic child is assigned to a special unit which is used for teaching children with literacy problems. Findings proved that phonological awareness deficits result from difficulties in encoding or retrieving phonological representations of words.

Developmental dyslexics often complain that small letters appear to blur and move around when they are trying to read. Anatomical, electrophysiological, psychophysical and brain-imaging studies have all contributed to elucidating the functional organization of these and other visual confusions. They emerge not from damage to a single visual relay but from abnormalities of the magnocellular component of the visual system, which is specialized for processing fast temporal information.The m-stream culminates in the posterior parietal cortex, which plays an important role in guiding visual attention. The evidence is consistent with an increasingly sophisticated account of dyslexia that does not single out either phonological, or visual or motor deficits. Rather, temporal processing in all three systems seems to be impaired. Dyslexics may be unable to process fast incoming sensory information adequately in any domain.

The development of literacy skills was studied in 20 dyslexic children (7 years 7 months to 12 years 7 months). At Time 1, the dyslexic children performed worse on tests of reading, spelling, and phonological processing than chronological age-matched normal readers, but their performance was qualitatively similar to that of younger reading age-matched controls. The dyslexic children made poor progress over the following 2 years and, in comparison with reading age controls at Time 2, showed specific difficulties in nonword reading and repetition and made more dysphonetic spelling errors. The authors argue that this typical dyslexic profile becomes more defined with development and provides support for the theory that phonological deficits in dyslexia compromise the development of reading skills.

The temporal-lobe motion-sensitive region V5/MT of the magnocellular visual subsystem shows defective visual motion processing in dyslexic individuals. Functional magnetic resonance imaging shows task-related functional activation of the V5/MT in response to a moving stimulus in normal individuals but not in dyslexic men. However, both groups show similar activation of the V1/V2 and extrastriate cortex in response to a stationary stimulus. This defect in visual motion processing may affect the coordination of temporal interaction with other motion-processing regions in dyslexics.

The right shift theory of handedness predicts two types of dyslexia with different distributions of handedness. This theory when tested on a sample of school students shows that dyslexics with poor phonology are less dextran than controls. Dyslexics, without poor phonology are however, more dextral than controls on measures of hand preference and hand skill. Relatives also differed for handedness as expected, if the relatives of phonological dyslexics are less likely to carry the rs+ gene.

Dyslexics' reading strategy may use visual more than phonological word features. The normally achieving and dyslexic readers were given the Woodcock Word Attack Subtest to measure their phonological skills, plus an orthographic awareness task. While normal readers did better than dyslexics in the word attack subtest, dyslexics scored higher in orthographic awareness. Thus, dyslexic and normal readers may be using different skills to reach their reading objectives.

In the Reicher-Wheeler paradigm, fluent readers can identify letters better when they appear in a word than when they appear in either a pronounceable pseudoword (a lexicality effect) or a single letter (a word-letter effect). It was predicted that if both of these effects involve a lexical factor, then adult acquired dyslexic subjects whose deficit prevents access to visual word form should show disruptions of the normal effects on the Reicher-Wheeler task. The results were that dyslexic subjects as well as matched control subjects showed a lexicality effect; however, while the control subjects showed a normal word-letter effect, the dyslexic subjects showed a reverse letter-superiority effect. Both effects, however, showed a systematic variation: As performance on lexical decision improved, the subjects' performance on words in the Reicher-Wheeler task was better than that for all the other conditions. These subject correlations were replicated by using data from a second lexical decision experiment, which utilized the same words and pseudowords that were used in the Reicher-Wheeler task. In addition, an item analysis showed that the words that the subjects had discriminated correctly in lexical decision showed a significant advantage over those that they had not, as well as an improvement relative to the other conditions. These results suggest that there is a lexical factor underlying the lexicality and word-letter effects, and it is proposed that the abnormal letter-superiority effect can be accounted for as the manifestation of other competing factors.

A peripheral retina, photoreceptor, or transient visual-system deficit has been suggested as a basis for dyslexia. We performed dark adaptation using a Goldmann-Weekers adaptometer on 41 dyslexic readers subjected to the Irlen Differential Perceptual Schedule for the Scotopic Sensitivity Syndrome and on 23 volunteers of normal reading ability, all aged between 10 and 20 years. 12 of the 41 disabled readers examined had abnormally poor dark adaptation at peripheral retinal locations consistent with a rod processing-system deficit.

One of the most intriguing and controversial observations in oculomotor research in recent years is the phenomenon of express saccades in monkeys and man. These are saccades with such short reaction times (100 msec in man, 70 msec in monkeys) that some experts on eye movements still regard them as artifacts or as anticipatory reactions that do not need any further explanation. On the other hand, some research groups consider them not only authentic but also a valuable means of investigating the mechanisms of saccade generation, the coordination of vision and eye movements, and the mechanisms of visual attention. This target article puts together pieces of experimental evidence in oculomotor and related research - with special emphasis on the express saccade - to enhance our present understanding of the coordination of vision, visual attention, and the eye movements subserving visual perception and cognition. We hypothesize that an optomotor reflex is responsible for the occurrence of express saccades, one that is controlled by higher brain functions involved in disengaged visual attention and decision making. We propose a neural network as the basis for more elaborate mathematical models or computer simulations of the optomotor system in primates.

The primary area of difficulty for dyslexic children is the phonological aspect of speech and print. Orthographic aspects of speech and print are a secondary area of difficulty. In a series of tests administered over the course of two years, the ability of dyslexic children to recognize words improved, but their capacity for phonemic analyses did not significantly improve. The reading skills of dyslexic children could be improved through increasing their phonological awareness.

Recently Stuart and Lovegrove questioned the receptor hypothesis of Grosser and Spafford which these authors used to account for the findings that dyslexic individuals have superior peripheral color discrimination to normal readers but also have poorer peripheral brightness discrimination than normal readers. Stuart and Lovegrove hypothesized that dyslexics instead have an impaired transient visual system. The receptor hypothesis is an attempt by Grosser and Spafford to link the functioning of the rods and cones to transient and sustained visual system functioning in a more specific manner than has been tried heretofore by suggesting that, while the parvocellular system is almost entirely fed by cones, both kinds of receptors drive magnocellular cells (but with the rapid onset of early transient system responding being due to the highly light sensitive rods). The rods are proposed to be the receptors initiating the rapid onset of responding in the magnocellular, transient pathway. In dyslexic individuals, they maintain, there are relatively fewer rods to provide for the rapid onset of transient system responses, resulting in a diminished capacity of the transient system to inhibit sustained system activity (as occurs with normal readers). Their receptor hypothesis supplements the concept of transient-vs-sustained system differences.

Speech perception was investigated in a carefully selected group of adult subjects with familial dyslexia. Perception of three synthetic speech continua was studied: /a/ - /[unkeyable]/, in which steady-state spectral cues distinguished the vowel stimuli; /ba/ - /da/, in which rapidly changing spectral cues were varied; and /sta/ - /sa/, in which a temporal cue, silence duration, was systematically varied. These three continua, which differed with respect to the nature of the acoustic cues discriminating between pairs, were used to assess subjects' abilities to use steady state, dynamic, and temporal cues. Dyslexic and normal readers participated in one identification and two discrimination tasks for each continuum. Results suggest that dyslexic readers required greater silence duration than normal readers to shift their perception from /sa/ to /sta/. In addition, although the dyslexic subjects were able to label and discriminate the synthetic speech continua, they did not necessarily use the acoustic cues in the same manner as normal readers, and their overall performance was generally less accurate.

A recurrent connectionist network was trained to output semantic feature vectors when presented with letter strings. When damaged, the network exhibited characteristics that resembled several of the phenomena found in deep dyslexia and semantic-access dyslexia. Damaged networks sometimes settled to the semantic vectors for semantically similar but visually dissimilar words. With severe damage, a forced-choice decision between categories was possible even when the choice of the particular semantic vector within the category was not possible. The damaged networks typically exhibited many mixed visual and semantic errors in which the output corresponded to a word that was both visually and semantically similar. Surprisingly, damaged near the output sometimes caused pure visual errors. Indeed, the characteristic error pattern of deep dyslexia occurred with damage to virtually any part of the network.

The precise neurological deficit which gives rise to dyslexia is not known. Studies have examined abnormalities in the electroencephalograms (EEGs) of dyslexic subjects, but the interpretation of the results remains quite controversial. One of the objections to some published research stems from the fact that dyslexia is often not pure, that is, it often occurs with hyperactivity, motor coordination problems, and difficulties in calculating. It is therefore difficult to attribute observed EEG changes to the dyslexia. To circumvent this problem, six patients were chosen according to strict criteria for pure dyslexia. Along with 10 control subjects, they were given a variety of visual and linguistic tasks while electroencephalographic recordings were being made. While viewing the Necker cube, a visual perception task, both the patients and controls showed greater right hemisphere negativity. However, when linguistic tasks were performed, the dyslexic patients did not show the left hemisphere negativity observed in the normal patients. While all dyslexics showed greater right-sided negativity than normal subjects on linguistic tasks, there was a striking amount of variability between individual dyslexics, and the individual responses were different for the different linguistic tasks. The results also revealed that while the clinical deficit of the dyslexics seemed limited to writing, that EEG abnormalities could be observed for oral tasks as well. This suggests that the abnormal neurological functioning associated with dyslexia may be more extensive than previously thought, and that the deficits in writing become apparent only because that task is especially elaborate and demanding. (Consumer Summary produced by Reliance Medical Information, Inc.)