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BackgroundT. J. Crow suggested that the genetic variance associated with the evolution in Homo sapiens of hemispheric dominance for language carries with it the hazard of the symptoms of schizophrenia. Individuals lacking the typical left hemisphere advantage for language, in particular for phonological components, would be at increased risk of the typical symptoms such as auditory hallucinations and delusions.Methodology/Principal FindingsTwelve schizophrenic patients treated with low levels of neuroleptics and twelve matched healthy controls participated in an event-related potential experiment. Subjects matched word-pairs in three tasks: rhyming/phonological, semantic judgment and word recognition. Slow evoked potentials were recorded from 26 scalp electrodes, and a laterality index was computed for anterior and posterior regions during the inter stimulus interval. During phonological processing individuals with schizophrenia failed to achieve the left hemispheric dominance consistently observed in healthy controls. The effect involved anterior (fronto-temporal) brain regions and was specific for the Phonological task; group differences were small or absent when subjects processed the same stimulus material in a Semantic task or during Word Recognition, i.e. during tasks that typically activate more widespread areas in both hemispheres.Conclusions/SignificanceWe show for the first time how the deficit of lateralization in the schizophrenic brain is specific for the phonological component of language. This loss of hemispheric dominance would explain typical symptoms, e.g. when an individual's own thoughts are perceived as an external intruding voice. The change can be interpreted as a consequence of “hemispheric indecision”, a failure to segregate phonological engrams in one hemisphere.

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Brain plasticity was investigated in 14 Italian children affected by developmental dyslexia after 6 months of phonological training. The means used to measure language reorganization was the recognition potential, an early wave, also called N150, elicited by automatic word recognition. This component peaks over the left temporo-occipital cortex and its amplitude depends on linguistic expertise. N150 elicited by written words was measured both in dyslexic children before and after training and in a sample of matched normal readers during phonological, semantic and orthographic tasks. After training, dyslexic children increased their reading speed. Normal readers showed a typical left posterior N150, whereas in dyslexic children it was equally distributed across hemispheres before and shifted to left posterior sites after training. In addition, dyslexics' left posterior N150 asymmetry on the phonological task after training was significantly correlated with reading speed improvement, that is, those children who showed the greatest left shift in phonological N150 also had the greatest reading speed improvement. Source localization of the N150 component was made with both the Standard Low Resolution Electromagnetic Tomography software and the classical dipole analysis method termed Brain Electrical Source Analysis. The N150 generator lies in the left occipito-temporal cortex (Brodmann areas 39, 37 and 19) in good readers, but in right homologous areas in dyslexic children before training. After the treatment, the dyslexics' main N150 generator shifted to the left occipito-inferotemporal cortex (namely Brodmann areas 37 and 19) with small differences between tasks. The two source location methods provided consistent, converging solutions. Results add to the current literature on the phonological hypothesis of dyslexia by showing hemispheric reorganization of linguistic networks at the level of early word recognition potential. Furthermore, the present work is the first to investigate brain reorganization in a regular/transparent language like Italian.

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The present study used delta EEG band to test the hypothesis of a cerebral maturational delay and a functional altered cerebral asymmetry for phonological processing in dyslexic children. A group of 14 children with dyslexia and 28 matched controls participated in a linguistic paradigm in which the same words were processed in three tasks: phonological, semantic, and orthographic. Delta amplitude was computed as an index of cortical inhibition in four different phases of word processing. In anterior sites, controls showed left activation (reduced delta) during the phonological task and bilateral activation in the other two tasks. Conversely, children with dyslexia showed greater overall delta amplitude, indexing a cerebral maturation delay and an altered language laterality pattern. In the phonological task they had larger left anterior delta (inhibition of left frontal linguistic locations) and smaller left posterior delta amplitude (activation of left posterior sites silent in controls). Results support the phonological deficit hypothesis of developmental dyslexia and the validity of EEG delta band as functional and clinical measure of language laterality.

BackgroundDespite the consistent information available on the physiological changes induced by head down bed rest, a condition which simulates space microgravity, our knowledge on the possible perceptual-cortical alterations is still poor. The present study investigated the effects of 2-h head-down bed rest on subjective and cortical responses elicited by electrical, pain-related somatosensory stimulation.Methodology/Principal FindingsTwenty male subjects were randomly assigned to two groups, head-down bed rest (BR) or sitting control condition. Starting from individual electrical thresholds, Somatosensory Evoked Potentials were elicited by electrical stimuli administered randomly to the left wrist and divided into four conditions: control painless condition, electrical pain threshold, 30% above pain threshold, 30% below pain threshold. Subjective pain ratings collected during the EEG session showed significantly reduced pain perception in BR compared to Control group. Statistical analysis on four electrode clusters and sLORETA source analysis revealed, in sitting controls, a P1 component (40–50 ms) in the right somatosensory cortex, whereas it was bilateral and differently located in BR group. Controls' N1 (80–90 ms) had widespread right hemisphere activation, involving also anterior cingulate, whereas BR group showed primary somatosensory cortex activation. The P2 (190–220 ms) was larger in left-central locations of Controls compared with BR group.Conclusions/SignificanceHead-down bed rest was associated to an overall decrease of pain sensitivity and an altered pain network also outside the primary somatosensory cortex. Results have implications not only for astronauts' health and spaceflight risks, but also for the clinical aspects of pain detection in bedridden patients at risk of fatal undetected complications.