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Previous research on working memory (WM) in children with poor mathematical skills has yielded heterogeneous results, possibly due to inconsistent consideration of the IQ-achievement discrepancy and additional reading and spelling difficulties. To examine the impact of both, the WM of 68 average-achieving and 68 low-achieving third-graders in mathematics was assessed. Preliminary analyses showed that poor mathematical skills were associated with poor WM. Afterwards, children with isolated mathematical difficulties were separated from those with additional reading and spelling difficulties. Half of each group fulfilled the IQ-achievement discrepancy, resulting in a 2 (additional reading and spelling difficulties: yes/no) by 2 (IQ-achievement discrepancy: yes/no) factorial design. Analyses revealed that not fulfilling the IQ achievement discrepancy was associated with poor visual WM, whereas additional reading and spelling difficulties were associated with poor central executive functioning in children fulfilling the IQ-achievement discrepancy. Therefore, WM in children with poor mathematical skills differs according to the IQ-achievement discrepancy and additional reading and spelling difficulties.
Current theories of schizophrenia suggest that the pathophysiology of the disorder may be the result of a deficit in the coordination of neural activity within and between areas of the brain, which may lead to impairments in basic cognitive functions such as contextual disambiguation and dynamic grouping (Phillips and Silverstein, 2003). This notion has been supported by recent studies showing that patients with schizophrenia are characterized by reduced synchronous, oscillatory activity in the gamma-frequency band during sensory processing (Spencer et al. 2003, Green et al. 2003, Wynn et al. 2005). However, it is currently unclear to what extent high-frequency gamma-band oscillations (> 60 Hz) contribute to impaired neural synchronization as research has so far focussed on gamma-band oscillations between 30 and 60 Hz. In addition, it is not known whether deficits in high-frequency oscillations are already present at the onset of the disorder and to what extent reductions may be related to the confounding influence of antipsychotic medication. Finally, the neural generators underlying impairments in synchronous oscillatory activity in schizophrenia have not been investigated yet. To address these questions, we recorded MEG activity during a visual closure task (Mooney faces task) in medicated chronic schizophrenia patients, drug-naive first-episode schizophrenia patients and healthy controls. MEG data were analysed for spectral power between 25 and 150 Hz, and beamforming techniques were used to localize the sources of oscillatory gamma-band activity. In healthy controls, we observed that the processing of Mooney faces was associated with sustained high-frequency gamma-band activity (> 60 Hz). A time-resolved analysis of the neural generators underlying perceptual closure revealed a network of distributed sources in occipito-temporal, parietal and frontal regions, which were differentially activated during specific time intervals. In chronic schizophrenia patients, we found a pronounced reduction of high-frequency gamma-band oscillatory activity that was accompanied by an impairment in perceptual organization and involved reduced source power in various brain regions associated with perceptual closure. First-episode patients were also characterized by a deficit in high-frequency gamma-band activity and reductions of source power in multiple areas; these impairments, however, were less pronounced than in chronic patients. Regarding behavioral performance, first-episode patients were not impaired in their ability to detect Mooney faces, but exhibited a loss in specificity of face detection. In conclusion, our results suggest that schizophrenia is associated with a widespread reduction in high-frequency oscillations that indicate local network abnormalities. These dysfunctions are independent of medication status and already present at illness onset, suggesting a possible progressive deficit during the course of the disorder.