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The study reported by Sharma et al. in this issue of Acta Psychiatrica Scandinavica (1) adds to increasing evidence that the cognitive deficits in schizophrenia are partially attributable to impairments in the coordination of neural activity across the brain, which is necessary to link networks of neurons collectively performing a particular task. The authors used an emotional Stroop task requiring participants to name the colour of a word that has either a positive, negative or neutral emotional valence. Patients were significantly slower than controls, but neither group showed the typical slowing in reaction times to negative words. Interestingly, however, they also examined the coherence (or synchronisation) of activity between two electrodes (at frontal and posterior locations), which reflects the degree to which activity at specific electrode sites form the part of common functional network of activity. The authors report that immediately following stimulus onset in comparison with controls, patients showed reduced connectivity in the delta (1–4 Hz) and theta (4–8 Hz) frequency range, which some researchers have attributed to long-range synchronisation in activity across brain areas. Interestingly, however, during the inter-trial interval (ITI) period when not directly performing the task patients had significantly higher coherence across all frequency ranges.

The results from the study highlight a number of issues that need to be considered in future studies.

First, the patients’ enhanced ITI activity indicates that researchers should exercise caution in the common practise of using this as a baseline from which to measure performance.

Second, the meaning of the ITI enhancement would warrant further investigations. Specifically, it would be important to look at coherence across a wider range of electrodes using data-driven measures (i.e. cluster statistics) during all periods of the task. In this way, the specific networks associated with the task could be identified, and it would be then possible to distinguish whether the ITI activity was related to either (i) compensatory maintenance of the specific task-related network (see for example 2, 3) or (ii) increases in activity in the default-mode network. The latter is a hypothesised network of areas reflecting a state into which the brain slips when not actively engaged in a specific task, which has shown to be increased in patients with schizophrenia and possibly reflect a difficulty in maintaining task-specific activity.

Third, the attenuation of low frequency (delta and theta) coherence in the early stimulus period in patients compared with controls might reflect the early sensory processing deficit reported in the disease (4). This could be investigated further by looking at measures that determine the direction of the connectivity (dynamic causal modelling), i.e. is the coherence driven by early posterior or later frontal activity. Finally, the study highlights the importance of neurophysiological measurements for probing the aetiology of schizophrenia by allowing a more sophisticated understanding of the underlying causes of behaviour deficits. Importantly, a considerable body of research is uncovering the neurochemical basis of oscillatory activity [i.e. network oscillation rely on GABAergic interneuron circuits (5)] which means oscillatory activity may provide a link between behavioural and neurochemical dysfunctions. As a consequence, this area of research holds considerable promise for the development and testing of targeted drug treatments.

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