Absence seizures are the most pure form of generalized epilepsy. They are characterized in the electroencephalogram by widespread bilaterally synchronous spike-wave discharges (SWDs), which are the reflections of highly synchronized oscillations in thalamocortical networks. To reveal network mechanisms responsible for the initiation and generalization of the discharges, we studied the interrelationships between multisite cortical and thalamic field potentials recorded during spontaneous SWDs in the freely moving WAG/Rij rat, a genetic model of absence epilepsy.Nonlinear association analysis revealed a consistent cortical "focus" within the peri-oral region of the somatosensory cortex.The SWDs recorded at other cortical sites consistently lagged this focal site, with time delays that increased with electrode distance (corresponding to a mean propagation velocity of 1.4 m/sec). Intra-thalamic relationships were more complex and could not account for the observed cortical propagation pattern. Cortical and thalamic sites interacted bi-directionally, whereas the direction of this coupling could vary throughout one seizure. However, during the first 500 msec, the cortical focus was consistently found to lead the thalamus.These findings argue against the existence of one common subcortical pacemaker for the generation of generalized spikewave discharges characteristic for absence seizures in the rat. Instead, the results suggest that a cortical focus is the dominant factor in initiating the paroxysmal oscillation within the corticothalamic loops, and that the large-scale synchronization is mediated by ways of an extremely fast intracortical spread of seizure activity. Analogous mechanisms may underlie the pathophysiology of human absence epilepsy.

Since the first reports of neurofeedback treatment in Attention Deficit Hyperactivity Disorder (ADHD) in 1976, many studies have investigated the effects of neurofeedback on different symptoms of ADHD such as inattention, impulsivity and hyperactivity. This technique is also used by many practitioners, but the question as to the evidence-based level of this treatment is still unclear. In this study selected research on neurofeedback treatment for ADHD was collected and a meta-analysis was performed. Both prospective controlled studies and studies employing a pre- and post-design found large effect sizes (ES) for neurofeedback on impulsivity and inattention and a medium ES for hyperactivity. Randomized studies demonstrated a lower ES for hyperactivity suggesting that hyperactivity is probably most sensitive to nonspecific treatment factors. Due to the inclusion of some very recent and sound methodological studies in this meta-analysis, potential confounding factors such as small studies, lack of randomization in previous studies and a lack of adequate control groups have been addressed, and the clinical effects of neurofeedback in the treatment of ADHD can be regarded as clinically meaningful. Three randomized studies have employed a semi-active control group which can be regarded as a credible sham control providing an equal level of cognitive training and client-therapist interaction. Therefore, in line with the AAPB and ISNR guidelines for rating clinical efficacy, we conclude that neurofeedback treatment for ADHD can be considered "Efficacious and Specific" (Level 5) with a large ES for inattention and impulsivity and a medium ES for hyperactivity.

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