Ongoing EEG artifact correction using blind source separation.

OBJECTIVE: Analysis of the electroencephalogram (EEG) for epileptic spike and seizure detection or brain-computer interfaces can be severely hampered by the presence of artifacts. The aim of this study is to describe and evaluate a fast automatic algorithm for ongoing correction of artifacts in continuous EEG recordings, which can be applied offline and online. METHODS: The automatic algorithm for ongoing correction of artifacts is based on fast blind source separation. It uses a sliding window technique with overlapping epochs and features in the spatial, temporal and frequency domain to detect and correct ocular, cardiac, muscle and powerline artifacts. RESULTS: The approach was validated in an independent evaluation study on publicly available continuous EEG data with 2035 marked artifacts. Validation confirmed that 88% of the artifacts could be removed successfully (ocular: 81%, cardiac: 84%, muscle: 98%, powerline: 100%). It outperformed state-of-the-art algorithms both in terms of artifact reduction rates and computation time. CONCLUSIONS: Fast ongoing artifact correction successfully removed a good proportion of artifacts, while preserving most of the EEG signals. SIGNIFICANCE: The presented algorithm may be useful for ongoing correction of artifacts, e.g., in online systems for epileptic spike and seizure detection or brain-computer interfaces.

[Relationship of polymorphism in CYP2C9 to genetic susceptibility to diclofenac-induced influenza-virus-associated encephalopathy].

The mechanism causing influenza-virus-associated encephalopathy is unclear, even though diclofenac metabolites may induce this pathogenesis. CYP2C9 is known as the major cytochrome P450 gene product that catalyzes diclofenac in human liver. It is uncertain whether the mutation of CYP2C9 is associated the pharmacologic effects of diclofenac in influenza infection. Therefore, we applied a simple and rapid procedure involving real-time fluorescence allele-specific PCR(TaqMan-ASA) assay and denaturing HPLC assay to detect the mutation of CYP2C9 gene. A single-base mutation in the CYP2C9 gene was found in one of thirty subjects in the healthy population. We suggest that this mutation in the CYP2C9 gene may be related to diclofenac-induced influenza-virus-associated encephalopathy.

Enhanced auditory brainstem response and parental bonding style in children with gastrointestinal symptoms.

BACKGROUND: The electrophysiological properties of the brain and influence of parental bonding in childhood irritable bowel syndrome (IBS) are unclear. We hypothesized that children with chronic gastrointestinal (GI) symptoms like IBS may show exaggerated brainstem auditory evoked potential (BAEP) responses and receive more inadequate parental bonding. METHODOLOGY/PRINCIPAL FINDINGS: Children aged seven and their mothers (141 pairs) participated. BAEP was measured by summation of 1,000 waves of the electroencephalogram triggered by 75 dB click sounds. The mothers completed their Children's Somatization Inventory (CSI) and Parental Bonding Instrument (PBI). CSI results revealed 66 (42%) children without GI symptoms (controls) and 75 (58%) children with one or more GI symptoms (GI group). The III wave in the GI group (median 4.10 interquartile range [3.95-4.24] ms right, 4.04 [3.90-4.18] ms left) had a significantly shorter peak latency than controls (4.18 [4.06-4.34] ms right, p = 0.032, 4.13 [4.02-4.24] ms left, p = 0.018). The female GI group showed a significantly shorter peak latency of the III wave (4.00 [3.90-4.18] ms) than controls (4.18 [3.97-4.31] ms, p = 0.034) in the right side. BAEP in the male GI group did not significantly differ from that in controls. GI scores showed a significant correlation with the peak latency of the III wave in the left side (rho = -0.192, p = 0.025). The maternal care PBI scores in the GI group (29 [26]-[33]) were significantly lower than controls (31 [28.5-33], p = 0.010), while the maternal over-protection PBI scores were significantly higher in the GI group (16 [12]-[17]) than controls (13 [10.5-16], p = 0.024). Multiple regression analysis in females also supported these findings. CONCLUSIONS: It is suggested that children with chronic GI symptoms have exaggerated brainstem responses to environmental stimuli and inadequate parental behaviors aggravate these symptoms.