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Abnormal slow wave mapping (ASWAM) : a tool for the investigation of abnormal slow wave activity in the human brain

Abnormal slow wave mapping (ASWAM) : a tool for the investigation of abnormal slow wave activity in the human brain

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WIENBRUCH, Christian, 2007. Abnormal slow wave mapping (ASWAM) : a tool for the investigation of abnormal slow wave activity in the human brain. In: Journal of Neuroscience Methods. 163, pp. 119-127

@article{Wienbruch2007Abnor-11188, title={Abnormal slow wave mapping (ASWAM) : a tool for the investigation of abnormal slow wave activity in the human brain}, year={2007}, doi={10.1016/j.jneumeth.2007.02.018}, volume={163}, journal={Journal of Neuroscience Methods}, pages={119--127}, author={Wienbruch, Christian} }

2007 Abnormal slow wave mapping (ASWAM) : a tool for the investigation of abnormal slow wave activity in the human brain application/pdf Wienbruch, Christian 2011-03-25T09:26:13Z Wienbruch, Christian First publ. in: Journal of Neuroscience Methods 163 (2007), pp. 119 127 2011-03-25T09:26:13Z eng Slow waves in the delta and theta frequency range, normal signs of deactivated networks in sleep stages, are considered 'abnormal' when prominent in the waking state and when generated in circumscribed brain areas. Structural cortical lesions, e.g. related to stroke, tumors, or scars, generate focal electric and magnetic slow wave activity in the penumbra. Focal concentrations of slow wave activity exceeding those of healthy subjects have also been found in individuals suffering from psychiatric disorders without obvious structural brain damage. Hence, identification and mapping of abnormal slow wave activity might contribute to the investigation of cortical indications of psychopathology. Here I propose a method for abnormal slow wave mapping (ASWAM), based on a 5 min resting magnetoencephalogramm (MEG) and equivalent current dipole fitting to sources in the 1-4 Hz frequency band (delta) in anatomically defined cortical regions. The method was tested in a sample of 116 healthy subjects (59 males), with the aim to provide a basis for later comparison with patient samples. As to be expected, delta dipole density was low in healthy subjects. However, its distribution differed between genders with fronto-central>posterior dipole density in male and posterior dominance in female participants, which was not significantly related to either age or head size. Results suggest that this method allows the identification of ASWA, so that comparison against Z-scores from a larger normal control group might assist diagnostic purposes in patient groups. As specific distributions seem to reflect differences between genders, this should be considered also in the analysis of patient samples. deposit-license

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