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At least 217 records · Page 12Linked to original sources
PubMed2004

EEG patterns in persons exposed to ionizing radiation as a result of the chernobyl accident. Part 2: quantitative EEG analysis in patients who had acute radiation sickness.

Cross-sectional quantitative electroencephalogram (qEEG) study (1996-2001) among Chernobyl accident survivors, who had confirmed acute radiation sickness and were irradiated in dose of 1-5 Gy, revealed the neurophysiological markers of ionizing radiation. Neuropsychological markers were: left fronto-temporal dominant frequency reduction; absolute delta-power lateralization to the left (dominant) hemisphere; relative delta-power increase in the fronto-temporal areas; absolute theta-power decrease in the left temporal region; absolute and relative alpha-power diffusive decrease, which may reflect cortico-limbic dysfunction lateralized to the left, dominant hemisphere, with the fronto-temporal cortical and hippocampal damage. Quantitative electroencephalogram proposed for differentiation of radiation and nonradiation brain damages and as a new biological dosymetry method. High radiosensitivity of the brain, neocortex, and dominant hemisphere higher radiosensitivity are discussed.

Brain Mapping↗
PubMed1998

Sleep-wake and eeg effects following adenosine a1 agonism and antagonism: similarities and interactions with sleep-wake and eeg effects following a serotonin reuptake inhibitor in rats.

Adenosine is currently being investigated as a possible mediator of a homeostatic sleep need. Reports from different laboratories suggest that both adenosine A1 agonists and selective serotonin reuptake inhibitors (SSRI) increase deep slow wave sleep (SWS-2) after an interval. In this study, the sleep-wake effects of the adenosine A1 agonist N6-cyclopentyladenosine (CPA) and the SSRI zimeldine are directly compared in the same animals. Since the SWS-2 increase following SSRIs may be secondary to increased adenosine levels during the initially increased waking, it was also investigated whether the adenosine A1 antagonist 8-cyclopentyltheofylline (CPT) would inhibit the SWS-2 increase following the serotonin reuptake inhibitor. Both the adenosine A1 agonist CPA and the SSRI zimeldine increased SWS-2 after an interval. Both drugs increased slow wave activity and decreased 9-20 Hz activity during SWS-2. Both the adenosine A1 antagonist CPT, zimeldine and the two drugs combined initially increased waking and subsequently increased SWS-2 after 2 or 4 h. All treatments increased 2-6 Hz activity in SWS-2 after 2h. Thus, CPT did not antagonize the SWS-2 increase of zimeldine. Based on the sleep and power spectral effects it is suggested that the adenosine A1 antagonist potentiated the zimeldine effect, possibly due to antagonism of adenosine A1 inhibition of serotonin release. The data indicate that the delayed SWS-2 and slow wave activity increases following zimeldine are not due to increased stimulation of adenosine A1 receptors following the initial sleep loss.

Analysis of Variance↗
PubMed2003

Preclinical data base of pharmaco-specific rat EEG fingerprints (tele-stereo-EEG).

An animal model is described which allows for differentiation of 8 common drug categories (antidepresssives, anticonvulsive, analgesic, neuroleptic, stimulant, narcotic, sedative and hallucinogenic drugs) by recording field potentials from stereotactically implanted electrodes and wireless transmission of the data. Four to five representatives of each drug category have been looked at in terms of changes of frequency content with respect to 6 different frequency ranges (delta, theta, alpha1, alpha2, beta1 and beta2). Basically all drugs within one category show a very similar pattern of changes providing a disease specific "fingerprint" of electrical activity. Discriminant analysis provides the statistical fundament for classification of single drugs into disease specific clusters. The data suggest that this type of analysis of the electrical activity of the brain not only allows for classification of unknown compounds but also can accelerate drug development to a major degree. Finally the recognition of new indications of already launched drugs not only becomes feasible but has resulted in filing of new indication patents.

Amphetamines↗