The relationship between neuron activity and cortical steady potentials.
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Biomedical subjects
Publications and source records attributed to G H Fromm.
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Since Berger's discovery of the electroencephalogram (EEG), its analysis has been generally restricted to the visual range (upmost 100Hz) and has ignored higher frequency components. One reason should be that there are no reliable methods to distinguish the brain potentials from muscle activity. We have introduced fluctuation analysis, which is popular method especially in the field of basic physiology to clinical electrophysiology. In our previous study, it was declared that power spectral density (PSD) of human high frequency EEG was composed of double Lorentzians and vanished into white level within 1kHz. Then the purpose of this study is to elucidate the "Automated Fluctuation Analysis," which enables us to evaluate these higher frequency components and its physiological meaning especially focused on conscious level from wakefulness to sleep stage 1. Seventy-four scalp recording EEGs in twenty normal subjects were studied. In short, "Automated Fluctuation Analysis" is made of three steps: amplification of EEG signal, A/D conversion and Fast Fourier Transform by signal processor and extraction of Lorentzian parameters. PSD of high frequency EEG was displayed on log-log graph and the algorithm fit to the following Lorentzian formula were mathematically based on Brown & Dennis. S(f) = S1/[1+(f/fc1)2]+S2/[1+(f/fc2)2], where S(f) is PSD (mu V2/Hz) at each frequency (f;Hz), S1 and S2 are the plateau level or zero-frequency power of the initial and second Lorentz, and fc1 and fc2 are the corner or half-power frequency of the initial and second Lorentz, respectively. As results, during wakefulness the PSD of high frequency EEG activity was composed of double Lorentzian fluctuations and the power distribution of S1 value in topographical display was frontal dominant. This pattern of S1 value disappeared and S2 value became lower during sleepiness and the second Lorentz disappeared during sleep.
The effect of the experimental antiepileptic gamma-aminobutyric acid (GABA) agonist drug progabide, [alpha-(chloro-4-phenyl)fluor-5-hydroxy-2-benzilideneamino]-4-buty ramide, on the trigeminal complex of cats was compared with the effect of established antiepileptic drugs and with the effect of various GABA agonists and antagonists. Intravenous administration of 10-40 mg/kg progabide depressed excitatory transmission and descending periventricular inhibition, similar to carbamazepine and phenytoin. However, progabide depressed, rather than facilitated, segmental inhibition. The serum levels of progabide were comparable with those in patients receiving long-term treatment with progabide. The GABA antagonist bicuculline had the opposite effect of progabide on our experimental model, but the other GABA agonists THIP (4,5,6,7-tetrahydroisoxazolo-5,4-C-pyridine-3-ol) and muscimol did not have the same effects as progabide. THIP had no effect on excitatory transmission, periventricular inhibition, or segmental inhibition, whereas muscimol facilitated periventricular inhibition and sometimes segmental inhibition and had no effect on excitatory transmission. Our experiments thus indicate that progabide, but not THIP or muscimol, should have antiepileptic properties, in agreement with the clinical experiences that have been reported. The reason for the differential effect of these three GABA agonists remains to be elucidated.
The effect of the experimental antiepileptic drug zonisamide (1,2-benzisoxazole-3-methanesulfonamide, ZNS) on the trigeminal complex of cats was compared with the effect of established antiepileptic drugs. Intravenous administration of 10-40 mg/kg ZNS significantly depresses descending excitatory mechanisms, as well as segmental and descending inhibitory mechanisms, but has only a minor effect on segmental excitatory mechanisms. This spectrum of activity is similar to that of valproate, and suggests that ZNS should also be a broad-spectrum antiepileptic drug. In agreement with our experimental observations, it has been found that ZNS is effective against complex partial, generalized tonic clonic, and myoclonic seizures. The antiepileptic profile of ZNS in conventional screening tests resembles that of carbamazepine (CBZ) and phenytoin. However, CBZ exacerbates rather than prevents myoclonic seizures. Our experimental model thus provides a more accurate prediction of ZNS's clinical spectrum of activity. The relationship of these findings to the mechanism of action of antiepileptic drugs is discussed.