Parasomnias (non-epileptic nocturnal episodic manifestations) in patients with magnesium deficiency.

Twenty seven patients with parasomnias (night terrors, nocturnal motor automatisms, nocturnal verbal automatisms and sometimes with bruxisms) associated with magnesium deficiency were selected. In all of them marked hypomagnesemia, clinical, EEG and EMG signs of spasmophilic syndromes were found. The 8 hours polysomnographical recordings of all cases (monitored in a system with infra-red video-TV cameras) showed severe sleep disorders and EEG nocturnal abnormalities occurring in the SWS (especially in the I b, II and III stages) with disappearance in the REM sleep. The authors suggest that these clinical and polysomnographic anomalies may be the expression of the brain damage caused by magnesium deficiency or of the clinical electrographic manifestations of the reticulate neuronal hypersynchrony exacerbated by sleep.

Computerized electroencephalographic mapping in hypomagnesian spasmophilic syndromes.

Out of 397 patients presenting hypomagnesaemia there were selected for this study only 107 cases with neurotic and neuromuscular clinical picture (sometimes with short and simple loss of consciousness) without any sign of organic cerebral lesion. The dosing of the seric and erythrocytic magnesium was performed by means of a colorimetric method of Mann and Yoe, modified by the authors. In all the cases, the EEG and EMG changes were studied by simultaneous recording of the EEG and EMG before, during and after hyperpnoea. In these 107 selected cases (divided into three groups: children, adolescents and adults) the computerized electroencephalographic maps (CEM) were carried out by an original method, transcribing the primary data of Hjorth's NSD parameters (Amplitudes and Frequencies) into a Romanian M-118 microcomputer, by a technique with analog-digital conversion. The CEM (in white-black and in colour cartography) were performed for various epochs, including the sequential ones (second by second, all along the EEG discharges during and after hyperpnoea). By these methods, we analyzed the dynamic fluctuation and temporo-spatial cortical distribution of the sinusoidal slow waves generated by the reticulate neuronal hypersynchrony. The CEM showed some differences in the three groups of hypomagnesemic syndromes selected.