守谷 俊

To evaluate the significance of an electrophysiologic monitoring system during brain hypothermia, we measured the brainstem auditory evoked potentials (BAEPs), somatosensory evoked potentials (SEPs), and topographic electroencephalography (EEG) in 29 critically ill patients (15 with severe head injury and 14 with encephalopathy following cardiopulmonary resuscitation). When the temperature measured in the internal jugular vein fell from 36 degrees C to 33 degrees C, the prolongation of latency in BAEPs was 0.1 +/-: 0.06 ms in wave I, 0.5 +/- 0.23 ms in wave III, and 0.92 +/- 0.86 ms in wave V. In addition, the prolongation of latency in SEPs was 1.2 +/- 0.2 ms in N13 and 2.1 +/- 0.4 ms in N20. The bifrontal fast wave responses, except for those of primary injured lesions, in the topographic EEG were recognized in 9 of 13 patients within 30 min after the injection of midazolam which was used as a sedative. When the temperature fell from 36 degrees C to 33 degrees C, the ratio of the delta and theta waves to the alpha waves recorded from 12 scalp electrodes increased. An electrophysiologic evaluation in critically ill patients should thus be considered an effective real-time monitoring system in patients experiencing brain hypothermia.

The role of Ca2+ in cellular injury has received particular attention in studies of acute spinal cord trauma. In this context, the spatial and temporal distribution of extracellular Ca2+ ([Ca2+](e)) may have an important bearing on the development of secondary tissue injury. We therefore studied the spatial-temporal distribution of [Ca2+](e) following moderate (25 g-cm) contusive injury to the rat thoracic (T9-T11) spinal cord. Double-barreled, Ca2+-selective microelectrodes were used to measure the magnitude and time course of [Ca2+](e) at increasing depths from the dorsal spinal cord surface. After 2 h, the tissue was frozen and later analyzed for total Ca concentration using atomic absorption spectroscopy. [Ca2+](e) fell at all depths, but the decrease was maximal at 250 and 500 mu m from the dorsal surface, where, at 0-10 min after injury, [Ca2+](e) averaged 0.09 +/- 0.03 and 0.06 +/- 0.03 mM respectively. By 2 h postinjury, [Ca2+](e) recovered to nearly 1 mM across all depths. Over this time, total tissue calcium concentration ([Ca](t)) was 4.54 +/- 0.16 mu mol/g in injured cords vs 2.75 +/- 0.1 mu mol/g in sham-operated controls. These data place emphasis on the dorsal gray matter as a principal site of ionic derangement in acute spinal cord injury. The implications of these findings are discussed with reference to secondary injury processes.