We present two patients with delayed neurological deterioration following apparent recovery from carbon monoxide poisoning in whom magnetic resonance imaging showed abnormalities. In the first patient, cortical grey matter abnormalities were seen without white matter changes. Visual evoked potentials were, however, abnormal. In the second, diffuse white matter lesions were detected. In neither patient were basal ganglia lesions seen.

SYNOPSIS In two subjects with paramyotonia congenita the isometric torque generated by the abductor digiti minimi and the surface EMG recorded over ADM decreased during prolonged or repetitive contractions, whether these were voluntarily or electrically induced. Isometric twitch times did not alter significantly during this muscle fatigue. Cooling greatly accelerated the fatiguing process. It is suggested that this local muscle weakness is due to a progressive decrease in excitability of the muscle cell membrane.

Circulatory arrest at 20° C is used during open heart surgery in infants. It has been stated that significant brain damage does not occur. Piglets between two and six weeks of age were cooled to 20° C using extracorporeal circulation and a membrane oxygenator. After one hour of circulatory arrest the perfusion system was used to rewarm the animals and restore normal circulation. Electroencephalogram was monitored throughout perfusion and surgery, and repeated on surviving animals on the third,fi/th, seventh and tenth postoperative days. On the tenth day the animals were killed by injection of pentobarbitone. Other groups were subjected to Continuous per fusion at 20° C, Continuous per fusion at 37° C, Thoracotomy and cannulation, Ischaemia, and Hypoxia. The return of E.E.C. activity was delayed after circulatory arrest compared with those continuously per/used. Lesions were found in the cerebral cortex in all the animals which had circulatory arrest and those subjected to ischaemia and hypoxia. The brains of animals of the other groups were indistinguishable from those killed without any experimental procedure. Despite apparent recovery, brain damage following hypothermic arrest during open heart surgery remains possible.

SYNOPSIS In two subjects with paramyotonia congenita myotonic delay in muscle relaxation, recorded electromyographically and with a displacement transducer, was found to increase with repeated forceful contractions. Myotonia was elicited readily in warm temperatures, was initially aggravated by cooling, but was invariably lost as muscle fatigue developed. The EMG evidence of myotonia usually subsided before complete muscle relaxation had occurred, suggesting that a defect of the contractile mechanism was present over and above any defect at membrane level.