Purpose. To compare closed intramedullary nailingto open reduction and internal fixation using a fixed angle blade plate for the management of subtrochanteric femoral fractures. Methods. 58 patients were equally randomised to undergo either an intramedullary nailing (IN) or fixed angle blade plating (BP). Results. There were no significant differences between the 2 groups with regard to age, time to surgery, operating time, receipt of blood transfusions, duration of hospital stay, or fracture classification. The revision rate was 28% (8/29) in the BP group and none in the IN group; the difference was statistically significant. Conclusion. Internal fixation using a fixed angle blade plate for subtrochanteric femoral fractures has higher implant failure and revision rates, compared to closed intramedullary nailing.

Trace element levels were measured by neutron activation analysis in spinal cord, liver and bone of 7 control patients dying of non-neurological disease and 15 patients dying of motor neurone disease (MND). The concentration of selenium was significantly elevated in the cervical cord, liver and bone in the MND group. Although spinal cord manganese levels were increased at both the cervical and thoracic levels, the hepatic concentration was reduced in the MND patients. These findings are discussed in relation to current understanding of the pathogenesis of MND.

SUMMARY Trace elements were estimated in the spinal cord, liver and bone of five patients dying of motor neuron disease and five control subjects dying of non-neurological disease. The content of selenium in cord and liver and the cord manganese level were significantly increased in the motor neuron disease patients. These findings are discussed in terms of the possible aetiology of motor neuron disease.Since the first description of motor neuron disease 150 years ago,'2 the possible role of lead in its pathogenesis has been a source of controversy. Its recognition as a distinct clinical entity emerged from reports ofpatients showing features similar to those of lead poisoning but lacking a history of exposure.2-4 Although it is clear that motor neuron disease-like syndromes can be seen in both lead58 and mercury910 toxicity, such patients improve either with chelation therapy or removal from the contaminated environment. Patients with motor neuron disease do not and the significance of reports of increased lead levels in the spinal cord of patients dying of motor neuron disease1112 is uncertain. It seems likely that these represent a secondary rather than a primary effect.12 13 The possibility remains that motor neuron disease arises as a result of a metabolic disturbance of motor neurons. The RNA content of motor neurons has been reported to be reduced14-16 and it has recently been suggested that these observations might reflect defective enzymatic DNA repair mechanisms.'7 While this is an attractive hypothesis there is no direct supporting evidence. Trace elements are of crucial importance in metabolism, particularly in respect of

The complication rate was not higher for operations performed by unsupervised trainees than those performed in the presence of a consultant.