The blood-sugar in convulsions of infancy and childhood.

It has long been recognized that severe convulsive attacks are followed by depletion of the carbohydrate reserves of the body. Indeed one of the experimental methods of exhausting the glycogen of the tissues is by inducing convulsions by the administration of strychnine or other similar drugs. Clearly in these circumstances the reduction of available carbohydrate is the result and not the cause of the convulsion. Following on the recogniitioni of hyperin sulinism as a cause of convulsions, however, the possibility has arisen that hypoglycaemia may be an etiological factor in the production of convulsions in infancy and childhood and there is no doubt that convulsions due to this occasionally occur. Two cases have been recorded by Kramer, Grayzel and Solomon', and Josephs2' ' has suggested that the combination of fever and a short fast may produce a state of hypoglyeaemia which may explain the convulsions occurring at the onset of an acute infection. Other workers, however, while notiing the presence of hypoglycaemia in the post-convulsive state have hesitated to attribute the seizure to the disturbance in carbohydrate metabolism. Griffiths' noted the association of hypoglyeaemia with convulsions but was not sure whether the low blood-sugar was the cause, the result or merely coincident with the convulsion. Higgins5 observed hypoglyeaemiia following convulsions in two new-born babies. Fleming, Herring and Morris6 reported three patients who were admitted to hospital comatose and had either glycosuria or a raised blood-sugar which in two of theni was followed by hypoglyeaemia, and Darrow7 recently reported two examples of recurring convulsions in mentally defective children in whom liypog,lycaenmia was frequently noted but on two occasions shortly after a convullsion the HIood-sugar was found to be high. It was found that in the hypoglyeaemic phase these children did not respond well to glucose. The suggestioni that idiopathic or epileptic convulsions of infancy and childhood are caused by a state of hypoglyeaemia at first sight seems unilikely, for true hypoglyeaemic convulsions arising, for example, from ovrer-dosage with or from an excessive productioni of insulin are of a different nature from the ordinary convulsions of childhood. Frequently the lbypoglyeaemic fit is preceded by a period of fatigue, malaise, hunger, fear, negativism, confused speech and automatism-none of which is a feature of convulsions due to other causes. 'While the convulsion itself is in(listinguishable from any other, these prodromal symptoms as well as the ready and complete recovery following the administration of