The frequency of symptomatic hypoglycaemic episodes was studied in 411 randomly selected conventionally treated Type 1 diabetic out-patients. Between two consecutive visits to the out-patient clinic each patient filled in a questionnaire at home. The number of hypoglycaemic episodes was then recorded prospectively in a diary for 1 week. From the questionnaires, the (retrospective) frequencies of mild and severe symptomatic hypoglycaemia were 1.6 and 0.029 episodes patient-1 week-1. From the diaries, the (prospective) frequencies of mild and severe hypoglycaemic episodes were 1.8 and 0.027 patient-1 week-1. Symptomatic hypoglycaemia was more frequent on working days than during weekends (1.8:1) and more frequent in the morning than during the afternoon, evening, and night (4.5:2.2:1.4:1). The symptoms of hypoglycaemia were non-specific, heterogeneous, and weakened with increasing duration of diabetes. During their diabetic life, 36% of the patients had experienced hypoglycaemic coma. The frequency of hypoglycaemia was positively, but only weakly, correlated with insulin dose, number of injections, percentage unmodified insulin of the total dose, and HbA1c (mild hypoglycaemia only). The frequency was also negatively, but weakly, correlated with age and HbA1c (episodes with coma only), but not correlated with sex, duration of diabetes, or patients' ratings of worries about mild and severe hypoglycaemia.

Eight insulin-dependent diabetic patients were studied to evaluate sleep patterns during normoglycemia and spontaneous and insulin-induced hypoglycemia. Two channels of electroencephalogram (EEG), electromyogram and actooculogram were recorded. The signals were analyzed off-line, using a polygraphic sleep analysis system. The scoring was mainly based on the color density spectral array of the EEG. Blood glucose and growth hormone were measured serially. Asymptomatic, spontaneous nocturnal hypoglycemia occurred in 38% of the nights. Conventional sleep analysis showed a tendency toward prolongation of the two first rapid eye movement cycles on hypoglycemic nights, although it was insufficient to explain the activities seen during hypoglycemia. Blood glucose values below 2.0 mmol/l were observed in some of the patients accompanied by EEG changes with increased theta and delta activity.

Eight Type 1 (insulin-dependent) diabetic patients with no diabetic complications were studied overnight for two consecutive and one subsequent night with continuous monitoring of electroencephalogram and serial hormone measurements. The aims were: 1) to evaluate the influence of spontaneous and insulin-induced hypoglycaemia on nocturnal electroencephalogram sleep-patterns and, 2) to evaluate counter-regulatory hormone responses. Spontaneous hypoglycaemia occurred on six nights (38%) with blood glucose concentrations less than 3.0 mmol/l and on four nights less than 2.0 mmol/l. All the patients experienced insulin-induced hypoglycaemia with a blood glucose nadir of 1.6 (range 1.4-1.9) mmol/l. The electroencephalogram was analysed by a new method developed for this purpose in contrast to the traditional definition of delta-, theta-, alpha- and beta-activity. The blood glucose concentration could be correlated to the rank of individual electroencephalogram-patterns during the whole night, and specific hypoglycaemic amplitude-frequency patterns could be assigned. Three of the eight patients showed electroencephalogram changes at blood glucose levels below 2.0 (1.6-2.0) mmol/l. The electroencephalogram classes representing hypoglycaemic activity had peak frequencies at 4 and 6 Hz, respectively, clearly different from the patients' delta- and theta-activity. The changes were not identical in each patient, however, they were reproducible in each patient. The changes were found equally in all regions of the brain. The three patients with electroencephalogram changes during nocturnal hypoglycaemia could only be separated from the other five patients by their impaired glucagon responses. Against this background the possibility of protection by glucagon, against neurophysiologic changes in the brain during hypoglycaemia may be considered.

The relationship between symptomatic (subjective feelings) and biochemical (blood glucose concentration less than 3 mmol l-1) hypoglycaemia was studied in 66 randomly selected insulin-dependent diabetic out-patients under normal conditions of daily life with conventional insulin injection regimens. The patients (a) collected 7-point diurnal blood glucose profiles at home on three consecutive days and then once weekly for 3 weeks, (b) indicated whether they felt hypoglycaemic at sampling times, and (c) collected extra samples if they felt hypoglycaemic at any time during the study period. The weekly frequencies of symptomatic and biochemical hypoglycaemia were 0.99 and 1.75 per patient, respectively. Biochemical hypoglycaemia was present in 29% of the symptomatic episodes, and symptomatic hypoglycaemia accompanied 16% of the biochemical episodes. Symptomatic hypoglycaemia was experienced at a median blood glucose concentration of 3.4 mmol l-1 (range 1.4-14.9 mmol l-1). Fifty per cent of both symptomatic and biochemical episodes occurred before lunch, while the remainder were evenly distributed throughout the day. The occurrence of biochemical hypoglycaemia, but not of symptomatic hypoglycaemia, was inversely correlated with HbA1c and median blood glucose concentration. Thus symptomatic hypoglycaemia is an unreliable indicator of biochemical hypoglycaemia and of the degree of glycaemic control. Blood glucose measurements are a prerequisite for the diagnosis of hypoglycaemia.

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despite sleep disturbances, nocturnal hypoglycaemia did not impair cognitive function the following morning in Type 1 (insulin-dependent) diabetic patients.

Objective: To compare two intensified insulin therapy regimenscontinuous subcutaneous insulin infusion (CSII) against multiple daily insulin injection (MDI) -in Danish adolescents examined in a prospective, matched controlled study design. Research design and methods: Thirty type 1 diabetic adolescents at CSII and 26 matched MDI controls were included in this open intention-totreat study. Actrapid was used in both groups. Before study entry, all participants followed a brush-up course in order to minimize study effect. At each visit, the following parameters were recorded: hemoglobin A1c (HbA1c), insulin dose, weight, number of hypoglycemic and diabetic ketoacidosis (DKA) events, and the time resources used. At entry and exit of the study, diet registration and validated quality-of-life (QoL) questionnaires were filled by the participants. Results: A non-significant decline in HbA1c was seen in both groups (p ¼ 0.468); HbA1c decreased from 9.5 to 8.9% and from 9.7 to 9.5% in the CSII and MDI group, respectively. The insulin dose and the number of severe hypoglycemic events per patient were lower (non-significant) in the CSII group. Both groups showed increased body mass index -highest in the CSII group -and mild to moderate DKA episodes were only seen among CSII users. No differences could be demonstrated within the QoL or diet registrations. Conclusions: CSII treatment is beneficial as an intensified insulin therapy for selected type 1 diabetic patients and both MDI and CSII can be offered by the professional diabetes team to better tailor therapy. In future, there is a strong need to identify the characteristics of responders to CSII treatment in order to increase the efficacy and safety of CSII treatment.