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PubMed2000

Does holiday hypoglycaemia exist?

BACKGROUND: To determine whether an excessive, prolonged and, above all, unusual physical exertion could be associated with episodes of mild hypoglycaemia in non-insulin-dependent diabetes mellitus (NIDDM) patients treated with glibenclamide. METHODS EXPERIMENTAL DESIGN: 11 months of observation with retrospective analysis of patient personal diaries to determine the hypoglycaemic risk. SETTING: Diabetic Unit-Department of Medicine and Aging-Chieti University School of Medicine. PATIENTS: We enrolled 340 NIDDM outpatients adjusted for sex, age, body mass index, alcohol intake and oral treatment regimen with glibenclamide. PATIENTS were tested monthly for circadian blood glucose profiles and glycosylated hemoglobin. Mild hypoglycaemia was defined on the basis of blood glucose values < 2.8 mmol/l associated with mild autonomic symptoms, without requiring external assistance. Each diabetic patient filled personal diary indicating the therapy regimen and the characteristics of eventual hypoglycaemic episodes occurring during the observation period. RESULTS: 21.8% of NIDDM patients experienced one or two episodes of mild hypoglycaemia during the observation period. The analysis of the patients' diaries showed that 60% of the hypoglycaemic episodes was associated with excessive, prolonged and unexpected physical exertions. Within this group, about 70% of the episodes occurred during a holiday ("holiday hypoglycaemia"). After analyzing the socio-demographic and clinical characteristics of the diabetic patients reporting hypoglycaemic events, we found a higher risk for "holiday hypoglycaemia" in patients with a lower educational level, with a sedentary occupation or among the ex-farmers. CONCLUSIONS: As resulted in the present study, unexpected physical exertions may represent a relevant cause of mild hypoglycaemia in diabetic patients receiving oral antidiabetic therapy. However, this hypoglycaemic cause may have been underestimated in the literature. Educational programs conducted by general practitioners or diabetologists could be useful for the patients in reducing the number of mild hypoglycaemic episodes.

Diabetes Mellitus, Type 2↗

PubMed2002

Mechanisms of impaired hypothalamic-pituitary-adrenal (HPA) function in diabetes: reduced counterregulatory responsiveness to hypoglycaemia.

In summary, our data suggest that in uncontrolled diabetes, increased HPA activity is caused by increased central drive at or above the level of the PVN. Insulin treatment only restores HPA activity at and below the pituitary level, presumably by GC-mediated suppression of ACTH secretion. We hypothesize that the defective HPA response to hypoglycaemia is at least in part due to a lack of a decrease in MR mRNA in response to hypoglycaemia, and diminished sensitivity of the pituitary and adrenal gland to stimulation. Interestingly, insulin treatment restores the HPA response, but not the defective epinephrine response. Therefore, defective epinephrine responses are not linked to defective HPA responses. Similarly, antecedent hypoglycaemia specifically impairs epinephrine responses, but not HPA responses to hypoglycaemia. These studies have revealed some of the mechanisms of impaired HPA function in diabetes and its impaired responsiveness to hypoglycaemia. Further investigations are essential for understanding poor counterregulation in insulin-treated diabetes and may lead to new strategies for preventing hypoglycaemia.

Adrenocorticotropic Hormone↗

PubMed1992

Responses of peripheral blood cells to acute insulin-induced hypoglycaemia in humans: effect of alpha-adrenergic blockade.

Acute hypoglycaemia provokes rapid changes in peripheral blood cell counts. To examine possible adrenergic mechanisms modulating these changes, counts of peripheral blood cells including lymphocytes, granulocytes and red cells were measured in response to acute hypoglycaemia in a group of six normal subjects in control conditions (study 1), and during alpha-adrenergic blockade with phentolamine (study 2). In study 1 hypoglycaemia provoked a biphasic white cell response, with an early rise in lymphocyte count and a later rise in granulocyte count. The red cell count increased modestly following hypoglycaemia. During alpha-adrenergic blockade, the rise in total white cell count was diminished, with the rise in the lymphocyte count being greatly obtunded. The rise in the granulocyte count was unchanged. The increment of the red cell count during acute hypoglycaemia was abolished. These findings suggest that the increments of peripheral lymphocyte and red cell counts in response to acute insulin-induced hypoglycaemia are mediated via alpha-adrenoreceptors.

Acute Disease↗

PubMed1989

A five year study of neonatal hypoglycaemia in Toa Payoh Hospital (1984-1988).

A total of 18,611 live births from 1984 to 1988 in Toa Payoh Hospital were screened for neonatal hypoglycaemia. 102 neonates developed hypoglycaemia which was asymptomatic in 83% of cases. Of the 91 neonates whose medical records were still available, all had at least a high risk factor for the development of hypoglycaemia. Infants of diabetic mother (IDM) that were also more than 4 kg birth weight had the highest risk of developing hypoglycaemia. 82% of these hypoglycaemic neonates developed hypoglycaemia within the first 4 hours of life. Since so many of them had asymptomatic hypoglycaemia, screening of high risk neonates must be stressed.

Humans↗

PubMed1987

Beta-and alpha-adrenergic blockade and metabolic responses to insulin induced hypoglycaemia in diabetics.

The metabolic, autonomic and symptomatic effects of labetalol and metoprolol in comparison with placebo, were studied during insulin induced hypoglycaemia in 5 non-insulin dependent diabetics. Both drugs suppressed the expected increase in heart rate during hypoglycaemia, but did not affect awareness of hypoglycaemic symptoms. Neither drug produced a rise in blood pressure during hypoglycaemia nor delayed the recovery from insulin-induced hypoglycaemia. In both there was no inhibition of release of gluconeogenic substrates such as free fatty acids. The results indicate that both metoprolol, a selective beta-blocker, and labetalol, a combined alpha beta-blocker, do not impair awareness of hypoglycaemia nor alter the metabolic response to hypoglycaemia in diabetics.

Blood Glucose↗

PubMed1987

Hormonal control of haemostasis during hypoglycaemia in diabetes mellitus.

Factor VIII (FVIII) and plasminogen activator activity (PAA) rise during hypoglycaemia, and this might contribute to the vascular complications of diabetes. Similar changes in haemostasis accompany raised plasma levels of vasopressin (aVP) and adrenaline. To investigate the effects of these hormones on haemostasis during hypoglycaemia and the role of plasma insulin concentrations, eight insulin-dependent diabetic patients underwent controlled hypoglycaemia for 20 min and 13 diabetic patients were investigated during hyperinsulinaemia with blood glucose maintained at 8.0 mmol/l. During hypoglycaemia, insulin levels increased to median values of 114 mU/l, a VP rose from 0.5 to 4.4 (p less than 0.005) pg/ml and adrenaline from 0.4 to 4.4 nmol/l (p less than 0.005). FVIII coagulant activity (FVIII:C) rose from 0.75 to 1.09 IU/ml (p less than 0.01) and the ristocetin co-factor (FVIIIR:Co) and von Willebrand factor antigen (vWF:Ag) showed similar responses. PAA increased from 156 to 745 units (p less than 0.005). During hyperinsulinaemia, insulin rose following infusion from 24 to 52 and 118 mU/l, maintained for an hour at each level. Despite this, plasma aVP, FVIII:C, FVIIIR:Co, vWF:Ag and PAA remained unchanged. This study indicates that the marked changes in FVIII, vWF and PAA concentrations which accompany hypoglycaemia depend on low blood glucose and not raised plasma insulin. The response in probably mediated by increases in adrenaline and aVP, which are part of the physiological response to hypoglycaemia.

Adolescent↗

PubMed1987

Sympathoadrenal and other responses to hypoglycaemia in the young foal.

The effects of insulin-induced hypoglycaemia on plasma catecholamines, cortisol and metabolites have been examined in newborn and 7-14-day-old foals. The fall in plasma glucose elicited by the highest dose of insulin (1.0 i.u./kg) given to the neonates was slower in onset and less severe in effect than 0.5 i.u./kg in the older foals. There was a significant inverse correlation between the concentrations of glucose and adrenaline (but not noradrenaline) in plasma once the glucose level had fallen below 2 mmol/l; the adrenergic response to hypoglycaemia was greater in the 7-14-day-old foals than in the neonates. No significant changes in glucose or catecholamines were seen after fasting alone. The adrenocortical response to hypoglycaemia was poor after birth, but significant changes occurred in the older foals with a 3-fold increase in plasma cortisol at 60 min after 0.5 i.u. insulin/kg. There were significant increases in plasma FFA after hypoglycaemia in both groups of animals, but the rise was less pronounced in the neonates. A significant positive correlation was found between plasma adrenaline and FFA values. Hypoglycaemia also resulted in a significant rise in plasma lactate and a slow fall in alpha-amino nitrogen. These findings show that hypoglycaemia in the foal is followed by stimulation of the adrenal medullary component of the sympathetic system and by activation of the adrenal cortex with a number of consequent metabolic changes. The hypoglycaemic effects of insulin were more intense and the response more rapid in the older foals than in the neonates, which exhibited some degree of insulin resistance.

Animals↗

PubMed1981

Effects of hypoglycaemia on ventilation and arousal responses to hypoxia, and newborn calves during active and quiet sleep.

Ventilatory and arousal responses to progressive, isocapnic hypoxia were assessed in five full-term calves, aged 1-8 d, during normo-glycaemia and insulin-induced hypoglycaemia; replicate tests were made during both quiet and active sleep. Hypoxia was produced by rebreathing 8-10% (W/V) oxygen; end-tidal PO2 and PCO2 confirmed the mask-seal, and the constancy of PCO2 achieved by a soda-lime CO2-absorber. Oxygen saturation was recorded continuously by aspirating aortic blood through a cuvette-oximeter. Airflow through a tightly fitting face-mask was digitized at 50 ms intervals to calculate breath-by-breath ventilation and rate. Sleep-state and arousal were characterized by EEG, electro-oculogram, nuchal electromyogram and behaviour. An intravenous dose of 2.5 units/kg of soluble insulin produced hypoglycaemia within 60 min (blood glucose less than 1 mmol/l). In the normoglycaemic control state, ventilation during quiet sleep increased linearly; typically the ventilation ratio to pre-hypoxic control was 1.5 at an arterial O2-saturation of 85-90%. In contrast, during active sleep, hypoxaemia progressed without any ventilatory response to a very low arterial O2-saturation of less than 70%. Severe hypoglycaemia did not alter these ventilatory responses during either quiet or active sleep. Thus, the relationship between ventilation ratio and arterial O2-saturation at a saturation of 75% did not differ significantly from control. In quiet sleep the mean ventilation ratio values at an arterial O2-saturation of 75% were 1.92 +/- 0.07 (SEM) and 1.62 +/- 0.07 (P greater than 0.05) for normoglycaemia and hypoglycaemia respectively; in active sleep these were 1.08 +/- 0.09 (SEM) and 1.06 +/- 0.04 (P greater than 0.20). The arterial O2-saturation at which reflex arousal occurred differed between sleep-states but was not altered by hypoglycaemia. In quiet sleep, values were 85.0 +/- 1.4 (SEM) and 84.4 +/- 2.5; in active sleep, 57.8 +/- 3.9 (SEM) and 60.4 +/- 1.4, for normoglycaemia and hypoglycaemia respectively.

Animals↗

PubMed1998

Quality of diabetes care, diabetes knowledge and risk of severe hypoglycaemia one and four years after participation in a 5-day structured treatment and teaching programme for intensified insulin therapy.

Intensification of insulin therapy in the Diabetes Control and Complications Trial led to an improvement in the quality of diabetes care, which was accompanied, however, by a threefold increase in the risk of severe hypoglycaemia. The present trial, a long-term evaluation of a structured 5-day treatment and teaching programme (DTTP) for intensified insulin therapy, was performed to clarify factors determining HbA1c, the incidence of severe hypoglycaemia, diabetes knowledge and quality of life. Ninety-four Type 1 diabetic patients were examined at baseline and 4 years after participation in a DTTP. Comparison of baseline data with measurements at the 4-year follow-up examination showed that relative HbA1c (= HbA1c/mean normal) improved (1.9 +/- 0.51 vs 1.55 +/- 0.3*, p < 0.001, *excluding 4 patients with diabetes manifestation at baseline) and that frequencies of daily insulin injections (3.73 +/- 1.23 vs 4.9 +/- 0.69*, p < 0.001) and weekly blood glucose self-tests (6.6 +/- 10.1 vs 25.5 +/- 8.7*, p < 0.001) increased, whereas the incidence of severe hypoglycaemia (intravenous glucose, glucagon injection) remained stable (0.19 vs 0.24, p = 0.48). Patients with less diabetes knowledge had higher HbA1c levels and a higher incidence of severe hypoglycaemia. In the group of patients with severe hypoglycaemia, certain crucial gaps in diabetes knowledge were identified concerning the effects of physical activity, nutrition and long-term complications of diabetes. In multivariate analysis. The most important factor associated with HbA1c was diabetes knowledge which, however, was not influenced by educational level or other factors. Interventions, such as the identification of psychosocial factors which may interact with diabetes knowledge, quality of life and successful self-management of diabetes by patients, are needed to improve the efficacy of DTTPs and to prevent severe side effects such as hypoglycaemia.

Adult↗

PubMed1996

Restitution of neurophysiological functions, performance, and subjective symptoms after moderate insulin-induced hypoglycaemia in non-diabetic men.

The restoration of cognitive function was studied in 10 healthy men aged 26 years (25.5 +/- 1.2 years; mean +/- SD) after insulin-induced hypoglycaemia (arterialized blood glucose 2.5 +/- 0.4 mmol l-1) for 62 +/- 8 min. Another group of six men participated in a single blind sham study for comparison. The hypoglycaemic event caused a significant increase (p = 0.006) in serum adrenaline levels. Ratings of adrenergically mediated symptoms increased during hypoglycaemia (p = 0.006), as did neuroglycopenic symptoms (p = 0.002), although neuroglycopenia ratings increased in both studies. During hypoglycaemia, P300 amplitudes in a relatively demanding visual search task decreased (p = 0.02), whereas easier tasks were unaffected. The amplitudes were restored after 40 min of normoglycaemia. Reaction time deteriorated after restoration of normoglycaemia, suggesting an effect of hypoglycaemia on learning. Thus, hypoglycaemia at a blood glucose level that is common among patients treated with insulin causes clear cognitive dysfunction, although restoration of the cognitive dysfunction to normal was fast.

Adult↗

PubMed1998

Counterregulatory hormones in insulin-treated diabetic patients admitted to an accident and emergency department with hypoglycaemia.

The aim of the study was (1) to describe hormone responses in insulin-induced hypoglycaemia and (2) to investigate if a combined treatment with intravenous glucose and intramuscular glucagon (group A) would improve glucose recovery as compared to treatment with intravenous glucose alone (group B). Eighteen adult patients with insulin-treated diabetes mellitus admitted to the Accident and Emergency Department with hypoglycaemia (plasma glucose 1.23 +/- 0.15 mmol l(-1) on admission) were randomized to one of the above treatments and plasma glucose and counterregulatory hormones were measured before and 30-120 min after treatment. Pre-treatment counterregulatory hormone concentrations were significantly lower than hormone concentrations during induced hypoglycaemia in healthy control subjects but significantly higher than healthy fasting concentrations for plasma adrenaline (p = 0.020), glucagon (p = 0.008), growth hormone (p = 0.011), and cortisol (p<0.00001). Thus, although glucagon and adrenaline responses may be absent when studying Type 1 diabetic patients in the experimental setting, both hormones increase to a significant extent in 'real-life' hypoglycaemia in this patient group, although to a lesser degree than might be expected. Plasma glucose did not differ significantly between the two treatments at any time point. Despite access to food, one of four patients in group B and one of five patients in group A had plasma glucose below 4.0 mmol l(-1) after 120 min. In conclusion, low yet significantly elevated concentrations of adrenaline and glucagon were found in diabetic patients admitted with severe hypoglycaemia to an Accident and Emergency Department.

Adult↗

PubMed1998

Estimates on the incidence of antidiabetic drug-induced severe hypoglycaemia in Hong Kong.

In order to estimate the incidence of severe hypoglycaemia (defined as episodes severe enough to require hospitalization in general medical wards) among known diabetics in Hong Kong in 1990, both the total number of such admissions to the Prince of Wales Hospital and the age and sex distribution and number of known diabetics among its catchment population were defined. The latter was derived from the 1991 census and two studies or the prevalence of diabetes mellitus in Chinese subjects in the New Territories East region in 1987 and 1990. The incidence of severe hypoglycaemia was generally higher in women than in men and in older than in younger subjects. The incidence was 15-19 times higher in subjects aged >or=60 years than in those aged <or=59 years (men 3.51 versus 0.17%, women 6.86 versus 0.43%, overall 5.16 versus 0.29%). As many as 24.16% of the subjects aged 70-74 years had severe hypoglycaemia in 1990. The overall incidence of severe hypoglycaemia in all known diabetics was 1.40%. Based on the data from a drug utilization study (70.24% and 5.93% of diabetics receiving sulphonylureas and insulins, respectively), it could be estimated that in 1990, the incidence of hypoglycaemia requiring hospitalization in general medical wards was 1.42% for sulphonylureas and 6.84% for insulins.

Journal Article↗

PubMedDate not supplied

Effects of insulin-induced hypoglycaemia on energy intake and food choice at a subsequent test meal.

BACKGROUND AND AIMS: Hypoglycaemia is assumed to increase food intake, but there is little data on the magnitude or qualitative nature of this effect. We have therefore investigated the effects of insulin-induced hypoglycaemia on food intake at a test meal. METHODS: Sixteen healthy men (age 29.8 +/- 11 years; mean +/- SD) were studied; either insulin (0.05 units/kg) or saline was given intravenously in a double-blind crossover design. Blood glucose was monitored at regular intervals. Participants were given an ad libitum breakfast 20 min after injections and food intake and appetite scores were recorded. RESULTS: Blood glucose was unchanged following saline (4.3 +/- 0.4 to 4.4 +/- 0.3 mmol/L). There was a transient decline in blood glucose after insulin with a nadir at 20 min (4.31 +/- 0.34 to 2.41 +/- 0.45 mmol/L, p < 0.0001), which returned to baseline at 40 min. Total energy intake was 17% higher (1701.1 +/- 895.3 kcal vs 1427.7 +/- 815 kcal, p = 0.026) following insulin administration compared to that following saline. Macronutrient analysis revealed a significant increase in high-fat foods (muffins) (69.2 +/- 54.1 vs 29 +/- 42.3 g, p = 0.009) after insulin. Appetite scores were similar after saline and insulin despite these changes in food intake. CONCLUSIONS: Transient insulin-induced hypoglycaemia increases energy intake. Participants consumed more fat after insulin compared to that after saline. High-fat foods can lead to passive overconsumption and have a low glycaemic index, which may prolong hypoglycaemia. Both factors could ultimately promote weight gain in individuals with recurrent hypoglycaemia.

Adult↗

PubMed1989

Effects of chronic sodium salicylate feeding on the impaired glucagon and epinephrine responses to insulin-induced hypoglycaemia in streptozotocin diabetic rats.

The potential role of endogenous prostaglandins in glucagon and epinephrine responses to insulin-induced hypoglycaemia was studied in streptozotocin-diabetic and age-matched control adult male rats. Rats made diabetic with a single intravenous injection of streptozotocin (65 mg/kg) developed impaired glucagon and epinephrine responses to insulin-induced hypoglycaemia by 80-100 days. Plasma glucagon levels in response to insulin-induced hypoglycaemia in streptozotocin-diabetic rats (167 +/- 67 pg/ml) were significantly lower (p less than 0.01) than those in control rats (929 +/- 272 pg/ml). Similarly, plasma epinephrine levels in hypoglycaemic state in streptozotocin-diabetic rats (11 +/- 8 pmol/ml) were also significantly lower (p less than 0.01) compared to control rats (37 +/- 13 pmol/ml). Streptozotocin-diabetic rats provided with sodium salicylate (25 mg/100 ml) in their drinking water from day one of diabetes exhibited prevention of the blunted glucagon and epinephrine responses to insulin-induced hypoglycaemia. About 80-100 days after the chronic sodium salicylate treatment in streptozotocin-diabetic rats, both plasma glucagon levels (1080 +/- 169 pg/ml) and plasma epinephrine levels (39 +/- 8 pmol/ml) were essentially identical to plasma glucagon levels (1074 +/- 134 pg/ml) and plasma epinephrine levels (37 +/- 5 pmol/ml) in control rats in hypoglycaemic state. These animals also exhibited an improvement in the diabetic state in that they had less severe hyperglycaemia and lack of weight gain. These results suggest that the blunted glucagon and epinephrine responses to insulin-induced hypoglycaemia may be related to altered prostaglandin levels in streptozotocin-diabetes.

Animals↗

PubMed1988

Counterregulatory hormonal responses to hypoglycaemia in type 1 (insulin-dependent) diabetes: evidence for diminished hypothalamic-pituitary hormonal secretion.

Acute insulin-induced hypoglycaemia in humans provokes autonomic neural activation and counterregulatory hormonal secretion mediated in part via hypothalamic stimulation. Many patients with Type 1 (insulin-dependent) diabetes have acquired deficiencies of counterregulatory hormonal release following hypoglycaemia. To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. To examine the effect of duration of diabetes these patients were subdivided into two groups (Group 1: 8 patients less than 5 years duration; Group 2: 8 patients greater than 15 years duration) and were compared with 8 normal volunteers (Group 3). The severity and time of onset of hypoglycaemia were similar in all 3 groups, but mean blood glucose recovery was slower in the diabetic groups (p less than 0.01). The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). The mean increments of glucagon and adrenaline in the diabetic groups were lower than the normal group, but these differences did not achieve significance; glucagon secretion was preserved in several diabetic patients irrespective of duration of disease. Various hormonal responses to hypoglycaemia were absent or diminished in individual diabetic patients, and multiple hormonal deficiencies could be implicated in delaying blood glucose recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1987

Cerebral blood flow increases during insulin-induced hypoglycaemia in type 1 (insulin-dependent) diabetic patients and control subjects.

The effect of insulin-induced hypoglycaemia on cerebral blood flow was examined using the intravenous xenon-clearance technique in 9 patients with Type 1 (insulin-dependent) diabetes (aged 20 to 43 years) and 9 age-matched control subjects before, during and after hypoglycaemia. Cerebral blood flow rose in both groups. The mean basal cerebral flood flow values were not significantly different and during hypoglycaemia mean cerebral blood flow increased by 17% (p = 0.008) in the diabetic patients and by 21% (p = 0.0003) in the control subjects. The results suggest that in young diabetic patients without autonomic neuropathy or microangiopathy cerebral vessels dilate normally in response to hypoglycaemia. The physiological importance of an increase in cerebral blood flow during hypoglycaemia is uncertain; but glucose availability is increased.

Adult↗

PubMed1993

Cognitive dysfunction in adults with type 1 (insulin-dependent) diabetes mellitus of long duration: effects of recurrent hypoglycaemia and other chronic complications.

To examine the long-term effects of recurrent severe hypoglycaemia and other biomedical complications on mental efficiency, a battery of cognitive tests was administered to 142 Type 1 (insulin-dependent) diabetic adult patients (age 33.5 +/- 5.6 years; mean +/- SD) and 100 demographically similar non-diabetic control subjects. All diabetic subjects had been diagnosed before the age of 17 years. Diabetic subjects with one or more complications (distal symmetrical polyneuropathy; advanced background or proliferative retinopathy; overt nephropathy; one or more episodes of severe hypoglycaemia) performed significantly (p < 0.001) more poorly than non-diabetic control subjects on tests requiring sustained attention, rapid analysis of visuospatial detail, and hand eye co-ordination. Regression analyses indicated that the best biomedical predictor of cognitive test performance was a diagnosis of polyneuropathy. Although severe recurrent hypoglycaemia was not associated with performance on any test, the neuropathy x recurrent hypoglycaemia interaction term was significant. These results suggest that in adults with Type 1 diabetes of long duration, recurrent hypoglycaemia does not appear to influence cognitive performance directly, but may interact with neuropathy to exaggerate or otherwise magnify the extent of neurobehavioural dysfunction.

Adult↗

PubMed1991

Nocturnal electroencephalogram registrations in type 1 (insulin-dependent) diabetic patients with hypoglycaemia.

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.

Adult↗