title: Nocturnal electroencephalogram registrations in type 1 (insulin-dependent) diabetic patients with hypoglycaemia.
abstract: 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.
authors.affiliation: Steno Memorial Hospital, Gentofte, Denmark.
authors.forename: I
authors.initials: I
authors.lastname: Bendtson
authors.forename: J
authors.initials: J
authors.lastname: Gade
authors.forename: A M
authors.initials: AM
authors.lastname: Rosenfalck
authors.forename: C E
authors.initials: CE
authors.lastname: Thomsen
authors.forename: G
authors.initials: G
authors.lastname: Wildschiødtz
authors.forename: C
authors.initials: C
authors.lastname: Binder
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000502:physiology*; D002096:C-Peptide / Q000097:blood; D002940:Circadian Rhythm; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D004562:Electrocardiography; D004569:Electroencephalography; D004837:Epinephrine / Q000097:blood; D005934:Glucagon / Q000097:blood; D006442:Glycated Hemoglobin / Q000032:analysis; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000503:physiopathology*; D007330:Insulin Antibodies / Q000032:analysis; D009638:Norepinephrine / Q000097:blood
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D004837:Epinephrine; D005934:Glucagon; D006442:Glycated Hemoglobin; D013006:Growth Hormone; D006854:Hydrocortisone; D007330:Insulin Antibodies; D009638:Norepinephrine