title: EEG abnormalities with and without relation to severe hypoglycaemia in adolescents with type 1 diabetes.
abstract: OBJECTIVE
  The aim of the present study was to identify whether adolescents with type 1 diabetes receiving modern multiple insulin injection therapy (MIT) have abnormal EEGs, and to elucidate possible correlations with a history of severe hypoglycaemia, poor metabolic control and nerve conduction defects.
  
  
  METHODS
  We investigated 35 patients (age 14-19 years) with disease duration 7.6+/-4.6 years, and 45 healthy control subjects. EEG spectral components were obtained from 15-min recordings in resting, awake subjects. Nerve conduction was measured bilaterally in motor and sensory fibres in the median, peroneal and sural nerves.
  
  
  RESULTS
  The EEGs of patients showed an increase in slow activity (delta and theta) and a reduction in alpha peak frequency, both of which were most pronounced in the frontal regions (p<0.001). They also showed a decrease in fast activity, which was most pronounced bilaterally in the posterior temporal regions (alpha p<0.001, beta p<0.01, gamma p<0.001). A history of severe hypoglycaemia was correlated with a global increase in theta activity (p<0.01-0.05). Poor metabolic control, measured as acute and long-term HbA1c levels, was correlated with an increase in delta activity and a decrease in alpha peak frequency. The decrease in fast activity in the temporal regions was a separate type of abnormality because it had a different distribution, and was not correlated with the increase in delta/theta power, poor metabolic control or with hypoglycaemia.
  
  
  CONCLUSIONS
  Recurrent severe hypoglycaemia and poor metabolic control are risk factors for EEG abnormalities in adolescents with type 1 diabetes receiving MIT treatment. In addition, we found pronounced abnormalities in the temporal regions that were not related to these risk factors.
authors.affiliation: Department of Clinical Neurophysiology, Karolinska University Hospital, Stockholm, Sweden. lars.hyllienmark@karolinska.se
authors.forename: L
authors.initials: L
authors.lastname: Hyllienmark
authors.forename: J
authors.initials: J
authors.lastname: Maltez
authors.forename: A
authors.initials: A
authors.lastname: Dandenell
authors.forename: J
authors.initials: J
authors.lastname: Ludvigsson
authors.forename: T
authors.initials: T
authors.lastname: Brismar
mesh_terms: D000293:Adolescent; D017668:Age of Onset; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D004569:Electroencephalography; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology*; D009046:Motor Neurons / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology; D010543:Peroneal Nerve / Q000503:physiopathology; D013497:Sural Nerve / Q000503:physiopathology
chemical_list: D001786:Blood Glucose
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