Loss of temporal lobe beta power in young adults with type I diabetes mellitus

被引:35
作者
Brismar, T [1 ]
Hyllienmark, L
Ekberg, K
Johansson, BL
机构
[1] Karolinska Hosp, Karolinska Inst, Dept Clin Neurophysiol, Sect Clin Physiol, S-17176 Stockholm, Sweden
[2] Karolinska Hosp, Karolinska Inst, Dept Surg Sci, Sect Clin Physiol, S-17176 Stockholm, Sweden
关键词
beta power; cognitive function; diabetic complications; EEG; encephalopathy; human; insulin; neuropathy; power spectrum; type I diabetes mellitus;
D O I
10.1097/00001756-200212200-00019
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cognitive defects have been reported in type I diabetes mellitus with possible correlation to recurrent episodes of hypoglycemia. The purpose of the present study was to identify signs of brain dysfunction with quantitative EEG in adults with insulin-dependent (type 1) diabetes. Patients (n = 49) with type I diabetes and controls (n 51) were recruited. All patients had good glycemic control, no diabetic polyneuropathy and a minor history of severe hypoglycaemia. EEG was recorded for 15 min following a standardized protocol, power spectra were obtained from 236-584 s of artefact-free EEG from each subject and EEG was repeated in diabetic patients after 3 and 9 months. The most pronounced finding was a loss of fast oscillations (alpha, beta and gamma activity) in both posterior temporal regions, with p < 0.001 for beta and p < 0.05 or 0.01 for alpha and gamma activity in the diabetes patients. A decrease in beta activity was also present bilaterally in the anterior temporal and occipital regions (p < 0.05 or 0.01). The alpha peak frequency was lower in patients than in controls, with reductions bilaterally in the temporo-central regions (p < 0.01). These changes were not found to correlate to a previous history of hypoglycaemia. The alpha and beta power showed a high test-retest reliability at both 3 and 9 months (0.88-0.92). The focal decrease in temporal lobe fast activity suggests that these brain regions are preferentially affected by type I diabetes. This abnormality may be related to the mechanism underlying the cognitive dysfunction described in diabetes.
引用
收藏
页码:2469 / 2473
页数:5
相关论文
共 23 条
[1]   Cerebral complications of diabetes: Clinical findings and pathogenetic mechanisms [J].
Biessels, GJ .
NETHERLANDS JOURNAL OF MEDICINE, 1999, 54 (02) :35-45
[2]  
Bjorgaas M, 1996, ACTA NEUROL SCAND, V93, P398
[3]   Cognitive function in Type 1 diabetic children with and without episodes of severe hypoglycaemia [J].
Bjorgaas, M ;
Gimse, R ;
Vik, T ;
Sand, T .
ACTA PAEDIATRICA, 1997, 86 (02) :148-153
[4]   SEVERE HYPOGLYCEMIA AND INTELLIGENCE IN ADULT PATIENTS WITH INSULIN-TREATED DIABETES [J].
DEARY, IJ ;
CRAWFORD, JR ;
HEPBURN, DA ;
LANGAN, SJ ;
BLACKMORE, LM ;
FRIER, BM .
DIABETES, 1993, 42 (02) :341-344
[6]   THE PREVALENCE BY STAGED SEVERITY OF VARIOUS TYPES OF DIABETIC NEUROPATHY, RETINOPATHY, AND NEPHROPATHY IN A POPULATION-BASED COHORT - THE ROCHESTER DIABETIC NEUROPATHY STUDY [J].
DYCK, PJ ;
KRATZ, KM ;
KARNES, JL ;
LITCHY, WJ ;
KLEIN, R ;
PACH, JM ;
WILSON, DM ;
OBRIEN, PC ;
MELTON, LJ .
NEUROLOGY, 1993, 43 (04) :817-824
[7]   Dynamic predictions: Oscillations and synchrony in top-down processing [J].
Engel, AK ;
Fries, P ;
Singer, W .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (10) :704-716
[8]   CHARACTERISTICS OF LEARNING AND MEMORY IN STREPTOZOCIN-INDUCED DIABETIC MICE [J].
FLOOD, JF ;
MOORADIAN, AD ;
MORLEY, JE .
DIABETES, 1990, 39 (11) :1391-1398
[9]   QUANTITATIVE EEG IN YOUNG DIABETICS [J].
HAUSER, E ;
STROHMAYER, C ;
SEIDL, R ;
BIRNBACHER, R ;
LISCHKA, A ;
SCHOBER, E .
JOURNAL OF CHILD NEUROLOGY, 1995, 10 (04) :330-334
[10]   Conventional versus intensive diabetes therapy in children with type 1 diabetes - Effects on memory and motor speed [J].
Hershey, T ;
Bhargava, N ;
Sadler, M ;
White, NH ;
Craft, S .
DIABETES CARE, 1999, 22 (08) :1318-1324