Effects of intensified metabolic control on CNS function in type 2 diabetes.
The mild cognitive decline associated with type 2 diabetes (T2DM) has been suggested to be reversible with improved glycemic control. In order to characterise this cognitive decline and study the effects of improved glycemic control we have studied patients with T2DM (N=28) and healthy control subjects (N=21). One group of patients with diabetes (N=15) were given a 2-month treatment of intensified glycemic control, whereas the other group (N=13) maintained their regular treatment. Cognitive function in four different domains, auditory event-related potentials (ERPs) and resting EEG power spectrum were studied in the two groups of patients and in healthy control subjects before and after the 2-month trial period. There were significant differences at baseline (p<0.02) between patients with T2DM and controls. Patients had lower scores in two cognitive domains: verbal fluency (p<0.01) and visuospatial ability (p<0.03). T2DM also affected ERP with a decrease in N100 amplitude (p<0.04) and an increase in P300 latency (p<0.03). Furthermore, resting EEG activity in the beta band (13-30Hz) was reduced (p<0.04). The change between 1st and 2nd investigation was significantly different in the three groups of patients/subjects (p<0.03). Patients receiving intensified treatment for glycemic control had an improvement of cognitive ability in visuospatial ability (p<0.02) and semantic memory performance (p<0.04) together with increased resting EEG activity in the alpha band (8-13Hz, p<0.02) and connectivity in the theta (4-8Hz, p<0.03) and alpha bands (p<0.03) over central and lateral regions. Furthermore, there was an increase in the connectivity in the beta band (p<0.04) over the central regions of the scalp. In conclusion, subjects with T2DM had a similar type of cognitive function impairment and EEG/ERP abnormality as previously demonstrated for subjects with type 1 diabetes (T1DM). Intensified therapy showed cognitive improvement not shown for regular treatment, suggesting that the negative effect of T2DM on cognition is reversible by means of improved glycemic control. Furthermore, there was an improvement in electro-physiological measures, suggesting increased availability of compensatory mechanisms in subjects with intensified treatment.
Cooray
Gerald
G
Department of Clinical Neurophysiology, Karolinska University Hospital (Solna), SE-17176 Stockholm, Sweden. gerald.cooray@ki.se
Nilsson
Erik
E
Wahlin
Ake
A
Laukka
Erika J
EJ
Brismar
Kerstin
K
Brismar
Tom
T
D000368:Aged; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism*; D016022:Case-Control Studies; D002490:Central Nervous System / Q000503:physiopathology*; D003071:Cognition / Q000187:drug effects; D003072:Cognition Disorders / Q000209:etiology / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D004569:Electroencephalography; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D013064:Speech Disorders / Q000453:epidemiology / Q000209:etiology
D001786:Blood Glucose; D007004:Hypoglycemic Agents