Research Article
Sherifa A. Hamed, Refaat F. Ab
Abstract
Central nervous system (CNS) abnormalities are known in patients with type 2 diabetes mellitus (T2DM) and attributed mostly to diabetic vasculopathy. We aimed to determine the direct effect of chronic hyperglycemia on the brain in absence of numerous potential vascular confounders. we systematically investigated markers of brain compromise in 57 patients with T2DM. Cognition was tested using a sensitive battery of psychometric testing [Mini-mental State Examination or MMSE, Stanford Binet Intelligence Scales 4th edition (SBIS) and Wechsler Memory Scale- Revised or WMS-R] and by recording P300 component of event related potentials [ERPs], a neurophysiological analogue for cognitive function. We also measured the serum levels of neuron specific enolase (NSE), a sensitive marker of neuronal cell damage. Compared to healthy subjects (n = 40), patients had lower total scores of cognitive testing (MMSE, SBIS and WMS-R) (p = 0.004), higher Beck Depression Inventory 2nd edition (BDI-II) scores (p = 0.001), prolonged latencies and reduced amplitudes of P300 component of ERPs (p = 0.0001 for both) and higher NSE concentrations (p = 0.001). No differences in clinical, lab and ERPs variables, scores of cognition testing and depression and NSE concentrations were identified regardless the degree of control on anti-diabetic treatments. Significant correlations had been identified between total score of cognitive testing and age (r = -0.370, p = 0.050), duration of illness (r = -0.658, p = 0.001), blood glucose level (r = -0.543, p= 0.010), ERPs latency (r = -0.560, p = 0.004) and amplitude ( r = 0.340, p = 0.053) and NSE concentrations (r = -0.698, p = 0.001). After adjustment of confounders, the total scores of cognitive testing was significantly correlated with NSE concentrations regardless the level of glycemic control. This study indicates that direct brain damage may result from poor glycemic control and chronic hyperglycemia and this contributes to progressive cognitive deficits with T2DM.