Abstract
Introduction: Hyperglycemia leads to a poor prognosis in acute stroke. We previously reported that neurological deterioration was related to larger variation of daily fasting blood glucose levels a week after acute stroke. In the present study, neurological worsening after stroke was correlated with delayed large fluctuation of glucose levels in the late half of week after admission. Methods: After excluding patients who underwent tPA or surgical treatment and had an NIHSS score at acute stroke admission exceeding 23, a total of 811 diabetic patients (267 females; mean age, 70.4±10.1 years; median age, 71 years) was enrolled. Blood glucose (BG) levels were measured three times a day at 6 AM, noon, and 6 PM for 7 days after admission. For the blood glucose levels, the average and successive variation (SV=[1/(n-1)*sigma{(BG i +1 -BG i )^2}]^0.5 while i denotes i th measurement of blood glucose), as an indicator of variation of BG levels, were calculated from two admission period, the early half (days 1 to 3, i=1 to 9) and the late half of week (days 4 to 7, i=10 to 21), respectively. Differences in BG and SV between the early and late half of week were evaluated. Patients whose NIHSS scores increased by ≥4 points from admission to discharge were classified into the exacerbation group. Results: The exacerbation group included 30 (3.7%) patients. The exacerbation group had a higher proportion of female and elderly patients and higher NIHSS scores on admission than the non-exacerbation group. From the early to late half of week, mean BG declines were 2.0±35.1 mg/dL in the exacerbation group and 7.9±24.4 mg/dL in the non-exacerbation group (p=0.287). While SV did not change (0.9±23.1) in the non-exacerbation group, it increased by 10.5±30.2 in the exacerbation group (p=0.017). Logistic regression analysis showed that a larger increase in SV difference was related to neurological exacerbation (HR=1.016, 95%CI=1.000-1.032, p=0.050). Conclusion: An increase in fluctuation of blood glucose levels a week after stroke, rather than its absolute reduction, was an independent risk factor of neurological deterioration in diabetic patients. These findings may suggest a vicious association between impaired glucose metabolism and symptom progression.
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