Insular lesions and hyperglycemia in acute stroke revisited.

Insular Lesions and Hyperglycemia in Acute Stroke Revisited To the Editor: I have read with interest the article by Allport et al1 reporting that insular cortical ischemia was associated with poststroke hyperglycemia. Previous studies have associated insular lesions with ECG abnormalities and have suggested a relation to cerebrogenic sudden death, possibly through the generation of fatal cardiac arrhythmias.2 It has further been hypothesized that this might come about either in an indirect manner by activation of the sympathicoadrenal system3 or by direct effects.4 Laterality of insular effects in humans has further been demonstrated.5 As increasing sympathicoadrenal tone causes hyperglycemia, the finding of higher blood glucose in patients with insular lesions may support this mechanism. We investigated s-cortisol levels in the light of insular lesions in 172 patients with acute stroke within 6 hours of admission, 42 of whom had unilateral insular lesions.6 In univariate analysis, we found that cortisol levels related significantly to insular damage, especially right insular damage. However, in multivariate analysis also including stroke severity on admission and early infarction signs on initial CT scan, this was no longer the case. On reading the article of Allport et al, I further tried to reproduce their findings concerning blood glucose and insular lesions in our 179 patients in whom blood glucose was measured on admission within 6 hours of stroke onset. Mean blood glucose in patients with insular lesions was 6.6 mmol/L in comparison to 6.4 mmol/L in patients with no insular lesions (P 0.317). In patients with right insular lesions, mean blood glucose was 7.0 mmol/L in comparison to 6.4 mmol/L in patients with left or no insular lesions (P 0.564). These findings support the idea of insular damage causing its effects in a direct manner rather than in an indirect manner by sympathicoadrenal activation.