Published online before print December 29, 2004, doi: 10.1161/01.STR.0000152959.64134.cf
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(Stroke. 2005;36:229.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Insular Lesions and Hyperglycemia in Acute Stroke Revisited
Bispebjerg Hospital, Copenhagen, Denmark
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.
References
- Allport LE, Butcher KS, Baird TA, MacGregor L, Desmond PM, Tress BM, Colman P, Davis SM. Insular cortical ischemia is independently associated with acute stress hyperglycemia. Stroke. 2004; 35: 1886–1891.
[Abstract/Free Full Text] - Cheung RTF, Hachinski VC. The insula and cerebrogenic sudden death. Arch Neurol. 2000; 57: 1685–1688.
[Abstract/Free Full Text] - Smith KE, Hachinski VC, Gibson CJ, Ciriello J. Changes in plasma catecholamine levels after insula damage in experimental stroke. Brain Res. 1986; 375: 182–185.[CrossRef][Medline] [Order article via Infotrieve]
- Oppenheimer S. The anatomy and physiology of cortical mechanisms of cardiac control. Stroke. 1993; 24 (suppl I): I-3–I-5.[Medline] [Order article via Infotrieve]
- Oppenheimer S, Hachinski VC. The cardiac consequences of stroke. Neurol Clin. 1992; 10: 167–176.[Medline] [Order article via Infotrieve]
- Christensen H, Boysen G, Johannesen HH. Serum-cortisol reflects severity and mortality in acute stroke. J Neurol Sci. 2004; 217: 175–180.[CrossRef][Medline] [Order article via Infotrieve]
Response
Royal Melbourne Hospital, Parkville, Victoria, Australia
We thank Dr Christensen for his interest in our study.1 Dr Christensen suggests that the cardiac effects of insular cortical (IC) infarction result from elevated sympathetic stimulation of the heart and not elevated sympathoadrenal activity. The IC does indeed contain chronotropic sites, but these are anatomically so closely related to more general sympathetic efferent regions that selective damage in ischemic stroke seems unlikely. Furthermore, IC sympathoadrenal and cardiac responses appear to share the same subcortical relays, which have been shown in animals to include the lateral hypothalamic area and ventrolateral medulla.2,3 Experimental IC ischemia has been shown to result in increases in extracardiac sympathetic nerve activity and epinephrine levels.4 It is therefore our hypothesis that cardiac perturbations after IC stroke are part of a more generalized sympathetic stress response, which ultimately culminates in hyperglycemia.
Nonetheless, Dr Christensen has reported a lack of elevation in acute glucose levels in his large cohort of acute ischemic stroke patients with IC involvement. We believe that this discordance between our 2 studies can be explained by 2 factors. The first is the difference in imaging techniques. Although we certainly agree that early ischemic changes can be readily appreciated with CT, even within 6 hours, the full extent of acute bioenergetic compromise is best visualized with diffusion-weighted imaging.5 The second factor is recognition that the posterior IC is an autonomic efferent region, whereas the anterior IC functions as visceral sensory cortex.6 For this reason, we analyzed our patients with respect to diffusion-weighted imaging changes in the anterior or posterior IC and indeed found elevated glucose levels only in the latter group. Dr Christensen’s cohort most certainly contains patients with isolated anterior IC involvement, as occurs in superior divisional middle cerebral artery infarction, in whom we would not expect to see autonomic changes that included glucose elevation.
References
- Allport LE, Butcher KS, Baird TA. Insular cortical ischemia is independently associated with acute stress hyperglycemia. Stroke. 2004; 35: 1886–1891.
[Abstract/Free Full Text] - Oppenheimer S. The anatomy and physiology of cortical mechanisms of cardiac control. Stroke. 1993; 24: I3–I5.[Medline] [Order article via Infotrieve]
- Cheung RT, Hachinski V. The insula and cerebrogenic sudden death. Arch Neurol. 2000; 57: 1685–1688.
[Abstract/Free Full Text] - Cechetto DF, Wilson JX, Smith KE, Wolski D, Silver MD, Hachinski VC. Autonomic and myocardial changes in middle cerebral artery occlusion: stroke models in the rat. Brain Res. 1989; 502: 296–305.[CrossRef][Medline] [Order article via Infotrieve]
- Barber PA, Darby DG, Desmond PM, Gerraty RP, Yang Q, Li T, Jolley D, Donnan GA, Tress BM, Davis SM. Identification of major ischemic change: diffusion-weighted imaging versus computed tomography. Stroke. 1999; 30: 2059–2065.
[Abstract/Free Full Text] - Cechetto DF. Identification of a cortical site for stress-induced cardiovascular dysfunction. Integr Physiol Behav Sci. 1994; 29: 362–373.[Medline] [Order article via Infotrieve]
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  F. C. Moreton, M. McCormick, and K. W Muir Insular Cortex Hypoperfusion and Acute Phase Blood Glucose After Stroke: A CT Perfusion Study Stroke, February 1, 2007; 38(2): 407 - 410. [Abstract] [Full Text] [PDF]
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