Published online before print January 3, 2008, doi: 10.1161/STROKEAHA.107.500967
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(Stroke. 2008;39:249.)
© 2008 American Heart Association, Inc.
Editorial |
Plus Ça Change ...
From the Vanderbilt University School of Medicine, Nashville, Tenn; and SMS Inc, Baltimore, Md.
Correspondence to Stephen Oppenheimer, MD, PhD, 10151 York Rd, Suite 120, Cockeysville, MD 21030. E-mail soppenh{at}hotmail.com
Key Words: radiology
See related article, pages 373–378.
Stroke progression is a noteworthy phenomenon. It may manifest radiologically, clinically or as both. Several systemic upheavals contribute including cardiovascular dysregulation, blood glucose disturbances and hyperthermia to name just three.1 No previous studies, however, have really assessed whether any particular stroke location might be especially prone to progression.
In this retrospective study of 61consecutive patients innocent of reperfusion therapy, Ay et al2 show that insular infarction is more prone to radiological extension over a median of 7 days (range 4.5 to 52.5 days) than stroke excluding the insular cortex. The contributions of various confounding variables including stroke volume and vascular territory as well as age and admission blood glucose were assessed using linear regression models.
Why is the insular cortex so attractive in this regard? This previously ill-understood region is a significant site of autonomic and nociceptive representation and integration. Insular strokes are associated with an increased risk of adverse cardiovascular outcomes including sudden death3 correlating with stroke-related cardiovascular autonomic abnormalities.4 Additionally, blood glucose dysregulation occurs significantly more frequently with insular stroke location.5 It would therefore be entirely reasonable to infer that insular stroke invokes cardiovascular and endocrine changes that compromise cerebral tissue when at its most vulnerable leading to stroke extension.
However, we do not yet know whether these radiological changes are functionally significant because no clinical assessments were reported. Additionally, whether the mechanistic explanations for stroke extension are relevant to the findings of this study is unclear. The authors did not gather blood glucose, inflammatory or cardiovascular data during follow-up. Therefore, some may question whether the location-related radiological changes are truly important. But if you ask me, there is little doubt in my mind that they are.
Acknowledgments
Disclosures
None.
Footnotes
The opinions in this editorial are not necessarily those of the editors or of the American Heart Association.
References
1. Oppenheimer SM, Hachinski VC. The complications of acute stroke. Lancet. 1992; 329: 721–724.
2. Ay H, Arsava EM, Koroshetz WJ, Sorensen AG. MCA infarcts encompassing the insula are more prone to growth. Stroke. 2008; 39: 373–378.
3. Laowattana S, Zeger S, Lima J, Goodman S, Wittstein I, Oppenheimer SM. Left insular stroke is associated with adverse cardiac outcome. Neurology. 2006; 66: 477–483.
4. Oppenheimer SM, Martin WM, Kedem G. Left insular cortex lesions perturb cardiac autonomic tone. Clinical Autonomic Research. 1996; 6: 131–140.[CrossRef][Medline] [Order article via Infotrieve]
5. 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.
Related Article:
Stroke 2008 39: 373-378.
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