This Article Full Text Full Text (PDF) All Versions of this Article: 39/2/249    most recent STROKEAHA.107.500967v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Oppenheimer, S. Search for Related Content PubMed PubMed Citation Articles by Oppenheimer, S. Related Collections Acute Cerebral Infarction Related Article

(Stroke. 2008;39:249.)
© 2008 American Heart Association, Inc.

Editorial

Plus Ça Change ...

Stephen Oppenheimer, MD, PhD

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@hotmail.com

Key Words: radiology

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 . . . [Full Text of this Article]

Related Article:

Middle Cerebral Artery Infarcts Encompassing the Insula Are More Prone to Growth

Hakan Ay, E. Murat Arsava, Walter J. Koroshetz, and A. Gregory Sorensen
Stroke 2008 39: 373-378. [Abstract] [Full Text] [PDF]