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Marc Fisher, MD; Andrew M. Blumenfeld, MD; Thomas W. Smith, MD
Worcester Memorial Hospital Departments of Neurology and Neuropathology University of Massachusetts Medical School Worcester, MA 01605

Arch Neurol. 1989;46(6):605.

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In Reply.—

We thank Norris and colleagues for their insightful comments. They observed the frequent presence of large intraplaque hemorrhages in carotid endarterectomy specimens from symptomatic patients. Yet, the intraplaque hemorrhages were not related to development of ischemic symptoms because the age of the hemorrhages appeared to predate symptom development. These results are similar to those of Lennihan et al¹ who observed plaque hematomas in 96 of 198 carotid endarterectomy specimens, but concluded that there was no significant association between ipsilateral ischemic symptoms and the presence of intraplaque hemorrhage. Neither study can directly answer the question as to whether intimal surface disruption initiates ischemic symptoms and promotes the development of intraplaque hemorrhage because sections were apparently not obtained at 100- to 200-µm intervals, and the time delay to pathologic analysis of subacute and chronic hematomas could have allowed for intimal repair. Additionally, the presence of intraplaque hemorrhage in both studies was . . . [Full Text PDF of this Article]

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