TIAs (carotid)

Seemant Chaturvedi MD (Dr. Chaturvedi of Wayne State University received grant support from Boehringer Ingelheim and consulting fees from Merck.)
Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released September 15, 1994; last updated September 4, 2015 expires September 4, 2018

This article includes discussion of carotid TIAs, transient hemispheric attack, transient ischemic attacks: carotid artery territory. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

The author provides an update on carotid transient ischemic attacks (TIAs), with description of new studies pertaining to carotid revascularization outcomes. Performance of carotid surgery after previous thrombolysis treatment is discussed. Finally, American Stroke Association recommendations for secondary stroke prevention are cited.

Key points

 

• Transient ischemic attacks are an important warning sign for stroke and deserve rapid evaluation and treatment.

 

• Risk stratification schemes can be useful for identifying the highest risk transient ischemic attack patients.

 

• Patients with transient ischemic attacks should receive rapid medical therapy (antithrombotic therapy for all, antihypertensives and statins for most) and carotid revascularization in select subjects.

Historical note and terminology

In 1951, Fisher described 7 patients with internal carotid artery occlusion and transient or permanent ischemic symptoms using the words "brief transient attacks of paralysis" (Fisher 1951b). In a separate publication that same year, Fisher linked occlusive disease at the internal carotid artery bifurcation to "transient episodes of blindness, aphasia, paresthesia and paralysis," "transient attacks," "premonitory fleeting," and "transient hemiplegia" (Fisher 1951a). Fisher went on to credit many other investigators who, earlier in this century, identified similar symptoms in relation to internal carotid artery bifurcation disease. He was unsure about the mechanism of symptom production and speculated about the roles of thrombosis, vasospasm, and embolism.

This review addresses all transient ischemic attacks in the territory of the internal carotid artery or its branches: the ophthalmic artery, posterior communicating artery, anterior choroidal artery, anterior cerebral artery, and middle cerebral artery (Mohr et al 1992). The discussion will not be limited to carotid territory transient ischemic attacks that are due solely to occlusive disease at the internal carotid artery bifurcation.

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