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Neurosurgery. 2018 Mar 1;82(3):322-328. doi: 10.1093/neuros/nyx173.

The Preservation of Cognition 1 Year After Carotid Endarterectomy in Patients With Prior Cognitive Decline.

Author information

1
Department of Neurological Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
2
Wisconsin Surgical Outcomes Center Research Program, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
3
Department of Medicine, Cardiovascular Medicine Division, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
4
Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
5
Department of Medical Physics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
6
Department of Electrical and Computer Engineering, University of Wisconsin-Madison, Madison, Wisconsin.
7
Department of Neurology, University of Wisconsin School of Medicine and Public Health, Centennial Building, Madison, Wisconsin.

Abstract

BACKGROUND:

Vascular cognitive decline is critically important in the course of atherosclerosis and stroke.

OBJECTIVE:

To explore the hypothesis that carotid endarterectomy (CEA) by removing an unstable plaque may slow the course of vascular cognitive decline in both symptomatic and asymptomatic patients.

METHODS:

Patients with clinically significant (>60%) carotid stenosis were studied preop and 1 yr post-CEA for clinical symptoms, vascular cognitive decline, instability of carotid plaque-presence of microemboli, brain white matter changes, and medical risk factors.

RESULTS:

Forty-six percent were classically symptomatic. All patients showed vascular cognitive decline at presentation which correlated with degree of plaque instability. Significant white matter hyperintensity changes (48.7%) and cerebral emboli (25%) were also seen at baseline in both classically symptomatic and asymptomatic. One year after CEA, both groups showed no decline in cognitive function and significant improvement in 2 tests (P = .028 and P = .013). Brain white matter hyperintensities were unchanged. Microemboli were reduced but remained present (17.86%). Improvement was predicted by the presence of hypertension (P = .001), or less advanced cognitive decline preoperatively (P = .009).

CONCLUSION:

This study demonstrates the importance of vascular cognitive decline in atherosclerotic disease. This is a function of the degree of instability of the atherosclerotic plaque more than the presence of stroke symptoms. It further suggests that atherosclerotic vascular cognitive decline need not be inevitable, and may be modified by treating hypertension and removal of the unstable plaque. This highlights the need for continued research on the cognitive effects of cerebrovascular disease and the synergistic benefits of intensive medical and surgical therapy.

PMID:
28575478
PMCID:
PMC5711632
[Available on 2019-03-01]
DOI:
10.1093/neuros/nyx173

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