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Abstract Details

Hemispheric Cortical Atrophy ipsilateral to Carotid Stenosis
Cerebrovascular Disease and Interventional Neurology
N5 - Neuroscience in the Clinic: Brain Health and the Neurovascular Unit (3:35 PM-3:45 PM)
001
Carotid stenosis has been associated with stroke and cognitive impairment. It remains unclear if cortical atrophy, a marker for neurodegeneration, may be in the mechanistic pathway in the association between carotid stenosis and cognitive decline. If so, carotid revascularization may potentially be a treatment option to slow cognitive decline.  

We aim to evaluate the association between carotid stenosis and brain atrophy (cortical thickness, gray matter volume, white matter volume) ipsilateral to the cervical carotid stenosis.

Patients age ≥40 years with carotid stenosis on carotid ultrasound who underwent MRI brain and intracranial angiogram from 2011-2015 were included. Severity of carotid stenosis was defined using NASCET criteria as 50-69% (moderate), 70-99% (high-grade) or occluded. Cortical thickness, gray matter volume and white matter volume were estimated on T1-weighted images using FreeSurfer software. Measures of brain atrophy were compared between hemisphere and across severity of carotid stenosis. 

Of the 168 patients, mean age was 71±10 years. Moderate and severe stenosis was present in 37.5% and 45.8%, respectively, and 16.7% had carotid occlusion. Mean cortical thickness was 2.5±0.01mm, gray matter volume was 211±1.6 cm3, and white matter volume was 241±2cm3. Gray matter volume was smaller on the side of stenosis compared to contralateral side (211 vs 212cm3,p=0.004). Cortical thickness and white matter volume were also smaller on the side of carotid stenosis but did not achieve statistical significance (p=0.099, p=0.070). There was a dose-dependent relationship between severity of carotid stenosis and hemispheric white matter volume:-0.29,-0.34,-3.54cm3 (trend-p=0.036).

We found a 0.5% reduction in cortical gray matter volume on the side of carotid stenosis. While the mean difference may seem small, it was 2.5-fold higher than yearly cortical thinning in healthy aging at midlife. Future analyses should consider whether the cortical thinning mediates cognitive impairment and if revascularization may slow cortical atrophy to prevent cognitive decline. 
Authors/Disclosures
Michelle P. Lin, MD (Mayo Clinic Florida)
PRESENTER
Dr. Lin has nothing to disclose.
Erik Middlebrooks No disclosure on file
No disclosure on file
Bhrugun Anisetti, MBBS Dr. Anisetti has nothing to disclose.
Ahamed M. Elkhair, MD (Mayo Clinic) Dr. Elkhair has nothing to disclose.
Hossam Youssef, MD Mr. Youssef has nothing to disclose.
No disclosure on file
Kevin M. Barrett, MD, FAAN (Mayo Clinic) Dr. Barrett has nothing to disclose.
Nilufer Taner, MD, PhD, FAAN (Mayo Clinic) The institution of Dr. Taner has received research support from NIH.
Thomas G. Brott, MD, FAAN (Mayo Clinic) Dr. Brott has nothing to disclose.
James F. Meschia, MD, FAAN (Mayo Clinic) The institution of Dr. Meschia has received research support from NINDS. The institution of Dr. Meschia has received research support from NINDS.