Jennifer Dearborn, MD 

Buratti L, Balucani C, Viticchi G, Falsetti L, Altamura C, Avitabile E, et al. Cognitive Deterioration in Bilateral Asymptomatic Severe CarotidStenosis. Stroke. 2014

Buratti et al. recently examined the question, what might the mechanism of cognitive impairment be in patients with large vessel (carotid) atherosclerosis? The authors had a hypothesis that cognitive dysfunction, if present, might be mediated by impaired cerebrovascular reactivity at the arteriolar level, as a result of more proximal, large vessel occlusion. To test this hypothesis, they evaluated patients presenting to a vascular ultrasound laboratory on a referral basis. Duplex sonography was used to evaluate neck and intracranial arteries. The major predictors were CVR (a measure of the arteriolar dilation in response to stimuli) using the breath holding index (BHI) test, and carotid intima media thickness (IMT). The outcome was change in Mini-mental status examination in the 3-year study period.



The authors found, after adjustments for hypertension age, sex and coronary artery disease that an abnormal BHI bilaterally was associated with a greater change in MMSE, and interestingly, this did not differ by carotid IMT. The authors suggest that the technique may show that chronic hypoperfusion contributes to cognitive decline. They acknowledge, however, that it is difficult to sort out the effects of generalized vascular disease, which may coexist with carotid disease and be the causual agent, rather than the presence of carotid disease itself. Therefore extrapolation of this studies results to suggestion of a mechanism of cognitive decline should be interpreted with caution, as it is difficult to adequately control for underlying vascular risk factors completely to show an independent association between BHI and hemodynamics and cognitive decline. However this study does suggest that the mechanism of cognitive decline should be investigated more carefully, perhaps by correlating hemodynamic measures with MRI markers of brain pathology in larger sample. For example, white matter hyperintesities, or more lacunes, may also be present in those with impaired BHI, and this would be an alternate and equally interesting explanation of the association.