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Neurovascular coupling is impaired in slow walkers: The MOBILIZE Boston Study
Author(s) -
Sorond Farzaneh A.,
Kiely Dan K.,
Galica Andrew,
Moscufo Nicola,
Serrador Jorge M.,
Iloputaife Ike,
Egorova Svetlana,
Dell'Oglio Elisa,
Meier Dominik S.,
Newton Elizabeth,
Milberg William P.,
Guttmann Charles R. G.,
Lipsitz Lewis A.
Publication year - 2011
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.22433
Subject(s) - neurovascular bundle , medicine , cardiology , hyperintensity , cerebral blood flow , middle cerebral artery , magnetic resonance imaging , quartile , confidence interval , anesthesia , psychology , anatomy , radiology , ischemia
Objective: Neurovascular coupling may be involved in compensatory mechanisms responsible for preservation of gait speed in elderly people with cerebrovascular disease. Our study examines the association between neurovascular coupling in the middle cerebral artery and gait speed in elderly individuals with impaired cerebral vasoreactivity. Methods: Twenty‐two fast and 20 slow walkers in the lowest quartile of cerebral vasoreactivity were recruited from the MOBILIZE Boston Study. Neurovascular coupling was assessed in bilateral middle cerebral arteries by measuring cerebral blood flow during the N‐Back task. Cerebral white matter hyperintensities were measured for each group using magnetic resonance imaging. Results: Neurovascular coupling was attenuated in slow compared to fast walkers (2.8%; 95% confidence interval [CI], −0.9 to 6.6 vs 8.2%; 95% CI, 4.7–11.8; p = 0.02). The odds ratio of being a slow walker was 6.4 (95% CI, 1.7–24.9; p = 0.007) if there was a high burden of white matter hyperintensity; however, this risk increased to 14.5 (95% CI, 2.3–91.1; p = 0.004) if neurovascular coupling was also attenuated. Interpretation: Our results suggest that intact neurovascular coupling may help preserve mobility in elderly people with cerebral microvascular disease. Ann Neurol 2011;