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Anatomy of executive deficit following ruptured anterior communicating artery aneurysm
Author(s) -
Martinaud O.,
Perin B.,
Gérardin E.,
Proust F.,
Bioux S.,
Gars D. Le,
Hannequin D.,
Godefroy O.
Publication year - 2009
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2009.02546.x
Subject(s) - lesion , medicine , stroop effect , executive functions , cognitive deficit , cognition , medial frontal gyrus , striatum , middle frontal gyrus , inferior frontal gyrus , neuroscience , prefrontal cortex , anterior communicating artery , psychology , aneurysm , pathology , psychiatry , radiology , cognitive impairment , dopamine
Background and purpose:  To evaluate behavioral and cognitive deficits following anterior communicating artery aneurysm rupture and determine critical lesion locations. Methods:  We investigated 74 patients with standardized cognitive tests and behavioral inventory. Two examiners rated MRI signal abnormalities in 51 predetermined regions of interest. Classification tree analysis was used to select regions associated with each cognitive deficit. Results:  Eleven patients presented behavioral executive deficits and 10 had cognitive executive deficit. Their presence depended on left hemisphere lesions only: (i) ventral striatum lesion was associated with behavioral executive deficit ( P  = 0.04), reduction of activities ( P  = 0.01), and hyperactivity ( P  = 0.02); (ii) superior frontal gyrus lesion, with cognitive executive deficit ( P  = 0.01), action initiation deficit ( P  = 0.02), and rule deduction deficit ( P  = 0.02); (iii) anterior half of centrum semiovale lesion, with Stroop inhibition deficit ( P  = 0.02); (iv) medial superior and middle frontal gyri lesions, with task coordination deficit ( P  = 0.01); and (v) middle frontal gyrus lesion, with words generation deficit ( P  = 0.02). Conclusion:  This study supports that (i) cognitive executive deficits depend mostly on lateral prefrontal lesions, (ii) with locations varying according to executive process, and (iii) behavioral executive deficits are mainly due to left ventral striatum lesion in post‐aneurysmal damage.

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