A neurysmal subarachnoid hemorrhage (aSAH) is a medical emergency with very high morbidity and mortality rates. 1-4 Advances in care have decreased mortality, 5 and survival rates after aneurysm rupture are reported at 65%. 6 Among survivors, ≤80% are considered to have good recovery 7 using the Glasgow Outcome Scale. 8 However, more sophisticated tools reveal that ≤50% have neurocognitive deficits, usually in the absence of structural lesions. 7,[9][10][11][12][13] In contrast to other types

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... stroke, aSAH affects a relatively young, productive population. 6 The combination of younger age and high morbidity yields substantial long-term personal and socioeconomic burden, with estimates that ≤50% of survivors will not return to the same level of work. 14,15 Impairments in memory are reported in ≈60% of survivors and executive function and language problems in 75%. 6,12 Deficits in visuospatial construction, memory, mental flexibility, and psychomotor speed are shown even in good-outcome patients 16 and can persist beyond 1 year. 7,12,17 Cognitive impairments are often more highly correlated with health-related quality-of-life scores than are physical impairments. 18 The cause of neurocognitive deficits remains unknown, 19 despite structural magnetic resonance imaging (MRI) investigations of lesion location and atrophy. 20-24 Theories of immediate damage include diffuse injury caused by decreased perfusion at time of rupture 16,25 and the presence of blood and its breakdown products in subarachnoid space. 11 Injury severity and volume of subarachnoid blood have been correlated with cognitive outcomes. 7,10,26 Reduced cerebral blood flow in the frontal lobes after clipping has also been correlated to cognitive function. 27 Because of variable impacts of hydrocephalus, aneurysm location, treatment method, vasospasm, and ischemia on cognitive function after aSAH, 10,12,16,28 a tool to describe patterns of neural activation in this population is justified. Reconstruction of white matter tracts in the vicinity Background and Purpose-Neurocognitive deficits are common among survivors of aneurysmal subarachnoid hemorrhage, even among those with good outcomes and no structural lesions. This study aims to probe the neurophysiological underpinnings of cognitive dysfunction among patients with ruptured intracranial aneurysms using magnetoencephalography (MEG). Methods-Thirteen patients who had undergone uncomplicated coiling for aneurysmal subarachnoid hemorrhage and 13 matched controls were enrolled. Neuropsychological tests were done before magnetoencephalography scans. Magnetoencephalography data were acquired in a 151-channel, whole-head magnetoencephalography system for resting state and 2 cognitive tasks (go-no-go and set-shifting). Mean time from treatment to test was 18.8 months. Results-Cognitive tasks of inhibition (go-no-go) indicated greater activation in the right anterior cingulate and inferior frontal gyrus, and cognitive set-shifting tasks (mental flexibility) indicated greater activity in the bilateral anterior cingulate cortex and right medial frontal gyrus among aneurysmal subarachnoid hemorrhage patients, with significantly different timing of activation between groups. Resting-state, beta-band connectivity of the anterior cingulate correlated negatively with Montreal Cognitive Assessment scores (left: r=−0.56; P<0.01 and right: r=−0.55; P<0.01): higher connectivity of this region was linked to poorer cognitive test performance. Conclusions-We have shown increased activation in areas of the anterior cingulate gyrus and frontobasal regions during the execution of more demanding tasks in good grade. The degree of activation in the anterior cingulate gyrus has a negative correlation with cognitive (Montreal Cognitive Assessment) scores. These subtle differences may be related to the common neurocognitive and behavioral complaints seen in this patient population. (Stroke. 2016;47:2503-2510. The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/