Visual Working Memory Encoding and Recognition in Good Outcome Aneurysmal Subarachnoid Patients. Front Neurol 2018;9:494
Date
07/13/2018Pubmed ID
29997567Pubmed Central ID
PMC6028596DOI
10.3389/fneur.2018.00494Scopus ID
2-s2.0-85049062685 (requires institutional sign-in at Scopus site) 5 CitationsAbstract
Objectives: Aneurysmal subarachnoid hemorrhage (aSAH) accounts for less than 5% of strokes but is associated with significant morbidity and mortality. Amongst survivors, neurocognitive complaints are common, often despite normal imaging. We used magnetoencephalography (MEG) to investigate neurophysiological function during a visual working memory task in aSAH survivors with good recovery and normal structural imaging. Methods: Patients with aSAH treated with coiling and exhibiting good outcome measured by Glasgow Outcome Scale (GOS) and without related parenchymal structural lesions in post-treatment MRI, were recruited and compared to age- and sex-matched controls. All participants underwent intelligence and cognitive screening, structural MRI, and MEG testing in conjunction with a 1-back visual working memory task. Sensor-level global field power and virtual electrode source analysis of neuronal activity and connectivity in aSAH were assessed. Results: Thirteen patients and 13 matched controls were enrolled (age: 56 ± 11 years, 19 female). The 1-back task was completed with similar accuracy despite a trend for a longer reaction time in aSAH patients (p = 0.054). During encoding and recognition phases, aSAH patients showed significantly increased neuronal activation and hyperconnectivity in periventricular areas, specifically the anterior and posterior cingulate gyri. Conclusions: Increased posterior and anterior cingulate gyri neuronal activity is demonstrated in aSAH patients during visual working memory tasks, in the absence of structural lesions. These areas work mainly as a hub to "organize" memory storage and retrieval. Increased activity in these areas might be compensatory due to injury and consequently loss of neuronal response in connected areas in the working memory networks.
