BACKGROUND: Cognitive sequelae frequently follow subarachnoid hemorrhage (SAH) and include deficits across multiple domains of executive function. This factor affects overall functional outcomes negatively, especially in younger patients. Several clinical correlates predict development and severity of cognitive dysfunction after SAH. Hypothetical mechanisms of cognitive dysfunction in the absence of radiographic lesion include cerebral hypoperfusion and blood breakdown products, resulting in perturbed interneuronal communication and network synchrony, excitotoxicity, and altered microRNA expression. METHODS: The PubMed database was searched for articles discussing cognitive outcomes in patients with unruptured and ruptured intracranial aneurysmal disease, sequelae of treatment, and modalities for neuropsychologic testing. RESULTS: Treatment of unruptured intracranial aneurysms, although capable of preventing SAH, comes with its own set of complications and may also affect cognitive function. Neuropsychological tests such as the Montreal Cognitive Assessment, Mini-Mental Status Examination, and others have proved useful in evaluating cognitive decline. Studies using functional neurologic imaging modalities have identified regions with altered activation patterns during various cognitive tasks. The sum of research efforts in this field has provided useful insights and an initial understanding of cognitive dysfunction after aneurysm treatment and SAH that should prove useful in guiding and rendering future investigations more fruitful. CONCLUSIONS: Development of finer and more sensitive neuropsychological tests in evaluating the different domains of cognitive function after aneurysm treatment and SAH in general will be useful in accurately determining outcomes after ictus and comparing efficacy of different therapeutic strategies.
BACKGROUND: Cognitive sequelae frequently follow subarachnoid hemorrhage (SAH) and include deficits across multiple domains of executive function. This factor affects overall functional outcomes negatively, especially in younger patients. Several clinical correlates predict development and severity of cognitive dysfunction after SAH. Hypothetical mechanisms of cognitive dysfunction in the absence of radiographic lesion include cerebral hypoperfusion and blood breakdown products, resulting in perturbed interneuronal communication and network synchrony, excitotoxicity, and altered microRNA expression. METHODS: The PubMed database was searched for articles discussing cognitive outcomes in patients with unruptured and ruptured intracranial aneurysmal disease, sequelae of treatment, and modalities for neuropsychologic testing. RESULTS: Treatment of unruptured intracranial aneurysms, although capable of preventing SAH, comes with its own set of complications and may also affect cognitive function. Neuropsychological tests such as the Montreal Cognitive Assessment, Mini-Mental Status Examination, and others have proved useful in evaluating cognitive decline. Studies using functional neurologic imaging modalities have identified regions with altered activation patterns during various cognitive tasks. The sum of research efforts in this field has provided useful insights and an initial understanding of cognitive dysfunction after aneurysm treatment and SAH that should prove useful in guiding and rendering future investigations more fruitful. CONCLUSIONS: Development of finer and more sensitive neuropsychological tests in evaluating the different domains of cognitive function after aneurysm treatment and SAH in general will be useful in accurately determining outcomes after ictus and comparing efficacy of different therapeutic strategies.