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      Cognitive domain deficits in patients with aneurysmal subarachnoid haemorrhage at 1 year

      1 , 1 , 1 , 2 , 3 , 1 , 2 , Cognitive Dysfunction after Aneurysmal Subarachnoid Hemorrhage Investigators

      (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab)

      Journal of Neurology, Neurosurgery, and Psychiatry

      BMJ Publishing Group

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          Cognitive domain deficits can occur after aneurysmal subarachnoid haemorrhage (aSAH) though few studies systemically evaluate its impact on 1-year outcomes.


          We aimed to evaluate the pattern and functional outcome impact of cognitive domain deficits in aSAH patients at 1 year.


          We carried out a prospective observational study in Hong Kong, during which, 168 aSAH patients (aged 21–75 years and had been admitted within 96 h of ictus) were recruited over a 26-month period. The cognitive function was assessed by a domain-specific neuropsychological assessment battery at 1 year after ictus. The current study is registered at ClinicalTrials.gov of the US National Institutes of Health (NCT01038193).


          Prevalence of individual domain deficits varied between 7% to 15%, and 13% had two or more domain deficits. After adjusting for abbreviated National Institute of Health Stroke Scale and Geriatric Depressive Scale scores, unfavourable outcome (Modified Rankin Scale 3–5) and dependent instrumental activity of daily living (Lawton Instrumental Activity of Daily Living<15) were significantly associated with two or more domain deficits and number of cognitive domain deficits at 1 year. Two or more domain deficits was independently associated with age (OR, 1.1; 95% CI 1.1 to 1.2; p<0.001) and delayed cerebral infarction (OR, 6.1; 95% CI 1.1 to 33.5; p=0.036), after adjustment for years of school education.


          In patients with aSAH, cognitive domain deficits worsened functional outcomes at 1 year. Delayed cerebral infarction was an independent risk factor for two or more domain deficits at 1 year.

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          Most cited references 26

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          Cerebral vascular accidents in patients over the age of 60. II. Prognosis.

           J S Rankin (1957)
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            Clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2).

            Clazosentan, an endothelin receptor antagonist, significantly and dose-dependently reduced angiographic vasospasm after aneurysmal subarachnoid haemorrhage (aSAH). We investigated whether clazosentan reduced vasospasm-related morbidity and all-cause mortality. In this randomised, double-blind, placebo-controlled, phase 3 study, we randomly assigned patients with aSAH secured by surgical clipping to clazosentan (5 mg/h, n=768) or placebo (n=389) for up to 14 days (27 countries, 102 sites, inpatient and outpatient settings) using an interactive web response system. The primary composite endpoint (week 6) included all-cause mortality, vasospasm-related new cerebral infarcts, delayed ischaemic neurological deficit due to vasospasm, and rescue therapy for vasospasm. The main secondary endpoint was dichotomised extended Glasgow outcome scale (GOSE; week 12). This trial is registered with ClinicalTrials.gov, number NCT00558311. In the all-treated dataset, the primary endpoint was met in 161 (21%) of 764 clazosentan-treated patients and 97 (25%) of 383 placebo-treated patients (relative risk reduction 17%, 95% CI -4 to 33; p=0·10). Poor functional outcome (GOSE score ≤4) occurred in 224 (29%) clazosentan-treated patients and 95 (25%) placebo-treated patients (-18%, -45 to 4; p=0·10). Lung complications, anaemia, and hypotension were more common with clazosentan. Mortality (week 12) was 6% in both groups. Clazosentan at 5 mg/h had no significant effect on mortality and vasospasm-related morbidity or functional outcome. Further investigation of patients undergoing endovascular coiling of ruptured aneurysms is needed to fully understand the potential usefulness of clazosentan in patients with aSAH. Actelion Pharmaceuticals. Copyright © 2011 Elsevier Ltd. All rights reserved.
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              Cognitive and functional outcome after aneurysmal subarachnoid hemorrhage.

              Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency characterized by the accumulation of blood in the subarachnoid space surrounding the brain. The acute treatment of aSAH is well documented but less is known about the long-term effects of aSAH on cognition and day-to-day functioning. We reviewed all studies in the past 10 years that have focused on the effects of aSAH on cognition and day-to-day functioning. Sixty-one empirical studies examining cognitive and functional outcome in patients with aSAH met inclusion criteria. Survivors of aSAH commonly experience deficits in memory, executive function, and language. These cognitive impairments interact to affect patients' day-to-day functioning, including activities of daily living, instrumental activities of daily living, return to work, and quality of life. Deficits in cognition and day-to-day functioning are further compounded by depression, anxiety, fatigue, and sleep disturbances. Much remains to be learned about the brain changes underlying cognitive and functional deficits, including the role of diffuse brain damage and secondary complications like vasospasm and elevated intracranial pressure. A consideration of these issues is necessary to obtain a better understanding of how aSAH affects cognition and day-to-day functioning in the long-term.

                Author and article information

                J Neurol Neurosurg Psychiatry
                J. Neurol. Neurosurg. Psychiatr
                Journal of Neurology, Neurosurgery, and Psychiatry
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                September 2013
                20 April 2013
                : 84
                : 9
                : 1054-1058
                [1 ]Division of Neurosurgery, Department of Surgery, Prince of Wales Hospital, The Chinese University of Hong Kong , Shatin, New Territories, Hong Kong
                [2 ]Division of Neurology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong , Shatin, New Territories, Hong Kong
                [3 ]Department of Imaging and Interventional Radiology, Prince of Wales Hospital, The Chinese University of Hong Kong , Shatin, New Territories, Hong Kong
                [4 ]Department of Psychological Studies, The Hong Kong Institute of Education , Tai Po, New Territories, Hong Kong
                Author notes
                [Correspondence to ] Dr George Kwok Chu Wong, Division of Neurosurgery, Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, 4/F Clinical Science Building, 30-32 Ngan Shing Street, Shatin, New Territories, Hong Kong; georgewong@ 123456surgery.cuhk.edu.hk
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

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