Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Docent Birgitta Johansson, University of Gotheburg, Sweden
- Second opponent: Neuropsychologist Anne Marie Buunk, University Medical Center Groningen (UMCG), The Netherlands
- Third member and chair of the evaluation committee: Professor II Ole Morten Rønning, University of Oslo
Chair of the Defence
Professor II Erik Taubøll, University of Oslo
Principal Supervisor
Associate Professor Tonje Haug Nordenmark, University of Oslo
Summary
Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening disease. With early aneurysm repair and modern intensive care, most patients recover without significant neurological deficits, but many endure persistent cognitive and emotional problems. Among these symptoms, fatigue is one of the most prominent and frequent sequelae. Hitherto, there is no standardized assessment of fatigue, and its underlying mechanisms are largely unknown. Further, no effective treatment of fatigue is known.
The overall aim of the thesis was to expand the knowledge about the phenomenology and underlying mechanisms behind post-aSAH fatigue, and to achieve a better understanding of how to assess and treat it. The thesis is based on a randomized, placebo-controlled, double-blind trial evaluating the effect of (−)-OSU6162 in the treatment of post-aSAH fatigue.
Post-aSAH fatigue was shown to be a frequent (70%) and relatively stable symptom over years. Its nature was mostly a mental type of fatigue (low motivation, mental exhaustion and a heightened sensitivity to stress) and to a lesser extent a physical type. Further, post-aSAH fatigue was related to poor health-related quality of life and partially to an inability to return to work. It was not related to neurological dysfunction or cognitive functioning. Post-aSAH fatigue was strongly related to emotional problems, especially depressive symptoms, but the overlap was incomplete and implied that the two constructs should be treated separately.
The odds of developing fatigue after aSAH were all more than doubled if the patient had a history of nicotine use, reduced consciousness (Glasgow Coma Scale score <14) at admission or severe vasospasm during the acute phase.
Fatigue was similarly alleviated by 12 weeks of treatment with (−)-OSU6162 and placebo. Recovery over time and placebo response may be exploited in developing non-pharmacological rehabilitation programs for post-aSAH fatigue.
Additional information
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