title: Mechanisms, predictors and clinical impact of early neurological deterioration: the protocol of the Trondheim early neurological deterioration study.
abstract: BACKGROUND
  10-40% of patients with acute ischemic stroke (AIS) suffer an early neurological deterioration (END), which may influence their long term prognosis. Multiple definitions of END exist, even in recently published papers. In the search for causes, various biochemical, clinical, and imaging markers have been found to be associated to END after AIS in some but not in other studies. The primary aim of this study is to assess the contribution of END to functional level at 3 months post stroke measured by modified Rankin Scale (mRS). Secondary aims are to identify factors and mechanisms associated with END and to define the prevalence, degree and timing of END in relation to stroke onset, and to compare Scandinavian Stroke Scale (SSS) and National Institute of Health Stroke Scale (NIHSS) based END-definitions. We hypothesized that END detected by changes in NIHSS and SSS (according to previously published criteria) at a threshold of 2 points indicate worsened prognosis, and that SSS is not inferior to NIHSS in predicting such a change. We further hypothesized that clinical deterioration has several causes, including impaired physiological homeostasis, vascular pathology, local effects and reactions secondary to the ischemic lesion, along with biochemical disturbances.
  
  
  METHODS
  Single-centre prospective observational study.
  
  
  METHODS
  Previously at home-dwelling patients admitted to our stroke unit within 24 hours after ictus of AIS are included into the study, and followed for 3 months. They are managed according to current procedures and national guidelines. A total of 368 patients are included by the end of the enrolment period (December 31(st) 2013), and the material will be opened for analysis by June 30(th) 2014. Frequent neurological assessments, continuous monitoring, and repeated imaging and blood samples are performed in all patients in order to test the hypotheses.
  
  
  CONCLUSIONS
  Strengths and weaknesses of our approach, along with reasons for the methods chosen in this study are discussed.
authors.affiliation: Research group for Geriatrics, Stroke and Movement (GeMS), Department of Neuroscience (INM), Norwegian University of Science and Technology, N-7489, Trondheim, Norway. Bernt.Harald.Helleberg@stolav.no.|Stroke Unit, Department of Internal Medicine, St. Olavs Hospital, University Hospital in Trondheim, N-7006, Trondheim, Norway. Bernt.Harald.Helleberg@stolav.no.
authors.forename: Bernt Harald
authors.initials: BH
authors.lastname: Helleberg
authors.affiliation: Stroke Unit, Department of Internal Medicine, St. Olavs Hospital, University Hospital in Trondheim, N-7006, Trondheim, Norway. Hanne.Ellekjer@stolav.no.
authors.forename: Hanne
authors.initials: H
authors.lastname: Ellekjær
authors.affiliation: Research group for Geriatrics, Stroke and Movement (GeMS), Department of Neuroscience (INM), Norwegian University of Science and Technology, N-7489, Trondheim, Norway. Gitta.Rohweder@stolav.no.|Stroke Unit, Department of Internal Medicine, St. Olavs Hospital, University Hospital in Trondheim, N-7006, Trondheim, Norway. Gitta.Rohweder@stolav.no.
authors.forename: Gitta
authors.initials: G
authors.lastname: Rohweder
authors.affiliation: Research group for Geriatrics, Stroke and Movement (GeMS), Department of Neuroscience (INM), Norwegian University of Science and Technology, N-7489, Trondheim, Norway. bent.indredavik@ntnu.no.|Stroke Unit, Department of Internal Medicine, St. Olavs Hospital, University Hospital in Trondheim, N-7006, Trondheim, Norway. bent.indredavik@ntnu.no.
authors.forename: Bent
authors.initials: B
authors.lastname: Indredavik
mesh_terms: D006801:Humans; D009422:Nervous System Diseases / Q000503:physiopathology*; D011379:Prognosis; D011446:Prospective Studies; D020521:Stroke / Q000453:epidemiology / Q000503:physiopathology*; D013997:Time Factors