title: Prospective study of apolipoprotein E genotype and functional outcome following ischemic stroke.
abstract: BACKGROUND
  The apolipoprotein E (APOE) epsilon 4 allele is a marker of adverse outcome following head injury and intracerebral hemorrhage. Transgenic animal data in a focal cerebral ischemia model suggest that the epsilon 4 allele increases infarct size and functional impairment.
  
  
  OBJECTIVE
  To determine if APOE genotype is associated with functional recovery from ischemic stroke.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Stroke service at a university teaching hospital.
  
  
  METHODS
  Patients with clinical and neuroimaging findings (computed tomography or magnetic resonance imaging) compatible with an acute ischemic stroke.
  
  
  RESULTS
  Functional outcome by Barthel index (BI) and modified Rankin scale (mRS) was compared for epsilon 3/epsilon 3 patients vs epsilon 4 carriers and vs epsilon 2 carriers at 1 and 3 months. Univariate predictors of 3-month outcome were examined in a multivariate analysis.
  
  
  RESULTS
  One hundred eighty nine patients were enrolled: 100 women, 89 men (mean +/- SD age, 69.4 +/- 11.0 years). There were 25 epsilon 2 alleles (frequency, 0.07), 292 epsilon 3 alleles (0.77), and 61 epsilon 4 alleles (0.16). Baseline National Institutes of Health Stroke Scale scores and Oxfordshire Community Stroke Project classifications were similar in all groups (epsilon 3/epsilon 3, epsilon 4, and epsilon 2 carriers). One-month (BI, P = .64; mRS, P = .59) and 3-month (BI, P = .87; mRS, P = .73) outcomes were not associated with possession of either epsilon 4 or the epsilon 2 allele. Baseline National Institutes of Health Stroke Scale scores (P < .001) and age (P = .002) were significant predictors of 3-month BI and mRS outcomes in multivariate analyses.
  
  
  CONCLUSIONS
  Although there is a robust influence of APOE polymorphism on functional recovery after some types of brain injury in humans, it does not exert a major influence on injury severity or functional recovery following ischemic stroke. Arch Neurol. 2000;57:1480-1484
authors.affiliation: Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, Scotland.
authors.forename: M O
authors.initials: MO
authors.lastname: McCarron
authors.forename: K W
authors.initials: KW
authors.lastname: Muir
authors.forename: J A
authors.initials: JA
authors.lastname: Nicoll
authors.forename: J
authors.initials: J
authors.lastname: Stewart
authors.forename: Y
authors.initials: Y
authors.lastname: Currie
authors.forename: K
authors.initials: K
authors.lastname: Brown
authors.forename: I
authors.initials: I
authors.lastname: Bone
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism*; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005838:Genotype; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D020127:Recovery of Function; D012720:Severity of Illness Index; D020521:Stroke / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology; D014057:Tomography, X-Ray Computed
chemical_list: D001057:Apolipoproteins E